Usmle2 Medicine

Front 1

What are the three cancers for which regular screening is recommended?

Back 1

Cancers of the colon, breast, and cervix.

Front 2

When should screening for colon cancer begin in the patient with no family history of colon cancer?

Back 2

Screening for colon cancer should begin at 50 with colonoscopy every 10 years. Annual fecal occult blood testing, sigmoidoscopy every 5 years, and barium enema are also options.

Front 3

What are the screening mammography recommendations for breast cancer?

Back 3

Every 1-2 years from age 40 and over. Breast examination by physician for ages 20-30, every 3 yrs. Patients with multiple first-degree relatives with breast cancer should receive prophylactic tamoxifen.

Front 4

What is the prophylaxis for hepatitis A for travelers?

Back 4

If a patient is leaving within 2 wks to a nonindustrialized country, vaccine and immune serum globulin are given. A booster shot given 6 months after the initial vaccination confers immunity for 10 years.

Front 5

What is the most common cause of hepatitis A?

Back 5

Hepatitis A is the most common vaccine-preventable disease in travelers; from fecal contamination of food or water.

Front 6

Which travelers should receive hepatitis B vaccine?

Back 6

Patients who will work with indigenous, engage in sex, receive medical/ dental care, on remain abroad >6 mth in a country where prevalence is intermediate or high.

Front 7

What is the recommended prophylaxis for malaria for travelers?

Back 7

Traveling to Mexico, Central America (except Panama), or Caribbean, chloroquine is prophylaxis for malaria. For travelers to areas where chloroquine resistance common, mefloquine recommended.

Front 8

What is the recommended prophylaxis for malaria for travelers?

Back 8

Rabies vaccination is recommended for patients traveling to areas where rabies is common (India, Asia, Mexico).

Front 9

What is the vaccination recommendation for yellow fever for travelers?

Back 9

Yellow fever vaccine is required for travel to sub-Saharan Africa and South American countries.

Front 10

What are the vaccination recommendations for meningococcal meningitis?

Back 10

Persons traveling to Nepal, sub-Saharan Africa, northern India should be immunized with the polysaccharide vaccine. Saudi Arabia requires immunization for pilgrims to Mecca.

Front 11

At what age is meningococcal vaccine usually given?

Back 11

Meningococcal is routinely given at age 11.

Front 12

What are the recommendations for prevention of traveler's diarrhea?

Back 12

Patients who experience loose stools without fever or blood may take loperamide. Treatment with a fluoroquinolone or azithromycin is reserved for patients with bloody diarrhea.

Front 13

What are the recommendations for tetanus and diphtheria vaccination in adults who were never vaccinated?

Back 13

Adults who were never vaccinated should receive three doses, the first two are given 1 to 2 months apart, with the third dose given 6 to 12 months later. A booster vaccination should be given every 10 years for life.

Front 14

What are the recommendations for influenza vaccination?

Back 14

Annually for adults >50. Cardiopulmonary disease, diabetes, hemoglobinopathy, or who are in chronic care facilities should receive annual. Pregnant women who will be in 2nd or 3rd trimester during influenza season.

Front 15

What are the indications for pneumococcal vaccination?

Back 15

Adults >65; sickle-cell, splenectomy, cardiopulmonary disease, alcoholism, cirrhosis, Alaskan natives, Native Americans; immunocomp (heme malignancies, CRF, nephrotic, HIV; immunosuppressives).

Front 16

What are the indications for hepatitis B vaccination?

Back 16

IV drug abuse, male homosexuality, household or sexual contact with hepatitis B carriers, frequent exposure to blood, chronic liver disease. Immunity can be confirmed serologically.

Front 17

What are the recommendations for hepatitis A vaccine?

Back 17

Hepatitis A vaccine is recommended for travelers to endemic areas, day-care employees, homosexual men, and chronic liver disease.

Front 18

What are the indications for varicella vaccine?

Back 18

Varicella vaccine is recommended for all adults who lack a history of childhood infection; should not be given to immunocompromised or pregnant because it is live attenuated.

Front 19

What are the recommendations for measles, mumps, rubella vaccine?

Back 19

Measles, mumps, rubella vaccine is a live attenuated vaccine given in childhood. Healthy adults should receive 1 dose if never vaccinated. Pregnant and immunocompromised not vaccinated.

Front 20

What are the recommendations for osteoporosis screening?

Back 20

All women older than age 65 should be given DEXA scans every 1-2 years. Begin at age 60, if there is low body weight or increased risk of fractures.

Front 21

What are the recommendations for screening for abdominal aortic aneurysm?

Back 21

Ultrasound should be given once in male smokers older than age 65.

Front 22

What are the recommendations for cholesterol screening?

Back 22

Cholesterol screening should begin at age 35 in men and 45 in women who have no risk factors. For patients with risk factors for coronary artery disease, screening should be done routinely after age 20.

Front 23

What are the recommendations for screening for diabetes?

Back 23

Obesity, impaired fasting glucose, African-Americans, native Americans and/or positive family history.

Front 24

What is the criteria for the diagnosis of diabetes?

Back 24

Diabetes mellitus is diagnosed when two fasting are greater than 126 mg/dL, or when a random glucose is >200 mg/dL.

Front 25

What clinical test should be used to screen for alcohol abuse?

Back 25

CAGE: Have you ever felt the need for Cut down? Have you ever felt Annoyed by criticism of your drinking? Have you ever Guilty about your drinking? Have you ever taken Eye opener? Positive is 2 "yes.?

Front 26

What pathological conditions are associated with hyperprolactinemia?

Back 26

Excess of prolactin occurs with prolactinomas (most common functioning pituitary adenomas, 60% of pituitary tumors.

Front 27

What medications cause hyperprolactinemia?

Back 27

Decreased inhibitory action of dopamine caused by drugs that block dopamine synthesis (phenothiazines, metoclopramide) and dopamine-depleting agents (alpha-methyldopa).

Front 28

What is the presentation of hyperprolactinemia?

Back 28

Women have galactorrhea, amenorrhea/oligomenorrhea, osteoporosis, infertility, gynecomastia; men have hypogonadism, erectile dysfunction, decreased libido, gynecomastia and infertility.

Front 29

How is hyperprolactinemia diagnosed?

Back 29

Always exclude pregnancy, lactation, hypothyroidism and medications before starting the evaluation of hyperprolactinemia. Prolactin levels >100 ng/mL suggest probable pituitary adenoma.

Front 30

What is the management of hyperprolactinemia?

Back 30

For prolactinomas: cabergoline or bromocriptine (dopamine agonist) reduce prolactin levels. Surgery for adenomas not responsive to cabergoline or bromocriptine, or if the tumor causes neurologic effects.

Front 31

What is acromegaly?

Back 31

Excessive secretion of growth hormone in an adult. In children, gigantism occurs. In adults acromegaly occurs, which is bony and soft tissue overgrowth. Pituitary adenoma that overproduces growth hormone. Only 1% are malignant.

Front 32

How is acromegaly diagnosed?

Back 32

The best initial test is insulin-like growth factor-1 levels. Confirmatory testing involves the measurement of GH after 100 g of glucose is given orally.

Front 33

What is the management of acromegaly?

Back 33

Transsphenoidal surgery. Hypopituitarism occurs after surgery in 10-20%. Octreotide is a somatostatin analog that reduces GH in two thirds of patients and causes partial tumor regression in 20-50% of patients.

Front 34

What are the causes of hypopituitarism?

Back 34

Tumors, cysts, sarcoidosis, Tb, syphilis, eosinophilic granuloma, Hashimoto, gastric atrophy. Trauma, radiation, surgery, infections, hypoxia. Sheehan postpartum necrosis, hemochromatosis, amyloidosis.

Front 35

What are the signs of hypopituitarism?

Back 35

Amenorrhea, genital atrophy, loss pubic hair. Growth fail. Thyrotropin deficiency: hypothyroidism. Adrenocorticotropin def: fatigue, anorexia, wt loss, decreased skin pigment, hypotension, hypoNa.

Front 36

How is hypopituitarism diagnosed?

Back 36

Measure GH, TSH, LH, and insulin-like-GF1.

Front 37

How is ACTH deficiency diagnosed?

Back 37

Insulin tolerance test: give insulin and measure serum cortisol. Metyrapone tests for decreased ACTH production. Metyrapone blocks cortisol production, which should increase ACTH levels.

Front 38

How is gonadotropin deficiency diagnosed?

Back 38

To diagnose gonadotropin deficiency in women, measure LH, FSH, and estrogen. In males, gonadotropin deficiency is detected by measuring LH, FSH, and testosterone.

Front 39

How is thyroid stimulating hormone deficiency diagnosed?

Back 39

To diagnose TSH deficiency, measure serum thyroxine (T4), and free triiodothyronine (T3), which are low, with a normal to low TSH.

Front 40

What is central diabetes insipidus?

Back 40

CDI is neurohypophyseal deficiency of vasopressin (ADH), which results in excessive, dilute urine and increased thirst with hypernatremia. Nephrogenic DL is caused by renal resistance to vasopressin.

Front 41

What are the causes of central diabetes insipidus?

Back 41

Adenomas, craniopharyngiomas; leukemias, sarcoid histocytosis. Pituitary/hypothalamic surgery, radiotherapy, severe head injuries, anoxia, hypertension, and meningitis. Idiopathic; encephalitis, TB, and syphilis.

Front 42

What are the causes of nephrogenic diabetes insipidus?

Back 42

Nephrogenic DL: idiopathic or caused by hyperCa, hypoK, sickle cell, amyloidosis, myeloma, pyelonephritis, sarcoidosis, Sjögren syndrome, lithium, demeclocycline, colchicine.

Front 43

What are the clinical signs of diabetes insipidus?

Back 43

Polyuria, excessive thirst, polydipsia (16-20 L/d), hypernatremia with high serum osmolarity, decreased urine specific gravity, dehydration, weakness, fever, altered mental status, and death.

Front 44

How is diabetes insipidus diagnosed?

Back 44

Water deprivation test: Uosm after dehydration versus Uosm after vasopressin. Normal response to fluid restriction is increased urine osm, decrease urine vol. DL urine vol remains high despite vol depletion.

Front 45

How is nephrogenic diabetes insipidus differentiated from central diabetes insipidus?

Back 45

ADH levels will be low in central DL and high in nephrogenic DL.

Front 46

What is the differential diagnosis of diabetes insipidus?

Back 46

Psychogenic polydipsia, drug-induced polydipsia from chlorpromazine, anticholinergic drugs, or thioridazine, and hypothalamic diseases.

Front 47

What is the management of central diabetes insipidus?

Back 47

Hormone replacement with vasopressin. For nephrogenic DL, HCTZ or amiloride increase the reabsorption of fluid from the proximal tubule.

Front 48

What are the causes of syndrome of inappropriate secretion of ADH?

Back 48

Small cell CA, pancreas CA, ectopic ADH; TB, pneumonia, lung abscess; head injury, stroke, encephalitis; chlorpropamide, clofibrate, vincristine, vinblastine, cyclophosphamide, carbamazepine.

Front 49

What are the clinical signs of syndrome of inappropriate ADH?

Back 49

Water retention and ECF expansion without edema or hypertension. Hyponatremia. Hyponatremia and concentrated urine (Uosm >300 mOsm), no edema or dehydration.

Front 50

What are the CNS signs of SIADH?

Back 50

Cerebral edema from hyponatremia causes irritability, confusion, seizures, coma.

Front 51

What are the laboratory findings in syndrome of inappropriate secretion of ADH?

Back 51

Hyponatremia <130 mEq/L, and Posm <270 mOsm/kg. Urine Na >20 mEq/L (inappropriate natriuresis). Low BUN, low creatinine, low urate, low albumin.

Front 52

What is the management of SIADH?

Back 52

Treat cause. Fluid restrict 800 mL/d. Demeclocycline. If severe confusion, convulsions, or coma: hypertonic saline (3%) 200-300 mL IV over 3-4 h. The rate of correction 0.5-1 mmol/L/h of serum Na.

Front 53

What is the most sensitive test for thyroid diseases?

Back 53

The most sensitive test in thyroid diseases is the TSH. If the TSH is normal, then the patient is euthyroid.

Front 54

What are the effects of thyroid binding globulin levels on the thyroxine levels?

Back 54

Increased TBG in pregnancy, OCP will increase total T4 but free T4 level is normal. Decreased TBG levels in nephrotic syndrome and androgens. Decreased TBG will decrease total T4, but free or active T4 normal.

Front 55

What are the signs of thyrotoxicosis?

Back 55

Graves disease, diffuse goiter, exophthalmos, dermopathy. More in women in the fourth decade.

Front 56

What is the cause of Grave disease?

Back 56

Autoantibodies bind to TSH receptor and stimulate thyroid. Intrinsic thyroid autonomy can result from a hyperfunctioning adenoma (toxic) or toxic multinodular goiter of the elderly.

Front 57

What are the causes of transient hyperthyroidism?

Back 57

Subacute thyroiditis (painful) and lymphocytic thyroiditis (painless, postpartum). Thyrotoxicosis factitia and ectopic thyroid tissue (struma ovarii, functioning follicular carcinoma).

Front 58

What are the cardiovascular signs of Graves disease?

Back 58

Anxiety, insomnia; atrial fibrillation, tremors, frequent bowel movements, excessive sweating, heat intolerance. Weight loss, increased appetite, weakness. Dyspnea, palpitations, angina, or cardiac failure.

Front 59

What are the dermatologic signs of Grave disease?

Back 59

Skin is warm and moist, palmar erythema; fine, silky hair. Staring, infrequent blinking, oligomenorrhea; osteoporosis and hypercalcemia.

Front 60

What are the laboratory findings in Graves disease?

Back 60

Low TSH; increased serum free T4 and T. RIAU is increased. Antithyroglobulin and antimicrosomal antibodies are elevated in Graves disease and autoimmune thyroiditis.

Front 61

What is the treatment of hyperthyroidism?

Back 61

Popranolol, propylthiouracil (safe in preg) or methimazole. Both can cause agranulocytosis. Ablation with radioactive iodine. Subtotal thyroidectomy only in pregnancy and children.

Front 62

What is a thyroid storm?

Back 62

Thyrotoxicosis precipitated by stress, infection, surgery, or trauma. Extreme irritability, delirium, coma, tachycardia, restlessness, vomiting, jaundice, diarrhea, hypotension, dehydration, and fever.

Front 63

What is the treatment for thyroid storm?

Back 63

Glucose, hydration, glucocorticoids, oxygen, cooling blanket. Propylthiouracil, beta-blockers, and iodine inhibit hormone release.

Front 64

What is the affect of antithyroid drugs on uptake of radioactive iodine?

Back 64

Antithyroid drugs should be stopped several days before radioactive iodine treatment because the antithyroid medications block the uptake of the radioactive iodine.

Front 65

What are the causes of primary hypothyroidism?

Back 65

Hypothyroidism is from thyroid in 95%. Can be caused by chronic thyroiditis (Hashimoto), postablative or radioactive iodine, heritable defects, iodine deficiency; lithium, aspirin, amiodarone, interferon, sulfonamides.

Front 66

What is the most common cause of goitrous hypothyroidism?

Back 66

Hashimoto disease is most common cause of goitrous hypothyroidism.

Front 67

What are the clinical signs in congenital hypothyroidism?

Back 67

Cretinism, jaundice, hoarse, constipation, somnolence, feeding problems; delayed milestones, dwarf, protruding tongue, broad flat nose, wide eyes, sparse hair, dry skin, potbelly, umbilical hernia, impaired mental.

Front 68

What are the signs and symptoms of hypothyroidism in the adult?

Back 68

Lethargy, constipation, cold intolerance, cramping, carpal tunnel, menorrhagia. Slow intellectual/motor; appetite decrease, weight increase; dry hair/skin. Deep voice, prolonged DTR. Myxedema: expressionless, sparse hair, periorbital puffiness, Lg tongue.

Front 69

What is the treatment of hypothyroidism?

Back 69

Levothyroxine (T4) should be administered with monitoring of TSH/T3 levels (6 weeks to steady state after dosing changes).

Front 70

What is myxedema coma?

Back 70

Severe hypothyroidism with hypothermic, stuporous state; frequently fatal; respiratory depression. Precipitated by cold exposure, trauma, infections, and CNS depressants. Treatment is very high doses of T4 and T3.

Front 71

What are the causes of subacute thyroiditis?

Back 71

Granulomatous, giant cell, and de Quervain thyroiditis. In the fourth and fifth decades. Viral origin and follows upper respiratory infection; malaise, fever, pain over the thyroid. Thyroid enlarged and firm.

Front 72

What are the laboratory findings in subacute thyroiditis?

Back 72

Elevated erythrocyte sedimentation rate (ESR), decreased radioactive iodine uptake, initial elevation in T4 and T3, followed by hypothyroidism.

Front 73

What is the treatment of subacute thyroiditis?

Back 73

Aspirin, prednisone, and Popranolol.

Front 74

What is Hashimoto thyroiditis?

Back 74

Chronic autoimmune inflammatory process with lymphocytic infiltration. Common disorder most frequently in middle-aged women; most common cause of sporadic goiter in children.

Front 75

What are the clinical signs of Hashimoto thyroiditis?

Back 75

Goiter that is painless, rubbery and hypothyroidism.

Front 76

How is Hashimoto thyroiditis diagnosed?

Back 76

TSH increases, and T4 and T decrease. Antimicrosomal and antithyroperoxidase antibodies.

Front 77

What is the management of Hashimoto thyroiditis?

Back 77

Replacement with L-thyroxine (T4).

Front 78

What is chronic lymphocytic thyroiditis?

Back 78

Self-limiting thyrotoxicosis; more common women. Thyroid is painless, nontender, firm, symmetrical, and enlarged. T4 and T3 are elevated, RAIU is low, ESR normal. Lasts for 2-5 months. Treatment with Popranolol.

Front 79

What is Reidel thyroiditis?

Back 79

Fibrosis of the thyroid and mediastinal and retroperitoneal fibrosis.

Front 80

What is papillary carcinoma?

Back 80

Most common thyroid CA; radiation exposure. 70% of all thyroid CA. Women 3 times more than men. Second decade and later. Treatment is surgery or suppression with levothyroxine.

Front 81

What is follicular carcinoma of the thyroid?

Back 81

Follicular carcinoma accounts for 15% of thyroid cancers. Elderly women. More malignant than papillary carcinoma. Spreads hematogenously.

Front 82

What is the treatment of follicular thyroid cancer?

Back 82

Treatment is near-total thyroidectomy with postoperative radioiodine ablation.

Front 83

What is anaplastic thyroid carcinoma?

Back 83

10% of all thyroid cancer. Elderly women. Highly malignant, painful enlargement. Eighty percent of patients die.

Front 84

What is medullary thyroid carcinoma?

Back 84

5% of all thyroid cancers. More malignant than follicular carcinoma. Often produces calcitonin. Medullary carcinoma is a component of two types of multiple endocrine neoplasias.

Front 85

What is the treatment of medullary thyroid cancer?

Back 85

Treatment is thyroidectomy. Calcitonin levels can also be increased from cancer of the lung, pancreas, breast, and colon.

Front 86

What are the clinical signs of thyroid carcinoma?

Back 86

Growth of thyroid or mass with no tenderness or hoarseness. History of radiation. Men and elderly have a higher incidence of thyroid malignancy. Solitary; may produce calcitonin.

Front 87

What is the significance of psammoma bodies in the thyroid?

Back 87

Calcifications such as psammoma bodies suggest papillary carcinoma; increased density is associated with medullary carcinoma.

Front 88

What is the significance of finding hyperthyroidism in association with a thyroid nodule?

Back 88

Hyperthyroidism is never associated with cancer.

Front 89

What is the diagnostic approach to solitary nonfunctioning nodule?

Back 89

Fine-needle aspiration for cytology is the initial procedure. The first test for a thyroid nodule is the TSH; if TSH is normal, then proceed to an FNA. If TSH is low, the nodule is benign. Ultrasound to distinguish cysts.

Front 90

What is the function of parathyroid hormone?

Back 90

Maintains calcium concentration. PTH acts on bone and kidney, indirectly on intestine (effects synthesis 1,25-dihydroxy-cholecalciferol) to increase serum calcium. Regulated by serum-ionized calcium.

Front 91

What is the effect of parathyroid hormone on the bones?

Back 91

PTH increases osteoclast, which releases Ca. PTH inhibits PO4 reabsorption kidney which decreases PO4 and favors Ca release from bones. PTH activates vitamin D, increases GI Ca absorption. Calcitonin decreases Ca.

Front 92

What is the most common cause of hypercalcemia?

Back 92

Primary hyperparathyroidism. Hypercalcemia of malignancy caused by PTH-like protein. Sarcoidosis, Tb, berylliosis, histoplasmosis, coccidioidomycosis increase vitamin D.

Front 93

What are the rare causes of hypercalcemia?

Back 93

Rare causes: vitamin D, thiazides, lithium, Paget, immobilization, hyperthyroidism.

Front 94

What are the signs of hypercalcemia?

Back 94

Lethargy, confusion, constipation, anorexia, nausea, vomiting. Pancreatitis because of precipitation of Ca pancreas. Polyuria, polydipsia. Ca precipitates kidney, resulting in nephrolithiasis. HTN in 50%.

Front 95

What are the ECG signs of hypercalcemia?

Back 95

ECG shows short QT.

Front 96

What is the treatment for hypercalcemia?

Back 96

Saline or half-normal and furosemide, which promote calcium loss. Bisphosphonates such as alendronate, zoledronate, risedronate, pamidronate inhibit osteoclasts and stimulate osteoblasts. Calcitonin.

Front 97

What are the causes of primary hyperparathyroidism?

Back 97

Gland adenoma (80%). Parathyroid CA rare (<1%). Hyperparathyroidism can be part of MEN type I: hyperparathyroidism, pituitary tumors, pancreatic tumors. MEN II: hyperparathy, pheo, medullary thyroid CA.

Front 98

What the effects of hyperparathyroidism on bone?

Back 98

Osteitis fibrosa cystica occurs because of osteoclastic bone resorption; bone pain, fractures, swelling, deformity, bone cysts, and brown tumors (punched-out lesions). One half asymptomatic.

Front 99

How is primary hyperparathyroidism diagnosed?

Back 99

Serum calcium >10.5 mg/dL, with elevated PTH level. In every other cause of hypercalcemia the PTH level will be low. Serum phosphate is low (<2.5 mg/dL).

Front 100

What is the management of primary hyperparathyroidism?

Back 100

Removal of parathyroids. Bisphosphonates if surgery is contraindicated or if serum Ca <11.5 mg/dL. Calcium reduced to 400 mg/d. 2-3 L of fluid/d. Phosphor-soda. Cinacalcet simulates effect of Ca parathyroid.

Front 101

What are the causes of hypocalcemia?

Back 101

Most common: hypoparathyroidism, renal failure, hyperphosphatemia, hypoMg. Loop diuretics, phenytoin, alendronate, foscarnet. Lack of renal activated 1,25-vitamin D, leads to decreased Ca absorption.

Front 102

What are the signs of hypocalcemia?

Back 102

Hypocalcemia results in neural hyperexcitability, seizures, tetany, circumoral numbness, and tingling. Cataracts.

Front 103

What are the ECG signs of hypocalcemia?

Back 103

Arrhythmias may develop because of a prolonged QT.

Front 104

What is the most common cause of hypoparathyroidism?

Back 104

Thyroidectomy. Low PTH levels are also seen in hereditary hypoparathyroidism and hypoMg. Mg deficiency prevents release of PTH. High PTH levels in renal failure because decreased active vitamin D.

Front 105

What are the neurologic signs of hypoparathyroidism?

Back 105

Neuromuscular irritability, tetany, laryngospasm, cramps, seizures, impaired memory. Chvostek sign: percussion of facial nerve contraction face. Trousseau: inflation of cuff elicits flexion metacarpophalangeal.

Front 106

What are the cardiovascular signs of hypocalcemia?

Back 106

QT prolongation, CHF, and/or hypotension. Circumoral tingling and tingling of the hands and feet.

Front 107

How is hypoparathyroidism diagnosed?

Back 107

Low calcium may be due to a low albumin. Ionized calcium is best test. PTH low. Low Ca with high PO4 can be due to renal failure, tissue destruction, hypoparathyroidism, pseudohypoparathyroidism.

Front 108

What are the causes of a low calcium with low phosphorous?

Back 108

Low calcium with low phosphorous is caused by low vitamin D.

Front 109

What is the management of hypoparathyroidism?

Back 109

Calcium gluconate IV. Maintenance oral calcium 2-4 g/d, vitamin D, and if there is hyperphosphatemia, diet restriction and phosphate binders (CaCO3).

Front 110

What is the usual age of onset of type 1 diabetes?

Back 110

The age of onset is usually <30 years. <10% of first-degree relatives are affected with a 50% occurrence in identical twins. Autoantibodies to islet cells. Lean body build.

Front 111

What is the usual age of onset of type 2 diabetes?

Back 111

Usually >40; males > females. >20% of first-degree relatives are affected with 90-100% occurrence in identical twins. Obese.

Front 112

What is the cause of type 2 diabetes?

Back 112

90% of diabetes is type 2, caused by abnormal insulin secretion and resistance to insulin.

Front 113

What are the clinical signs of diabetes?

Back 113

Hyperglycemia causes polyuria, polydipsia, polyphagia, coma (ketoacidosis for type I diabetes and hyperosmolar coma for type 2 diabetes).

Front 114

How is diabetes diagnosed?

Back 114

Polyuria, polydipsia, ketonuria, weight loss, plasma glucose >200 mg/dL in these patients is sufficient for diagnosis. In asymptomatic patients, fasting plasma glucose 126 mg/dL on two occasions is diagnostic of diabetes.

Front 115

What is glycosylated hemoglobin A1c?

Back 115

HgA1c is condensation of glucose with free amino groups on Hb. It is used to follow glucose control. HgA1C is high in diabetics with chronic hyperglycemia during the preceding 8-12 weeks.

Front 116

What is the glycosylated hemoglobin A1c goal?

Back 116

The goal of therapy is to have an HgA1c <7%.

Front 117

What is the management of type 2 diabetes?

Back 117

Metformin in obese. Contraindicated: renal insufficiency. Does not cause hypoglycemia. If diabetes is not controlled with metformin, add a sulfonylurea; then either switch to insulin or add glitazone.

Front 118

What is the dosage for insulin in type 2 diabetes?

Back 118

0.5 U/kg, with two-thirds given AM (2/3 NPH, 1/3 reg) and one-third in PM (½ NPH, ½ reg). Glucose measurements before each meal and at bedtime.

Front 119

What is the dosage for glargine insulin?

Back 119

Once-a-day injection along with 2-3 times/day ultra short-acting insulin (such as lispro or aspart before meals). Glargine causes less hypoglycemia compared with NPH.

Front 120

What is the acute complication of uncontrolled type 1 diabetes mellitus?

Back 120

Diabetic ketoacidosis results from severe insulin insufficiency in type 1 diabetics. Precipitating factors of DKA include interrupted insulin therapy, infection, emotional stress, and excessive alcohol.

Front 121

What are the clinical signs of diabetic ketoacidosis?

Back 121

Anorexia, nausea, vomiting, abdominal pain, rapid breathing (Kussmaul), "fruity" breath odor (acetone), dry skin/mucous membranes, poor skin turgor, altered consciousness to coma. Arrhythmias, hyperkalemia fatal.

Front 122

What is the treatment of diabetic ketoacidosis?

Back 122

K is low because of the urinary loss of K. As soon as K <4 mEq/L, KCl given. Normal saline should be given in high volume. Bolus with 5-10 units of regular insulin then infuse.

Front 123

What acid-base disorder is associated with uncontrolled diabetes?

Back 123

Elevated blood glucose, increased acetoacetate, acetone, hydroxybutyrate result in metabolic acidosis (low serum bicarbonate and low blood pH), and increased anion gap [sodium - (bicarbonate + chloride)].

Front 124

What is hyperosmolar nonketotic coma?

Back 124

HONK occurs in type 2 diabetes; severe hyperglycemia without ketosis. Precipitated by noncompliance plus inability to drink. Elderly, infections, strokes, steroids, immunosuppressants, diuretics.

Front 125

What is the presentation of hyperosmolar nonketotic coma?

Back 125

Profound dehydration results from hyperglycemic diuresis. Weakness, polyuria, polydipsia, lethargy, confusion, convulsions, and coma.

Front 126

What are the laboratory findings in hyperosmolar nonketotic coma?

Back 126

Elevated blood glucose (>1,000 mg/dL) and extremely high serum osmolality.

Front 127

What is the treatment of hyperosmolar non-ketotic coma?

Back 127

High-volume fluid and electrolyte replacement and insulin.

Front 128

What are the chronic ocular complications of diabetes?

Back 128

Retinopathy is the leading cause of blindness; background or proliferative (microaneurysms, hemorrhages, exudates, retinal edema).

Front 129

What are the ophthalmic screening recommendations for diabetes?

Back 129

Diabetics should be screened for retinopathy once a year. Proliferative retinopathy is treated with laser photocoagulation.

Front 130

What are the renal complications of diabetes?

Back 130

Nephropathy affects 40% of type 1 and 30% of type 2 diabetics. Proteinuria and end-stage renal disease can develop. Diffuse widening of glomerular basement membrane and mesangial thickening.

Front 131

What is the treatment of diabetic nephropathy?

Back 131

Management of nephropathy involves strict control of diabetes, angiotensin-converting enzyme inhibitors, and dialysis or renal transplantation.

Front 132

What are the screening recommendations for proteinuria in diabetics?

Back 132

All diabetics should be screened for proteinuria annually. Microalbuminuria is >30/day. Treated with ACE inhibitors. Diabetes is the most common cause of end stage renal disease.

Front 133

What are the cardiovascular complications of diabetes?

Back 133

75% of deaths in diabetes are from myocardial infarction, congestive failure, or stroke. Coronary artery bypass should be performed in a diabetic patient even if there is only two-vessel coronary disease.

Front 134

What is the lipid management of diabetes?

Back 134

Diabetes is equivalent of coronary disease for management of hyperlipidemia. The target LDL in a diabetes is <100 mg/dL. Diet and exercise should be initiated if LDL >100 mg/dL. Statin for an LDL >100 mg/dL.

Front 135

What is the management of diabetic retinopathy?

Back 135

Screening for retinopathy annually. In type 1 diabetes, the first screening should take place 5 years after diagnosis, then annually. Proliferative retinopathy with vitreous hemorrhages or neovascularization is treated with laser.

Front 136

What is the treatment of diabetic gastroparesis?

Back 136

Metoclopramide or erythromycin.

Front 137

What is the treatment of diabetic erectile dysfunction?

Back 137

Occurs in 50% of patients after 10 years of diabetes. Treatment is sildenafil.

Front 138

What is the screening for diabetic peripheral neuropathy?

Back 138

Podiatric examination annually. Neuropathy leads to increased injury. Diabetes is responsible for 50% of all nontraumatic amputations.

Front 139

What are the characteristics of diabetic peripheral neuropathy?

Back 139

Peripheral neuropathy is symmetrical, with numbness, paresthesia, pain; absent reflexes and loss of vibratory. Mononeuropathy (mononeuritis multiplex) is foot drop, wrist drop, or paralysis of 3, 4, 6 cranial nerve.

Front 140

What are the signs of diabetic autonomic neuropathy?

Back 140

Difficulty swallowing, delayed gastric emptying (gastroparesis), constipation, or diarrhea. Bladder dysfunction or paralysis.

Front 141

What is the treatment for peripheral neuropathy?

Back 141

Analgesics, gabapentin, pregabalin, amitriptyline, and carbamazepine

Front 142

What is the Somogyi effect?

Back 142

Rebound hyperglycemia in the morning because of counterregulatory hormone release after hypoglycemia at night.

Front 143

What is the dawn phenomenon?

Back 143

Early morning rise in plasma glucose, requiring increased amounts of insulin to maintain euglycemia.

Front 144

What are the symptoms of hypoglycemia?

Back 144

Sweating, tremor, tachycardia, anxiety, hunger. Dizziness, headache, clouding vision, blunted mental, fine motor loss, confusion, abnormal behavior, convulsions, loss consciousness. Major symptoms <20 mg/dL.

Front 145

What are the causes of hypoglycemia?

Back 145

Panhypopituitarism, adrenal insufficiency, enzyme defects, malnutrition, pregnancy, liver disease, alcohol, Popranolol, salicylates. Insulinoma, exogenous insulin, sulfonylureas, quinine, endotoxic shock, insulin receptor Ab.

Front 146

What are the clinical signs of insulinoma?

Back 146

Insulinoma (pancreatic B-cell tumor) can cause hypoglycemia. Benign symptoms of hypoglycemia are blurred vision, headache, feelings of detachment, slurred speech, and weakness.

Front 147

How is insulinoma diagnosed?

Back 147

Serum insulin level of >8 mg/mL in the presence of blood glucose values <40 mg/dL.

Front 148

What are the causes of factitious hyperinsulinism?

Back 148

Administration of insulin or ingestion of Equal or oral sulfonylureas. It is common.

Front 149

What are the laboratory abnormalities in factitious hyperinsulinism?

Back 149

Hypoglycemia, high insulin and suppressed plasma C peptide is pathognomonic of exogenous insulin. Ethanol-hypoglycemia with starvation.

Front 150

What is Cushing syndrome?

Back 150

Group of abnormalities. Glucocorticoid therapy is most common cause. Others: adrenal hyperplasia, which can be caused by pituitary ACTH in pituitary dysfunction or pituitary ACTH-adenomas

Front 151

What is Cushing disease?

Back 151

Pituitary adenoma that secretes ACTH, causing hypercortisolism.

Front 152

What percentage of Cushing syndrome is caused by ACTH-producing pituitary adenomas?

Back 152

ACTH-producing pituitary adenomas cause 40% of Cushing cases.

Front 153

What types of cancers can cause adrenal hyperplasia by producing ACTH?

Back 153

ACTH or corticotropin-releasing hormone is secreted by bronchogenic, thymus, or pancreatic CA. Adrenal adenoma or carcinoma and adrenal nodular hyperplasia account for 30% Cushing.

Front 154

What are the clinical signs of Cushing syndrome?

Back 154

Moon face, buffalo hump, truncal obesity; HTN, weakness, osteoporosis; striae, bruises. Acne, hirsutism, oligomenorrhea. Depression, psychosis. Hyperglycemia, delayed healing, nephrolith; glaucoma, polyuria, infections.

Front 155

What are the laboratory signs of Cushing syndrome?

Back 155

Cushing's is associated with hypokalemia and leukocytosis. Hypokalemia occurs because of the mineralocorticoid effect of steroids.

Front 156

How is Cushing syndrome diagnosed?

Back 156

1- mg overnight dexamethasone suppression test and the 24-hour urine free cortisol. The tests used to establish the etiology of the cortisol excess are the ACTH level, high-dose Dex suppress test, MRI.

Front 157

What is the 1-mg overnight dexamethasone suppression test?

Back 157

Best initial diagnostic test of glucocorticoid excess. Give dexamethasone 11 PM; cortisol at 8 AM should be normal. Single random cortisol levels are not reliable. Abnormal 1-mg test confirmed with 24h urine cortisol.

Front 158

How is the etiology of the Cushing syndrome established?

Back 158

ACTH levels are elevated with either a pituitary source of ACTH (adenoma or ectopic). If the ACTH level is low, then the etiology is adenoma, cancer, or adrenal hyperplasia.

Front 159

When there is a high ACTH level, how is the precise etiology of Cushing syndrome determined?

Back 159

MRI of the pituitary for an adenoma or a CT scan of the chest looking for an ectopic focus.

Front 160

What is hyperaldosteronism?

Back 160

Aldosterone reabsorbs sodium and excretes K and acid (H+). Hyperaldosteronism is caused by: primary aldosteronism from the adrenal; and secondary aldosteronism, in which the stimulus is extraadrenal.

Front 161

What are the causes of primary hyperaldosteronism?

Back 161

Unilateral adrenal adenoma (70%). Bilateral hyperplasia accounts for 25-30%. Excessive licorice ingestion (licorice has aldosterone-like qualities).

Front 162

How is primary hyperaldosteronism diagnosed?

Back 162

High urine aldosterone and low plasma renin levels confirm a diagnosis of primary hyperaldosteronism. High-salt diet before the test should suppress aldosterone. Confirm the diagnosis with a CT scan of the adrenals.

Front 163

What is the treatment of bilateral adrenal hyperplasia?

Back 163

Bilateral adrenal hyperplasia is treated with spironolactone, which blocks aldosterone.

Front 164

What is Bartter syndrome?

Back 164

Secondary hyperaldosteronism without edema or hypertension; defect in the loop of Henle; severe hypokalemic alkalosis, defect in renal conservation of sodium or chloride.

Front 165

What is congenital adrenal hyperplasia?

Back 165

Most common adrenal disorder of infancy and childhood. CAH is an autosomal recessive mutation, which produce deficiencies of enzymes that are necessary for the synthesis of cortisol.

Front 166

What are the common enzymatic defects associated with congenital adrenal hyperplasia?

Back 166

Enzymatic defects include alpha-21 hydroxylase deficiency in 95% of all cases. Alpha-21 hydroxylase deficiency is associated with reduction in aldosterone secretion in one third of patients.

Front 167

What are the signs of congenital adrenal hyperplasia?

Back 167

Adrenal virilization with salt-losing tendency caused by aldosterone deficiency (hyponatremia, hyperkalemia, dehydration, hypotension). Ambiguous genitalia, enlarged clitoris, labial fusion, virilization. Males have macrogenitosomia, precocious puberty.

Front 168

How is congenital adrenal hyperplasia diagnosed?

Back 168

Failure to thrive, adrenal insufficiency, salt wasting, HTN. Decreased testosterone, androstenedione, dehydroepiandrosterone, 17-hydroxy-progesterone, urinary 17-ketosteroid,, pregnanetriol.

Front 169

What is the management of congenital adrenal hyperplasia?

Back 169

Glucocorticoid (hydrocortisone) replacement.

Front 170

What are the two types of adrenal deficiency disorders?

Back 170

Adrenal insufficiency is divided into primary adrenocorticoid deficiency (Addison disease) and secondary failure in elaboration of ACTH. Primary adrenocortical insufficiency results from adrenal hypofunction.

Front 171

What are the causes of Addison disease?

Back 171

Caused by destruction of gland. Autoimmune destruction accounts for 80%. Destruction by surgical removal, Tb, fungal, CMV, Mycobacterium avium complex, hemorrhagic, trauma, metastatic invasion.

Front 172

What are the clinical signs of Addison disease?

Back 172

Weakness, paresthesias, cramping, stress intolerance, irritability. Small heart, wt loss, sparse axillary hair. Hyperpigmentation only with primary insufficiency. Addisonian crisis is fever, hypotension, low Na, high K, acidosis.

Front 173

How is primary adrenocortical insufficiency diagnosed?

Back 173

Rapid ACTH, then measurement of cortisol. Moderate neutropenia, lymphocytosis, eosinophilia; elevated K, BUN; low Na; low blood glucose; low plasma cortisol and urinary 17-hydroxycorticosteroid.

Front 174

What is the cosyntropin or ACTH stimulation test?

Back 174

A cortisol level is obtained before and after administering ACTH. A normal person should show a rise in cortisol level after ACTH administration.

Front 175

What is the management of Addison disease?

Back 175

Glucocorticoid, mineralocorticoid, and sodium chloride replacement.

Front 176

What is an adrenal crisis?

Back 176

Fever, vomiting, abdominal pain, altered mental, vascular collapse. Previously undiagnosed adrenal insufficiency after surgery, serious infection, stress; bilateral adrenal infarction/hemorrhage, withdrawal from glucocorticoids.

Front 177

What is the treatment of adrenal crisis?

Back 177

Measure cortisol level, then rapidly administer fluids and IV hydrocortisone.

Front 178

What is pheochromocytoma?

Back 178

Pheochromocytoma is a rare, usually benign, tumor that arises from the chromaffin cells of the sympathetic nerves. 90% in adrenals; 10% extraadrenal, 10% malignant, 10% in children, 10% bilateral, 10% not HTN.

Front 179

What substances are secreted by pheochromocytomas?

Back 179

Epinephrine secretion causes tachycardia, sweating, flushing, and hypertension. Norepinephrine is secreted by all extraadrenal pheochromocytomas.

Front 180

What are the clinical signs of pheochromocytoma?

Back 180

Paroxysms lasting a few minutes to several hours, with headache, profuse sweating, palpitations, and apprehension. Pain in the chest or abdomen, nausea and vomiting. Hypertension with tachycardia.

Front 181

How is pheochromocytoma diagnosed?

Back 181

24-h urine collection for free catecholamines, urinary metanephrines and vanillylmandelic acid, plasma catecholamine. Plasma metanephrine is initial test. Chromogranin levels correlate tumor size. CT/MRI.

Front 182

What is the management of pheochromocytomas?

Back 182

Control BP with alpha-adrenergic blocker (phentolamine, phenoxybenzamine). No other antihypertensive drugs should be used before adequate control of blood pressure. Surgery after BP stabilization.

Front 183

What are the causes of primary hypogonadism?

Back 183

Primary hypogonadism (hypergonadotropic: increased LH, FSH) from Klinefelter syndrome (small testes, eunuchoid, XXY), anorchia, castration or radiotherapy, mumps, TB, leprosy, or chemotherapeutic agents.

Front 184

What are the causes of secondary hypogonadism?

Back 184

Secondary hypogonadism (low LH, FSH) can result from hypopituitarism caused by idiopathic, tumors, hypothalamic lesions, Kallmann syndrome (hypergonadotrophic hypogonadism, decreased smell).

Front 185

What are the clinical signs of prepubertal hypogonadism?

Back 185

External genitalia are underdeveloped, voice is high-pitched, beard does not grow, lacks libido and potency. Youthful appearance, with obesity, long extremities, small Adam's apple, gynecomastia.

Front 186

What are the laboratory abnormalities in hypogonadism?

Back 186

Urinary 17-ketosteroid is low to normal, and serum testosterone low. Serum FSH and LH are low in hypothalamic or pituitary origin and elevated in primary testicular failure. Treatment is testosterone.

Front 187

What are the causes of postpubertal hypogonadism?

Back 187

Pituitary lesion or testes damage by trauma, radiation, infection, drugs. Loss of libido, potency, hair; sterility. Testosterone low. FSH, LH are low with pituitary lesions and high with testicular failure. Rx testosterone.

Front 188

What is Klinefelter syndrome?

Back 188

1 of every 500 males. Caused by a supernumerary X chromosomes. 47,XXY. Gynecomastia with elevated levels of LH and FSH. Sterility and lack of libido. The testes are small. Mental retardation may be present.

Front 189

What are the laboratory abnormalities in Klinefelter syndrome?

Back 189

Urinary 17-ketosteroids are low normal; serum testosterone is low to normal, LH and FSH are elevated, and serum estradiol is elevated. 20x increased risk of breast cancer. Treatment is testosterone.

Front 190

What are the basic synovial fluid tests?

Back 190

Cell count, crystals, cultures, and Gram stain.

Front 191

What are the synovial fluid cell count in osteoarthritis?

Back 191

OA and traumatic arthritis have 200-2,000 white blood cells (WBC)/mm3 in the synovial fluid. Inflammatory diseases (RA, gout) have 5,000-50,000 WBC/mm3. Septic arthritis has >50,000 WBC/mm3.

Front 192

What are antinuclear antibodies?

Back 192

Antinuclear antibodies are Ab that bind to structures within nucleus. ANAs are found in SLE, Sjögren syndrome, and systemic sclerosis, and 5% of normal people.

Front 193

How is the ANA test performed?

Back 193

The ANA test is performed by exposing the antibodies in the serum to laboratory test cells. It is then determined whether the antibodies react with various parts of the nucleus.

Front 194

What subsets of ANAs are associated with systemic lupus erythematosus?

Back 194

Anti ds-DNA and anti-SM antibodies are found in patients with SLE; anti-histone antibodies are found in patients with drug-induced lupus.

Front 195

What is the significance of a positive ANA test?

Back 195

95% of SLE have positive ANA. Neg ANA excludes SLE. Pos ANA in asymptomatic patient is a false pos (5% of population); a positive ANA with arthritis, proteinuria, pleural effusion is likely SLE.

Front 196

What are rheumatoid factors?

Back 196

Autoantibody against Fc portion of IgG. RF found in 70% of RA. Not specific for RA and are found in 5% of healthy. RF is neither sensitive nor specific for the diagnosis of RA. High titers causes more aggressive disease.

Front 197

What is the significance of a positive cyclic citrullinated peptide?

Back 197

Cyclic citrullinated peptide is associated with rheumatoid arthritis.

Front 198

What are antineutrophil cytoplasmic antibodies?

Back 198

ANCAs are antibodies directed against cytoplasm of neutrophils in Wegener granulomatosis. Perinuclear ANCA is found in polyarteritis nodosa and Churg-Strauss syndrome.

Front 199

What is antiphospholipid antibody syndrome?

Back 199

Hypercoagulable state with Ab against phospholipids or cardiolipins (lupus anticoagulant or anticardiolipin antibodies). Elevated PTT, false-positive VDRL.

Front 200

What is the presentation of antiphospholipid antibody syndrome?

Back 200

Presents with spontaneous abortions or thromboembolism. If two first-trimester spontaneous abortions occur, antiphosolipid antibodies should be checked.

Front 201

A 28-year-old woman with joint swelling and stiffness. Stiffness for 2 h in morning. Fatigue, fever. Wrist, MCPs, and PIPs red and swollen. DIPs are not involved. Fluid in wrist joints. What is the diagnosis?

Back 201

Rheumatoid arthritis.

Front 202

What is rheumatoid arthritis?

Back 202

Chronic, symmetric, inflammatory synovitis. Inflammation destroys cartilage and causes bone erosions, deforming joint. Triggered by infectious agent. Women 3x more than men; 35-50 years.

Front 203

What is the diagnostic criteria for rheumatoid arthritis?

Back 203

4 of the following: Morning stiffness. Swelling of wrists, MCPs, PIPs. Swelling of three joints. Symmetric joint swelling. Joint erosions on x-rays. RF positive. Rheumatoid nodules.

Front 204

Which joints are never involved in rheumatoid arthritis?

Back 204

Distal interphalangeal joints and joints of the lower back.

Front 205

What are the systemic symptoms of rheumatoid arthritis?

Back 205

Two-thirds of the patients present with fatigue, anorexia, weight loss, generalized weakness before the onset of the arthritis.

Front 206

What are the extraarticular manifestations of rheumatoid arthritis?

Back 206

Damage to the ligaments and tendons. Radial deviation of the wrist with ulnar deviation of the digits. Boutonniere deformity. Swan-neck deformity. Rheumatoid nodules.

Front 207

What are the laboratory findings in rheumatoid arthritis?

Back 207

Rheumatoid factor, anemia, increased ESR, X-rays erosions.

Front 208

What is the initial treatment for rheumatoid arthritis?

Back 208

Nonsteroidal antiinflammatory drugs (NSAIDs) have fewer side effects than aspirin.

Front 209

What is the mechanism of selective COX-2 inhibitors?

Back 209

Cyclooxygenase 2 inhibitors selectively block the COX-2 enzyme at the site of inflammation. Benefit of COX-2 inhibitors is not inhibiting COX-1, an enzyme that produces protective stomach lining.

Front 210

What is the mechanism of action of nonselective NSAIDS?

Back 210

Nonselective of NSAIDs block both COX-2 and COX-1, which can lead to increased risk for gastrointestinal side effects (bleeding).

Front 211

What is the beneficial effect of selective NSAID COX-2 inhibitors?

Back 211

Selective COX-2 inhibitors (celecoxib) reduce risk of gastric ulcers, but COX-2 inhibitors double risk of MI and stroke because COX-2 enzyme creates protective fatty acids that prevent thromboses.

Front 212

What is the treatment of rheumatoid arthritis that does not respond to NSAIDs?

Back 212

Glucocorticoids. Disease-modifying agents: antimalarials, gold, sulfasalazine, methotrexate, and tumor necrosis factor receptor inhibitors: infliximab (Remicade), adalimumab (Humira), etanercept (Enbrel)

Front 213

What is atlantoaxial subluxation?

Back 213

Occurs in rheumatoid arthritis when there is excessive movement between atlas (Cl) and axis (C2). Neck pain, C2 radicular pain (hands), myelopathy, paraplegia, quadriplegia.

Front 214

What is a ruptured Baker cyst?

Back 214

Extension of inflamed synovium into the popliteal space; swollen, painful calf.

Front 215

34-year-old woman with confusion, malar rash, HTN, symmetrical joint swelling of wrists and MCPs. Creatinine of 2.5, proteinuria. What is the diagnosis?

Back 215

Systemic lupus erythematosus.

Front 216

What is systemic lupus erythematosus?

Back 216

Systemic disease in which tissues and multiple organs are damaged by autoantibodies and immune complexes. Ninety percent of cases are women. Ultraviolet light may cause flares.

Front 217

What is the diagnostic criteria for systemic lupus erythematosus?

Back 217

4 required: malar/discoid rash, photosensitivity, oral ulcers, arthritis, serositis, renal; neurologic (seizures, psychosis); hematologic (hemolysis, leukopenia); immunologic (ANA).

Front 218

What are the skin manifestations of systemic lupus erythematosus?

Back 218

Malar rash and photosensitivity (diffuse, maculopapular) flare with exposure to UV-B light and resolve with no scarring. Discoid lupus is a circular rash with a raised rim over scalp and face; central atrophy and scarring.

Front 219

What are the joint manifestations of systemic lupus erythematosus?

Back 219

Arthritis is systemic, non-erosive of wrists, MCPs, PIPs.

Front 220

What are the psychiatric manifestations of systemic lupus erythematosus?

Back 220

Change in personality and psychosis with CNS lupus. Libman-Sacks endocarditis is noninfectious endocarditis that is rare in lupus

Front 221

What are the laboratory findings in lupus?

Back 221

Positive ANA supports diagnosis but is not specific. Complement levels are decreased in lupus. ds-DNA antibodies with active lupus are very specific: increase likelihood of nephritis, and active SLE.

Front 222

What is the treatment for systemic lupus?

Back 222

NSAIDs for arthritis, pleurisy. Corticosteroid for rashes. Hydroxychloroquine and corticosteroids for arthritis. Cytotoxics (azathioprine, cyclophosphamide) for nephritis, carditis, pleuritis. Sunscreen.

Front 223

What drugs cause drug-induced lupus?

Back 223

Hydralazine, isoniazid, procainamide, quinidine.

Front 224

What is the presentation of drug-induced lupus?

Back 224

Arthritis, fatigue, fever, and rarely pleurisy. There is no skin disease, kidney disease, and milder symptoms than SLE. Causes positive ANA. Symptoms resolve within 2 weeks.

Front 225

35-year-old woman with skin tightness and painful fingertips with exposure to cold. BP 170/100; shiny, thickened skin. Elevated creatinine. What is the diagnosis?

Back 225

Scleroderma.

Front 226

What is systemic sclerosis?

Back 226

Thickening of the skin caused by accumulation of connective tissue; involvement of GI, lungs, kidneys. All scleroderma patients have Raynaud phenomenon.

Front 227

What are the gastrointestinal signs of systemic sclerosis?

Back 227

Esophageal dysmotility and achalasia, hypomotility of the small intestine with bacterial overgrowth and malabsorption, and dilatation of the large intestine with diverticula.

Front 228

What are the pulmonary manifestations of scleroderma?

Back 228

Pulmonary fibrosis with restrictive lung disease and cor pulmonale.

Front 229

What are the renal manifestations of scleroderma?

Back 229

Renal crisis in which malignant hypertension acute renal failure. Treated with angiotensin-converting enzyme inhibitors.

Front 230

What is limited scleroderma (CREST syndrome)?

Back 230

Variant of scleroderma: Calcinosis, Raynaud, Esophageal dysfunction, Sclerodactyly, Telangiectasias. Calcium deposits in fingers, knees, elbows, ulcerate. Sclerodactyly is skin thickening of fingers, toes.

Front 231

What are the laboratory findings in limited scleroderma?

Back 231

Limited scleroderma has positive ANA test. Antibodies to Sc-70 are negative in limited scleroderma and positive in diffuse scleroderma.

Front 232

What is Raynaud phenomenon?

Back 232

Pallor, cyanosis in cold. Vasoconstriction. Raynaud disease is not associated underlying disease. Secondary Raynaud phenomenon is associated with disease (scleroderma). 5% population Raynaud disease. Young women.

Front 233

What is the treatment for systemic sclerosis?

Back 233

No cure. D-penicillamine may be used. Raynaud phenomenon: use calcium-channel blockers; for hypertension use angiotensin-converting enzyme inhibitors.

Front 234

A 43-year-old woman with dry eyes and sensation of sand in her eyes; painful swallowing. Parotid enlargement. ANA positive. What is the diagnosis?

Back 234

Sjögren syndrome.

Front 235

What is Sjögren syndrome?

Back 235

Autoimmune lymphocytic infiltration of exocrine glands; xerostomia, dry eyes. Sjögren syndrome may be primary or with autoimmune diseases (secondary), RA or SLE. Lungs, kidneys, malignant lymphoma.

Front 236

What is the presentation of Sjögren syndrome?

Back 236

Itchy eyes, sandy feeling under their eyes destruction of the corneal epithelium (keratoconjunctivitis sicca), and dysphagia.

Front 237

What are diagnostic tests for Sjögren syndrome?

Back 237

Schirmer's test shows decreased tear production. ANA positive; anti-Ro (SSA) and anti-La (SSB) are positive. Treatment is artificial tears.

Front 238

Which autoimmune diseases have arthritis plus multiple organ involvement?

Back 238

SLE, systemic sclerosis (scleroderma), and Sjögren syndrome.

Front 239

25-year-old man with lower back stiffness and pain in morning >2 h, improving with exercise. Murmur over second right intercostal space and decreased range-of-motion of lumbar spine. What is the diagnosis?

Back 239

Ankylosing spondylitis.

Front 240

What allele is associated with the spondyloarthropathies?

Back 240

B-27 allele.

Front 241

What is ankylosing spondylitis?

Back 241

Inflammatory disorder that affects axial skeleton and peripheral joints. Second to third decade (rare after 40). Men 3-4 times that of women. Positive for HLA B-27.

Front 242

What is the presentation of ankylosing spondylitis?

Back 242

Chronic lower back pain, young man (20s-30s). Morning stiffness 1 h, improves with exercise. Cervical spine not affected. Anterior uveitis, aortic insufficiency, CHF, heart block. Decreased spine mobility, fractures.

Front 243

What are the x-ray abnormalities in ankylosing spondylitis?

Back 243

Sacroiliitis and fusing of the sacroiliac joint. Bamboo spine and squaring of the vertebral bodies.

Front 244

What is the treatment for ankylosing spondylitis?

Back 244

NSAIDs, physical therapy, exercise. TNF blockers (infliximab, adalimumab, etanercept).

Front 245

What is reactive arthritis?

Back 245

Seronegative arthropathy after infection, non-gonococcal urethritis. Keratoderma blennorrhagica (waxy, palms/soles), circinate balanitis, oral/genital ulcers, conjunctivitis, arthritis. Campylobacter, Salmonella.

Front 246

What is the treatment for reactive arthritis?

Back 246

Severe form of reactive arthritis in HIV patients improves with antiretroviral medications. NSAIDS, tumor necrosis factor blockers.

Front 247

What is psoriatic arthritis?

Back 247

Arthritis involves the DIP joints and associated with psoriatic nail disease (pitting of the nails); sausage-shaped digit.

Front 248

What is enteropathic arthropathy?

Back 248

Joint arthropathy with ulcerative colitis or Crohn disease; associated with pyoderma gangrenosum and erythema nodosum.

Front 249

A 66-year-old man with knee pain and pain in distal interphalangeal joints. Knee crepitations. What is the diagnosis?

Back 249

Osteoarthritis

Front 250

What is osteoarthritis?

Back 250

Most common joint disease. Articular cartilage destruction with hypertrophy of bone. Osteoarthritis, unlike RA, is not an inflammatory disease. Knee osteoarthritis is leading cause of chronic disability in elderly.

Front 251

What are the major risk factors for osteoarthritis?

Back 251

Age, female sex, genetic factors, major joint trauma, repetitive stress, and obesity. The most common joint to be affected is the knee; base of the thumb.

Front 252

What is the presentation of osteoarthritis?

Back 252

Weight-bearing joints (hip, knee), small finger joints (PIPs, DIPs). Oligoarticular-asymmetric. Progressive, irreversible. Pain with exercise, relieved by rest. Morning stiffness <30 min. Crepitations, no systemic.

Front 253

What X-ray findings are associated with osteoarthritis?

Back 253

Osteophytes and unequal joint space PIP osteophytes are called Bouchard's nodes, in the DIP are called Heberden's nodes.

Front 254

What is the treatment of osteoarthritis?

Back 254

Acetaminophen, analgesic ibuprofen is 1,200 mg/d, antiinflammatory dose is 2,400 mg/d. Caution in elderly with NSAIDs. COX-2 inhibitors may be used in patients at high risk for ulcers (celecoxib).

Front 255

What are the crystal-induced arthropathies?

Back 255

Monosodium urate, calcium pyrophosphate, calcium oxalate, calcium hydroxyapatite caused by deposition in joints; they have identical presentations and can only be distinguished by synovial fluid analysis.

Front 256

What is gout?

Back 256

Gout affects middle-aged men and presents with acute monoarthritis. Deposition of urate crystals in connective tissue (tophi) and kidneys.

Front 257

What is the presentation of acute gout?

Back 257

First toe is commonly affected (podagra); knee, ankle, PIPs, or DIPs may be initially involved. First episode occurs at night with severe joint pain. Warm, red, tender. Pain resolves within 3-14 days.

Front 258

What are the factors that can precipitate gout?

Back 258

Excessive alcohol, trauma, surgery, infection, steroid withdrawal, hydrochlorothiazide, furosemide; pyrazinamide and ethambutol, and serious medical illnesses.

Front 259

How is gout diagnosed?

Back 259

Uric acid maybe normal. Many have elevated uric acid levels and never develop gout. Serum uric acid level is of no value in diagnosis of gout. Synovial fluid: negatively birefringent needles. WBCs 5000-50000.

Front 260

What is the treatment of acute gouty arthritis?

Back 260

Indomethacin 50 mg three times a day. Colchicine, 0.6 mg every hour until symptoms resolve. Steroids, intraarticular or oral in elderly patients who cannot tolerate NSAIDs, colchicine or in renal impairment.

Front 261

What is the treatment of recurrent gouty attacks?

Back 261

Hypouricemic therapy in recurrent gouty. Probenecid used in undersecretors (>80%). Allopurinol in overproducers, undersecretors, with renal failure/stones. Allopurinol should not be initiated during attack.

Front 262

What is pseudogout?

Back 262

Calcium pyrophosphate crystal deposition is more common in the elderly population and preexisting joint damage. Hyperparathyroidism, hemochromatosis, hypophosphatemia, hypomagnesemia.

Front 263

What are the clinical signs of pseudogout?

Back 263

The knee is the most commonly affected joint; other joints are the wrist, shoulder, and ankle.

Front 264

How is pseudogout diagnosed?

Back 264

Rhomboid, positive birefringent crystals on synovial fluid evaluation. Linear radiodense deposits in joint menisci or articular cartilage (chondrocalcinosis).

Front 265

What is the treatment for calcium pyrophosphate crystal deposition disease?

Back 265

NSAIDS, colchicine, corticosteroid. Prevent frequent recurrences with low doses of colchicine.

Front 266

A 65-year-old woman with history of rheumatoid arthritis with left shoulder pain for 2 days; low-grade fever. decreased range of motion, erythema. What is the next step?

Back 266

Perform arthrocentesis

Front 267

What is the most common cause of infectious arthritis in patients younger than 40 years old?

Back 267

Gonorrhea, which accounts for 70% of episodes in patients younger than 40 years old.

Front 268

What is the most common cause of infectious arthritis in older patients?

Back 268

Staphylococcus aureus is most common cause of infectious arthritis and occurs in preexisting joint destruction from other rheumatic diseases. RA is highest risk.

Front 269

What are the synovial fluid findings in gonococcal infectious arthritis?

Back 269

Infected joints with gonococci will not have positive cultures, and the Gram stain will be negative.

Front 270

What treatment should be prescribed for a young woman with acute monoarticular arthritis with >50,000 WBCs in synovial fluid without crystals?

Back 270

A young woman with acute monoarticular arthritis who is found to have >50,000 WBCs in the synovial fluid without crystals should be treated with ceftriaxone.

Front 271

What treatment should be ordered for an elderly man with RA and acute monoarticular arthritis and >50,000 WBCS in synovial fluid?

Back 271

An elderly man with infectious arthritis should be treated with IV nafcillin or vancomycin.

Front 272

What is Wegener granulomatosis?

Back 272

Small vessel vasculitis of any organ, but mainly the sinuses, nose, trachea, lungs and kidneys. Rhinitis, sinusitis, and nasal ulcers. Cough, hemoptysis, and dyspnea. Kidney involvement in 80%. Arthritis in 60%.

Front 273

How is Wegener granulomatosis diagnosed?

Back 273

Associated with antineutrophil cytoplasmic antibodies (C-ANCA). Confirm diagnosis by biopsy of an involved organ (nasal septum), vasculitis and granulomas.

Front 274

What is the treatment of Wegener granulomatosis?

Back 274

Glucocorticoid and immunosuppressive agent (cyclophosphamide).

Front 275

What is polyarteritis nodosa?

Back 275

Multisystem disease with fever, malaise, weight loss, anorexia, and abdominal pain. Affects any site in the body, except the lungs. Predisposition for skin, kidney, nerves, GI.

Front 276

What is the presentation of polyarteritis nodosa?

Back 276

Peripheral neuropathies. abdominal pain and gastrointestinal bleeding. Biopsy of skin, symptomatic nerves, or muscles medium-size arteritis.

Front 277

What is the treatment of polyarteritis nodosa?

Back 277

Corticosteroids, immunosuppressive drugs (cyclophosphamide).

Front 278

What is Churg-Strauss syndrome?

Back 278

Vasculitis can involve any organ; asthma, eosinophilia, lung involvement.

Front 279

What is the presentation of Churg-Strauss syndrome?

Back 279

Middle aged individual with new-onset asthma, mononeuropathy, transient pulmonary infiltrates, paranasal sinus abnormalities, nasal polyps, allergic rhinitis.

Front 280

What are the biopsy findings in Churg-Strauss syndrome?

Back 280

Biopsy: medium arteritis. Treatment is prednisone and cytotoxic agent.

Front 281

What is temporal arteritis?

Back 281

Temporal arteritis is a vasculitis of large arteries that supply the head, eyes, and optic nerves. New-onset headache in any patient older than 50 years; may cause permanent vision loss.

Front 282

What is the presentation of temporal arteritis?

Back 282

Headache, pain in temples. Scalp tenderness, jaw claudication, decreased vision, tongue numbness, sudden loss of vision. 25% also have polymyalgia rheumatica.

Front 283

How is temporal arteritis diagnosed?

Back 283

ESR is first test (100% sensitive); always confirm by biopsy of temporal artery for giant cells. If temporal arteritis is suspected and the ESR elevated, prednisone should be started immediately (before biopsy).

Front 284

A 73-year-old woman with new right-sided headache, fever, decreased vision. What is the first step?

Back 284

Check the ESR; if elevated, start prednisone 60 mg daily.

Front 285

43-year-old woman with proximal weakness for 2 months. Diffuse lilac rash over sun-exposed areas. Weakness in upper and lower proximal muscles. CPK and aldolase positive. What is the diagnosis?

Back 285

Dermatomyositis

Front 286

What are the inflammatory myopathies?

Back 286

Inflammatory muscle diseases with progressive muscle weakness. Polymyositis, dermatomyositis, and inclusion body myositis.

Front 287

What are the clinical signs of inflammatory myopathies?

Back 287

Proximal muscle weakness: lifting objects, combing hair, rising from chair. Ocular muscles never involved, which differentiates inflammatory myopathies from myasthenia.

Front 288

What is the presentation of dermatomyositis?

Back 288

Dermatomyositis will have weakness with heliotrope rash, which is a purple-lilac discoloration of the face, eyelids, and sun-exposed areas of body.

Front 289

What are the laboratory findings in inflammatory myopathies?

Back 289

Inflammatory destruction of muscles causes an elevation of the muscle enzymes creatine kinase and aldolase. EMG shows of myopathic potentials; confirmed by biopsy.

Front 290

What is the treatment for polymyositis and dermatomyositis?

Back 290

Steroids are useful in polymyositis and dermatomyositis.

Front 291

What is achalasia?

Back 291

Idiopathic loss of nerves of lower esophageal sphincter; inhibitory neurons lost, inability to relax LES. Unknown etiology. Very small number can be from Chagas disease, gastric carcinoma, lymphoma.

Front 292

What is the presentation of achalasia?

Back 292

Achalasia presents with progressive dysphagia to both solids and liquids; regurgitation.

Front 293

How is achalasia diagnosed?

Back 293

Barium esophagography shows dilation of esophagus, which narrows into "bird's beak" at end. Esophageal manometry shows increased lower esophageal sphincter resting pressure. Treatment is dilation.

Front 294

A 65-year-old man with difficulty swallowing solids, weight loss. reflux esophagitis, smoking, enlarged left supraclavicular lymph node. What is the diagnosis?

Back 294

Esophageal cancer.

Front 295

What are the causes of esophageal cancer?

Back 295

Alcohol, tobacco for squamous cell cancer in proximal two-thirds of esophagus. Adenocarcinoma in the distal third, associated with gastroesophageal reflux disease and Barretts esophagus.

Front 296

What is the presentation of esophageal cancer?

Back 296

Progressive dysphagia first for solid food, then liquids, weight loss. Halitosis, regurgitation, hoarseness, and hypercalcemia.

Front 297

How is esophageal cancer diagnosed?

Back 297

Barium swallow first; endoscopy is mandatory for biopsy. CT scan assesses local spread; bronchoscopy detects spread into the bronchi. Endoscopic ultrasound for staging.

Front 298

What is the presentation of esophageal spasm?

Back 298

Intermittent chest pain, dysphagia, with no relationship to exertion or eating. The pain is precipitated by drinking cold liquids.

Front 299

How is esophageal spasm diagnosed?

Back 299

Barium studies show a "corkscrew" pattern. The most accurate test is manometric studies.

Front 300

What is the treatment of esophageal spasm?

Back 300

Nifedipine and nitrates.

Front 301

What is Schatzki's ring?

Back 301

Schatzki's rings are thin, epithelial membranes; intermittent dysphagia; painless. More distal and located at the squamocolumnar junction proximal to the lower esophageal sphincter.

Front 302

What is Plummer-Vinson syndrome?

Back 302

Plummer-Vinson syndrome causes a more proximal ring in the hypopharynx. Associated with iron-deficiency anemia and progression to squamous cell cancer. Middle-aged women.

Front 303

How is Plummer-Vinson syndrome diagnosed?

Back 303

Diagnosed with a barium swallow.

Front 304

What is the treatment of Plummer-Vinson syndrome?

Back 304

May respond to treatment of iron deficiency. Dilation procedures are used.

Front 305

What is the most common infectious cause of esophagitis?

Back 305

Candida albicans. HIV positive with a CD4 <200/mm3. Diabetes mellitus is the second most common risk. Herpes simplex, cytomegalovirus, aphthous ulcers.

Front 306

What is the treatment of esophagitis?

Back 306

If the patient is HIV positive, empiric treatment is with fluconazole.

Front 307

What medications are associated with esophagitis?

Back 307

Pills that cause esophagitis are alendronate, quinine, risedronate, vitamin C, potassium chloride, doxycycline, NSAIDs, and iron sulfate.

Front 308

What is a Zenker diverticulum?

Back 308

Outpocketing of posterior pharynx. Older patients have bad breath and difficulty initiating swallowing. Repeated clearing of throat; regurgitation of food eaten several days ago.

Front 309

How is Zenker diverticulum diagnosed?

Back 309

The diagnosis is made by barium studies. Treated with surgical resection.

Front 310

What is Mallory-Weiss syndrome?

Back 310

Tear of the lower esophagus caused by retching and vomiting. Painless upper gastrointestinal bleeding. Melena or hematemesis. Diagnosed by upper endoscopy.

Front 311

What is the treatment for Mallory-Weiss tears?

Back 311

Resolve spontaneously. Injection of the tear with epinephrine or cauterization.

Front 312

What are the causes of epigastric pain?

Back 312

Ulcer disease, pancreatitis, gastroesophageal reflux disease, gastritis, and gastric cancer.

Front 313

What organism causes gastric ulcers, duodenal ulcers, and gastritis?

Back 313

Helicobacter pylori is most strongly associated with the development of duodenal ulcers, gastric ulcers, and gastritis.

Front 314

What is the most common cause of epigastric tenderness?

Back 314

Pancreatitis is the most common cause for epigastric tenderness and pain. Ulcer disease is associated with epigastric tenderness in <20% of patients.

Front 315

What is the most common cause of epigastric pain?

Back 315

The most common etiology of epigastric pain is nonulcer dyspepsia, a functional disorder of persistent pain with normal tests.

Front 316

How is Helicobacter pylori disease diagnosed?

Back 316

H. pylori can be diagnosed with serology, urea breath testing, stool antigen detection. Endoscopy not needed, but biopsy and is the most accurate. When testing for eradication, use breath test or stool antigen.

Front 317

When is endoscopy indicated for patients with ulcer disease?

Back 317

All patients with epigastric pain and >45 years or alarm symptoms, such as weight loss, dysphagia, odynophagia, or heme-positive stool, should undergo endoscopy to exclude gastric cancer.

Front 318

What is the treatment of Helicobacter pylori disease?

Back 318

Ulcers, reflux disease, and gastritis treated empirically. Young, healthy patients can be treated empirically with H2 blockers, antacids, or proton-pump inhibitors, and then endoscopy if there is no improvement.

Front 319

What is the cause of gastroesophageal reflux disease?

Back 319

Abnormal flow of the acid gastric contents backward from the stomach up into the esophagus through the lower esophageal sphincter.

Front 320

What factors decrease tone of the lower esophageal sphincter?

Back 320

Nicotine, alcohol, caffeine, peppermint, chocolate, anticholinergics, calcium-channel blocking agents, and nitrates.

Front 321

What is the clinical presentation of GERD?

Back 321

Epigastric pain, sore throat; a bad, metal-like taste in the mouth; hoarseness; and cough and wheezing. Pain in the substernal area. 24-hour pH monitoring is not necessary.

Front 322

What is the treatment for GERD?

Back 322

PP-inhibitors: omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole increase pH. Avoid nicotine, alcohol, caffeine, chocolate, late meals. Elevate bed. 5% require Nissen fundoplication.

Front 323

What is Barrett esophagus?

Back 323

Complication of long-standing reflux disease where epithelium of lower esophagus changes from normal squamous epithelium to columnar epithelium. Treatment is proton-pump inhibitors.

Front 324

What are the causes of peptic ulcer disease?

Back 324

Ulcers are caused by NSAIDs, H pylori, stomach CA, Zollinger-Ellison, Crohn, burns, head trauma, mechanical ventilation. Ulcers not caused by smoking, alcohol, steroids.

Front 325

What is the pathophysiology of peptic ulcer disease?

Back 325

Prostaglandins stimulate mucous production that forms a protective barrier. Prostaglandins are inhibited by NSAIDs. Parietal cells produce acid.

Front 326

What hormones stimulate acid production?

Back 326

Stimulants of acid production are gastrin, acetylcholine, histamine. Histamine is released by stomach cells and stimulates acid release.

Front 327

What is the mechanism of action of H2 blockers?

Back 327

H2 blockers, such as cimetidine, famotidine, and ranitidine, inhibit acid release by blocking histamine effect on parietal cells.

Front 328

What is Zollinger-Ellison syndrome?

Back 328

Zollinger-Ellison syndrome is the excessive production and release of gastrin from G cells.

Front 329

What is the most common cause of ulcer disease?

Back 329

The most common cause of ulcer disease is Helicobacter pylori followed by the use of NSAIDs. Eighty to 90% of duodenal ulcers and 70 to 80% of gastric ulcers are associated with H. pylori.

Front 330

How is ulcer disease diagnosed?

Back 330

Ulcer is best diagnosed with endoscopy. In patients <45 with epigastric pain, endoscopy performed only if symptoms persist. If >45, wt loss, anemia, or heme-positive, endoscopy should be performed.

Front 331

How is H. pylori disease diagnosed?

Back 331

Diagnosis of H. pylori is based on serology, urea breath test, stool antigen, or biopsy. Serology is the least expensive and has high sensitivity. Serology does not distinguish between old disease and new disease.

Front 332

What is the advantage of breath testing for H pylori over serology?

Back 332

Advantage of breath testing and stool antigen detection is same sensitivity as serology and are able to distinguish new versus old disease. After treatment, breath/stool tests become neg and used as a test for cure.

Front 333

What is the treatment of H pylori ulcer disease?

Back 333

PPI, clarithromycin and amoxicillin. Omeprazole, lansoprazole, pantoprazole, rabeprazole, and esomeprazole are all equal. PPI/clarithromycin/amoxicillin is >90% effective. Therapy 10-14 d.

Front 334

What is the approach to patients who fail therapy for H pylori?

Back 334

In those who fail therapy, a urea breath test should be performed. If the organism was not eradicated, then re-treat with PPI, tetracycline, metronidazole and bismuth subsalicylate.

Front 335

What is gastritis?

Back 335

Inflammation, erosion of the gastric lining. Unlike ulcer disease, gastritis can be caused by alcohol; also NSAIDs, Helicobacter, head trauma, burns, mechanical ventilation. Associated with increased gastric acid.

Front 336

What is the presentation of gastritis?

Back 336

Most patients with gastritis present with asymptomatic bleeding. Other patients have epigastric pain, nausea and vomiting, hematemesis or melena.

Front 337

How is gastritis diagnosed?

Back 337

The diagnosis of H. pylori is based on either serology, urea breath testing, stool antigen testing, or biopsy with histology.

Front 338

When should endoscopy be performed in patients with gastritis?

Back 338

If <45 years of age with epigastric pain, endoscopy can be performed if the symptoms persist. In those older than 45 years or with weight loss, anemia, heme-positive stools, dysphagia, endoscopy should be performed.

Front 339

How is gastritis treated?

Back 339

PPI combined with clarithromycin and amoxicillin. Omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole are equal. Duration of therapy is 10 to 14 days.

Front 340

How is pernicious anemia diagnosed?

Back 340

B12 deficiency and pernicious anemia are diagnosed with low B12 level and increased methylmalonic acid level. Pernicious anemia is confirmed by antiparietal cell Ab and anti-intrinsic factor Ab.

Front 341

What is Zollinger-Ellison syndrome?

Back 341

Hypergastrinemia caused by cancer of gastrin-producing cells. Half of gastrinomas are in duodenum, and quarter are in pancreas. <20% are associated with MEN 1 or parathyroid, pituitary, pancreatic tumors.

Front 342

What is the presentation of Zollinger-Ellison syndrome?

Back 342

Present with ulcer. <1% of ulcer disease has a Zollinger-Ellison syndrome or gastrinoma. Ulcers are recurrent after therapy, multiple in number, and occur in the distal duodenum, or resistant to routine therapy. Diarrhea.

Front 343

How is Zollinger-Ellison syndrome diagnosed?

Back 343

Gastrin level must be elevated while the patient is off antisecretory therapy for several days. Nuclear somatostatin-receptor scintigraphy is sensitive metastatic disease. Most sensitive test endoscopic ultrasound.

Front 344

What is gastroparesis?

Back 344

Weak stomach. Cause is diabetes. Presents with early satiety, postprandial nausea, and sense of increased abdominal fullness. Abdominal pain and bloating and diabetes, with retinopathy, neuropathy, nephropathy.

Front 345

What is the treatment for gastroparesis?

Back 345

Increase motility of the stomach with erythromycin or metoclopramide.

Front 346

What are the symptoms of inflammatory bowel disease?

Back 346

Fever, diarrhea, weight loss, and abdominal pain and bleeding. Episcleritis, scleritis and iritis, sclerosing cholangitis, joint pains, and pyoderma gangrenosum or erythema nodosum.

Front 347

What are skip lesions in inflammatory bowel disease?

Back 347

"Skip lesions" are areas of normal tissue in between the areas of disease; associated with Crohn disease.

Front 348

What are the characteristics of ulcerative colitis?

Back 348

UC that is a mucosal disease which is limited to the large bowel. UC has no skip lesions, no fistula formation, and no oral or perianal involvement. UC is more likely to cause bloody diarrhea.

Front 349

Which type of inflammatory bowel disease can lead to colon cancer?

Back 349

Both forms of IBD can lead to colon cancer after 8 to 10 years of involvement of the colon.

Front 350

What are the complications of Crohn disease?

Back 350

Complications of Crohn disease are calcium oxalate kidney stones, diarrhea, and cholesterol gallstones.

Front 351

How is inflammatory bowel disease diagnosed?

Back 351

Colonoscopy. Antineutrophil cytoplasmic antibody is associated with UC.

Front 352

What laboratory abnormalities are associated with Crohn disease?

Back 352

B12, calcium, vitamin K, iron deficiencies because malabsorption. Anti-saccharomyces cerevisiae antibodies. PT increased because vitamin K malabsorption. Kidney stones because increased absorption oxalate.

Front 353

What is the treatment of inflammatory bowel disease?

Back 353

Pentasa is a form of mesalamine released in upper and lower bowel; hence, it is used in CD. Asacol is a form of mesalamine released in the large bowel, and it is most useful for UC. Rowasa is used for rectal disease.

Front 354

What is the treatment of exacerbations of inflammatory bowel disease?

Back 354

Acute exacerbations of IBD are treated with high-dose steroids. Budesonide has a strong local effect when used orally, but is largely cleared by the liver in a first-pass effect.

Front 355

What is the treatment of Crohn perianal disease?

Back 355

Ciprofloxacin and metronidazole are used for CD with perianal disease. Infliximab is used for CD fistulae or refractory disease.

Front 356

What is the role of surgery in inflammatory bowel disease?

Back 356

Surgery is curative in UC; almost 60% will require surgery within 5 years after the diagnosis of UC due to refractory symptoms or severe disease. Surgery is less effective in CD and the disease reoccurs after surgery.

Front 357

What is the laboratory evaluation of inflammatory bowel disease?

Back 357

Stool should be evaluated for fecal leukocytes, culture, and ova and parasite examination. Clostridium difficile toxin and stool Giardia-antigen testing.

Front 358

What are the most common causes of infectious diarrhea?

Back 358

Campylobacter and Salmonella.

Front 359

What is the presentation of Bacillus cereus diarrhea?

Back 359

Ingestion of refried Chinese food. Short incubation period (1-6 hours). Vomiting is prominent. Blood is never present.

Front 360

What type of diarrhea is associated with reactive arthritis and Guillain-Barre syndrome?

Back 360

Campylobacter

Front 361

What type of diarrhea occurs in HIV-positive patients with <100/mm3 CD4 cells?

Back 361

Cryptosporidium and Isospora.

Front 362

What type of food is associated with E. coli 0157:H7?

Back 362

Hamburger meat. Shiga toxin may cause hemolytic uremic syndrome when organism dies; therefore, antibiotics are contraindicated. Platelet transfusions exacerbate the disease.

Front 363

What type of ingestion is associated with Giardia diarrhea?

Back 363

Unfiltered water on a camping trip. Giardia never causes blood in stool. There is abdominal fullness, bloating, and gas. Giardia can also simulate celiac disease by causing a fat and vitamin malabsorption.

Front 364

What type if diarrhea is associated with ingestion of chicken and eggs, dairy products?

Back 364

Salmonella

Front 365

What type of ingestion is associated with scombroid poisoning?

Back 365

Contaminated fish, resulting in vomiting, diarrhea, flushing, wheezing within minutes. Bacteria invade, producing and then releasing histamine into the flesh of fish, such as tuna, mahi mahi, mackerel and amberjack.

Front 366

What is the presentation of Yersinia diarrhea?

Back 366

Yersinia can mimic appendicitis. Also common in people with iron overload, e.g., hemochromatosis.

Front 367

What type of ingestion is associated with Vibrio parahaemolyticus?

Back 367

Ingestion of raw shellfish, such as mussels, oysters, and clams.

Front 368

What type of ingestion is associated with Vibrio vulnificus?

Back 368

Raw shellfish; high incidence in people with underlying liver disease or disorders of iron metabolism. Associated with the development of skin bullae.

Front 369

What population is predisposed to viral diarrhea?

Back 369

Children in day-care centers; absence of blood and white cells

Front 370

Ingestion of what type of foods is associated with Staphylococcus aureus gastroenteritis?

Back 370

Ingestion of dairy products, eggs, salads. Short incubation period (1-6 hours); nausea/vomiting predominate; rarely diarrhea.

Front 371

Ingestion of what type of food is associated with ciguatera-toxin?

Back 371

2-6 hours after ingestion of grouper fish, red snapper, and barracuda. Neurological symptoms include paresthesia, weakness, and reversal of heat and cold.

Front 372

How is acute diarrhea diagnosed?

Back 372

Fecal leukocytes is most useful test. Found when there has been invasion of the intestinal mucosa, as in dysentery, which is a bacterial infection of the bowel, producing diarrhea and bloody stool.

Front 373

What are the invasive organisms that cause infectious diarrhea?

Back 373

Salmonella, Shigella, Campylobacter, V parahaemolyticus, Yersinia, E coli, Vibrio vulnificus. Invasive organisms need 24 h to produce effect. The most definitive test for these bacteria is stool culture.

Front 374

How is cryptosporidiosis diagnosed?

Back 374

Cryptosporidiosis is diagnosed with a modified acid-fast test.

Front 375

How is giardia diagnosed?

Back 375

Giardia is diagnosed with an ELISA stool antigen test. 90% sensitivity.

Front 376

What is the treatment of acute infectious diarrhea?

Back 376

Antibiotics are used if there is abdominal pain, blood in the stool, and fever. Empiric therapy for infectious diarrhea is ciprofloxacin.

Front 377

What is the treatment for scombroid poisoning?

Back 377

Scombroid poisoning is treated with diphenhydramine.

Front 378

What is the treatment of Giardia?

Back 378

Giardia is treated with metronidazole. A newer agent for Giardia is tinidazole, which is effective in a single dose.

Front 379

What is the treatment of Cryptosporidiosis?

Back 379

Cryptosporidiosis is treated with paromomycin and raise the CD4 count to >100/mm3 with antiretrovirals.

Front 380

What is antibiotic-associated diarrhea?

Back 380

Most common cause is Clostridium difficile. Any antibiotic may cause diarrhea, although clindamycin may have one of the highest frequencies. Stool test for C. difficile toxin.

Front 381

What is the treatment for antibiotic-associated diarrhea?

Back 381

Metronidazole. Oral vancomycin only if not resolve with metronidazole.

Front 382

What is the presentation of lactose intolerance?

Back 382

Diarrhea with gas and bloating; never has blood or leukocytes. Weight loss does not occur. High prevalence. Increased stool osmolality and increased osmolar gap.

Front 383

How is lactase deficiency diagnosed?

Back 383

Remove milk, cheese, ice cream, and all other dairy products (except yogurt) from the diet; resolution of symptoms should occur within 24 to 36 hours. Dietary changes are the best therapy; lactase supplements.

Front 384

What is irritable bowel syndrome?

Back 384

Pain syndrome in which there is increased frequency of peristaltic contractions.20% have constipation. Some have diarrhea alone or diarrhea alternating with constipation. No nocturnal symptoms. History of abuse.

Front 385

How is irritable bowel syndrome diagnosed?

Back 385

No specific diagnostic test. Exclude lactose intolerance, inflammatory bowel disease, celiac disease, carcinoid, Giardia infection, and anatomic defects of the bowel.

Front 386

What is the Rome criteria for irritable bowel syndrome?

Back 386

Pain relieved by a bowel movement or by a change in bowel habit. Fewer symptoms at night. Diarrhea alternating with constipation. No fever, weight loss, anorexia, or anemia.

Front 387

What is the treatment for irritable bowel syndrome?

Back 387

High-fiber, loperamide, diphenoxylate. Antispasmodics: hyoscyamine, dicyclomine, belladonna. Tricyclics. Tegaserod in constipation-predominant; may cause diarrhea. Alosetron reduces diarrhea.

Front 388

What is carcinoid syndrome?

Back 388

Tumors that cause neuroendocrine syndrome. Located in appendix and ileum. Symptoms appear after liver has been overwhelmed by metastatic disease. Bronchial carcinoids are rare but are highly symptomatic.

Front 389

What is the presentation of carcinoid syndrome?

Back 389

Diarrhea, flushing, tachycardia, hypotension. Tricuspid insufficiency and pulmonic stenosis.

Front 390

How is carcinoid syndrome diagnosed?

Back 390

Urinary 5-hydroxyindolacetic acid level (5-HIAA).

Front 391

What is the treatment of carcinoid syndrome?

Back 391

Control diarrhea with octreotide (somatostatin analog). Very few carcinoids are localized enough for surgical resection.

Front 392

What are causes of fat malabsorption?

Back 392

Celiac disease and chronic pancreatitis; tropical sprue and Whipple disease are extremely rare causes.

Front 393

What is the presentation of fat malabsorption?

Back 393

Greasy diarrhea, oily, floating, foul smelling. Weight loss. Malabsorption of the fat-soluble vitamins A, D, E, K. Hypocalcemia, easy bruising; prolongation PT. Iron malabsorption, macrocytic anemia.

Front 394

What type of malabsorption causes Vitamin B12 deficiency?

Back 394

Vitamin B12 malabsorption occurs from damage or loss of the mucosal surface of the terminal ileum from celiac disease.

Front 395

What is the most common presentation of celiac disease?

Back 395

Iron deficiency anemia. Dermatitis herpetiformis is a vesicular skin rash on the extensor surfaces of the body in 10%.

Front 396

What is the most common cause of fat malabsorption?

Back 396

Celiac disease is the most likely cause of fat malabsorption because it is the most common.

Front 397

What is the presentation of malabsorption caused by chronic pancreatitis?

Back 397

Patients with chronic pancreatitis will give a history steatorrhea with repeated episodes of pancreatitis from alcohol or gallstones.

Front 398

What type of malabsorption is associated with travel to a tropical country?

Back 398

Tropical sprue is suspected when there is a history of being in a tropical country.

Front 399

What is the presentation of Whipple disease?

Back 399

Whipple disease is the rarest cause of fat malabsorption; dementia (10%), arthralgias (80%), and ophthalmoplegia. Caused by the bacterium Tropheryma whipplei.

Front 400

How is celiac disease diagnosed?

Back 400

Antigliadin, antiendomysial, and antitransglutaminase antibodies. Small bowel biopsy shows flattening of villi. Just removing gluten (wheat, oats) from diet is not effective for diagnosis because antibodies.

Front 401

What is the presentation of chronic pancreatitis?

Back 401

Chronic pancreatitis is diagnosed from the history of repeated episodes of pancreatitis and is confirmed by finding calcification of the pancreas on x-ray and CT scan.

Front 402

How is tropical sprue diagnosed?

Back 402

Tropical sprue and Whipple disease are diagnosed by finding organisms on a bowel-wall biopsy. A positive Tropheryma Whippelii biopsy shows foamy macrophages that are PAS positive.

Front 403

What is the treatment of malabsorption?

Back 403

Chronic pancreatitis can be managed by orally replacing, amylase, lipase, trypsin. Tropical sprue is treated with sulfamethoxazole/trimethoprim or doxycycline.

Front 404

What is the treatment of Whipple disease?

Back 404

Whipple disease is treated with sulfamethoxazole/trimethoprim or doxycycline or ceftriaxone for 1 year.

Front 405

What is diverticulosis?

Back 405

Diverticulosis is caused by a lack of fiber in the diet and an increase in intracolonic pressure, leading to outpocketing of the colon. 50% of persons are over the age of 50.

Front 406

What is the presentation of diverticulosis?

Back 406

Asymptomatic. Left lower quadrant abdominal pain that can be colicky in nature.

Front 407

How is diverticulosis diagnosed?

Back 407

Colonoscopy. Diverticula are more on left in sigmoid, but bleeding occurs more often from diverticula on the right because of thinner mucosa and more fragile blood vessels. Bleeding is painless.

Front 408

What is the treatment for diverticulosis?

Back 408

Dietary fiber in bran, or bulking agents, such as psyllium husks.

Front 409

What is the presentation of diverticulitis?

Back 409

Fever, tenderness, pain, and elevation of white blood cell count.

Front 410

How is diverticulitis diagnosed?

Back 410

CT scanning. Barium studies and endoscopy are relatively contraindicated in diverticulitis.

Front 411

What is the treatment for diverticulitis?

Back 411

Cipro and metronidazole. Other choices are ampicillin/sulbactam, piperacillin/ tazobactam, or the combination of cefotetan or cefoxitin with gentamicin. Mild disease treated with amoxicillin/ clavulanate.

Front 412

What are the causes of constipation?

Back 412

Lack of fiber; calcium-channel blockers, oral ferrous sulfate, hypothyroidism, opiate analgesics, anticholinergics, and tricyclic antidepressants.

Front 413

What is the lifetime risk of colon cancer?

Back 413

>6%. Most cases occur sporadically. Diets that are high in red meat, fat and smoking increase the risk.

Front 414

What is the presentation of colon cancer?

Back 414

Heme-positive, brown stool; chronic anemia when the cancer in right side of colon. Left-sided lesions cause obstruction and decreased stool caliber.

Front 415

What type of cancer is associated with endocarditis caused by Streptococcus bovis?

Back 415

Colon cancer is associated with endocarditis by Streptococcus bovis and Clostridium septicum.

Front 416

What is the treatment for colon cancer?

Back 416

Localized disease easily be cured. Once the disease has spread, then surgical resection will not be effective. Widespread disease is treated with resection and 5-FU.

Front 417

What is the screening for colon cancer?

Back 417

Annual fecal occult blood testing, colonoscopy every 10 years, and sigmoidoscopy every 5 years. Screening should occur after the age of 50 years.

Front 418

What are the causes of a false-positive stool guaiac test?

Back 418

False-positive stool guaiac tests can be caused by aspirin, NSAIDs, red meat, and poultry. False-negative tests can be caused by vitamin C.

Front 419

What is hereditary polyposis colorectal cancer syndrome?

Back 419

Genetic defect causing colon cancer. 3 family members in at least 2 generations with colon CA. 30% develop endometrial/ovarian cancer. Screening should start at the age of 25 with colonoscopy every 1 to 2 years.

Front 420

What is familial adenomatous polyposis?

Back 420

100% adenomas by 35 yrs and of colon cancer by 50. Polyps by age 25. Screening flexible sigmoidoscopy should be done every 1 to 2 years beginning at age 12. If polyps are found, a colectomy should be performed.

Front 421

What is the colon cancer risk in juvenile polyposis syndrome?

Back 421

Juvenile polyposis syndrome has 10% risk of colon cancer. Hamartomas have very little risk of developing into cancer.

Front 422

What is Gardner syndrome?

Back 422

Gardner syndrome is colon cancer with multiple, osteomas, lipomas, cysts, and fibrosarcomas. The osteomas have predilection for the mandible.

Front 423

What is Peutz-Jeghers syndrome?

Back 423

Hamartomatous polyps in the large and small intestine with hyperpigmented spots. Melanotic spots on lips, buccal, skin. Risk of cancer increased. Intussusception, obstruction.

Front 424

What is the usual outcome of gastrointestinal bleeding?

Back 424

80% of cases of gastrointestinal bleeding will resolve spontaneously with supportive management, irrespective of etiology.

Front 425

What is the initial management of gastrointestinal bleeding?

Back 425

Fluid resuscitation with NS. CBC, PT, T&C. If PT is elevated, give FFP. Platelets if count is <50,000. NG tube is only useful to determine site of bleeding.

Front 426

What medications should be given to patients with gastrointestinal bleeding?

Back 426

Patients with gastritis or ulcer disease should be treated with PPIs empirically. H2 blockers have no efficacy in acute gastrointestinal bleeding.

Front 427

What medication reduces portal hypertension in patients with cirrhosis of the liver and gastrointestinal bleeding?

Back 427

If a history of cirrhosis of the liver, or if long-term alcoholic, octreotide should be added to this initial management plan to decrease portal hypertension.

Front 428

What are the indications for transfusion in acute bleeding?

Back 428

Hematocrit should be maintained >30% in older patients or CAD. Younger patients do not need to be transfused, unless their hematocrit is <20%.

Front 429

What is the treatment of bleeding esophageal varices?

Back 429

Octreotide to lower portal pressure. If ineffective, endoscopy to place bands. If banding is not effective, then transjugular intrahepatic portosystemic shunting.

Front 430

What is transjugular intrahepatic portosystemic shunting?

Back 430

Creates shunt between the systemic circulation of hepatic vein and portal circulation of portal vein.

Front 431

What is the primary complication of TIPS?

Back 431

Complication of transjugular intrahepatic portosystemic shunting is worsening of encephalopathy.

Front 432

What are the indications for a Blakemore tube?

Back 432

A Blakemore tube tamponades the site of bleeding in the stomach or esophagus; rarely used and is only a temporary bridge to surgery.

Front 433

What medication reduces risk of bleeding in portal hypertension?

Back 433

Propranolol is a nonselective beta-blocker that used in the long-term management of portal hypertension to decrease the frequency of bleeding.

Front 434

What are the most common causes of upper gastrointestinal bleeding?

Back 434

Ulcers, gastritis, Mallory-Weiss, esophagitis, gastric cancer. Variceal bleeding is common in portal hypertension from cirrhosis.

Front 435

What is the anatomic definition of upper gastrointestinal bleeding?

Back 435

Upper gastrointestinal bleeding is defined as bleeding proximal to the ligament of Treitz.

Front 436

What are the causes of lower gastrointestinal bleeding?

Back 436

Diverticulosis, angiodysplasia, hemorrhoids, cancer, and inflammatory bowel disease.

Front 437

What is the clinical presentation of lower gastrointestinal bleeding?

Back 437

Red blood in stools; upper gastrointestinal bleeding presents with black stool or melena.

Front 438

What degree of blood loss is indicated by the finding of orthostasis?

Back 438

Orthostasis is a >10 rise in pulse or >20 drop in systolic BP when the patient goes from supine to standing or sitting. Orthostasis indicates a 15-20% blood loss.

Front 439

If the resting pulse is >100 bpm, what amount of blood loss has occurred?

Back 439

Pulse above 100/min or a systolic blood pressure under 100 indicates >30% blood loss.

Front 440

How is lower gastrointestinal bleeding diagnosed?

Back 440

Endoscopy is the most accurate test for upper and lower GI bleeding. If endoscopy is unrevealing, nuclear bleeding scan can detect low volume bleeds 0.1-0.5 mL/min. Small bowel bleeding detected capsule endoscopy.

Front 441

What are the causes of acute pancreatitis?

Back 441

Majority from alcoholism/gallstones. Pentamidine, didanosine, azathioprine, sulfas (sulfamethoxazole/trimethoprim thiazides). Hypercalcemia, hypertriglyceridemia. ERCP, trauma, mumps.

Front 442

What is the pathophysiology of pancreatitis?

Back 442

Premature activation of trypsinogen into trypsin while in the pancreas. Autodigestion of the pancreas.

Front 443

What is the clinical presentation of acute pancreatitis?

Back 443

Midepigastric pain with tenderness, nausea, and vomiting; radiates to the back. Septic shock; fever, hypotension, respiratory distress from ARDS, elevation of the white cell count; rigid abdomen.

Front 444

How is acute pancreatitis diagnosed?

Back 444

Lipase is more specific than amylase. Elevated WBC, hypoxia, glucose, LDH, AST. Calcium decreases because malabsorption of fat allows fat to bind with Ca. BUN increases because volume depletion.

Front 445

What test determines the severity of pancreatitis?

Back 445

The most accurate test to determine the severity of pancreatitis is the CT scan, which will demonstrate inflammation, necrosis, pseudocysts, abscesses, and ductal stones. Findings on the CT scan are a more

Front 446

What are the signs of severe necrotizing pancreatitis?

Back 446

Cullen sign: blue around umbilicus caused by hemoperitoneum. Turner's: Purple flanks caused by tissue Hb. Best test for biliary/ pancreas is ERCP. Urinary trypsinogen activation peptide predicts severity.

Front 447

What are the complications of pancreatitis?

Back 447

Ascites (high in amylase); pleural effusion (transudate, amylase); splenic vein thrombosis.

Front 448

What is the treatment of pancreatitis?

Back 448

Intravenous fluids, bowel rest, and pain medication. ERCP removes stone in the pancreatic duct or and to dilate a stricture.

Front 449

What as the management of pancreatic necrosis?

Back 449

Necrosis on CT is an indication imipenem or cefuroxime. Fever is an indication to perform a percutaneous needle biopsy. Infection of the pancreas and necrosis requires debridement.

Front 450

What is the management of pancreatic pseudocysts?

Back 450

Pseudocysts develop 2 weeks after pancreatitis. Pseudocysts should be drained if pain, fistula, rupture, or if expanding. Small, asymptomatic pseudocysts <5 cm do not need drainage.

Front 451

What is the pathophysiology of cirrhosis of the liver?

Back 451

Cirrhosis develops when there is chronic inflammation of the liver. When at least 70 to 80% of liver function has been lost, the synthetic capacity of the liver is diminished.

Front 452

What are the causes of cirrhosis of the liver?

Back 452

The most common cause of cirrhosis is alcohol. Other causes of cirrhosis are primary biliary cirrhosis, sclerosing cholangitis, alpha-1 antitrypsin deficiency, hemochromatosis, and Wilson disease.

Front 453

What are the signs of hepatic cirrhosis?

Back 453

Esophageal varices, ascites, edema; spider angiomata, palmar erythema, asterixis, encephalopathy, jaundice, low albumin. PT prolonged because of inability to make clotting factors.

Front 454

What is spontaneous bacterial peritonitis?

Back 454

Idiopathic infection of ascites. Gram stain is rarely positive. Culture of the fluid is the most specific test. White cell count of >500 or the presence of >250 neutrophils are criteria for infection.

Front 455

What is the treatment of spontaneous bacterial peritonitis?

Back 455

Cefotaxime and ceftriaxone are the drugs of choice for SBP and albumin infusion decreases risk of hepatorenal syndrome.

Front 456

What is the serum-ascites albumin gradient?

Back 456

Ascitic albumin is normally < serum. The difference is the serum-ascites albumin gradient. When SAAG is >1.1, portal hypertension is cause. When SAAG is <1.1, cancer or infection is cause.

Front 457

What is the treatment of cirrhotic edema?

Back 457

Edema and fluid overload in third spaces, such as ascites, are managed with spironolactone.

Front 458

What is the treatment of cirrhotic portal hypertension?

Back 458

Portal hypertension and varices are managed with propranolol to prevent bleeding. Encephalopathy is managed with neomycin or lactulose. Vitamin K is not effective.

Front 459

What is primary biliary cirrhosis?

Back 459

Idiopathic autoimmune disorder in middle-aged women. Bilirubin levels do not elevate until 5 years. Association with Sjögren syndrome, rheumatoid arthritis, and scleroderma.

Front 460

What is the presentation of primary biliary cirrhosis?

Back 460

Fatigue, pruritus. Asymptomatic with an elevated alkaline phos. Osteoporosis. Transaminases normal. GGTP, IgM elevated. Antimitochondrial Ab specific. Biopsy diagnostic.

Front 461

What is the treatment for primary biliary cirrhosis?

Back 461

Bile acid-binding medication, such as ursodeoxycholic acid and cholestyramine. Ultraviolet light. Liver transplant.

Front 462

What is the presentation of primary sclerosing cholangitis?

Back 462

Fatigue, pruritus; increased alkaline phos. Idiopathic disorder of biliary system associated more often ulcerative colitis, also with Crohn. Cancer of biliary system in 15%.

Front 463

How is primary sclerosing cholangitis diagnosed?

Back 463

Elevated alkaline phosphatase; the antimitochondrial antibody test is negative. The most specific test for primary sclerosing cholangitis is an ERCP or transhepatic cholangiogram.

Front 464

What is the treatment for primary sclerosing cholangitis?

Back 464

Bile acid-binding resins. Liver transplant.

Front 465

What is hemochromatosis?

Back 465

Common genetic disease of overabsorption of iron in duodenum. Hepatic inflammation, fibrosis, cirrhosis. Hepatocellular CA in 20%. Restrictive cardiomyopathy 15%. Arthralgias, skin hyperpigmentation, diabetes.

Front 466

What are the laboratory findings in hemochromatosis?

Back 466

Decreased iron-binding capacity. Ferritin is elevated. Liver biopsy.

Front 467

What is the treatment of hemochromatosis?

Back 467

Phlebotomy to remove iron.

Front 468

What is Wilson disease?

Back 468

Autosomal recessive; diminished ability to excrete copper. Copper in liver, brain, cornea. Basal ganglia movement disorder. Kayser-Fleischer rings in eye on slit-lamp. Fanconi syndrome and type II RTA.

Front 469

How is Wilson disease diagnosed?

Back 469

Low ceruloplasmin level. High urinary copper level. Liver biopsy is most specific.

Front 470

What is the treatment for Wilson disease?

Back 470

Penicillamine is a copper chelator. Liver transplantation is curative.

Front 471

What is alpha-1 antitrypsin deficiency?

Back 471

Autosomal recessive disorder leading to deficient alpha-1 antitrypsin levels. Cirrhosis, emphysema developing at a young age in a nonsmoker.

Front 472

How is alpha-1 antitrypsin deficiency diagnosed?

Back 472

Low level of the enzyme in a person with COPD confirms diagnosis.

Front 473

What is the treatment of alpha-1 antitrypsin deficiency?

Back 473

Replacement of the enzyme and stop smoking.

Front 474

How is chronic hepatitis B and C diagnosed?

Back 474

Persistence of hepatitis B surface antigen for more than 6 mth confirms chronic hepatitis B. Ab to hepatitis C and elevated viral load by PCR confirms chronic hepatitis C. Liver biopsy most accurate.

Front 475

What is the treatment for chronic hepatitis B?

Back 475

Chronic hepatitis B is treated with interferon, lamivudine, or adefovir.

Front 476

What is the treatment for chronic hepatitis C?

Back 476

Chronic hepatitis C is treated with the combination of pegylated interferon and ribavirin.

Front 477

What are the important aspects of the chest pain history?

Back 477

Duration, quality, location, radiation, frequency, alleviating or precipitating factors (exercise), associated symptoms. For acute coronary syndromes the quality of chest pain is described as "tightness," or "pressure."

Front 478

What is the clinical presentation of inferoposterior myocardial ischemia?

Back 478

Nausea and vomiting are sometimes the main symptoms in inferoposterior wall ischemia. In inferoposterior wall ischemia, vagal reflexes may cause bradycardia and hypotension.

Front 479

What are the characteristics of pain that is less likely to be caused by ischemia?

Back 479

"Sharp" chest pain that the patient can pinpoint is not likely caused by ischemia, especially if pain is reproduced by position or palpation. Diaphoresis, tachypnea, anxiety indicate a life-threatening process.

Front 480

What is the usual amount of time that myocardial infarction pain is present?

Back 480

Myocardial infarction lasts more than 20-30 minutes.

Front 481

What etiology is suggested if pain is relieved by nitroglycerine?

Back 481

Relief of chest pain with nitroglycerin indicates ischemia or esophageal spasm. Chest pain that worsens with nitroglycerin occurs with gastroesophageal reflux disease.

Front 482

What is the presentation of acute coronary syndrome in women?

Back 482

Acute coronary syndromes in women present with atypical symptoms: dyspnea, shortness of breath, fatigue.

Front 483

What are the physical examination findings that suggest aortic dissection?

Back 483

Blood pressure a difference between arms of over 20 mm Hg systolic suggests aortic dissection.

Front 484

What etiologies of chest pain are suggested by hypotension?

Back 484

Massive pulmonary embolism or cardiac shock. Fever may suggest pneumonia or esophageal rupture. Corneal lipid rings, narrowed retinal arteries, murmurs; pigment and hair-loss on legs indicate coronary syndrome.

Front 485

What etiology is suggested by wide splitting of the second heart sound?

Back 485

Wide physiologic splitting of the second heart sound (splitting wider with inspiration) can be found in right ventricular infarction.

Front 486

What is the significance of fourth heart sound in patients with chest pain?

Back 486

A new fourth heart sound can occur with angina or infarction. An S3 is may be caused by underlying heart failure.

Front 487

What etiology is suggested by the finding of a murmur of aortic regurgitation in patients with ischemic chest pain?

Back 487

Significant aortic regurgitation occurs in over half of patients with aortic dissection, while mitral regurgitation can occur in patients with angina or infarction and is due to papillary muscle dysfunction.

Front 488

What are the 12-lead ECG signs of an acute myocardial infarction?

Back 488

50% of persons with acute MI will have diagnostic findings (ST elevation or Q waves >0.04 sec), while 35% will have findings consistent with ischemia (ST depression and/or T wave inversion).

Front 489

What is the role of creatine kinase MB isoenzyme in patients with an acute coronary syndrome?

Back 489

CK-MB isoenzyme is cardiac specific and is useful for early diagnosis of MI.

Front 490

At what time after an acute myocardial infarction does the CK-MB become elevated?

Back 490

CK-MB detectable 4-6 hrs after ischemia onset, peaks 12-24 hrs, normalizes 2-3 d; can be used to detect early reinfarction. CK-MB levels are obtained at admission to ED and repeated 6-12 hrs.

Front 491

What are cardiac troponins?

Back 491

Troponins (T, I, C) are in striated and cardiac muscle. T and I are preferred markers for diagnosis of myocardial injury. Troponin T and I have similar sensitivity and specificity for MI.

Front 492

What is the difference between troponin T and I?

Back 492

Unlike troponin I levels, troponin T levels may be elevated in patients with renal disease, polymyositis, or dermatomyositis.

Front 493

What is the significance of an elevated troponin level and a normal CK-MB in a patient with chest pain?

Back 493

Patients with a normal CK-MB level but elevated troponin levels have sustained minor myocardial damage, or microinfarction. Elevations of both CK-MB and troponins is acute MI.

Front 494

How much time is required before cardiac troponins return to normal after an acute myocardial infarction?

Back 494

The cardiac troponins may remain elevated up to two weeks after symptom onset, which makes them useful as late markers of recent acute myocardial infarction.

Front 495

What is the role of the chest x-ray in patients with chest pain?

Back 495

Pneumothorax, pneumomediastinum, effusion, infiltrates. Aortic dissection can cause widening of mediastinum. Loss of lung volume or unilateral loss of vascular markings suggest PE.

Front 496

What are the symptoms of aortic dissection?

Back 496

Pain is sharp, tearing, severe; radiates to back; loss of pulses; aortic insufficiency murmur; mediastinum is widened; confirmed by MRI, CT scan, transesophageal echocardiogram, or aortography.

Front 497

What are the symptoms of pulmonary embolism?

Back 497

Dyspnea, tachycardia, hypoxemia; pleuritic pain.

Front 498

How is pulmonary embolism diagnosed?

Back 498

ECG may show an S wave in lead I, Q wave in lead III, or inverted T wave in lead III. Diagnosis is confirmed by spiral chest CT, lung scan, or pulmonary angiogram.

Front 499

What are the symptoms of pericarditis?

Back 499

Pain is sharp, positional, pleuritic, and relieved by leaning forward; preceded by viral illness; pericardial rub.

Front 500

What are the ECG signs of acute pericarditis?

Back 500

Diffuse ST elevation occurs without evolution of Q waves; CK level usually normal.

Front 501

What are the symptoms of myocarditis?

Back 501

Pain is vague and mild if present preceded by viral illness; MB fraction of CK are often elevated; tachycardia, conduction abnormalities and sometimes Q waves occur.

Front 502

What are the musculoskeletal causes of chest pain?

Back 502

Musculoskeletal causes are the most common cause of chest pain. Costochondritis, cervical osteoarthritis, radiculitis; pain is stabbing, localized; pleuritic; reproduced by motion or palpation; ECG changes absent.

Front 503

What are the gastrointestinal causes of chest pain?

Back 503

Esophageal reflux is worse with recumbency or meals; regurgitation; relieved by antacids, nitroglycerin. Ulcers, cholecystitis. Pancreatitis causes abdominal tenderness, with radiation to back, hyperamylasemia.

Front 504

What are the symptoms of pneumothorax?

Back 504

Onset abrupt with sharp pleuritic chest pain and dyspnea; breath sounds are absent, chest x-ray confirms.

Front 505

What are the symptoms of pleuritis?

Back 505

Pain is sharp and increases on inspiration; pleural friction rub; underlying pulmonary infection.

Front 506

What are the major modifiable risk factors for ischemic heart disease?

Back 506

Hypercholesterolemia, smoking hypertension, physical inactivity, obesity, diabetes.

Front 507

What subgroup of hypercholesterolemia is the most important risk factor for ischemic heart disease?

Back 507

LDL cholesterol is single most important subgroup that carries risk for ischemic heart disease. Low HDL cholesterol, hypertriglyceridemia, increased total-to-HDL-cholesterol ratio, and increased lipoprotein A increase risk.

Front 508

What is the risk of myocardial infarction in smokers?

Back 508

Cigarette smoker's risk of heart attack is more than twice that of a nonsmoker. The risk for myocardial infarction in patients who quit smoking is reduced to that of nonsmokers within two years of cessation.

Front 509

What degree of hypertension is a risk factor for cardiovascular events?

Back 509

Risk for cardiovascular events increases at BP above 110/75 mm Hg. HTN is a risk factor for myocardial ischemia, stroke, kidney failure, and heart failure.

Front 510

What percentage of patients with diabetes die of cardiovascular disease?

Back 510

Almost 75% of patients with diabetes die of some form of cardiovascular disease. Elevated blood glucose levels and insulin resistance are associated with ischemic heart disease and overall cardiovascular events.

Front 511

What are the clinical signs of stable angina?

Back 511

Substernal pressure lasting 5-15 min; not affected by respiration/position. Stable angina occurs when myocardium becomes ischemic during exercise, hypotension, anemia.

Front 512

What is the most common ECG sign in patients with angina?

Back 512

Most commonly ST segment depression is seen. ST segment elevation typically occurs in variant angina (Prinzmetal angina) where coronary artery spasm is responsible.

Front 513

How is ischemic heart disease diagnosed?

Back 513

The exercise treadmill test is the most useful test in the evaluation of the cause of chronic chest pain when ISCHEMIC HEART DISEASE (stable angina) is a consideration.

Front 514

What is the criteria for a positive exercise stress test for myocardial ischemia?

Back 514

>2 mm ST-segment depressions or hypotension (a drop of more than 10 mm Hg in systolic pressure) occur either alone or in combination.

Front 515

What type of noninvasive test for ischemic heart disease is indicated for patients who are unable to exercise?

Back 515

Patients who are unable to exercise or walk should be considered for chemical stress testing, such as dipyridamole (Persantine) or dobutamine stress tests.

Front 516

What type of noninvasive test for ischemic heart disease is indicated for patients with bundle branch block?

Back 516

Nuclear stress imaging. These tests may also be used in patients who are taking digoxin or beta-blockers. Beta-blockers may blunt the heart rate during exercise.

Front 517

What is a nuclear stress test?

Back 517

Radioactive substance is injected and perfusion of heart tissue is visualized at rest and after exercise. Abnormal amount of thallium in areas of heart that have decreased blood.

Front 518

What are the dobutamine and adenosine stress tests?

Back 518

This test is used in people who are unable to exercise. A drug is given to induce tachycardia.

Front 519

What is a stress echocardiogram?

Back 519

The stress echocardiogram combines a treadmill stress test and an echocardiogram (ECHO). Abnormal movement of the walls of the left ventricle are induced by exercise.

Front 520

What are the indications for cardiac catheterization?

Back 520

Patients with stable angina for (1) diagnosis and (2) prognosis/risk stratification. Angiography is also used after stress test are positive to identify patients that will benefit form stent or bypass.

Front 521

What is the treatment of ischemic heart disease?

Back 521

Nitroglycerin SL alleviates pain. Long-acting nitrates, beta blockers. Aspirin and statins. All patients with stable angina need cardiac angiography or stress testing.

Front 522

What are the target goals for treatment of hyperlipidemic patients with coronary artery disease?

Back 522

LDL less than 100 mg/dL. HDL 40 mg/dL or greater. Triglycerides less than 150 mg/dL.

Front 523

What is the optimal LDL-cholesterol goal for patients at very high risk of coronary artery disease?

Back 523

<70 mg/dL for very high risk with cardiovascular disease plus diabetes, smoking, HTN; metabolic syndrome (triglycerides >200, HDL <40); and patients with ACS. Statin therapy regardless of levels.

Front 524

What are the indications for coronary bypass graft in ischemic heart disease?

Back 524

Left main coronary disease or three vessel disease and left ventricular (LV) dysfunction. More efficacious in diabetes. More beneficial in low ejection fraction.

Front 525

What are the types of acute coronary syndromes?

Back 525

Acute coronary syndromes (ACS) include a range of thrombotic coronary diseases, including unstable angina (UA), non-ST elevation myocardial infarction, and STEMI.

Front 526

What is a non ST-segment elevation myocardial infarction?

Back 526

Ischemia causes damage detectable by troponin I, troponin T, or CK-MB. If there are no detectable serum markers after 24 h, the patient has UA. UA and NSTEMI may be indistinguishable.

Front 527

What are the indications for thrombotic therapy in patients with acute coronary syndrome?

Back 527

Thrombolytic therapy is beneficial for ST elevation MI (STEMI), but is not effective in UA or NSTEMI because the infarct-related artery is not occluded.

Front 528

What is unstable angina?

Back 528

Angina of increasing severity, frequency, duration; angina with increasing resistance to nitrates; or angina occurring at rest or new-onset angina. Untreated unstable angina progresses to MI in 50% of cases.

Front 529

What are the ECG findings in non-segment elevation MI?

Back 529

Dynamic ST-segment depression (>5 mm), or new T-wave inversion ( 2 mm), but the ECG may be normal or show minor changes.

Front 530

What are the high-risk features for patients with UA/NSTEMI?

Back 530

Repetitive or prolonged chest pain (>10 min), elevated markers, persistent ST depression >0.5 mm or new T-wave inversion, SBP <90, VT; syncope, ejection fraction <40%, prior PTCA or CABG, diabetes, kidney disease.

Front 531

What is the general management of NSTEMI?

Back 531

Aspirin is recommended in all patients unless contraindicated. High-risk patients should be treated with aggressive medical management and arrangements should be made for coronary angiography.

Front 532

What are the drugs that are used in NSTEMI?

Back 532

Aspirin, clopidogrel, heparin, tirofiban, metoprolol, nitroglycerine.

Front 533

What antiplatelet therapy should be given to patients with NSTEMI?

Back 533

Aspirin and clopidogrel. Clopidogrel should be avoided if likely to require bypass surgery (severe ST-segment depression, SBP <90). Clopidogrel should be given before percutaneous coronary intervention.

Front 534

What are the indications for anticoagulants in NSTEMI?

Back 534

Unfractionated heparin or subcutaneous enoxaparin should be given until angiography or for 48-72 hours. Enoxaparin dose must be reduced in patients with impaired renal function.

Front 535

What is the mechanism of the glycoprotein (GP) Hb/IIIa inhibitors?

Back 535

Inhibit platelet function by blocking a receptor involved in platelet aggregation, providing a more comprehensive platelet blockade than the combination of aspirin and heparin.

Front 536

What is the indication for tirofiban or eptifibatide in NSTEMI?

Back 536

High-risk patients in whom an invasive strategy is planned. Tirofiban is particularly beneficial and recommended in patients with diabetes. Complications are bleeding and thrombocytopenia.

Front 537

What are the indications for a beta-blocker in patients with NSTEMI?

Back 537

A beta-blocker should be given unless contraindicated. Intravenous nitroglycerin is given for refractory pain.

Front 538

Which patients with NSTEMI should receive invasive management?

Back 538

Early angiography (48 h) and revascularization is recommended in NSTEMI with high-risk features. Refractory ischemia, and high-risk features on early exercise testing need early invasive.

Front 539

What are the clinical signs of ST elevation myocardial infarction?

Back 539

Substernal, diffuse, pressure pain. Radiation neck, jaw, shoulders, arms. Lightheadedness, nausea, vomiting, diaphoresis, dyspnea. Pain lasts longer than 20 min, does not respond completely to nitroglycerin.

Front 540

What are the signs of STEMI in elderly and diabetic patients?

Back 540

Elderly and diabetic patients are prone to atypical symptoms, such as nausea or dyspnea. 20% of MI are "silent".

Front 541

What are the physical signs of ST elevation myocardial infarction?

Back 541

Bradycardia in inferior MI. Tachycardia with large MI. BP elevated. Left ventricular failure, valve dysfunction. S4 of stiffened ventricle. Mitral regurgitation if papillary muscle malfunction. S2 paradoxical split as LV contraction time increases due to

Front 542

What are the ECG criteria for STEMI?

Back 542

Persistent ST-segment elevation of >1 mm in two contiguous limb leads. ST-segment elevation of >2 mm in two contiguous chest leads. New LBBB. Initially, markers are not elevated in STEMI (eventually positive).

Front 543

What is the initial nonspecific management of acute coronary syndrome?

Back 543

Initial nonspecific management for all patients with possible MI (chest pain) is oxygen therapy, aspirin (unless contraindicated), nitroglycerin and morphine.

Front 544

What is the management of STEMI in patients who present within 12 hours of the onset of ischemic symptoms?

Back 544

Completely occluded coronary artery with thrombus at the site of a ruptured plaque. Reperfusion strategy with fibrinolytic therapy or percutaneous coronary intervention.

Front 545

Which ECG leads have ST elevation in an inferior myocardial infarction?

Back 545

II, III, aVF

Front 546

Which coronary artery is occluded in an inferior myocardial infarction?

Back 546

Right coronary.

Front 547

Which ECG leads have ST elevation in an anteroseptal myocardial infarction?

Back 547

V1-V3

Front 548

Which coronary artery is occluded in an anteroseptal myocardial infarction?

Back 548

Left anterior descending

Front 549

Which ECG leads have ST elevation in an anterior myocardial infarction?

Back 549

V2-V4

Front 550

Which coronary artery is occluded in an anterior myocardial infarction?

Back 550

Left anterior descending artery.

Front 551

Which ECG leads have ST elevation in a lateral myocardial infarction?

Back 551

I, aVL, V4, V5, and V6

Front 552

Which coronary artery is occluded in an anterior myocardial infarction?

Back 552

Left anterior descending or circumflex artery.

Front 553

Which ECG leads have ST elevation in a posterior MI?

Back 553

V1-V2: Tall broad initial R wave, ST depression, tall upright T wave; usually occurs in association with inferior or lateral MI.

Front 554

Which coronary artery is occluded in a posterior myocardial infarction?

Back 554

Posterior descending

Front 555

What is the time of onset of hyperacute T waves (tall, peaked T waves) after a myocardial infarction?

Back 555

Immediately. Disappear in 6-24 hours.

Front 556

What is the time of onset of ST-segment elevations after a myocardial infarction?

Back 556

Immediately

Front 557

At what time do ST-segment elevations disappear after a myocardial infarction?

Back 557

1-6 weeks

Front 558

What is the time of onset of Q waves longer than 0.04 seconds after a myocardial infarction?

Back 558

One to several days. 0.04 seconds is one small ECG box.

Front 559

At what time do Q waves longer than 0.04 seconds disappear after a myocardial infarction?

Back 559

Years to never

Front 560

What is the time of onset of T wave inversions after a myocardial infarction?

Back 560

6-24 hours

Front 561

At what time do T wave inversions disappear after a myocardial infarction?

Back 561

Disappear months to years later.

Front 562

What is the best emergent reperfusion therapy?

Back 562

PCI is the best available treatment because of improved short-term and long-term reduction of deaths and MI in patients with STEMI presenting within 12 hours when compared with thrombolytic therapy.

Front 563

What are the indications for thrombolytics?

Back 563

tPA is the most common agent used in the US. Thrombolytic agent is an alternative to primary PCI in suitable candidates with: ST-elevation MI (>1 mm ST elevation in two contiguous leads). New LBBB

Front 564

What are the contraindications to thrombolytic therapy?

Back 564

Active bleeding or bleeding diathesis, head or facial trauma within 3 months, suspected aortic dissection, prior intracranial hemorrhage, ischemic stroke within 3 months.

Front 565

What are the relative contraindications to thrombolytic therapy?

Back 565

Recent major surgery (<3 weeks); traumatic or prolonged cardiopulmonary resuscitation; recent internal bleeding; active peptic ulcer. Severe, poorly controlled HTN. Ischemic stroke.

Front 566

What are the indications for antiplatelet agents in STEMI?

Back 566

Aspirin (300 mg) should be given to all STEMI; 75 mg/d long term. Clopidogrel (300-600 mg loading) in addition to aspirin if undergoing PCI. If fibrinolytic therapy, clopidogrel given in addition to ASA. If CABG planned, clopidogrel withheld.

Front 567

What are the indications for antithrombin in STEMI?

Back 567

With PCI: Antithrombin therapy should be used in conjunction with PCI. Enoxaparin in acute STEMI in conjunction with PCI is effective.

Front 568

What are the indications for enoxaparin with fibrinolysis?

Back 568

Enoxaparin may be used in conjunction with fibrin-specific fibrinolytic agents in patients under the age of 75 years if there is no significant renal dysfunction.

Front 569

What are the indications for glycoprotein IIb/IIIa inhibitors in STEMI?

Back 569

Use abciximab with primary PCI in patients with STEMI.

Front 570

What are the recommended discharge medications after ACS?

Back 570

Aspirin, clopidogrel, beta-blocker, statin, nitrates.

Front 571

What discharge antiplatelet therapy should be given to patients after ACS?

Back 571

Aspirin: All patients should take 75-325 mg daily unless contraindicated. Clopidogrel should be prescribed for up to 9-12 months after ACS, particularly after stent placement.

Front 572

What are the indications for a beta-blocker after ACS?

Back 572

Beta-blocker should be prescribed for all patients after an ACS unless contraindicated, and continued indefinitely. Metoprolol and carvedilol should be used in patients after ACS who have heart failure.

Front 573

What are the indications for ACE inhibitors after ACS?

Back 573

ACE inhibitors should be given in patients with ACS in congestive heart failure, left ventricular dysfunction (ejection fraction 40%).

Front 574

What are the indications for statin therapy after ACS?

Back 574

Statin therapy should be initiated in the hospital in all patients with ACS.

Front 575

What are the indications for nitrates after ACS?

Back 575

All patients should be prescribed short-acting nitrates. Long-acting nitrates (isosorbide) are given if there is continuous and frequent chest pain.

Front 576

What are the indications for warfarin after ACS?

Back 576

Warfarin is recommended after ACS only for those at high risk of systemic thromboembolism because of atrial fibrillation, mural thrombus, or congestive heart failure.

Front 577

What are the recommendations for exercise ECG testing after ACS?

Back 577

Submaximal testing 4-7 days after infarction. A maximal test can be performed at 3-6 weeks postinfarction. Myocardial perfusion imaging can be performed before hospital discharge to assess residual ischemia.

Front 578

What are the complications of ACS?

Back 578

Pump dysfunction, ischemia, pericarditis (Dressler syndrome), thromboembolism, sudden cardiac death due to arrhythmia (most commonly ventricular fibrillation). Ventricular tachycardia.

Front 579

What is right ventricular infarction?

Back 579

Accompanies 30% of inferior MIs. It is diagnosed with right side leads and treated with fluids.

Front 580

What is Prinzmetal angina?

Back 580

Uncommon condition: episodes of angina are triggered when a coronary artery goes into spasm with ST-segment elevation. May cause acute MI, ventricular arrhythmias, sudden death.

Front 581

What is the treatment of Prinzmetal angina?

Back 581

Calcium channel blockers or nitrates.

Front 582

81-year-old with HTN, dyslipidemia dyspnea, edema. Jugular venous distention 8 cm, S3 gallop, apical impulse displaced. Cardiomegaly. Dilated left ventricle with an EJECTION FRACTION 30%. Diagnosis?

Back 582

Congestive heart failure

Front 583

What is systolic heart failure?

Back 583

Systolic dysfunction is caused by a loss of contractile strength of the myocardium with ventricular dilatation. Ischemic cardiomyopathy and dilated cardiomyopathy.

Front 584

What is diastolic heart failure?

Back 584

Filling of one or both ventricles is impaired while the emptying capacity is normal (the ejection fraction is normal). Infiltrative cardiomyopathies (amyloidosis).

Front 585

What are the causes of decompensated heart failure?

Back 585

Exacerbation of HF can be caused by nonadherence to medication, increase in dietary salt, acute ischemia, tachycardia or pulmonary infection, arrhythmias, hypertension, thyrotoxicosis, and anemia.

Front 586

What are the causes of congestive heart failure?

Back 586

Ischemic heart disease causes 70%. Other:: hypertensive heart disease, cardiomyopathies (idiopathic, alcohol), valvular, congenital. With exacerbation of HF, always check troponin to exclude myocardial infarction.

Front 587

What are the symptoms of left ventricular heart failure?

Back 587

Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, and weakness.

Front 588

What is the New York Heart Association Functional Classification of heart failure?

Back 588

Class I: no limitation. Class II: slight, mild limitation of activity. Class III: marked limitation. Class IV: confined to bed or chair.

Front 589

What is the best test to confirm the diagnosis of heart failure?

Back 589

Echocardiography is the test-of-choice for diagnosis and to classify the type (systolic vs. diastolic). Echocardiography measures ejection fraction.

Front 590

What are the chest x-ray findings in congestive heart failure?

Back 590

The chest x-ray may show cardiomegaly, vascular redistribution, Kerley B-lines, and interstitial edema.

Front 591

What are the ECG findings in congestive heart failure?

Back 591

Electrocardiogram identifies ventricular hypertrophy, ischemic heart disease, arrhythmias or conduction delays which may cause HF.

Front 592

What is B-type natriuretic peptide?

Back 592

BNP is a polypeptide secreted by the heart in response to excessive stretching of the myocytes. The BNP is elevated (97% sensitivity) in decompensated HF.

Front 593

What are the beneficial effects of ACE inhibitors in congestive heart failure?

Back 593

ACE reduce preload and afterload through vasodilation, reducing right atrial, pulmonary arterial, pulmonary capillary wedge pressures. Angiotensin receptor blockers if unable to tolerate ACEI (cough).

Front 594

What are the side effects of captopril?

Back 594

Rash, nonproductive cough, proteinuria, renal failure, taste disturbance, agranulocytosis, hypotension

Front 595

What are the side effects of enalapril?

Back 595

Hypotension, angioedema, renal failure, laryngeal edema, cough.

Front 596

What are the side effects of lisinopril?

Back 596

Hypotension, proteinuria, renal insufficiency, rash, cough.

Front 597

What are the side effects of nitroprusside?

Back 597

Thiocyanate toxicity, methemoglobinemia.

Front 598

What are the side effects of nitroglycerin?

Back 598

Headache, postural hypotension, methemoglobinemia.

Front 599

What are the side effects of isosorbide dinitrate?

Back 599

Headache, postural hypotension

Front 600

What are the side effects of hydralazine?

Back 600

Headache, positive ANA, SLE-like syndrome (10-20%) drug fever, rash.

Front 601

What is the treatment of congestive symptoms in heart failure?

Back 601

Loop diuretics. Furosemide is most commonly used. Spironolactone and eplerenone (aldosterone antagonists) are used as add-on therapy to ACE inhibitors in severe heart failure.

Front 602

What is the mechanism of action of thiazides?

Back 602

Inhibits NaCl cotransport; used mostly for treatment of hypertension; hydrochlorothiazide, chlorothiazide

Front 603

What are the side effects of thiazides?

Back 603

HypoNa, hypoK, hyperlipidemia, hyperCa, metabolic alkalosis, hyperuricemia, reduced GFR, allergy, thrombocytopenia, agranulocytosis, leukopenia, anemia, pancreatitis, sexual dys, glucose intolerance.

Front 604

What are the side effects of indapamide?

Back 604

Hypokalemia and lipid abnormalities are less common than with other thiazides. Hyponatremia, hypercalcemia, metabolic alkalosis, hyperuricemia, reduced glomerular filtration rate, allergy.

Front 605

What are the side effects of phthalimidine derivatives?

Back 605

Similar to thiazides, but hypokalemia may be profound. Chlorthalidone, metolazone.

Front 606

What is the mechanism of action of loop diuretics?

Back 606

Inhibitors of Na/K/Cl cotransport; most commonly used diuretics in heart failure; furosemide, ethacrynic acid, bumetanide.

Front 607

What are the side effects of loop diuretics?

Back 607

Hyponatremia, hypokalemia, hypocalcemia, metabolic alkalosis, hyperuricemia, interstitial nephritis, ototoxicity, thrombocytopenia, agranulocytosis, leukopenia, anemia.

Front 608

What are the side effects of potassium-sparing diuretics?

Back 608

Hyperkalemia, mental confusion, nausea, and gynecomastia (spironolactone only).

Front 609

What is the initial therapy for congestive heart failure?

Back 609

ACE inhibitor and furosemide is considered first line for all HF. Once stable, add on carvedilol or metoprolol. Chronic adrenergic activation is associated with HF.

Front 610

What treatment is recommended for black patients with severe heart failure who have already been treated with the standard therapy?

Back 610

Reduction in death and a decrease in hospitalization occurs with the combination of hydralazine and isosorbide.

Front 611

What is the treatment of severe HF if there is no improvement of the EJECTION FRACTION and/or symptoms on standard therapy (diuretic, ACE inhibitor and beta blocker)?

Back 611

Addition of spironolactone significantly reduces death and hospitalizations.

Front 612

What is the treatment of severe refractory heart failure?

Back 612

Inotropic agents for severe heart failure improves symptoms, quality of life and reduces hospitalizations, but does not improve survival.

Front 613

What is the mechanism of digitalis?

Back 613

Inhibits Na+/K+ - ATPase pump which results in increased intracellular Na+ and decreased intracellular Ca. Increase in intracellular Ca results in improved cardiac contractility.

Front 614

What is the effect of potassium levels on the effect of digitalis?

Back 614

Hyperkalemia will decrease digitalis activity, whereas hypokalemia results in toxicity.

Front 615

What conditions predispose to digitalis toxicity?

Back 615

Renal insufficiency, hypokalemia, hypercalcemia, hypomagnesemia, advanced age, sinoatrial and atrioventricular block; hypothyroidism, hypoxic states, pulmonary disease; multiple drug therapy.

Front 616

What drug interaction occurs with digoxin and quinidine?

Back 616

Decreases renal clearance of digoxin.

Front 617

What drug interaction occurs with digoxin and verapamil/diltiazem?

Back 617

Decreases renal clearance of digoxin.

Front 618

What drug interaction occurs with digoxin and cholestyramine/colestipol?

Back 618

Binds digoxin in gastrointestinal tract; interferes with enterohepatic circulation.

Front 619

What drug interaction occurs with digoxin and spironolactone?

Back 619

Inhibits tubular secretion of digoxin.

Front 620

What drug interaction occurs with digoxin and thiazides/furosemide?

Back 620

Diuretic-induced hypokalemia and/or bumetanide. Hypomagnesemia potentiates digitalis action.

Front 621

What are the side effects of digoxin?

Back 621

Nausea, vomiting, gynecomastia, blurred vision; yellow halo around objects; paroxysmal atrial tachycardia with block, PVCs, and bradycardia.

Front 622

What is the treatment for digoxin toxicity?

Back 622

Stop the drug. K+ administration if needed. Lidocaine and phenytoin. Digibind only for acute overdose.

Front 623

What is the treatment of severe heart failure that does not respond to standard therapy?

Back 623

Sympathomimetic amines (dopamine, dobutamine) and phosphodiesterase inhibitors (amrinone, milrinone) IV infusion. Other options: pacing, implantable defibrillator, heart transplantation.

Front 624

What is the treatment of diastolic heart failure?

Back 624

Diastolic HF may worsen when diuretics and vasodilators. Reducing the heart rate with beta blockers and calcium channel blockers (verapamil, diltiazem) to allow adequate diastolic filling.

Front 625

What are the signs of pulmonary edema?

Back 625

Increased respiratory rate, nocturnal dyspnea, cough with expectoration of pink frothy sputum, cyanosis, crackles, rhonchi, wheezing.

Front 626

What are the chest x-ray findings in pulmonary edema?

Back 626

Prominent pulmonary vasculature, enlarged cardiac silhouette, Kerley B lines, effusions.

Front 627

What is the treatment of pulmonary edema?

Back 627

Morphine sulfate. Furosemide reduces preload. Nitroglycerin reduces preload. Digoxin if atrial fibrillation. Intravenous ACE inhibitors.

Front 628

What is mitral stenosis?

Back 628

Thickened valve leaflets impede left ventricular filling; increased left atrial pressure causes pulmonary congestion; cardiac output reduced, secondary pulmonary vasoconstriction and RV failure occurs

Front 629

What is the most common lesion caused by rheumatic fever?

Back 629

Mitral stenosis is the most common lesion caused by rheumatic fever. Rarely congenital.

Front 630

What are the early clinical signs of mitral stenosis?

Back 630

Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, wasting, hemoptysis (rupture of pulmonary vessels); systemic embolism from stasis of blood in an enlarged left atrium

Front 631

What are the late clinical signs of severe mitral stenosis?

Back 631

Hoarseness due to impingement of an enlarged left atrium on recurrent laryngeal nerve; right-sided heart failure; hepatomegaly, ascites; peripheral edema.

Front 632

What are the physical signs of mitral stenosis?

Back 632

Atrial fibrillation (irregular rhythm); pulmonary rales; decreased pulse pressure; loud S1, opening snap following S2, diastolic rumble, sternal lift (right ventricular enlargement).

Front 633

What are the ECG findings in mitral stenosis?

Back 633

Right ventricular hypertrophy; left and right atrial enlargement; atrial fibrillation may occur.

Front 634

What are the chest x-ray findings in mitral stenosis?

Back 634

Large left atrium (double-density right heart border, straightening of the left heart border). Signs of pulmonary hypertension, including Kerley B lines and increased vascular markings. Large pulmonary artery.

Front 635

What is the treatment of mitral stenosis?

Back 635

Diuretics and salt-restricted diet; digitalis, anticoagulants if atrial fibrillation; when symptomatic: mitral commissurotomy or valve replacement.

Front 636

What are the hemodynamic findings in mitral regurgitation?

Back 636

LV stroke volume is pumped backward into LA, resulting in decreased CO. Volume overload, increased preload. LV failure causes dyspnea, orthopnea, paroxysmal nocturnal dyspnea. Pulmonary HTN.

Front 637

What are the acute causes of mitral regurgitation?

Back 637

Rupture chordae tendineae; papillary muscle rupture; endocarditis, trauma.

Front 638

What are the chronic causes of mitral regurgitation?

Back 638

Rheumatic heart disease, papillary muscle dysfunction, mitral prolapse/calcification, endocarditis; HCM; endocardial cushion defect, corrected transposition; endocardial fibroelastosis; LV dilatation.

Front 639

What are the physical signs of mitral regurgitation?

Back 639

Hyperdynamic and downward left ventricular impulse. Holosystolic apical murmur radiating to the axilla with a thrill (palpable turbulence). S3 with a soft S1 and widely split S2. Distended neck veins.

Front 640

What are the ECG signs of mitral regurgitation?

Back 640

Left ventricular hypertrophy and left atrial enlargement. Chest x-ray: cardiac enlargement vascular congestion.

Front 641

What is the treatment of mitral regurgitation?

Back 641

Digitalis, diuretics, arteriolar vasodilators (ACE inhibitors), warfarin; mitral valve replacement when symptoms.

Front 642

What is mitral valve prolapse?

Back 642

Most common congenital valvular abnormality; also in young women with connective tissue disease (e.g., Marfan or idiopathic).

Front 643

What is the presentation of mitral valve prolapse?

Back 643

Asymptomatic. Lightheadedness, palpitations, syncope, chest pain. Arrhythmias. Mid-to-late systolic click, late systolic murmur at apex which worsens with Valsalva; improves with squatting.

Front 644

What are the complications of mitral valve prolapse?

Back 644

Serious arrhythmias, sudden death, congestive heart failure, bacterial endocarditis, calcifications, transient cerebral ischemic attacks, mitral regurgitation.

Front 645

What is the treatment of mitral valve prolapse?

Back 645

Endocarditis prophylaxis only in severe cases. Beta-blocker for chest pain. Mitral valve replacement is rarely necessary.

Front 646

What is aortic stenosis?

Back 646

Calcification and degeneration; more common in elderly. Calcification and fibrosis of a congenitally bicuspid aortic valve. Rheumatic valvular disease.

Front 647

What is the pathophysiology of aortic stenosis?

Back 647

Elevation LV systolic pressure and LV hypertrophy. Noncompliant left ventricle causes a prominent S4 gallop. LV diastolic pressure increases; pulmonary congestion.

Front 648

What are the clinical signs of aortic stenosis?

Back 648

Angina, syncope, dyspnea. Pulsus tardus et parvus (carotid pulse weak, late), carotid thrill. Systolic ejection murmur aortic area; harsh, S4 gallop; A2 decreased, S2 single or paradoxically split; aortic ejection click.

Front 649

What are the ECG signs of aortic stenosis?

Back 649

Left ventricular hypertrophy. Chest x-ray: calcification, cardiomegaly, pulmonary congestion.

Front 650

What is the treatment of aortic stenosis?

Back 650

Endocarditis prophylaxis is not recommended. Valve replacement when the valve area is reduced below 0.8 cm or symptoms. Balloon valvuloplasty if too ill to tolerate surgery.

Front 651

What is aortic valve sclerosis of the elderly?

Back 651

Systolic murmur may mimic aortic stenosis. Systolic murmur ends early and does not peak late. Carotids do not have delayed upstrokes. No left ventricular hypertrophy by ECG. There is no stenosis on echo.

Front 652

What are the clinical signs of hypertrophic obstructive cardiomyopathy?

Back 652

Brisk bifid carotid. Systolic crescendo-decrescendo-murmur at left sternal border, which does not radiate to neck. Murmur increases with Valsalva (all other murmurs decrease). Pseudoinfarct (large septal Q).

Front 653

What are the clinical sings of mitral regurgitation?

Back 653

Murmur is holosystolic and radiates to axilla and not carotids. Carotid upstroke is normal; dilated left ventricle.

Front 654

What are the clinical signs of pulmonic stenosis?

Back 654

Murmur does not radiate into neck; loudest along the left sternal border; increases with inspiration.

Front 655

What are the causes of aortic regurgitation?

Back 655

Hypertension is the most common cause; infectious endocarditis, syphilis, ankylosing spondylitis; Marfan syndrome, rheumatic fever, aortic dissection, aortic trauma.

Front 656

What is the pathophysiology of aortic regurgitation?

Back 656

Aortic regurgitation results in a volume overload of the left ventricle.

Front 657

What are the clinical signs of aortic regurgitation?

Back 657

Dyspnea is most common. Diastolic decrescendo murmur. Systolic flow murmur. S3 in left ventricular failure, Austin-Flint murmur: low pitched, late diastolic apex murmur

Front 658

How is aortic regurgitation diagnosed?

Back 658

ECG: LV hypertrophy; chest x-ray: LV and aortic dilation; echocardiogram

Front 659

What is the treatment of aortic regurgitation?

Back 659

Endocarditis prophylaxis is not recommended. Salt restriction, diuretics, ACE inhibitors. Aortic valve replacement when symptoms worsen.

Front 660

What is hypertrophic obstructive cardiomyopathy?

Back 660

Marked hypertrophy of left ventricle; usually disproportionate hypertrophy of septum

Front 661

What is restrictive cardiomyopathy?

Back 661

Reduced ventricular compliance; usually caused by infiltration of myocardium (by amyloid, hemosiderin, or glycogen deposits).

Front 662

What is obliterative cardiomyopathy?

Back 662

Thickened endocardium or mural thrombi, or both, act as space-occupying lesions and reduce left ventricular filling.

Front 663

What is dilated cardiomyopathy?

Back 663

Characterized by diminished myocardial contractility, usually involving both ventricles; most common cause for heart transplants.

Front 664

What are the causes of dilated cardiomyopathy?

Back 664

Idiopathic, alcoholic, peripartum; viruses, parasites, mycobacteria, Rickettsiae; toxins (cobalt, lead, arsenic); doxorubicin cyclophosphamide, vincristine. Hypophosphatemia, hypoK, hypoCa, uremia.

Front 665

What are the clinical signs of dilated cardiomyopathy?

Back 665

Symptoms of left and right ventricular failure: dyspnea, orthopnea; peripheral edema.

Front 666

What are the x-ray signs of dilated cardiomyopathy?

Back 666

Cardiomegaly with pulmonary congestion. ECG: sinus tachycardia, arrhythmias, conduction disturbances.

Front 667

What is the cause of hypertrophic obstructive cardiomyopathy?

Back 667

Hypertrophic cardiomyopathy can develop sporadically; it is hereditary in 60%; autosomal dominant.

Front 668

What is the pathophysiology of hypertrophic obstructive cardiomyopathy?

Back 668

Thickening of interventricular septum. LV compliance reduced. Heart is hypercontractile. EJECTION FRACTION 80% (normal is 60%). Obstruction worsened by increased contractility.

Front 669

What is the effect of digitalis glycosides on hypertrophic obstructive cardiomyopathy?

Back 669

Increase obstruction because of increased contractility.

Front 670

What is the effect of beta-adrenergic stimulation (eg, isoproterenol, epinephrine) on hypertrophic obstructive cardiomyopathy?

Back 670

Increase obstruction because of increased contractility.

Front 671

What is the effect of premature beats on hypertrophic obstructive cardiomyopathy?

Back 671

Increase obstruction because of increased contractility.

Front 672

What is the effect of Valsalva maneuver on hypertrophic obstructive cardiomyopathy?

Back 672

Increase obstruction because of decreased preload.

Front 673

What is the effect of decrease in intravascular volume (eg, hemorrhage, diuresis, gastrointestinal losses) on hypertrophic obstructive cardiomyopathy?

Back 673

Increase obstruction because of decreased preload.

Front 674

What is the effect of standing on hypertrophic obstructive cardiomyopathy?

Back 674

Increase obstruction because of decreased preload.

Front 675

What is the effect of nitroglycerin on hypertrophic obstructive cardiomyopathy?

Back 675

Increase obstruction because of decreased preload.

Front 676

What is the effect of vasodilator drugs on hypertrophic obstructive cardiomyopathy?

Back 676

Increase obstruction because of decreased preload.

Front 677

What is the effect of tachycardia on hypertrophic obstructive cardiomyopathy?

Back 677

Increase obstruction because of decreased preload and increased contractility.

Front 678

What is the effect of hypovolemia on hypertrophic obstructive cardiomyopathy?

Back 678

Increase obstruction because of decreased afterload.

Front 679

What is the effect of nitroglycerin and related drugs on hypertrophic obstructive cardiomyopathy?

Back 679

Increase obstruction because of decreased afterload.

Front 680

What is the effect of vasodilator drugs on hypertrophic obstructive cardiomyopathy?

Back 680

Increase obstruction because of decreased afterload.

Front 681

What is the effect of beta-adrenergic blockade (eg, propranolol) on hypertrophic obstructive cardiomyopathy?

Back 681

Decreased obstruction because of decreased contractility.

Front 682

What is the effect of heavy sedation and general anesthesia on hypertrophic obstructive cardiomyopathy?

Back 682

Decreased obstruction because of decreased contractility.

Front 683

What is the effect of calcium channel blockers, disopyramide, and other drugs that depress myocardial function on hypertrophic obstructive cardiomyopathy?

Back 683

Decreased obstruction because of decreased contractility.

Front 684

What is the effect of intravascular volume expansion on hypertrophic obstructive cardiomyopathy?

Back 684

Decreased obstruction because of increased preload.

Front 685

What is the effect of squatting on hypertrophic obstructive cardiomyopathy?

Back 685

Decreased obstruction because of increased preload.

Front 686

What is the effect of bradycardia on hypertrophic obstructive cardiomyopathy?

Back 686

Decreased obstruction because of increased preload.

Front 687

What is the effect of beta-adrenergic blockade on hypertrophic obstructive cardiomyopathy?

Back 687

Decreased obstruction because of increased preload.

Front 688

What is the effect of intravascular volume expansion on hypertrophic obstructive cardiomyopathy?

Back 688

Decreased obstruction because of increased afterload.

Front 689

What is the effect of squatting on hypertrophic obstructive cardiomyopathy?

Back 689

Decreased obstruction because of increased afterload.

Front 690

What is the effect of alpha-adrenergic stimulation (e.g., phenylephrine, mephentermine) on hypertrophic obstructive cardiomyopathy?

Back 690

Decreased obstruction because of increased afterload.

Front 691

What is the effect of handgrip exercise on hypertrophic obstructive cardiomyopathy?

Back 691

Decreased obstruction because of increased afterload.

Front 692

What are the symptoms of hypertrophic obstructive cardiomyopathy?

Back 692

Dyspnea, angina, presyncope, syncope, and palpitations.

Front 693

What are the physical signs of hypertrophic obstructive cardiomyopathy?

Back 693

Large jugular A wave, bifid carotid pulse, palpable S4 gallop, systolic murmur and thrill, mitral regurgitation murmur; sudden death.

Front 694

What are the ECG signs of hypertrophic obstructive cardiomyopathy?

Back 694

Left ventricular hypertrophy, pseudo Q waves (V1-V3), ventricular arrhythmias.

Front 695

What is the treatment of hypertrophic obstructive cardiomyopathy?

Back 695

Beta-blockers, calcium channel blockers, surgery.

Front 696

What is restrictive cardiomyopathy?

Back 696

Least common cause of cardiomyopathy; rigid noncompliant ventricular walls.

Front 697

What are the causes of restrictive cardiomyopathy?

Back 697

Sarcoidosis; amyloidosis, hemochromatosis, neoplasia, scleroderma, radiation

Front 698

What is the pathophysiology of restrictive cardiomyopathy?

Back 698

Myocardium is rigid and noncompliant, impeding ventricular filling and raising cardiac filling pressures. Systolic performance reduced.

Front 699

What are the signs of restrictive cardiomyopathy?

Back 699

Dyspnea, exercise intolerance, weakness. Elevated jugular venous pressure, edema, hepatomegaly, ascites, S4 and S3 gallop, Kussmaul sign.

Front 700

What are the x-ray signs of restrictive cardiomyopathy?

Back 700

Mild cardiomegaly, pulmonary congestion. Echocardiogram is diagnostic.

Front 701

What is the treatment of restrictive cardiomyopathy?

Back 701

Heart transplantation; death from congestive heart failure or arrhythmias.

Front 702

What are the causes of acute pericarditis and myopericarditis?

Back 702

Idiopathic, infections (viral), vasculitis (connective tissue disease), disorders of metabolism, neoplasms, trauma, drug reactions.

Front 703

What are the clinical symptoms of acute pericarditis?

Back 703

Chest pain at left of sternum, worsened by lying down, coughing, and deep inspiration, relieved by sitting up and leaning forward.

Front 704

What are the physical signs of acute pericarditis?

Back 704

Scratchy, high-pitched rub that has 1-3 components. The rub is best heard with the diaphragm of the stethoscope as the patient sits forward at forced-end expiration.

Front 705

What are the ECG signs of acute pericarditis?

Back 705

Diffuse ST-segment elevation with upright T waves. The diffuseness of the ST-segment elevation, and absence of Q waves distinguish pericarditis from acute MI.

Front 706

What is the treatment of acute pericarditis?

Back 706

NSAIDs, aspirin, corticosteroids.

Front 707

What are the types of pericardial effusions?

Back 707

Transudates, serosanguineous, blood.

Front 708

What are the causes of transudative pericardial effusions?

Back 708

Transudates occur with congestive heart failure, overhydration, or hypoproteinemia. Exudates occur in the presence of pericardial injury.

Front 709

What are the causes of serosanguineous pericardial effusions?

Back 709

Serosanguineous pericardial fluid is sign in tuberculosis and neoplastic diseases.

Front 710

What are the causes of bloody pericardial effusions?

Back 710

Blood in the pericardial space may occur in aortic aneurysm or aortic dissection, trauma, rupture of the heart in acute MI, and bleeding caused by coagulation defects.

Front 711

How is pericardial effusion diagnosed?

Back 711

Echocardiography. Chest x-ray may show a "water-bottle" cardiac silhouette.

Front 712

What is the treatment of pericardial effusion?

Back 712

Pericardial fluid aspiration.

Front 713

What is cardiac tamponade?

Back 713

A life-threatening condition in which a pericardial effusion compresses the heart.

Front 714

What are the causes of cardiac tamponade?

Back 714

Neoplasia, idiopathic (viral) pericarditis, tuberculosis, suppurative, intrapericardial hemorrhage, central line extravasation, surgery, postpericardiotomy syndrome, uremia, radiation therapy, vasculitis.

Front 715

What are the clinical manifestations of pericardial tamponade?

Back 715

Dyspnea, fatigue, orthopnea. Pulsus paradoxus (decrease in systolic blood more than 10 with inspiration or disappearance pulse with inspiration).

Front 716

What is the triad of pericardial tamponade?

Back 716

Triad of neck vein distension with clear lung, hypotension, and muffled heart sounds.

Front 717

What is the treatment of cardiac tamponade?

Back 717

Pericardiocentesis; subxiphoid surgical drainage.

Front 718

What is constrictive pericarditis?

Back 718

Diffuse thickening of the pericardium caused by inflammation; reduced distensibility of the cardiac chambers. Cardiac output is limited and filling pressures are increased; abnormal diastolic filling.

Front 719

What are the causes of constrictive pericarditis?

Back 719

Idiopathic; following open-heart surgery; thoracic radiation; postviral infection.

Front 720

What are the clinical manifestations of constrictive pericarditis?

Back 720

Dyspnea on exertion, orthopnea; ascites, edema, jaundice, hepatic tenderness, and hepatomegaly (right-side failure). Jugular venous distension that increases with inspiration (Kussmaul sign).

Front 721

How is constrictive pericarditis diagnosed?

Back 721

CT: thickened pericardium; pericardial calcifications in tuberculous constriction. Left ventricular ejection fraction is decreased in restrictive cardiomyopathy, but not in constrictive pericarditis.

Front 722

What is the treatment of constrictive pericarditis?

Back 722

Sodium restriction, diuretics, pericardiectomy.

Front 723

What is sinus bradycardia?

Back 723

Ventricular complexes are normal width, evenly spaced, rate is <60/min.

Front 724

What are the causes of sinus bradycardia?

Back 724

Acute MI, carotid sinus pressure, vomiting, Valsalva maneuver, phenothiazines, digitalis glycosides, beta-adrenergic blocking agents, calcium blockers, marathoners and swimming, hypothyroidism, normal variant.

Front 725

What is the treatment of sinus bradycardia?

Back 725

Atropine if symptoms. Pacemaker.

Front 726

What are the types of atrioventricular block?

Back 726

The three classic clinical types are first-, second-, and third-degree (or complete) atrioventricular block.

Front 727

What is first-degree atrioventricular block?

Back 727

PR interval greater than 0.20 s at a heart rate of 70 beats/min.

Front 728

What are the causes of first-degree heart block?

Back 728

Digitalis; exaggerated vagal tone after tracheal suctioning; ischemia, inflammation (myocarditis, acute rheumatic fever), cardiomyopathies.

Front 729

What are the types of second-degree atrioventricular block?

Back 729

Type I (Mobitz I, Wenckebach) and type II (Mobitz II).

Front 730

What is type I atrioventricular block (Mobitz I, Wenckebach)?

Back 730

There is progressive prolongation of the PR interval until a P wave is blocked and a ventricular beat is dropped. The PR interval of the next conducted beat is shorter than the preceding PR interval.

Front 731

What is type II (Mobitz II) atrioventricular block?

Back 731

An intermittent blocked beat occurs suddenly and is not preceded by a change in the duration of the PR interval.

Front 732

What is the site of the block in type I second-degree atrioventricular block?

Back 732

Usually AV nodal (supra-Hisian)

Front 733

What is the site of the block in type II second degree atrioventricular block?

Back 733

Infranodal (infra- or infra-Hisian).

Front 734

What are the causes of type I second degree atrioventricular block?

Back 734

Degenerative changes in AV node; diaphragmatic myocardial infarct; digitalis toxicity; myocarditis; rheumatic fever; increased vagal tone.

Front 735

What are the causes of type II second degree AV block?

Back 735

Extensive anterior myocardial infarct; degenerative changes in His-Purkinje system; calcification of mitral or aortic valve annulus.

Front 736

What are the ECG findings in type I second degree AV block?

Back 736

PR interval lengthens progressively until ventricular beat dropped. PR shortens after dropped beat. RR narrows progressively up to the dropped beat. RR after blocked beat is < twice the RR interval of conducted beats.

Front 737

What are the ECG findings in type II second degree AV block?

Back 737

PR interval is normal duration and constant length; blocked beats occur suddenly without progressive lengthening of PR. RR interval of conducted beats is constant or a multiple of a basic RR interval.

Front 738

What is third-degree atrioventricular block?

Back 738

In 3rd degree block, all atrial beats are blocked, and ventricles are driven by an escape focus.

Front 739

What are the most common causes of 3rd degree atrioventricular block?

Back 739

Most common is fibrous degeneration of conduction system from aging; inferior/ posterior infarction; infection, inflammation, digitalis, ankylosing spondylitis, Adams-Stokes, heart failure.

Front 740

What are Adams-Stoke attacks?

Back 740

Sudden asystole or transient ventricular tachycardia or ventricular fibrillation.

Front 741

What is the treatment of third degree AV block?

Back 741

Pacing.

Front 742

What is sinus tachycardia?

Back 742

Rhythm with a rate >100. Ventricular complexes are normal width, evenly spaced, normal P precedes a QRS. Caused by fever, hypotension, volume depletion, anxiety, pain. Thyrotoxicosis, anemia, beta-agonists.

Front 743

What is paroxysmal supraventricular tachycardia?

Back 743

Group of ectopic tachyarrhythmias that are characterized by sudden onset and abrupt termination. Includes paroxysmal atrial tachycardia. 80% are caused by re-entry, mainly in the AV node.

Front 744

What are the ECG signs of paroxysmal supraventricular tachycardia?

Back 744

Paroxysmal supraventricular tachycardia has an absolutely regular rhythm at a rate between 130 and 220 beats/min. P-wave is abnormal.

Front 745

What is the treatment of paroxysmal supraventricular tachycardia?

Back 745

Right side carotid sinus massage to increase vagal tone; adenosine is effective in more than 90%. IV propranolol, esmolol, digitalis; synchronized external cardioversion if patient is unstable.

Front 746

What are the ECG signs of multifocal atrial tachycardia?

Back 746

Irregular supraventricular rhythm rate 100-200. At least 3 different P wave morphologies; PR interval varies. Each QRS complex is preceded by a P wave. Occurs in elderly patients or chronic lung disease.

Front 747

What are the causes of atrial flutter?

Back 747

Chronic obstructive lung disease, pulmonary embolism, thyrotoxicosis, mitral valve disease, alcohol.

Front 748

What are the ECG signs of atrial flutter?

Back 748

Atrial flutter has an absolutely regular rhythm with a ventricular rate of 125-150 beats/min and an atrial rate of 250-300 beats/min (ie, 2:1 block).

Front 749

What is the initial treatment of atrial flutter?

Back 749

Cardioversion if hemodynamically unstable (e.g., hypotension); digitalis, verapamil, diltiazem, beta-blockers.

Front 750

What is the most common sustained cardiac rhythm disturbance?

Back 750

Atrial fibrillation, which is often associated with heart disease but occurs commonly in patients with no disease. AF may cause thromboembolic events and hemodynamic impairment.

Front 751

What are the ECG signs of atrial fibrillation?

Back 751

No p waves. Fibrillatory waves with an irregular, rapid ventricular response (irregularly, irregular).

Front 752

What is the sign of Wolf-Parkinson White syndrome with atrial fibrillation?

Back 752

Extremely rapid rates (over 200 bpm) suggest the presence of an accessory pathway (W-P-W syndrome), which may manifest as AF. There is a delta wave.

Front 753

What is the rate of ischemic stroke in atrial fibrillation?

Back 753

The rate of ischemic stroke among patients with nonrheumatic atrial fibrillation averages 5% per year.

Front 754

What are the signs of atrial fibrillation?

Back 754

Elderly patients with shortness of breath, dizziness, or palpitations. Acute fatigue or exacerbation of congestive heart failure. Irregularly irregular pulse.

Front 755

What is "lone atrial fibrillation"?

Back 755

Atrial fibrillation with no evidence of structural heart disease.

Front 756

What are the causes of atrial fibrillation?

Back 756

Rheumatic mitral disease, CAD, CHF, HTN (atrial dilation). Hyperthyroidism, hypoxemia, alcohol. In younger patients, 30-45% of paroxysmal cases and 20-25% of persistent cases of AF occur as lone AF.

Front 757

What tests are use in the evaluation of atrial fibrillation?

Back 757

ECG: AF, left ventricular hypertrophy, pre-excitation, prior myocardial infarction. Echocardiogram: identifies LVH, valvular disease, atrial size, and left atrial thrombus. Thyroid function tests.

Front 758

What drugs are effective for pharmacologic cardioversion of atrial fibrillation?

Back 758

Amiodarone, dofetilide, flecainide, ibutilide, propafenone, and quinidine.

Front 759

Which drugs are used to maintain sinus rhythm in patients with atrial fibrillation?

Back 759

Drugs used to maintain sinus rhythm in patients with atrial fibrillation include amiodarone, disopyramide, dofetilide, flecainide, propafenone, and sotalol.

Front 760

What is the first step in managing atrial fibrillation?

Back 760

Control rate to <100 with beta-blockers, calcium-blockers, or digoxin. These agents do not convert AF to sinus rhythm. Digoxin is the drug of choice in HF. Diltiazem, atenolol, metoprolol, verapamil.

Front 761

What is the recommended treatment strategy for atrial fibrillation?

Back 761

Rate control with chronic anticoagulation for the majority of patients with chronic AR. Rhythm control has not been shown to be superior to rate control in reducing morbidity and mortality.

Front 762

A 40-year-old man with shortness of breath. Blood pressure is 70/50 mm Hg. Jugular vein distention and bilateral crackles on exam. ECG atrial fibrillation waves. What is the next appropriate step in management?

Back 762

Electrical cardioversion.

Front 763

What is Wolff-Parkinson-White syndrome?

Back 763

Ventricle is activated by atrial impulses early by accessory pathway (Kent bundle). Short PR interval followed by a wide QRS complex with a slurred initial deflection (delta), which represents early ventricular activation.

Front 764

What is the treatment of Wolff-Parkinson-White syndrome?

Back 764

If unstable, then synchronized cardioversion. If stable, then procainamide. Ablation.

Front 765

What drugs should be avoided in Wolff-Parkinson-White syndrome?

Back 765

Avoid digoxin, beta-blockers, calcium-blockers because inhibit conduction in the normal conduction pathway and cause ventricular or supraventricular tachycardia via in the aberrant conduction pathway.

Front 766

What is ventricular tachycardia?

Back 766

VT is three or more consecutive beats of ventricular origin at a rate greater than 120 beats/min. QRS complexes are wide and bizarre.

Front 767

What are the causes of ventricular tachycardia?

Back 767

Ischemic heart disease after an acute MI; cardiomyopathies, hypokalemia, hypercalcemia, hypomagnesemia, hypoxia, digitalis toxicity and thioridazine drugs.

Front 768

What are the clinical manifestations of ventricular tachycardia?

Back 768

Hypotension, congestive heart failure, syncope, or cardiac arrest.

Front 769

What are the ECG signs of torsade de pointes ventricular tachycardia?

Back 769

Undulating rotations of QRS complexes around baseline. Initiated by a PVC in setting of abnormal ventricular repolarization, characterized by prolongation of QT interval. Episodes of dizziness or syncope.

Front 770

What are the causes of torsade de pointes ventricular tachycardia?

Back 770

Antiarrhythmics that prolong ventricular repolarization (prolong QT); quinidine, procainamide, disopyramide, phenothiazines, thioridazine, tricyclics, lithium, hypoK hypoMg, intracerebral hemorrhage.

Front 771

What is the treatment of torsade de pointes ventricular tachycardia?

Back 771

Treat underlying electrolyte disorders. Magnesium and potassium are first-line therapies. Isoproterenol and short-acting beta-blockers. Overdrive pacing. If unstable, perform electrical cardioversion.

Front 772

What are the indications for amiodarone?

Back 772

Amiodarone is a very effective antiarrhythmic drug, used in ventricular tachycardia, AF, and atrial flutter. Amiodarone has a very long half-life (over 50 days).

Front 773

What are the side effects of amiodarone?

Back 773

Cough, fever; painful breathing can be fatal. 20% neurotoxicity with imbalance, tremor, numbness, weakness. Hypothyroidism/ hyperthyroidism; blue-gray skin; halos, blurred vision; corneal deposits.

Front 774

What are the indications for disopyramide?

Back 774

Ventricular ectopic activity and atrial ectopic activity.

Front 775

What are the adverse effects of disopyramide?

Back 775

Anticholinergic effects; hypotension, heart failure, heart block, tachyarrhythmia.

Front 776

What are the indications for lidocaine?

Back 776

Ventricular ectopic activity

Front 777

What are the adverse effects of lidocaine?

Back 777

Drowsiness, agitation, seizures; rarely congestive heart failure or heart block.

Front 778

What are the cardiac indications for phenytoin?

Back 778

Ventricular ectopic activity.

Front 779

What are the adverse effects of phenytoin?

Back 779

Ataxia, nystagmus, drowsiness; hypotension and heart block with rapid IV injection

Front 780

What are the indications for procainamide?

Back 780

Ventricular ectopic activity, atrial ectopic activity

Front 781

What are the adverse effects of procainamide?

Back 781

Lupus-like syndrome; nausea/vomiting; insomnia; rash; hypotension; aggravation of arrhythmia; blood, dyscrasias

Front 782

What are the indications for quinidine?

Back 782

Ventricular ectopic activity, atrial ectopic activity

Front 783

What are the adverse effects of quinidine?

Back 783

Aggravation of arrhythmias; thrombocytopenia; fever, rash; cinchonism; nausea; digoxin-quinidine interaction (elevation of digoxin levels).

Front 784

What are the antiarrhythmic indications for beta-adrenergic blocking agents?

Back 784

Atrial ectopic activity, ventricular ectopic activity.

Front 785

What are the adverse effects of beta-blockers?

Back 785

Heart block, hypotension, heart failure, asthma, hypoglycemia, lethargy, impotence.

Front 786

What are the antiarrhythmic indications for verapamil?

Back 786

Atrial ectopic activity.

Front 787

What are the adverse effects of verapamil?

Back 787

Congestive heart failure, asystole, constipation

Front 788

What are the indications for adenosine?

Back 788

Ventricular tachycardia

Front 789

What are the adverse effects of adenosine?

Back 789

Transient dyspnea, noncardiac chest pain, rarely hypotension.

Front 790

What are the indications for mexiletine?

Back 790

Ventricular ectopic activity

Front 791

What is mexiletine?

Back 791

Lidocaine-like drug. Local anesthetic; half-life, 8-14 h.

Front 792

What are the indications for tocainide?

Back 792

Ventricular ectopic activity

Front 793

What is tocainide?

Back 793

Lidocaine-like drug. Half-life 14-16 h in patients with high-grade ventricular ectopic activity.

Front 794

What are the indications for amiodarone?

Back 794

Atrial ectopic activity (especially WPW), ventricular ectopic activity.

Front 795

What are the adverse effects of amiodarone?

Back 795

Very long half-life (20-40 d). May increase digoxin level. May worsen existing cardiac conduction disturbances. May prolong Coumadin effect.

Front 796

What are the indications for encainide?

Back 796

Ventricular tachycardia, Wolff-Parkinson-White syndrome.

Front 797

What are the adverse effects of encainide?

Back 797

Negative inotropism; QRS and PR prolongation. Hepatic metabolism to active metabolites.

Front 798

What are the indications for flecainide?

Back 798

Ventricular tachycardia, supraventricular tachycardia, Wolff-Parkinson-White syndrome.

Front 799

What are the adverse effects of flecainide?

Back 799

Negative inotropism, QRS, PR prolongation

Front 800

What are the indications for propafenone?

Back 800

Ventricular tachycardia, atrial fibrillation

Front 801

What the adverse effect of propafenone?

Back 801

Negative inotropism

Front 802

What are the physiologic effects of low doses of nitrates?

Back 802

In low doses, nitrates increase venous dilation and reduce preload.

Front 803

What are the physiologic effects of medium doses of nitrates?

Back 803

In medium doses, nitrates increase arteriolar dilatation and decrease afterload and preload.

Front 804

What are the physiologic effects of high doses of nitrates?

Back 804

In high doses, nitrates increase coronary artery dilatation and increase oxygen supply.

Front 805

What are the side effects of nitrates?

Back 805

Vasodilation can lead to orthostatic hypotension, reflex tachycardia, throbbing headache, and blushing.

Front 806

What is the contraindication to nitrates?

Back 806

Contraindicated if systolic blood pressure is <90 mm Hg.

Front 807

What is the dosing pattern for nitrates?

Back 807

Requires a window-free period of more than 8 hours with nitrate therapy to reduce tachyphylaxis.

Front 808

What are the beneficial effects of beta-blockers?

Back 808

Beta-blockers have been shown to improve survival after an acute myocardial infarction and in CHF.

Front 809

What are the adverse effects of beta-blockers?

Back 809

Fatigue, mental depression, insomnia, adverse effects on lipid panel; hallucinations, Raynaud phenomenon, bronchoconstriction, mask signs and symptoms of insulin-induced hypoglycemia, sexual dysfunction.

Front 810

What are the adverse effects of nonselective beta-blockers?

Back 810

Nonselective beta-blockers may mask hypoglycemic symptoms in insulin-dependent diabetics.

Front 811

What is the contraindication to beta-blockers?

Back 811

Contraindicated in severe asthma.

Front 812

What are the physiologic effects of calcium-channel blockers?

Back 812

Produces decreases in preload and afterload. May be harmful in postinfarction period, especially if left ventricular failure.

Front 813

What are the adverse effects of calcium channel blockers?

Back 813

Congestive heart failure, reflex tachycardia, hypotension, lightheadedness; flushing, headache, weakness, nausea, constipation, nasal congestion, wheezing, peripheral edema.

Front 814

What is anemia?

Back 814

A hematocrit less than 41% in men or less than 36% in women, or a hemoglobin less than 13.5 gm/dL in men or less than 12 gm/dL in women.

Front 815

What is microcytic anemia?

Back 815

Microcytic anemia is a low mean corpuscular volume (MCV) less than 80; caused by iron deficiency, thalassemia, sideroblastosis, and lead poisoning. Anemia of chronic disease can be either microcytic or normocytic.

Front 816

What is macrocytic anemia?

Back 816

Elevated MCV >100 caused by vitamin B12 or folic acid deficiency, alcohol, liver disease, methotrexate, zidovudine, phenytoin. Normal MCV in early micro/macrocytic anemia and hemolysis.

Front 817

What is the presentation of anemia?

Back 817

Fatigue, tiredness, poor exercise tolerance. Dyspnea on exertion and light-headedness, confusion. Anemia may cause death from myocardial ischemia. Older patient will develop dyspnea or angina at a Hct <30%.

Front 818

What is the first step in diagnosing anemia?

Back 818

First step is to determine the MCV. Iron studies, reticulocyte count, peripheral smear, red cell distribution of width (RDW), Coombs test, B12, folate levels, and occasionally a bone marrow biopsy.

Front 819

What is the treatment for anemia?

Back 819

Packed red blood cells are used to maintain a hematocrit >25-30%. A healthy young patient can have transfusion withheld until the Hct is in the low 20%s. Older patient needs Hct >30%.

Front 820

How does one unit of packed red blood cells affect the hematocrit?

Back 820

The hematocrit should rise three points for every unit of packed red blood cells given.

Front 821

What is iron deficiency anemia?

Back 821

Diminished RBC production and an MCV <80, hypochromic cells, low iron. Iron deficiency anemia is caused by blood loss, either GI or menstrual. Hematuria, malabsorption, hemolysis, poor intake.

Front 822

What is the presentation of iron deficiency anemia?

Back 822

Hct 30% causes fatigue, poor exercise tolerance. Hct 25% cause tachycardia, palpitations, dyspnea, pallor. Older and CAD dyspneic at 30%. Lightheadedness, confusion, syncope, chest pain, death.

Front 823

What are the physical signs of iron deficiency?

Back 823

Brittle nails, spoon shaped nails, glossitis, and pica.

Front 824

How is iron deficiency anemia diagnosed?

Back 824

Low serum ferritin <10 ng/mL. MCV is low. The serum iron is low and the total iron binding capacity is high. The RDW is elevated. The reticulocyte count is low.

Front 825

What is anemia of chronic disease?

Back 825

A defect in the ability to use iron; either microcytic or normocytic; caused by any chronic inflammatory, infectious, or neoplastic condition.

Front 826

How is anemia of chronic disease diagnosed?

Back 826

Serum ferritin level is normal or elevated. The serum iron level and total iron binding capacity (TIBC) are low. The reticulocyte count is low.

Front 827

What is the treatment for anemia of chronic disease?

Back 827

Correct underlying disease. Iron and erythropoietin are not effective, except in renal disease and anemia caused by chemotherapy or radiation therapy for malignancies.

Front 828

What is sideroblastic anemia?

Back 828

A microcytic anemia caused by a disorder in the synthesis of hemoglobin. Hereditary and acquired forms from chloramphenicol, isoniazid, or alcohol. Lead poisoning.

Front 829

How is sideroblastic anemia diagnosed?

Back 829

Ferritin is elevated. Transferrin saturation very high, and TIBC very low. Serum iron level is high. Prussian Blue stain of red blood cells in the marrow reveals ringed sideroblasts.

Front 830

What is thalassemia?

Back 830

Hereditary underproduction of either the alpha or beta globin chains of the hemoglobin molecule, resulting in a hypochromic, microcytic anemia.

Front 831

What populations more commonly have thalassemia?

Back 831

Alpha thalassemia is more common in Asian populations. Beta thalassemia is more common in Mediterranean populations.

Front 832

What is the presentation of thalassemia?

Back 832

Individuals with two genes deleted have a mild anemia with hematocrits ranging from 30-40% with a low MCV. In beta thalassemia there is a mild anemia with microcytosis (low MCV).

Front 833

How is thalassemia diagnosed?

Back 833

Thalassemia trait: mild anemia with microcytosis. Beta thalassemia major has severe symptoms, large spleen, bone abnormalities.

Front 834

How is thalassemia diagnosed?

Back 834

Microcytic anemia with normal iron studies, and hemoglobin electrophoresis. Beta thalassemia shows an increased level of hemoglobin F and hemoglobin A2.

Front 835

What is the treatment for thalassemia?

Back 835

Thalassemia traits do not require treatment. Beta thalassemia major patients require blood transfusions once or twice a month.

Front 836

A 73-year-old alcoholic man memory loss and tingling in his feet. Hematocrit of 32% with an MCV of 110. What is the diagnosis?

Back 836

Folic acid deficiency.

Front 837

What are the causes of vitamin B12 deficiency?

Back 837

Most common cause: pernicious anemia (hereditary, autoimmune, decreased intrinsic factor). Gastrectomy, atrophic gastritis, sprue, enteritis, blind loop. Pancreatic insufficiency, tapeworm. Decreased intake.

Front 838

What is the presentation of vitamin B12 deficiency?

Back 838

Peripheral neuropathy, decreased position and vibratory sense; psychiatric, autonomic, motor, cranial nerve, bowel, bladder, and sexual dysfunction. Glossitis, diarrhea, and abdominal pain.

Front 839

How is vitamin B12 deficiency diagnosed?

Back 839

Anemia with macrocytosis (increased MCV). Hypersegmented neutrophils. Indistinguishable from folate deficiency. Reticulocyte count is reduced. Pancytopenia. Most specific test is low B12 level.

Front 840

How is pernicious anemia diagnosed?

Back 840

Antibodies to intrinsic factor and parietal cells confirm the etiology as pernicious anemia. The Schilling test is not necessary if there is a low B12 level combined with the presence of antibodies to intrinsic factor.

Front 841

What is the treatment for vitamin B12 deficiency?

Back 841

Replace the vitamin B12 by the intramuscular route.

Front 842

What is folic acid deficiency?

Back 842

Deficiency in folic acid levels leading to anemia because of decreased dietary intake. Alcoholics have decreased folate intake.

Front 843

How is folic acid deficiency diagnosed?

Back 843

The hematologic presentation of folic acid deficiency is identical to B12 deficiency. Low red-blood-cell folic-acid level. Treatment is oral replacement of folic acid.

Front 844

What are some chronic causes of hemolytic anemia?

Back 844

Sickle cell disease, paroxysmal nocturnal hemoglobinuria, and hereditary spherocytosis

Front 845

What are some acute causes of hemolytic anemia?

Back 845

Drug-induced hemolysis, auto-immune hemolysis, or glucose 6-phosphate dehydrogenase deficiency.

Front 846

What is the presentation of hemolytic anemia?

Back 846

Fatigue and weakness. Dyspnea and confusion. Jaundice and dark urine. Fever, chills, chest pain, tachycardia, and backache may occur.

Front 847

How is hemolytic anemia diagnosed?

Back 847

Hemolytic anemias have a normal MCV. The reticulocyte count is elevated. LDH and indirect bilirubin are elevated. Peripheral smear shows fragmented cells. Hemoglobinuria.

Front 848

What is the treatment of hemolytic anemia?

Back 848

Transfusion when the hematocrit becomes low. Hydration prevents toxicity to the kidney tubule from free hemoglobin.

Front 849

What is sickle cell disease?

Back 849

A hereditary chronic hemolysis ranging from asymptomatic to severe crisis; irreversibly sickled cells and recurrent painful crises. Autosomal recessive.

Front 850

What is the pathophysiology of sickle cell disease?

Back 850

Hemoglobin S is due to a substitution of a valine for glutamic acid as the sixth amino acid of the beta globin chain.

Front 851

What is the prevalence of sickle cell disease?

Back 851

The heterozygous trait is present in 8% of the African-American population, and the homozygous form (disease) is present in 1 in 400 African Americans.

Front 852

What conditions may precipitate a painful crisis?

Back 852

Painful crisis can be precipitated by hypoxia, dehydration, acidosis, infection, and fever. Sudden drops in hematocrit may also be caused by Parvovirus B19 infection or folate deficiency.

Front 853

What is the presentation of sickle cell disease?

Back 853

Renal concentrating defects, ulcerations of legs, bilirubin gallstones, aseptic necrosis of femoral head, osteomyelitis, retinopathy, recurrent infections from Pneumococcus, Haemophilus, growth retardation, splenomegaly, autosplenectomy.

Front 854

What is an acute painful crisis of sickle cell disease?

Back 854

Back, rib, chest, leg pain. Acute chest syndrome is chest pain, fever, leukocytosis, hypoxia, and infiltrates. Stroke and TIA. Priapism, blindness, MI, cardiomyopathy. Spontaneous abortion, low birth weight.

Front 855

How is sickle cell disease diagnosed?

Back 855

Anemia with a normal MCV. Reticulocyte count 10-20%. LDH, bilirubin elevated. Hb electrophoresis most specific. Peripheral smear shows sickled cells. UA blood. WBC elevated.

Front 856

What is the treatment of acute sickle cell pain crisis?

Back 856

Fluids, analgesics, and oxygen. Antibiotics with infection, fever; leukocytosis. Ceftriaxone and cefotaxime are preferred because cover Pneumococcus and Haemophilus influenza.

Front 857

What is the treatment of sickle cell acute chest syndrome, CNS manifestations, priapism, and acute cardiac ischemia?

Back 857

PRBC if Hct low. Folic acid and vaccinations against Pneumococcus and influenza. Hydroxyurea to decrease frequency of pain crises. Bone marrow transplantation can be curative.

Front 858

What are autoimmune, cold agglutinin, and drug-induced hemolytic anemias?

Back 858

Various forms of acquired hemolytic anemias resulting from production of IgG, IgM, or activation of complement C3 against the red cell membrane. Often sudden and idiopathic.

Front 859

What are the causes of autoimmune hemolytic anemias?

Back 859

Antibodies in leukemia, viral infections, lymphoma, collagen vascular diseases or penicillins, cephalosporins, sulfa drugs, quinidine, alpha methyldopa, procainamide, rifampin, and thiazides.

Front 860

What percentage of autoimmune hemolytic anemias are idiopathic?

Back 860

50% do not have an underlying disorder.

Front 861

What is cold agglutinin disease?

Back 861

IgM against the red cell in association with lymphoma, Waldenstrom macroglobulinemia, Mycoplasma or mononucleosis.

Front 862

Which inflammatory bowel disease is associated with autoimmune hemolytic anemia?

Back 862

Ulcerative colitis.

Front 863

What is the presentation of autoimmune hemolysis?

Back 863

Sudden fever, syncope, congestive failure, hemoglobinuria. Splenomegaly; cold agglutinin disease results in cyanosis of the ears, nose, fingers, and toes. Weakness, pallor, jaundice, and dark urine.

Front 864

How is autoimmune hemolysis diagnosed?

Back 864

Normocytic anemia, reticulocytosis, increased LDH, increased indirect bilirubin. Coombs test is specific for autoimmune, cold agglutinin, drug-induced hemolysis. Spherocytes on smear.

Front 865

What is the treatment for autoimmune hemolysis?

Back 865

Steroids. Splenectomy for those unresponsive to steroids. Cold agglutinin disease is managed by avoiding cold.

Front 866

What is hereditary spherocytosis?

Back 866

Hemolysis with spherocytes, jaundice, splenomegaly. Autosomal dominant; loss of spectrin in RBC membrane results in spheres, which are not able to pass spleen. Anemia; splenomegaly jaundice; bilirubin stones.

Front 867

How is hereditary spherocytosis diagnosed?

Back 867

Decreased MCV anemia, elevated LDH, indirect bilirubin, reticulocytes. Hemolysis; negative Coombs. RBC sensitivity to lysis in osmotic fragility test. The mean corpuscular hemoglobin concentration is elevated.

Front 868

What is the treatment for hereditary spherocytosis?

Back 868

Folate replacement. Splenectomy.

Front 869

What is paroxysmal nocturnal hemoglobinuria?

Back 869

A red cell membrane defect leading to intermittent dark urine and venous thrombosis and a chronic hemolysis. A red cell membrane defect allows binding of complement to the red cell.

Front 870

What is the presentation of paroxysmal nocturnal hemoglobinuria?

Back 870

Dark urine from intravascular hemolysis. Thrombosis of the hepatic vein (Budd-Chiari syndrome). Hemoglobinuria in the first morning urine.

Front 871

How is paroxysmal nocturnal hemoglobinuria diagnosed?

Back 871

Increased LDH, bilirubin, and reticulocyte count, hemoglobinuria. Sugar-water test and the acidified-hemolysis (Ham) test. Decay accelerating factor is diminished in PNH.

Front 872

What is the treatment for paroxysmal nocturnal hemoglobinuria?

Back 872

Iron replacement. Corticosteroids.

Front 873

What is glucose-6-phosphate dehydrogenase deficiency?

Back 873

Hereditary deficiency of an enzyme for neutralizing oxidant stress to the red cell, resulting in acute hemolysis. Oxidant stress from infections, sulfa drugs, primaquine, dapsone, quinidine, and nitrofurantoin.

Front 874

What is the presentation of glucose-6-phosphate dehydrogenase deficiency?

Back 874

Sudden, severe, intravascular hemolysis; jaundice, dark urine, weakness, and tachycardia.

Front 875

How is glucose-6-phosphate dehydrogenase deficiency diagnosed?

Back 875

High LDH, bilirubin, and reticulocyte count with a normal MCV and hemoglobinuria. Heinz bodies are inclusions in red cells. Definitive test is the G6PD level.

Front 876

What is the treatment for glucose-6-phosphate dehydrogenase deficiency?

Back 876

Hydration and transfusion. Avoid oxidant stress.

Front 877

What is aplastic anemia?

Back 877

Failure of bone marrow, resulting in anemia, leukopenia, and thrombocytopenia (pancytopenia). The marrow is empty.

Front 878

What are the causes of aplastic anemia?

Back 878

Radiation, benzene, NSAIDs, chloramphenicol, alcohol, chemotherapeutics. Tb, lymphoma. Hepatitis, HIV, CMV, EBV, Parvovirus B19. The most common etiology is idiopathic.

Front 879

What is the presentation of aplastic anemia?

Back 879

Bleeding from thrombocytopenia. Fatigue from anemia and infections from neutropenia. Pancytopenia on CBC. Marrow biopsy confirms.

Front 880

What is the treatment for aplastic anemia?

Back 880

Bone marrow transplantation or immunosuppressive agents.

Front 881

What is acute leukemia?

Back 881

Derangement of pluripotent stem cell, resulting in the destruction of marrow. Leukemic blasts crowd out marrow cells, resulting in pancytopenia. Blood cells lose the ability to mature and function.

Front 882

What are the causes of acute leukemia?

Back 882

Most cases are idiopathic; radiation exposure, benzene, melphalan and etoposide, retroviruses.

Front 883

What is the presentation of acute leukemia?

Back 883

Fatigue from anemia. Bleeding from thrombocytopenia. Infection from the underproduction of white blood cells.

Front 884

Which type of anemia is more common in children?

Back 884

Acute lymphocytic leukemia (ALL) is more common in children. Acute myelogenous leukemia (AML) is more common in adults. Enlargement of the liver, spleen, and lymph nodes and bone pain are common at presentation.

Front 885

How is acute leukemia diagnosed?

Back 885

WBC can be low, normal, or elevated. Thrombocytopenia, anemia; leukemic blasts in peripheral blood. Marrow biopsy >20% blasts confirms.

Front 886

What are the markers of acute myelogenous leukemia?

Back 886

AML is characterized by Auer rods, myeloperoxidase, and esterase.

Front 887

What are the markers of acute lymphocytic leukemia?

Back 887

ALL is characterized by common ALL antigen and terminal deoxynucleotidyl transferase (TdT).

Front 888

What is chronic myelogenous leukemia (CML)?

Back 888

Massive overproduction of myeloid cells. Philadelphia chromosome is characteristic, producing tyrosine kinase.

Front 889

What is the presentation of chronic myelogenous leukemia?

Back 889

Markedly elevated white blood cell count fatigue, night sweats, and low-grade fever. Abdominal pain from massive enlargement of the spleen. Bone pain.

Front 890

How is chronic myelogenous leukemia diagnosed?

Back 890

Elevated WBC consisting of neutrophils. Leukocyte alkaline phosphatase score is diminished. Basophilia characteristic of CML and all myeloproliferative disorders such as polycythemia vera. Platelets elevated.

Front 891

What is the treatment for chronic myelogenous leukemia?

Back 891

Imatinib which is direct inhibitor of the tyrosine kinase produced by the Philadelphia chromosome. 90% hematologic response.

Front 892

What is chronic lymphocytic leukemia?

Back 892

Massive overproduction of mature; lymphocytes from production of B lymphocytes.

Front 893

What is the presentation of chronic lymphocytic leukemia?

Back 893

CLL can often present as an asymptomatic elevation of white cells. 90% being over the age of 50. Fatigue, lethargy, and enlargement of lymph nodes. Infiltration of spleen, liver, and bone marrow.

Front 894

How is chronic lymphocytic leukemia diagnosed?

Back 894

Older patient with a marked elevation in the white cell count with a marked lymphocytic predominance. The marrow is infiltrated with the leukemic lymphocytes with CD19 antigen.

Front 895

What is multiple myeloma?

Back 895

Plasma cell overproduction, replacing the bone marrow; large quantities of functionless immunoglobulins.

Front 896

What is the presentation of multiple myeloma?

Back 896

Bone pain. Pain in back, ribs; fractures. Radiculopathy. Encapsulated organisms (Pneumococcus, Haemophilus). Renal failure, anemia. Hypercalcemia: polyuria, polydipsia, altered mental. Weakness, pallor.

Front 897

How is multiple myeloma diagnosed?

Back 897

Normochromic, normocytic anemia. Protein electrophoresis monoclonal immunoglobulin spike. Skull punched out lesions. beta2 microglobulin. Hypercalcemia from bone destruction. Elevated BUN, creatinine from kidney damage. Biopsy: 10% plasma cells.

Front 898

What is Bence-Jones protein?

Back 898

Urinary Bence-Jones protein is nonfunctional gamma globulin found in multiple myeloma. It will not react with urine dipstick test.

Front 899

What is the treatment for multiple myeloma?

Back 899

Bone marrow transplantation. Older patients should receive melphalan and prednisone.

Front 900

What is monoclonal gammopathy of uncertain significance?

Back 900

Overproduction of immunoglobulin by plasma cells without manifestations MGUS is present in 1% > 50 and in 3% of those > age 70. Monoclonal immunoglobulin spike on electrophoresis. Treatment is not necessary.

Front 901

What is Hodgkin disease?

Back 901

A neoplastic transformation of lymphocytes in the lymph node with Reed-Sternberg cells; spread to contagious areas of lymph nodes. Bimodal age peaks in the 20s and 60s.

Front 902

What is the presentation of Hodgkin disease?

Back 902

Enlarged, rubbery, nonerythematous, nontender lymph nodes. "B" symptoms are night sweats, weight loss, fevers. Pruritus; cervical, supraclavicular, axillary lymphadenopathy most common. Spleen, skin, gastric, lung, CNS.

Front 903

What is the treatment for Hodgkin disease?

Back 903

Localized disease is managed with radiation. All patients with "B" symptoms and stage III or stage IV disease are managed with chemotherapy.

Front 904

What is non-Hodgkin lymphoma?

Back 904

Neoplastic transformation of B and T lymphatic cells. Accumulation of neoplastic cells in both the lymph nodes and diffusely in extra-lymphatic organs and the bloodstream. Reed-Sternberg cell is absent.

Front 905

What conditions predispose to non-Hodgkin lymphoma?

Back 905

Infections such as HIV, hepatitis C, Epstein-Barr, HTLV-I, and Helicobacter pylori predispose to the development of NHL.

Front 906

What is the presentation of non-Hodgkin lymphoma?

Back 906

Enlarged, rubbery, nonerythematous, nontender lymph nodes. "B" symptoms are night sweats, weight loss, fevers. Pruritus may occur.

Front 907

What sites are affected by non-Hodgkin lymphoma?

Back 907

NHL is the same as HD except that HD is localized to cervical and supraclavicular nodes. NHL involves extra-lymphatic sites and blood. CNS is more common NHL. HIV patients often have CNS NHL.

Front 908

What is the treatment for non-Hodgkin lymphoma?

Back 908

Local disease is treated with radiation, and those with "B" symptoms or Stages III and IV receive combination chemotherapy.

Front 909

A 21-year-old woman with epistaxis and heavy periods. She has a PT of 12 seconds, a PTT of 40 seconds (prolonged), and 200,000/mm3 platelets. What is the diagnosis?

Back 909

Idiopathic thrombocytopenic purpura. Also known as primary immune thrombocytopenic purpura.

Front 910

What is idiopathic thrombocytopenic purpura?

Back 910

Thrombocytopenia caused by idiopathic production of an antibody to platelets; often associated with lymphoma, chronic lymphocytic leukemia, HIV, and connective tissue diseases.

Front 911

What is the presentation of idiopathic thrombocytopenic purpura?

Back 911

Bleeding skin, nasal, oral, GI, urine, vagina. Young, female; epistaxis, bruising, hematuria, uterine and GI bleeding. Petechiae, purpura, ecchymoses. Splenomegaly absent.

Front 912

How is idiopathic thrombocytopenic purpura diagnosed?

Back 912

Thrombocytopenia. Antiplatelet Ab have a high sensitivity, poor specificity. Marrow filled with megakaryocytes, indicating platelet destruction. Smear and creatinine are normal, excluding HUS, TTP, DIC.

Front 913

What is the treatment for idiopathic thrombocytopenic purpura?

Back 913

Prednisone. Splenectomy if very low platelet counts.

Front 914

What is Von Willebrand disease?

Back 914

Platelet-type bleeding, autosomal dominant, decreased von Willebrand factor; VWD is the most common congenital disorder of hemostasis. Decreased ability of platelets to adhere to endothelial lining of blood vessels.

Front 915

What is the presentation of Von Willebrand disease?

Back 915

Epistaxis, petechiae, bruising, and menstrual abnormalities; gastrointestinal and urinary tract bleeding.

Front 916

How is Von Willebrand disease diagnosed?

Back 916

Platelet count is normal. The bleeding time is increased. Von Willebrand factor is low. Ristocetin platelet aggregation test is abnormal. PTT may be elevated.

Front 917

What is the treatment for von Willebrand disease?

Back 917

Desmopressin acetate (DDAVP) for mild bleeding. Factor VIII replacement is used if desmopressin is not effective and the bleeding continues. Aspirin contraindicated. FFP is not useful.

Front 918

Which coagulopathies cause a prolonged prothrombin time?

Back 918

Factor VII deficiency, vitamin K deficiency, liver disease, warfarin use, factor VII inhibitor.

Front 919

Which coagulopathies cause a prolonged PTT?

Back 919

vWF and factors VIII, IX, XI, or XII deficiencies; heparin, antiphospholipid antibody

Front 920

Which coagulopathies cause a prolonged PT and PTT?

Back 920

Prothrombin, fibrinogen, factor V, factor X or combined factor deficiencies, liver disease, DIC, supratherapeutic heparin or warfarin; combined heparin and warfarin.

Front 921

What is hemophilia?

Back 921

Deficiency of clotting factor 8 in hemophilia A and deficiency of factor 9 in hemophilia B resulting in increased bleeding. X-linked recessive, resulting in disease in males. Females are carriers. Hemophilia A is far more common than B.

Front 922

Why does hemophilia not express in females?

Back 922

Females do not express the disease because homozygosity results in intrauterine death of the fetus.

Front 923

What is the presentation of hemophilia?

Back 923

Mild deficiencies result in absence of symptoms or with symptoms only during surgery or trauma. Severe deficiency results in spontaneous bleeding. Factor-type bleeding is deeper than bleeding caused by platelets.

Front 924

What type of bleeding is associated with factor deficiency?

Back 924

Factor deficiencies cause hemarthrosis, hematoma, gastrointestinal bleeding, urinary bleeding, bruising, CNS bleeding. Severe hemophilia presents by age two or circumcision.

Front 925

How is hemophilia diagnosed?

Back 925

A prolonged PTT with a normal PT. Specific factor VIII or IX levels allow for a precise diagnosis of hemophilia A or B.

Front 926

What is the treatment of hemophilia?

Back 926

Mild hemophilia can be treated with desmopressin (DDAVP). Severe deficiencies are treated with replacement of the specific factor. Desmopressin is ineffective for hemophilia B.

Front 927

What factor deficiency results from vitamin K deficiency?

Back 927

The deficiency of vitamin K results in decreased production of factors 2, 7, 9, and 10. Caused by dietary deficiency, malabsorption, and antibiotics that kill the colon bacteria that produce vitamin K.

Front 928

What is the presentation of vitamin K deficiency?

Back 928

Bleeding may occur at any site. Oozing at venipuncture sites.

Front 929

How is vitamin K deficiency diagnosed?

Back 929

PT and PTT are elevated. A correction of PT and PTT in response to giving vitamin K is the most common method of confirming the diagnosis.

Front 930

What is the treatment for vitamin K deficiency?

Back 930

Severe bleeding is treated with fresh frozen plasma. Vitamin K is given at the same time.

Front 931

Why do patients with liver disease have increased PT and PTT?

Back 931

Coagulopathy is caused by decreased production of clotting factors by the liver. Any severe liver disease or cirrhosis can cause decreased production of clotting factors.

Front 932

What are the effects of coagulopathy of liver disease?

Back 932

Bleeding at any site, gastrointestinal tract is the most common site. Vitamin K does not result in improvement. Low platelet counts are often caused by hypersplenism that accompanies the liver disease.

Front 933

What is the treatment of coagulopathy of liver disease?

Back 933

Fresh frozen plasma severe bleeding.

Front 934

What is disseminated intravascular coagulation?

Back 934

Consumptive coagulopathy from major illness, resulting in consumption of platelets and clotting factors; bleeding with a microangiopathic hemolysis and fibrin products; occasionally thrombosis.

Front 935

What are the causes of disseminated intravascular coagulation?

Back 935

Sepsis is most common. Any cell destruction and release of tissue factor. Rhabdomyolysis, adenocarcinomas, heatstroke, transfusion reactions, burns, head trauma, abruption, amniotic embolism, trauma, pancreatitis, snakebites, leukemia.

Front 936

What is the presentation of disseminated intravascular coagulation?

Back 936

Bleeding from any site. Thrombosis is less common. Hemolysis often may lead to acute renal failure, jaundice, confusion.

Front 937

How is disseminated intravascular coagulation diagnosed?

Back 937

Serious underlying disorder with bleeding, elevation PT, PTT; decrease platelets. Fibrinogen low. D-dimers and fibrin- split products are increased. Schistocytes with intravascular hemolysis.

Front 938

What is the treatment for disseminated intravascular coagulation?

Back 938

Fresh frozen plasma and platelet transfusions. Heparin is rarely used except in thrombosis.

Front 939

What are the names of the semisynthetic penicillinase-resistant penicillins?

Back 939

Oxacillin, cloxacillin, dicloxacillin, methicillin, nafcillin

Front 940

Which bacteria are susceptible to the semisynthetic penicillins?

Back 940

Staphylococci and streptococci. Oxacillin, nafcillin, dicloxacillin, cloxacillin. Exclusively effective against Gram-pos cocci, particular staph. Methicillin not used because interstitial nephritis.

Front 941

What are the indications for the semisynthetic penicillins?

Back 941

Used when Staphylococcus is sensitive to the semisynthetic penicillins and if concurrent Gram-negative infection is not suspected. More efficacious than vancomycin when the organism is sensitive.

Front 942

What antibiotic is used to treat resistant-resistant Staph aureus?

Back 942

MRSA is treated primarily with vancomycin. Oral linezolid or IV quinupristin-dalfopristin are alternatives for MRSA.

Front 943

What is the coverage of linezolid?

Back 943

Drug-resistant enterococcus, staphylococcus, and pneumococcus.

Front 944

Which bacteria are sensitive to penicillin G, penicillin VK, ampicillin, and amoxicillin?

Back 944

Effective against streptococci, such as S. pyogenes, viridans group streptococci, and S. pneumonia, but not against staphylococci.

Front 945

When can ampicillin and amoxicillin be used against staphylococcal infections?

Back 945

Ampicillin and amoxicillin are only effective against staph when ampicillin is combined with the beta-lactamase inhibitor sulbactam or when amoxicillin is combined with clavulanate.

Front 946

What is the coverage of ampicillin against E coli?

Back 946

Ampicillin also has some activity against E. coli. Ampicillin and amoxicillin are effective against enterococci and Listeria. Useful against Gram-negative bacteria, such as Neisseria.

Front 947

What are the first-generation cephalosporins?

Back 947

Cefazolin, cefadroxil, cephalexin.

Front 948

What are the second-generation cephalosporins?

Back 948

Cefoxitin, cefotetan, cefuroxime, cefprozil, loracarbef.

Front 949

What is the coverage of the first-generation cephalosporins?

Back 949

Same organisms that the semisynthetic penicillins will cover. In addition to staphylococci and streptococci, 1st and 2nd gen cephalosporins will also cover some Gram-neg. 1st gen agents will only reliably cover Gram-neg Moraxella and E. coli.

Front 950

What is the coverage of second-generation cephalosporins?

Back 950

Cover everything a first-generation cephalosporin covers, as well as a few more Gram-negative bacilli such as Providencia, Haemophilus, Klebsiella, Citrobacter, Morganella, and Proteus.

Front 951

What is the coverage of the third-generation cephalosporins?

Back 951

3rd gen, particularly ceftazidime, are not reliable against staphylococcus. 4th gen cephalosporin, cefepime, will cover staph and strep, but should not be used for exclusively Gram-pos infections.

Front 952

What is the allergic cross-reactivity of penicillins with cephalosporins?

Back 952

For persons allergic to penicillin, there is only 5% risk of cross-reaction with cephalosporins. When the allergic reaction was a rash, a cephalosporin can be used. When the reaction was anaphylaxis, a cephalosporin should not be used.

Front 953

What antibiotic should be used in patients with a history of an anaphylactic reaction to a penicillin?

Back 953

A macrolide (clarithromycin or azithromycin) or levofloxacin, gatifloxacin, or moxifloxacin can be used. For serious infections, use vancomycin, linezolid, or daptomycin.

Front 954

What are the indications for macrolides (erythromycin, clarithromycin, azithromycin), extended fluoroquinolones (levofloxacin, gatifloxacin, moxifloxacin), and clindamycin?

Back 954

Alternatives to penicillin and cephalosporins for Gram-pos infection. Macrolides should not be used for serious staph. Extended quinolones very good for strep, particularly S pneumoniae in absence of penicillin resistance. Good against staph; not MRSA.

Front 955

Why should ciprofloxacin not be used to treat pneumonia?

Back 955

Ciprofloxacin does not cover Strep pneumoniae.

Front 956

What are the indications for vancomycin, linezolid, quinupristin, dalfopristin?

Back 956

Alternatives for Gram-pos infections when penicillin allergy or MRSA. Linezolid is the only oral MRSA.

Front 957

What is the coverage of linezolid, quinupristin, dalfopristin?

Back 957

Linezolid, quinupristin, dalfopristin are effective against MRSA and vancomycin-resistant enterococci.

Front 958

What is the activity of antipseudomonal penicillins (piperacillin, ticarcillin, mezlocillin) against Gram-negative bacilli?

Back 958

Fully active against range of Gram-negative bacilli, such as the Enterobacteriaceae including Pseudomonas. Enterobacteriaceae include E. coli, Proteus, Enterobacter, Citrobacter, Morganella, Serratia, Klebsiella.

Front 959

What is the activity of ticarcillin and mezlocillin against MSSA?

Back 959

Antipseudomonal penicillins are only active against staph when combined with a beta-lactamase inhibitor, such as piperacillin/tazobactam or ticarcillin/clavulanate. Not MRSA.

Front 960

What is the coverage of ampicillin/sulbactam and amoxicillin/clavulanate?

Back 960

Cover strep and staph and Gram-neg bacilli, but not Pseudomonas. All penicillins will cover sensitive streptococci.

Front 961

What are the third-generation cephalosporins?

Back 961

Ceftazidime, cefotaxime, ceftriaxone, cefotaxime.

Front 962

What is the fourth generation cephalosporin?

Back 962

Cefepime

Front 963

What is the coverage of third- and fourth-generation cephalosporins?

Back 963

Fully active against full range of Gram-neg bacilli, such as the Enterobacteriaceae. Only ceftazidime and cefepime will cover Pseudomonas. Cefepime also covers staph.

Front 964

What is the Gram-negative coverage of second-generation agents?

Back 964

Cover some of the Enterobacteriaceae, but not Pseudomonas.

Front 965

What is the coverage of the third generation cephalosporins?

Back 965

Predominantly for use against Gram-negative organisms. Ceftriaxone and cefotaxime cover best for penicillin-insensitive pneumococci which cause meningitis or pneumonia.

Front 966

What is the coverage of quinolones (ciprofloxacin, levofloxacin, gatifloxacin, moxifloxacin, ofloxacin)?

Back 966

Cover most Enterobacteriaceae, such as E. coli, Proteus, Enterobacter, Haemophilus, Moraxella, Citrobacter, Morganella, Serratia, and Klebsiella. Only ciprofloxacin will cover Pseudomonas.

Front 967

What is the coverage of extended-spectrum quinolones?

Back 967

Moxifloxacin, levofloxacin, gatifloxacin are also active against Gram-positive cocci, in particular Strep pneumoniae. Good for pneumonia because also cover Mycoplasma, Chlamydia, Legionella.

Front 968

What is the coverage of aminoglycosides (gentamicin, tobramycin, amikacin)?

Back 968

Gram-negative coverage. Aminoglycosides are synergistic with ampicillin in treatment of staph.

Front 969

What is the coverage of monobactams?

Back 969

Aztreonam is exclusively a Gram-negative agent, with no strep or staph coverage.

Front 970

What is the coverage of carbapenems (imipenem, meropenem, ertapenem)?

Back 970

Enterobacteriaceae and Pseudomonas with Gram-neg coverage. Excellent staph and anaerobic coverage. Used in Gram-negative infections, but also effective polymicrobial. Ertapenem not cover Pseudomonas.

Front 971

What agent is most active against intraabdominal anaerobes?

Back 971

Metronidazole. Clindamycin is less active against intraabdominal anaerobes. Metronidazole has good anaerobic Gram- neg in bowel, such as B fragilis. Metronidazole is first-line against C difficile.

Front 972

What is the coverage of clindamycin?

Back 972

Clindamycin may have some advantages over metronidazole against the anaerobic streptococci found in the mouth.

Front 973

What agents have intraabdominal anaerobic coverage?

Back 973

Metronidazole, carbapenems and beta-lactam/beta-lactamase combinations (piperacillin/tazobactam, ticarcillin/clavulanate, ampicillin/sulbactam, or amoxicillin/clavulanate). 2nd gen cephalosporins cefoxitin and cefotetan, have fair activity against.

Front 974

A 15-year-old male with fever, headache, nausea, and vomiting. Neck stiffness and photophobia. What is the next step?

Back 974

Lumbar puncture.

Front 975

What is the most common cause of meningitis after the neonatal period?

Back 975

Streptococcus pneumoniae is the most common cause of meningitis for all patients beyond the neonatal period. Neisseria meningitidis is the most common cause of meningitis in adolescents.

Front 976

What factors predispose to listeria monocytogenes meningitis?

Back 976

Listeria monocytogenes is more common with immune system defects, HIV, steroid use, leukemia, lymphoma, and various chemotherapeutic agents. Neonates and the elderly.

Front 977

What is the most common cause of meningitis in the elderly and infants?

Back 977

Streptococcus pneumoniae is the most common etiology. Listeria is more common in the very old and infants.

Front 978

Which patients are at risk for staphylococcal meningitis?

Back 978

Staphylococcus aureus is more common in those who have had any form of neurosurgery.

Front 979

Which patients are at risk for cryptococcus meningitis?

Back 979

Cryptococcus is more common in those who are HIV positive and who have profound decreases in their T-cell counts to levels less than 100 cells/mm3.

Front 980

Which persons are at risk for Rocky Mountain spotted fever meningitis?

Back 980

Rocky Mountain spotted fever is common in those who have been exposed to ticks in the mid-Atlantic areas, such as the Carolinas, Kentucky, Tennessee, Delaware, Maryland, Virginia, Georgia, Florida, Oklahoma, etc.

Front 981

What area is associated with Lyme meningitis?

Back 981

Lyme disease can also cause meningitis and is more common in the Northeast. Tuberculosis and syphilis are also associated with meningitis.

Front 982

What are the CSF characteristics in aseptic meningitis?

Back 982

CSF has lymphocytic pleocytosis and bacterial cultures are negative.

Front 983

What are the causes of aseptic meningitis?

Back 983

Enteroviruses, arboviruses (St. Louis encephalitis virus, West Nile virus), HIV, herpes simplex, and lymphocytic choriomeningitis virus.

Front 984

What is the most common cause of neonatal meningitis?

Back 984

Group B Streptococcus (Streptococcus agalactiae) is the most common cause of meningitis in the neonatal period.

Front 985

What is the clinical presentation of meningitis?

Back 985

Fever, photophobia, headache, nuchal rigidity (Kernig, Brudzinski), nausea, vomiting, seizures. The most common deficit from meningitis is damage to 8th cranial nerve (hearing).

Front 986

What type of meningitis is associated with a petechial rash?

Back 986

Neisseria. A rash on the wrists and ankles with centripetal spread toward the body suggests Rocky Mountain spotted fever.

Front 987

What type of meningitis is associated with facial palsy?

Back 987

Facial nerve palsy is suggestive of Lyme disease. Pulmonary symptoms or an abnormal chest x-ray suggest tuberculosis.

Front 988

When should a CT scan be done before lumbar puncture in patients with suspected meningitis?

Back 988

CT should be done before lumbar puncture if papilledema, focal motor deficits, new onset seizures, mental status abnormalities, or immunocompromise (HIV, immunosuppressive).

Front 989

What should be done if the lumbar puncture is delayed more than 20-30 minutes?

Back 989

An empiric dose of antibiotics should be given.

Front 990

What are the CSF findings in bacterial meningitis?

Back 990

Protein elevated with bacterial meningitis. Opening pressure elevated. Gram stain has a limited sensitivity; positive 50%. The most useful test is the cell count. Only bacterial meningitis causes thousands of cells, all neutrophils.

Front 991

What types of meningitis are associated with an elevation in lymphocytes?

Back 991

Viral infection, Rickettsia, Lyme disease, tuberculosis, syphilis, or fungal (cryptococcal) etiology. Normal CSF cell count is <5 cells, lymphocytes.

Front 992

What is the empiric treatment of bacterial meningitis in adults?

Back 992

Vancomycin (pneumococci are resistant penicillin) plus a 3rd gen cephalosporin, such as ceftriaxone. Ampicillin is added to cover Listeria if immune defects, >50, or <1 month. Listeria is resistant cephalosporins.

Front 993

What is the treatment of Lyme meningitis?

Back 993

Lyme disease is treated with ceftriaxone.

Front 994

What is the treatment of Cryptococcal meningitis?

Back 994

Cryptococcus is treated with amphotericin. Followed by fluconazole in HIV-positive patients for life or until the patient is on HAART and is asymptomatic with a CD4 count >100.

Front 995

What is the treatment of neurosyphilis?

Back 995

Neurosyphilis is treated with high-dose intravenous penicillin.

Front 996

What is the treatment of tuberculosis meningitis?

Back 996

TB meningitis is treated the same as pulmonary tuberculosis (though a longer duration of 9-12 months).

Front 997

What are the indications for corticosteroid in meningitis?

Back 997

Steroid use in adult meningitis is appropriate for TB meningitis and bacterial meningitis.

Front 998

What are the recommendations for adjunctive dexamethasone for bacterial meningitis?

Back 998

Reduces inflammatory response to bacterial lysis; given with antibiotics for 4 days if bacterial meningitis is confirmed by positive Gram stain or >1000 WBCs in CSF.

Front 999

What is encephalitis?

Back 999

Infection of brain parenchyma usually caused by any viruses. The most common cause is HSV type 1. Varicella-zoster virus, CMV, enteroviruses, Eastern and Western equine encephalitis, St. Louis, and West Nile.

Front 1000

What is the presentation of encephalitis?

Back 1000

Altered mental status with fever and headache. Confusion to lethargy or coma. Focal deficits. Neck stiffness. Seizures.

Front 1001

How is HSV encephalitis diagnosed?

Back 1001

Lumbar puncture PCR has eliminated the need for biopsy. PCR for HSV has a 98% sensitivity and >95% specificity. HSV has a predilection for temporal lobes.

Front 1002

What is the treatment for HSV encephalitis?

Back 1002

Intravenous acyclovir.

Front 1003

What is the treatment of cytomegalovirus encephalitis?

Back 1003

Ganciclovir or foscarnet are active against CMV.

Front 1004

An HIV-negative man with a seizure. Aphasia and weakness of the right hand and leg. A CT scan of the head with contrast shows a ring enhancing lesion. What is the diagnosis?

Back 1004

Brain abscess.

Front 1005

What are the causes of brain abscesses?

Back 1005

Bacteria can spread into the brain from otitis media, sinusitis, mastoiditis, or dental infections. Organisms may also spread through the bloodstream from endocarditis or pneumonia.

Front 1006

Which organisms cause brain abscesses?

Back 1006

Brain abscesses most commonly Streptococcus 60-70%, Bacteroides 20-40%, Enterobacteriaceae 25-35% and Staph 10%, often polymicrobial. Toxoplasmosis can reactivate in HIV when CD4 <100.

Front 1007

What is the presentation of brain abscess?

Back 1007

Headache. Fever, focal neurologic deficits, seizures.

Front 1008

How is brain abscess diagnosed?

Back 1008

Brain abscess and malignancy enhance with contrast. MRI more accurate than CT. Stereotactic aspiration for Gram stain, culture. In HIV, 90% of brain lesions will be toxoplasmosis or lymphoma.

Front 1009

What is the treatment for brain abscess?

Back 1009

Surgical drainage. Penicillin, metronidazole, and a third-generation cephalosporin, such as ceftazidime. HIV patients are treated empirically with pyrimethamine and sulfadiazine.

Front 1010

What are the causes of otitis media?

Back 1010

The most common organisms are Strep pneumoniae (35-40%), H. influenzae (nontypeable; 25-30%), and Moraxella catarrhalis (15-20%). Viruses.

Front 1011

What is the presentation of otitis media?

Back 1011

Ear pain, fever, and decreased hearing. Immobility of the membrane on insufflation.

Front 1012

What is the treatment for otitis media?

Back 1012

High-dose amoxicillin. Amoxicillin-clavulanate is used if recent amoxicillin or if no response to amoxicillin. Alternatives: Cefuroxime, loracarbef, cefprozil, or cefdinir or cefixime.

Front 1013

What is the treatment for otitis media in severe allergy to penicillin?

Back 1013

Macrolides, such as azithromycin or clarithromycin. Levofloxacin, moxifloxacin or gatifloxacin are acceptable. TMP/SMZ is poorly active against Streptococcus pneumoniae.

Front 1014

What is the most common site of sinusitis?

Back 1014

The most common site of infection is the maxillary sinus.

Front 1015

What are the cause of sinusitis?

Back 1015

Viruses are responsible for most cases. Bacterial organisms are strep pneumonia, H influenza (non-typable), Moraxella catarrhalis.

Front 1016

What is the presentation of sinusitis?

Back 1016

Facial pain, headache, postnasal drainage, and purulent nasal drainage. Headache, fever, tooth pain.

Front 1017

How is sinusitis diagnosed?

Back 1017

If imaging is required because of concern of complications, a CT scan is the best test.

Front 1018

What is the treatment for sinusitis?

Back 1018

High-dose amoxicillin. Amoxicillin-clavulanate if recent amoxicillin use or if no response amoxicillin. Alternatives: cefuroxime, loracarbef, cefprozil, cefdinir, cefixime.

Front 1019

What is the treatment of sinusitis in patients with severe penicillin allergies?

Back 1019

Patients with severe penicillin allergies should receive azithromycin or clarithromycin. Levofloxacin, moxifloxacin, or gatifloxacin are acceptable.

Front 1020

What are the causes of pharyngitis?

Back 1020

Usually viruses; group A beta-hemolytic streptococci (S. pyogenes) may cause rheumatic fever or glomerulonephritis. S. pyogenes causes 15-20% of cases of pharyngitis.

Front 1021

What is the presentation of pharyngitis?

Back 1021

Sore throat with cervical adenopathy and inflammation of the pharynx with an exudate is highly suggestive of S. pyogenes. Viruses do not cause an exudate.

Front 1022

How is pharyngitis diagnosed?

Back 1022

Rapid Streptococcal antigen test is 60-100% sensitive and >95% specific. A positive test can be considered the equivalent of a positive culture, whereas a negative test should be confirmed with a culture.

Front 1023

What is the treatment for pharyngitis?

Back 1023

Penicillin or amoxicillin. Azithromycin, clarithromycin, and oral, second-generation cephalosporins are alternatives in penicillin-allergic.

Front 1024

What is influenza?

Back 1024

A systemic viral illness from influenza A or B, usually occurring in an epidemic pattern, leading to sinusitis, otitis media, bronchitis, and pneumonia.

Front 1025

What is the presentation of influenza?

Back 1025

Fever, myalgias, headache, and fatigue. Upper respiratory symptoms predominate. Coryza, nonproductive cough, sore throat, and conjunctival injection.

Front 1026

How is influenza diagnosed?

Back 1026

Rapid antigen detection methods of swabs or washings of nasopharyngeal secretions. Viral culture.

Front 1027

What is the treatment for influenza?

Back 1027

Specific antiviral medications for both influenza A and B are the neuraminidase inhibitors: oseltamivir and zanamivir. Amantadine and rimantadine are only effective against influenza A.

Front 1028

What are the indications for influenza vaccinations?

Back 1028

>50 chronic lung and cardiac disease, pregnant in the second and third trimesters; chronic facilities, health-care workers, immunosuppressed, diabetes, renal dysfunction. Contraindicated in allergy to eggs.

Front 1029

A 63-year-old man with a cough sputum smoked 30 years. Temperature of 100 degrees F. Chest x-ray is normal. What is the diagnosis?

Back 1029

Bronchitis

Front 1030

What are the causes of bronchitis?

Back 1030

Viruses. Small percentage caused by M. pneumoniae, C. pneumoniae, B. pertussis. Most common organisms responsible for chronic bronchitis are S pneumoniae, H influenzae, and Moraxella. CXR normal.

Front 1031

What is the treatment for acute exacerbations of chronic bronchitis?

Back 1031

Amoxicillin, doxy, or TMP/SMZ. Patients not responding to amoxicillin should be treated with amoxicillin/clavulanate, clarithromycin, azithromycin, 2nd/3rd-gen cephalosporins, or gatifloxacin, levofloxacin, or moxifloxacin.

Front 1032

A 65-year-old alcoholic with cough, sputum, fever. Lost 15 pounds. Febrile. Poor dentition. Putrid, foul breath. CXR: cavitary lesion. What is the diagnosis?

Back 1032

Lung abscess.

Front 1033

What is a lung abscess?

Back 1033

Necrosis of the pulmonary parenchyma caused by microbial infection.

Front 1034

What is the bacteriology of lung abscesses?

Back 1034

90% anaerobes. Peptostreptococcus, Prevotella, and Fusobacterium species (oral anaerobes). Aerobic bacteria, most frequently are S. aureus, E. coli, Klebsiella, and Pseudomonas.

Front 1035

What conditions predispose to lung abscess?

Back 1035

Association with periodontal disease or aspiration (e.g., altered sensorium, seizures).

Front 1036

What is the presentation of lung abscess?

Back 1036

Fever, cough, chest pain; putrid, foul-smelling sputum in 60-70%; chronic course with weight loss and fatigue.

Front 1037

How is lung abscess diagnosed?

Back 1037

Sputum Gram stain and culture. Cavitary lesion. Lower lobes in upright patients, and the posterior right upper lobe in supine patients. Aspiration of abscess fluid is necessary for diagnosis.

Front 1038

What is the treatment of lung abscess?

Back 1038

Clindamycin has good empiric coverage for the "above the diaphragm" anaerobes. Penicillin is also acceptable.

Front 1039

What conditions predispose to pneumonia?

Back 1039

Cigarette smoking, diabetes, alcoholism, malnutrition, obstruction from tumors, and immunosuppression. Neutropenia and steroid use predispose to Aspergillus infection.

Front 1040

What is the most common cause of community-acquired pneumonia in all groups?

Back 1040

S. pneumoniae (viruses <5 years). Hospital-acquired or ventilator-associated pneumonia: Gram-neg bacilli such as E. coli, the other Enterobacteriaceae, or Pseudomonas, and MRSA.

Front 1041

What conditions predispose to Haemophilus influenzae pneumonia?

Back 1041

Smokers, COPD.

Front 1042

What factors are associated with Mycoplasma pneumonia?

Back 1042

Young, otherwise healthy patients.

Front 1043

What conditions predispose to Legionella?

Back 1043

Epidemic infection in older smokers, particularly when located near infected water sources, such as air-conditioning systems.

Front 1044

What conditions predispose to Pneumocystis jiroveci pneumonia?

Back 1044

HIV-positive persons with <200 CD4 cells/mm3 not on PJP prophylaxis.

Front 1045

What conditions predispose to Coxiella burnetii (Q-fever) pneumonia?

Back 1045

Exposure to animals, particularly at the time the animals are giving birth.

Front 1046

What condition predisposes to Klebsiella pneumonia?

Back 1046

Alcoholics

Front 1047

What condition predisposes to Staphylococcus aureus pneumonia?

Back 1047

Occurs after viral syndromes or viral bronchitis, especially influenza

Front 1048

What condition predisposes to Coccidioidomycosis pneumonia?

Back 1048

Exposure to the deserts of the American Southwest, particularly Arizona

Front 1049

What conditions predispose to Chlamydia psittaci pneumonia?

Back 1049

Bird exposure.

Front 1050

What conditions predispose to Histoplasma capsulatum pneumonia?

Back 1050

Exposure to bat or bird droppings, spelunking (recreational cave exploration)

Front 1051

What are the clinical signs of Bordetella pertussis pneumonia?

Back 1051

Cough with whoop and post-tussive vomiting.

Front 1052

What conditions predispose to Francisella tularensis pneumonia?

Back 1052

Hunters or exposure to rabbits, bioterrorism.

Front 1053

What activity predisposes to severe acute respiratory syndrome (SARS, Avian influenza pneumonia)?

Back 1053

Travel to southeast Asia.

Front 1054

Which bacteria may be utilized in bioterrorism?

Back 1054

Bacillus anthracis, Yersinia pestis, and Francisella tularensis.

Front 1055

What is the clinical presentation of pneumonia?

Back 1055

Cough, fever, sputum, dyspnea. Bacterial infections (pneumoniae, Haemophilus, Klebsiella) have purulent sputum. S. pneumoniae causes rusty hemoptysis.

Front 1056

What are the characteristics of the sputum in Klebsiella pneumonia?

Back 1056

Klebsiella pneumoniae sputum is like currant jelly.

Front 1057

What are the characteristics of pneumonia caused by Pneumocystis jiroveci, viruses, Mycoplasma, and Legionella?

Back 1057

Interstitial infections are caused by Pneumocystis jiroveci pneumonia, viruses, Mycoplasma, and Legionella; often cause nonproductive or "dry" cough.

Front 1058

What type of pain is associated with pneumococcal pneumonia?

Back 1058

Pleuritic pain is associated with lobar pneumonia, caused by Pneumococcus, because of inflammation of the pleura. S. pneumoniae usually causes a lobar pneumonia with pleural effusion.

Front 1059

What are the physical signs of pneumonia?

Back 1059

Rales, rhonchi, lung consolidation, dullness to percussion, bronchial breath sounds, increased vocal fremitus, egophony. Severe pneumonia leads to hypoxia.

Front 1060

What is the presentation of Mycoplasma pneumonia?

Back 1060

Dry cough and chest soreness. Bullous myringitis; anemia from hemolysis from cold agglutinins. Rarely need to be admitted to the hospital.

Front 1061

What is the presentation of Legionella pneumonia?

Back 1061

Confusion, headache, and lethargy. Diarrhea and abdominal pain.

Front 1062

What is the presentation of Pneumocystis jiroveci pneumonia?

Back 1062

Marked dyspnea, particularly on exertion, with chest soreness with cough in an HIV-positive person with a CD4 count of <200/mm3.

Front 1063

Which types of pneumonia are associated with interstitial infiltrates?

Back 1063

Interstitial infiltrates are associated with PJP, viral, Mycoplasma, Chlamydia, Coxiella, and Legionella pneumoniae.

Front 1064

What is the most specific test for lobar pneumonia?

Back 1064

Sputum culture and Gram stain. S pneumoniae, Staph, Klebsiella, Haemophilus. Viral, Mycoplasma, Chlamydia, Coxiella ("atypicals") will not appear on a Gram stain or bacterial culture.

Front 1065

What is the best diagnostic method for Mycoplasma pneumonia?

Back 1065

Specific serologic antibody titers. Cold agglutinins have limited specificity and sensitivity.

Front 1066

What are the diagnostic methods for Legionella pneumonia?

Back 1066

Charcoal yeast extract media, urine antigen tests, direct fluorescent antibodies, and antibody titers.

Front 1067

What is the best diagnostic method for Pneumocystis jiroveci pneumonia?

Back 1067

Bronchoalveolar lavage; increased LDH.

Front 1068

What is the best diagnostic method for Chlamydia pneumoniae, Coxiella, Coccidioidomycosis, and Chlamydia psittaci?

Back 1068

Specific antibody titers.

Front 1069

What are the signs of severe pneumonia?

Back 1069

pO2 <60 mm Hg, O2 sat <94%, resp >30, disorientation, uremia, systolic BP <90. High fever, hypothermia, leukopenia (<4,000), tachycardia (>125), hyponatremia, dehydration, elevated BUN.

Front 1070

Which pneumonia patients should be hospitalized?

Back 1070

Patients with severe pneumonia or serious underlying diseases such as cancer, liver disease, renal disease, or chronic lung disease should be hospitalized for intravenous medications.

Front 1071

What is the empiric therapy for outpatient pneumonia?

Back 1071

Macrolide, azithromycin or clarithromycin. Levofloxacin, moxifloxacin, gatifloxacin are alternatives. Cephalosporins and amoxicillin/clavulanate do not cover atypical pathogens.

Front 1072

What is the treatment for hospitalized patients with community-acquired pneumonia?

Back 1072

Levofloxacin, moxifloxacin, or gatifloxacin or cefotaxime or ceftriaxone combined with a macrolide such as azithromycin or clarithromycin (or doxycycline).

Front 1073

What organisms cause hospital-acquired pneumonia?

Back 1073

Drug-resistant, Gram-negative bacilli (Pseudomonas, Klebsiella, E. coli), or gram-positives, including methicillin-resistant Staphylococcus aureus.

Front 1074

What is the treatment of hospital-acquired pneumonia?

Back 1074

3rd gen cephalosporin with antipseudomonal activity (ceftazidime, cefotaxime) or carbapenems (imipenem) or beta-lactam/beta-lactamase combinations (piperacillin/tazobactam), and vancomycin or linezolid. Gentamicin added for Gram-neg synergy.

Front 1075

What is the specific coverage for Haemophilus influenzae?

Back 1075

Second- or third-generation cephalosporin.

Front 1076

What is the specific coverage for Mycoplasma pneumoniae?

Back 1076

Macrolide, doxycycline, or a quinolone.

Front 1077

What is the specific coverage for Legionella?

Back 1077

Macrolide, doxycycline, or a quinolone

Front 1078

What is the specific coverage for pneumocystis jiroveci pneumonia?

Back 1078

Trimethoprim/sulfamethoxazole. Steroids should be used if arterial pO2 <70 mm Hg. If the patient is allergic to TMP/SMZ, intravenous pentamidine or atovaquone should be used.

Front 1079

What is the specific coverage for Coxiella burnetii (Q-fever)?

Back 1079

Doxycycline (or erythromycin)

Front 1080

What is the specific coverage for klebsiella?

Back 1080

Third-generation cephalosporin.

Front 1081

What is the specific coverage for staphylococcus aureus?

Back 1081

Semisynthetic penicillin (nafcillin) if methicillin sensitive. In the nosocomial setting, isolates are methicillin-resistant, and vancomycin or linezolid is used.

Front 1082

What is the specific coverage for coccidioidomycosis?

Back 1082

Treatment only for disseminated disease or pulmonary disease with immunosuppression. Life-threatening disease is treated with amphotericin. Mild disease is treated with fluconazole or itraconazole.

Front 1083

Which patients should receive pneumococcal vaccine?

Back 1083

>65. Lung, cardiac, liver, renal disease. Immunocompromised. Re-dosing in 5 y is only necessary with severe immunocompromise or if vaccinated <65. >65, a single dose confers lifelong immunity.

Front 1084

What is bacillus Calmette-Guerin?

Back 1084

Bacillus Calmette-Guerin vaccination is used outside the United States to prevent tuberculosis. Only 50% effective and is never used in the US. BCG vaccination does not alter PPD test interpretation.

Front 1085

Which persons are at risk for tuberculosis infection?

Back 1085

Immigrants, alcoholics, healthcare workers, prisoners, homeless shelters, nursing homes, chronically debilitated, impairment of T-cell immunity. Steroid use, organ transplantation, leukemia, lymphoma, and HIV.

Front 1086

What is the clinical presentation of tuberculosis?

Back 1086

Cough, sputum, fever, and an abnormal lung examination. Weight loss. Tuberculosis usually takes up to five years to become fatal. Night sweats. TB occurs outside of the lungs in 15-20%.

Front 1087

What sites may be affected by extrapulmonary tuberculosis?

Back 1087

Any part of the body, although the lymph nodes, meninges, GI and GU are the most frequent extrapulmonary TB. Adenitis is the most common extrapulmonary site.

Front 1088

How is tuberculosis diagnosed?

Back 1088

CXR: apical infiltrates, cavitation. Adenopathy, effusion, calcified nodules (Ghon). 3 sputum smears 90% sensitive. Culture is most specific; 4 wks. PPD not used to diagnose acute TB unless other tests neg.

Front 1089

What is the treatment of tuberculosis?

Back 1089

Initial 4-drug: INH, rifampin, pyrazinamide, ETB. 4 drugs continued for 2 mo or until sensitivity known. PZA/ETB are discontinued, and continue INH, rifampin for 4 mo. ETB given if sensitivity not known.

Front 1090

What is the length of treatment of tuberculosis meningitis?

Back 1090

12 mths. TB in pregnancy is treated for 9 mths. HIV- positive treated for 6-9 months.

Front 1091

What drug should be taken with isoniazid?

Back 1091

INH use should generally be combined with vitamin B6 (pyridoxine) to prevent peripheral neuropathy.

Front 1092

Which antituberculosis drugs are contraindicated in pregnancy?

Back 1092

Pregnant patients should not receive PZA or streptomycin.

Front 1093

When are steroids used in tuberculosis?

Back 1093

Steroids are used for TB meningitis and TB pericarditis.

Front 1094

What are the side effects of antituberculosis medications?

Back 1094

All TB medications can cause liver toxicity, except streptomycin. INH causes peripheral neuropathy because of pyridoxine deficiency. Rifampin is associated with orange/red bodily fluids .

Front 1095

What are the adverse effects of ethambutol?

Back 1095

Ethambutol is associated with optic neuritis, color blindness and other visual disturbances. PZA can cause a benign hyperuricemia, which does not require treatment.

Front 1096

What is the PPD test?

Back 1096

PPD test is used to screen asymptomatic populations at risk of TB to determine if they have been exposed and are at increased risk of re-activating. PPD should not be used to diagnose TB in an acutely ill patient.

Front 1097

What is the physical indication of a positive PPD?

Back 1097

A PPD test is positive if there is induration of the skin 48-72 h after intradermal injection. A positive PPD test indicates a 10% risk of TB in HIV-negative. BCG vaccination does not alter recommendations.

Front 1098

What is two-stage PPD testing?

Back 1098

Those in whom there has not been a recent PPD test and now show some reactivity that is <10 mm should have a second test within two weeks. This ensures that the first test was not a false negative.

Front 1099

What is the criteria for a positive PPD in close contacts of active TB cases, HIV-positive persons, persons with an abnormal chest x-ray consistent with old TB, and steroid use or organ transplantation recipients?

Back 1099

>5 mm

Front 1100

What is the criteria for a positive PPD in high-risk groups, such as healthcare workers, prisoners, nursing home residents; immigrants; homeless; leukemia, lymphoma, diabetics, dialysis, IVDU who are HIV-neg; and children exposed to adults at high risk?

Back 1100

>10 mm

Front 1101

What is the criteria for a positive PPD in low risk populations?

Back 1101

>15 mm

Front 1102

What is the management of a positive PPD?

Back 1102

Chest x-ray to determine if they have early signs of TB. Those with abnormal chest x-rays should have sputum AFB stains to see if they have active disease. Positive AFB smears need the start of four TB drugs.

Front 1103

What is the treatment for patients with positive PPD and no evidence of active disease (negative chest x-ray)?

Back 1103

9 months of INH and vitamin B6. A normal chest x-ray or an abnormal x-ray and three negative AFB stains of sputum are sufficient to exclude active disease.

Front 1104

What is the cause of most infectious diarrhea?

Back 1104

Contaminated food and water. Bacillus cereus and Staphylococcus aureus, food poisoning present predominantly with vomiting. Food poisoning is most commonly Campylobacter.

Front 1105

What type of diarrhea is associated with poultry and eggs?

Back 1105

Salmonella is most commonly associated with contaminated poultry and eggs.

Front 1106

What is the most common cause of travelers' diarrhea?

Back 1106

E. coli is the most common cause of travelers' diarrhea. E. coli 0157:H7 is associated with eating undercooked hamburger meat.

Front 1107

What organism is associated with fried rice?

Back 1107

Bacillus cereus is associated with fried rice.

Front 1108

What types of diarrhea are associated with water from streams?

Back 1108

Giardia lamblia and cryptosporidiosis are acquired from contaminated water from streams.

Front 1109

What type of diarrhea is associated with AIDS?

Back 1109

Cryptosporidiosis is associated with HIV, particularly when the CD4 count has dropped below 50 cells. Vibrio cholera is very rare in the United States.

Front 1110

What type of diarrhea is associated with shellfish?

Back 1110

Vibrio parahaemolyticus is associated with contaminated shellfish.

Front 1111

What is the most common cause of diarrhea in children?

Back 1111

Viral infections such as with rotavirus or Norwalk agents are associated with outbreaks in children.

Front 1112

What type of diarrhea is associated with previous antibiotic use?

Back 1112

Clostridia difficile is associated with previous antibiotic use.

Front 1113

What type of food is associated with clostridia botulinum?

Back 1113

Clostridia botulinum is associated with ingestion of infected canned foods, and Clostridia perfringens is associated with meats that have been contaminated with spores.

Front 1114

What organisms are associated with blood in the stool?

Back 1114

Blood in the stool is most commonly associated with invasive enteric pathogens, such as Salmonella, Shigella, Yersinia, invasive E. coli, and Campylobacter.

Front 1115

What type of diarrhea is associated with Guillain-Barre syndrome?

Back 1115

Campylobacter is rarely associated with Guillain-Barre syndrome.

Front 1116

What are the symptoms of ciguatera toxin poisoning?

Back 1116

Ingestion of barracuda, red snapper, grouper within 2 h; paresthesias, numbness, nausea, vomiting, cramps; weakness, reversal of hot-cold, hypotension.

Front 1117

What is the treatment for ciguatera toxin poisoning?

Back 1117

No therapy.

Front 1118

Which infectious agents are associated with hemolytic uremic syndrome?

Back 1118

E. coli 0157:H7 and Shigella are associated with hemolytic uremic syndrome.

Front 1119

What is the presentation of staphylococcal food poisoning?

Back 1119

Bacillus cereus and Staphylococcus predominantly present with vomiting within 1-6 hours of their ingestion because they contain a preformed toxin. Diarrhea occurs later.

Front 1120

What is the characteristic of viral diarrhea?

Back 1120

Viruses can cause voluminous watery diarrhea but do not result in bloody diarrhea.

Front 1121

What type of diarrhea occurs after ingestion of tuna, mackerel, or mahi mahi?

Back 1121

Scombroid poisoning from histamine in flesh. Minutes: rash, diarrhea, vomiting, wheezing, burning in mouth, dizziness, paresthesias.

Front 1122

How is infectious diarrhea diagnosed?

Back 1122

Test the stool for white blood cells with methylene blue testing. WBCs indicate an invasive pathogen. Culture is necessary to determine specific type.

Front 1123

Which test is used to detect Giardia and Cryptosporidium?

Back 1123

Giardia and Cryptosporidium are detected by direct examination for ova and parasites, as well as for their eggs. A special modified AFB stain is necessary to detect Cryptosporidium.

Front 1124

What is the treatment of infectious diarrhea?

Back 1124

More severe infections with high fever, abdominal pain, tachycardia and hypotension, require intravenous fluids and oral ciprofloxacin.

Front 1125

What are the causes of viral hepatitis?

Back 1125

Viral hepatitis is an infection of the liver caused by hepatitis A, B, C, D, or E.

Front 1126

What are the symptoms of hepatitis A?

Back 1126

Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice.

Front 1127

What are the symptoms of hepatitis B?

Back 1127

Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice, 10-20% with serum sickness-like (joint pain, rash).

Front 1128

What are the symptoms of hepatitis C?

Back 1128

Only 20% are acutely symptomatic with fever, malaise, headache, jaundice.

Front 1129

What are the symptoms of hepatitis D?

Back 1129

Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice

Front 1130

What are the symptoms of hepatitis E?

Back 1130

Fever, malaise, headache, anorexia, vomiting, dark urine, jaundice

Front 1131

What types of hepatitis have a carrier state?

Back 1131

Hepatitis B, C, D. There is no carrier state for hepatitis A or hepatitis E.

Front 1132

What is the serology of hepatitis A?

Back 1132

Anti-HAV, IgM fraction, IgG fraction.

Front 1133

What is the serology of hepatitis B?

Back 1133

HBsAg, HBsAb, HBeAg, anti-HBs, anti-HBc, anti-HBe

Front 1134

What is the serology of hepatitis C?

Back 1134

Antibody to hepatitis C, PCR-RNA

Front 1135

What is the serology of hepatitis D?

Back 1135

Anti-delta, IgM fraction, IgG fraction

Front 1136

What is the serology of hepatitis E?

Back 1136

Anti-Hep E IgM, IgG

Front 1137

What is the mode of transmission of hepatitis A and E?

Back 1137

Transmitted by contaminated food and water. Incubation period 2-6 weeks. Hepatitis A and E cause symptomatic disease for several days to weeks, no chronic form, cause cirrhosis or hepatocellular CA.

Front 1138

What is the mode of transmission of hepatitis B, C and D?

Back 1138

Transmitted parenterally, perinatally, or through sexual contact; blood transfusion, needlestick, and needle sharing. Hepatitis B and C cause a chronic form, cirrhosis and hepatocellular carcinoma.

Front 1139

What is the most common disease leading to the need for liver transplantation?

Back 1139

Hepatitis C. All forms of hepatitis can occasionally present with fulminant hepatic necrosis and acute liver failure.

Front 1140

What is the presentation of acute hepatitis?

Back 1140

Jaundice, dark urine, light stool, fatigue, malaise, weight loss, tender enlarged liver. B and C can also cause joint pain, rash, vasculitis, glomerulonephritis. B with polyarteritis nodosa.

Front 1141

How is acute hepatitis diagnosed?

Back 1141

Viral and drug hepatitis cause elevated bilirubin. Viral hepatitis causes elevation of ALT and AST, but the ALT is greater than AST. AST is more elevated in alcohol hepatitis.

Front 1142

What is the significance of a positive IgM antibody in the diagnosis of hepatitis?

Back 1142

Hepatitis A, C, D, and E are diagnosed by acute IgM antibody. IgG antibody to hepatitis A, C, D, and E indicates old, resolved. Hepatitis C can be followed with a PCR-RNA viral load.

Front 1143

What is the first hepatitis B marker to elevate?

Back 1143

Hepatitis B is diagnosed as acute with the presence of the hepatitis B surface antigen, which is the first viral marker to elevate. The hepatitis B e antigen and the IgM core antibody also indicate an acute infection.

Front 1144

What is the significance of the hepatitis B e antigen?

Back 1144

The e antigen indicates high levels of viral replication and increased infectivity.

Front 1145

What laboratory findings indicate resolution of hepatitis B?

Back 1145

Resolution of the infection is definitively indicated by the loss of surface antigen activity and the development of hepatitis B surface antibody.

Front 1146

What is the significance of the hepatitis B core IgG antibody?

Back 1146

B core IgG and e antibody indicate that the acute infection is about to resolve and may be the only markers present in window period 2-6 weeks between loss of surface antigen and development of surface Ab.

Front 1147

What is the treatment for chronic hepatitis B?

Back 1147

Interferon, entecavir, adefovir, or lamivudine.

Front 1148

What is the treatment of chronic hepatitis C?

Back 1148

Chronic hepatitis C is treated with interferon combined with ribavirin. The only therapy for cirrhosis is liver transplantation.

Front 1149

What is the postexposure prophylaxis after hepatitis B needlestick?

Back 1149

If surface-antigen-positive patient, the person stuck should receive hepatitis B immunoglobulin (HBIg) and B vaccine. If the person stuck already has protective levels of surface antibody, then no therapy.

Front 1150

What is the postexposure prophylaxis for hepatitis C?

Back 1150

There is no effective postexposure prophylaxis to hepatitis C, and there is no vaccine?

Front 1151

What are the indications for hepatitis B vaccine?

Back 1151

All healthcare workers, IV drug users, and others at risk should be vaccinated. Newborn children are vaccinated.

Front 1152

What are the causes of urethritis?

Back 1152

Neisseria gonorrhoeae or nongonococcal urethritis is caused by either Chlamydia trachomatis (50%), Ureaplasma urealyticum (20%), Mycoplasma hominis (5%), Trichomonas (1%), or herpes simplex.

Front 1153

What are the clinical signs of urethritis?

Back 1153

Purulent urethral discharge; dysuria, urgency, and frequency in urination

Front 1154

How is urethritis diagnosed?

Back 1154

Urethral smear Gram-neg intracellular, coffee bean-shaped diplococci. Fluorescent antibodies for chlamydia by urethral swab, or by ligase chain reaction test of urine. Culture is the most specific test for gonorrhea.

Front 1155

What is the treatment of urethritis?

Back 1155

Combination of ceftriaxone IM and single-dose azithromycin PO. An alternative regimen is ceftriaxone and PO doxycycline for 7 d. Gonorrhea can also be treated with single-dose Cipro or cefixime.

Front 1156

What is pelvic inflammatory disease?

Back 1156

Infection of the fallopian tubes, uterus, ovaries, or ligaments of the uterus caused by N. gonorrhoeae, Chlamydia, Mycoplasma, anaerobic bacteria or Gram-negative bacteria. Intrauterine devices predispose to PID.

Front 1157

What are the clinical signs of pelvic inflammatory disease?

Back 1157

Pelvic pain on palpation of the cervix, uterus, or adnexa; fever, and leukocytosis. Cervical motion tenderness. Discharge from the cervix.

Front 1158

How is pelvic inflammatory disease diagnosed?

Back 1158

Cervical culture on Thayer-Martin for gonococcus. Laparoscopy. A pregnancy test should be done.

Front 1159

What is the therapy for pelvic inflammatory disease?

Back 1159

Doxycycline and cefoxitin (or cefotetan) IV. Outpatient therapy is single-dose ceftriaxone intramuscularly and doxycycline orally for 2 weeks. Outpatient therapy can also be 2 weeks ofloxacin and metronidazole.

Front 1160

What are the sequelae of pelvic inflammatory disease?

Back 1160

Infertility and ectopic pregnancy.

Front 1161

A 22-year-old man with painless, ulcerated genital lesion, adenopathy. What is the next step?

Back 1161

Dark-field microscopy for syphilis, VDRL.

Front 1162

What are the clinical signs of primary syphilis?

Back 1162

Chancre within 3 weeks; disappears 10-90 days; regional lymphadenopathy is painless, nontender. Chancres on penis, anus, rectum, vulva, cervix, perineum. Caused by the spirochete, Treponema pallidum.

Front 1163

What are the signs of secondary syphilis?

Back 1163

6-12 wks after infection, symmetrical rash more on flexor and volar (pinkish in whites; copper blacks). Lymphadenopathy; papules at mucocutaneous junctions and moist areas are condylomata lata (extremely infectious), alopecia.

Front 1164

What are the signs of latent syphilis?

Back 1164

Asymptomatic; persist for life, and one-third develop late or tertiary syphilis.

Front 1165

What are the signs of late or tertiary syphilis?

Back 1165

Most neurologic. Symptomatic but not contagious. Tertiary develops 3-20 y after initial infection, and the typical lesion is the gumma (chronic granulomatous reaction); any tissue or organ. Cardiovascular syphilis.

Front 1166

What is the Argyll Robertson pupil?

Back 1166

Small irregular pupil that accommodates but does not react to light.

Front 1167

What are the signs of tabes dorsalis?

Back 1167

Tabes dorsalis (locomotor ataxia) is pain, ataxia, sensory changes, and loss of tendon reflexes.

Front 1168

How is syphilis diagnosed?

Back 1168

Screening tests are VDRL and RPR; specific tests are FTA-ABS, MHA-TP, and Darkfield exam of chancre.

Front 1169

What are the causes of a false positive VDRL?

Back 1169

False positives VDRL occurs with EBV, collagen vascular disease, TB, subacute bacterial endocarditis.

Front 1170

What is the Jarisch-Herxheimer reaction?

Back 1170

Malaise, fever, headache, sweating rigors, and temporary exacerbations of the syphilitic lesions 6-12 hours after initial treatment.

Front 1171

What is the treatment of primary, secondary, and latent syphilis?

Back 1171

Im benzathine penicillin once a week. Primary and secondary syphilis require one week of therapy. Late latent syphilis is treated for three weeks and diagnosed when VDRL or RPR >1:8 without symptoms.

Front 1172

What is the treatment for tertiary syphilis?

Back 1172

Penicillin 10-20 million units/day IV for 10. Penicillin-allergics receive doxycycline for primary and secondary syphilis, but must be desensitized in tertiary syphilis. Pregnant must also undergo desensitization.

Front 1173

What is chancroid?

Back 1173

Acute, localized, contagious disease of painful genital ulcers and suppuration of the inguinal lymph nodes caused by Haemophilus ducreyi (Gram negative bacillus)

Front 1174

What are the clinical signs of chancroid?

Back 1174

Small, soft, painful papules that become shallow ulcers with ragged edges. Inguinal lymph nodes become very tender and enlarged.

Front 1175

How is chancroid diagnosed?

Back 1175

Gram stain shows Gram-negative bacillus, culture; PCR testing.

Front 1176

What is the treatment of chancroid?

Back 1176

Azithromycin single dose or ceftriaxone intramuscularly (single dose). Erythromycin for 7 days or Cipro for 3 days are alternatives.

Front 1177

What is lymphogranuloma venereum?

Back 1177

Contagious, sexually transmitted disease with primary lesion followed by suppurative lymphangitis caused by chlamydia trachomatis.

Front 1178

What are the clinical signs of lymphogranuloma venereum?

Back 1178

Small, transient, nonindurated, ulcerates, heals; tender, unilateral enlargement inguinal nodes; multiple draining sinuses (buboes); scar, sinuses; fever, malaise, joint pains, headaches.

Front 1179

How is lymphogranuloma venereum diagnosed?

Back 1179

Complement fixing antibodies; isolate chlamydia from pus in buboes

Front 1180

What is the treatment of lymphogranuloma venereum?

Back 1180

Doxycycline or erythromycin.

Front 1181

What is granuloma inguinale?

Back 1181

Chronic granulomatous condition, spread by sexual contact; caused by Donovania granulomatis, Calymmatobacterium granulomatis

Front 1182

What are the clinical signs of granuloma inguinale?

Back 1182

A painless, red nodule that develops into an elevated granulomatous mass. In males, on penis, scrotum, groin, thighs; in females on vulva, vagina, perineum. In homosexual males, the anus and buttocks. Scar formation.

Front 1183

How is granuloma inguinale diagnosed?

Back 1183

Giemsa or Wright stain (Donovan bodies) or smear of lesion; punch biopsy. Treatment with doxycycline ceftriaxone, TMP/SMZ, or erythromycin.

Front 1184

What virus causes genital herpes?

Back 1184

Herpes virus, type II; type I can be seen in genital herpes.

Front 1185

What are the clinical signs of genital herpes?

Back 1185

Vesicles skin or mucous membranes; become painful, circular ulcers, red areola. Soreness precedes lesions. Inguinal lymphadenopathy. Lesions on penis or labia, clitoris, perineum, vagina, cervix.

Front 1186

How is genital herpes diagnosed?

Back 1186

Tzanck test and viral culture.

Front 1187

What is the treatment of genital herpes?

Back 1187

Acyclovir, famciclovir, or valacyclovir. Herpes may recur; sexual contacts should be examined. Acyclovir-resistant herpes is treated with foscarnet.

Front 1188

What are genital warts?

Back 1188

Also known as condylomata acuminata; papilloma virus. Soft, moist, minute, pink, or red; grow rapidly and become pedunculated. Cauliflower appearance. Differentiate from flat warts and condylomata lata.

Front 1189

What is the treatment of genital warts?

Back 1189

Destruction (curettage, trichloroacetic acid), cryotherapy, podophyllin, imiquimod for 14 weeks (an immune stimulant), laser.

Front 1190

What conditions predispose to cystitis?

Back 1190

Predisposed by tumors, stones, strictures, prostatic hypertrophy, neurogenic bladder. Sexual intercourse in women. Catheters.

Front 1191

What is the etiology of cystitis?

Back 1191

E. coli in >80%; second are other coliforms (Gram-negative bacilli) such as Proteus, Klebsiella, Enterobacter; enterococci occasionally; Staph saprophyticus in young women.

Front 1192

What are the symptoms of cystitis?

Back 1192

Dysuria, frequency, urgency, and suprapubic pain. Hematuria, low-grade fever; foul-smelling and cloudy urine. Suprapubic tenderness without flank tenderness.

Front 1193

How is cystitis diagnosed?

Back 1193

Urinalysis for WBCs, RBCs, protein, bacteria. Nitrites indicate Gram-negative. Urine culture with >100,000 colonies/mL of urine is confirmatory but not always necessary.

Front 1194

What is the treatment of cystitis?

Back 1194

Uncomplicated cystitis: 3 days of trimethoprim/sulfamethoxazole, or any quinolone. Seven days of therapy for cystitis in diabetes. Quinolones should not be used in pregnancy.

Front 1195

What are the predisposing factors for pyelonephritis?

Back 1195

Strictures, tumors, calculi, prostatic hypertrophy, or neurogenic bladder, vesicoureteral reflux; more common in women, childhood, pregnancy, after urethral catheterization or instrumentation

Front 1196

What are the clinical signs of pyelonephritis?

Back 1196

Chills, fever, flank pain, nausea, vomiting, costovertebral angle tenderness, increased frequency in urination, and dysuria.

Front 1197

How is pyelonephritis diagnosed?

Back 1197

Clean-catch urine for urinalysis, culture; >100,000 bacteria/mL of urine. If the patient does not improve in 48-72 hours, ultrasound or CT scan can be done to detect obstruction renal or perinephric abscess.

Front 1198

What is the treatment of pyelonephritis?

Back 1198

Antibiotics for 10-14 days with fluoroquinolone, or ampicillin and gentamicin, or a third-generation cephalosporin. Most treated as outpatients. Resistance to TMP/SMZ 20%.

Front 1199

What is the bacteriology of pyelonephritis?

Back 1199

E. coli is the most common pathogen, others include: Klebsiella, Proteus, and Enterococcus. Immunosuppressed and indwelling catheters are more prone to Candida.

Front 1200

What is perinephric abscess?

Back 1200

Infected material surrounding kidney and within the Gerota fascia; from pyelonephritis. Stones in 20-60%. Other structural abnormalities, recent surgery, trauma, diabetes.

Front 1201

What is the microbiology of perinephritic abscess?

Back 1201

E. coli most common, then Klebsiella, Proteus; Staph aureus sometimes accounts for hematogenous cases.

Front 1202

How is perinephritic abscess diagnosed?

Back 1202

Urinalysis normal 30% and culture normal 40%. Fever, pyuria with a negative culture or a polymicrobial culture. Ultrasound; CT or MRI scan are better tests. Aspiration of the abscess.

Front 1203

What is the treatment of perinephric abscess?

Back 1203

Third-generation cephalosporins, antipseudomonal penicillin, or ticarcillin/clavulanate with an aminoglycoside percutaneous drainage

Front 1204

What is impetigo?

Back 1204

Superficial, pustular skin infection in children (ecthyma is ulcerative form of impetigo), oozing, crusting, draining; S. aureus (bullous impetigo) and group A beta-hemolytic Streptococcus

Front 1205

What are the clinical signs of impetigo?

Back 1205

Arms, legs, and face after skin trauma. Maculopapules, rapidly progresses to vesicular pustular lesions or bullae. Progress to lymphangitis, furunculosis, or cellulitis, and acute glomerulonephritis.

Front 1206

What is the treatment of impetigo?

Back 1206

Oral first-generation cephalosporin or semisynthetic penicillin (oxacillin, cloxacillin, dicloxacillin). Topical mupirocin or bacitracin. Penicillin-allergic: clarithromycin or azithromycin.

Front 1207

What is erysipelas?

Back 1207

Superficial cellulitis caused by group A beta-hemolytic Streptococcus.

Front 1208

What are the clinical signs of erysipelas?

Back 1208

Bilateral, shiny, red, indurated, edematous, tender lesions on the face, arms, and legs. Lesions are sharply demarcated.

Front 1209

What is the treatment of erysipelas?

Back 1209

Semisynthetic penicillin or first-generation cephalosporin; penicillin.

Front 1210

What are dermatophyte infections?

Back 1210

Superficial infection caused by a dermatophyte fungus that invades outer layer of skin nails, hair, stratum corneum; caused by microsporum, Trichophyton, and Epidermophyton

Front 1211

How are dermatophyte infections diagnosed?

Back 1211

Potassium hydroxide (10%) prep; culture.

Front 1212

What are the signs of tinea corporis?

Back 1212

Papulosquamous annular lesions of the body with a raised border, which expands peripherally and clear centrally.

Front 1213

What are the signs of tinea pedis?

Back 1213

Macerated and scaling borders (third and fourth interdigital space) of the foot.

Front 1214

What are the signs of tinea unguium?

Back 1214

Thickened and lusterless nails.

Front 1215

What are the signs of tinea capitis?

Back 1215

Small, scaly, semi-bald, grayish patches with broken lusterless hair on head

Front 1216

What are the signs of tinea cruris?

Back 1216

Ringed lesion that extends from the crural folds over the adjacent inner thigh

Front 1217

What are the signs of tinea barbae?

Back 1217

Inflammatory, deep plaques and noninflammatory patches on the bearded area of the face.

Front 1218

What is the treatment for dermatophyte infections?

Back 1218

Terbinafine or itraconazole orally for capitis, corporis, and unguium. Miconazole, clotrimazole and ketoconazole in cream or lotion for mild cruris, pedis, and corporis.

Front 1219

What is candidiasis?

Back 1219

Infection of skin, mucous membranes by Candida albicans. Immunodeficiency antibacterial therapy, obesity, diabetes, corticosteroid, antimetabolite, pregnancy, debilitate, blood dyscrasias, HIV.

Front 1220

What are the clinical signs of candidiasis?

Back 1220

Intertriginous infection: Well-demarcated, erythematous, itchy, exudative patches, rimmed with small red-based pustules in the groin, gluteal folds (diaper rash), axilla, umbilicus, and inframammary areas

Front 1221

What are the signs of candida vulvovaginitis?

Back 1221

White discharge with inflammation of the vaginal and vulva. Pregnancy and diabetes mellitus.

Front 1222

What are the signs of oral candidiasis (thrush)?

Back 1222

White patches of exudates on tongue or buccal mucosa.

Front 1223

What is candidal paronychia?

Back 1223

Painful red swelling around the nail.

Front 1224

How is candidiasis diagnosed?

Back 1224

Potassium hydroxide exam. Culture is definitive.

Front 1225

What is the treatment of candidiasis?

Back 1225

Topical nystatin, clotrimazole, miconazole, ciclopirox, econazole, terconazole. Amphotericin for invasive infection. Fluconazole for less serious infections and paronychia.

Front 1226

What is tinea versicolor?

Back 1226

Multiple macules (usually asymptomatic), varying in color from white to brown caused by Pityrosporum orbiculare (Malassezia furfur)

Front 1227

What are the clinical signs of tinea versicolor?

Back 1227

Tan, brown, white, scaling macular lesions that tend to coalesce; found on chest, neck, abdomen, or face. Lesions do not tan.

Front 1228

How is tinea versicolor diagnosed?

Back 1228

Skin scrapings with 10% KOH. "spaghetti and meatballs," appearance of hyphae and spores.

Front 1229

What is the treatment of tinea versicolor??

Back 1229

Topical selenium sulfide, clotrimazole, ketoconazole, or oral itraconazole.

Front 1230

What are the signs of scabies?

Back 1230

Skin infection with superficial burrows, intense pruritus, and secondary infections, caused by Sarcoptes scabiei; skin-to-skin transmission.

Front 1231

What are the clinical signs of scabies?

Back 1231

Pruritus, burrows, papules on flexor surfaces of wrists, finger webs, elbows, axilla, areola of breast and genitals. Immunocompromised may develop severe, crusted Norwegian scabies.

Front 1232

How is scabies diagnosed?

Back 1232

Parasite in scrapings in mineral oil.

Front 1233

What is the treatment of scabies?

Back 1233

Permethrin, lindane (Kwell). Ivermectin oral therapy if the disease is extensive. Lindane in contraindicated in pregnancy.

Front 1234

What is pediculosis?

Back 1234

Skin infestation caused by lice. Itching, excoriations, erythematous macules and papules; secondary bacterial infection

Front 1235

How is pediculosis diagnosed?

Back 1235

Examination of the pubic area, axillae, scalp, and other hair-bearing surfaces for the louse or nits.

Front 1236

What is the treatment for pediculosis?

Back 1236

Permethrin or lindane (Kwell).

Front 1237

What is molluscum contagiosum?

Back 1237

Skin-colored, waxy, papules caused by poxvirus. Small papules anywhere on the skin (genital and pubic area). Transmitted by skin-to-skin contact or sexually. Seen in children; increased with HIV.

Front 1238

What is the treatment of molluscum contagiosum?

Back 1238

Freezing, curettage, electrocautery, or cantharidin.

Front 1239

61-year-old man with painful leg for 2 weeks. Ulcer over the proximal portion of his tibia just below the knee. Peripheral vascular disease and diabetes. Sinus tract in the ulcer draining purulent material. What is the diagnosis?

Back 1239

Osteomyelitis

Front 1240

What is acute hematogenous osteomyelitis?

Back 1240

S aureus. Long bones of lower extremities children; tibia, femur, metaphyseal. In adults, hematogenous osteomyelitis accounts for 20%, lumbar vertebrae. Fever, back tenderness. Injection drugs.

Front 1241

What is the most common organism in osteomyelitis that is caused by spread of a contiguous infection?

Back 1241

A contiguous infection after recent trauma or placement of a prosthetic joint may cause osteomyelitis. S. aureus is the most common organism; sometimes polymicrobial.

Front 1242

What is vascular insufficiency osteomyelitis?

Back 1242

Majority over 50, with diabetes or peripheral vascular disease. Bones of the lower extremities. Polymicrobial, but most common organism is S. aureus.

Front 1243

What is the presentation of osteomyelitis?

Back 1243

Pain, erythema, swelling, and tenderness. Nearby ulceration or wound. Draining sinus tract.

Front 1244

How is osteomyelitis diagnosed?

Back 1244

Technetium bone scan and MRI. Plain x-ray: Periosteal elevation. Bone biopsy and culture is the best test.

Front 1245

What is the treatment of osteomyelitis?

Back 1245

Children treated with antibiotics; osteomyelitis in adults requires surgery and nafcillin or vancomycin (MRSA) plus an aminoglycoside or a 3rd gen cephalosporin for 12 weeks.

Front 1246

70-year-old woman with a swollen right knee; effusion and decreased mobility. Redness and tenderness. What is the next step?

Back 1246

Arthrocentesis.

Front 1247

What are the causes of septic arthritis?

Back 1247

Neisseria gonorrhoeae, staphylococci or streptococci; Rickettsia, viruses, spirochetes. Bacterial arthritis is divided into gonococcal and nongonococcal types?

Front 1248

What is the pathogenesis of gonococcal septic arthritis?

Back 1248

Sexual activity is risk factor for gonococcal septic arthritis. 1-5% of people with gonorrhea will develop disseminated disease.

Front 1249

What is the pathogenesis of nongonococcal bacterial arthritis?

Back 1249

Hematogenous spread. Bites, surgery, trauma, spread from surrounding infection. Normal or damaged joints can be infected after rheumatoid arthritis, osteoarthritis, surgery, prosthesis, gout; sickle, IVDU, diabetes, HIV.

Front 1250

What is the microbiology of nongonococcal arthritis?

Back 1250

Gram-positive (>85); (S. aureus [60%], Streptococcus [ 15%], Pneumococcus [5%]), Gram-negative (10-15%), polymicrobial (5%).

Front 1251

What is the presentation of nongonococcal septic arthritis?

Back 1251

Monoarticular in >85%, with a swollen, tender, erythematous joint with decreased range of motion. Knee most common. Petechiae or purpura?

Front 1252

How is nongonococcal septic arthritis diagnosed?

Back 1252

Nongonococcal. Culture of joint aspirate fluid and Gram stain. The cell count of the synovial fluid is high (>50,000) and is predominantly PMNs with a low glucose. Blood culture is positive in 50%.

Front 1253

How is gonococcal septic arthritis diagnosed?

Back 1253

Only 50% of aspirates have positive culture. Less than 10% of blood cultures are positive. Cervix, pharynx, rectum, and urethra may be positive.

Front 1254

What is the treatment for nongonococcal septic arthritis?

Back 1254

Good empiric coverage is nafcillin or oxacillin (or vancomycin if MRSA is suspected) combined with an aminoglycoside or a third-generation cephalosporin.

Front 1255

What is the treatment for gonococcal septic arthritis?

Back 1255

Ceftriaxone is the drug of choice.

Front 1256

What is gas gangrene (clostridial myonecrosis)?

Back 1256

Necrotizing infection of muscle by gas-producing organisms with sepsis. 80% caused by the spread of infection from C perfringens after traumatic wound (50%). Postoperative (30%), nontraumatic (20%).

Front 1257

What are the signs and symptoms of clostridial myonecrosis?

Back 1257

<1-4 days of incubation after the wound, then pain, swelling, and edema. Hypotension, tachycardia, and fever. Crepitation, renal failure, death.

Front 1258

How is clostridial myonecrosis diagnosed?

Back 1258

Gram-positive rods, but no white cells. Culture positive for C. perfringens.

Front 1259

What is the treatment for clostridial myonecrosis?

Back 1259

High-dose penicillin or clindamycin; surgical debridement or amputation. Hyperbaric oxygen 38-year-old man with fever, intravenous drug use, systolic murmur at the lower left sternal border?

Front 1260

What is the next step?

Back 1260

Blood cultures for infective endocarditis.

Front 1261

Which heart valves are most frequently affected by endocarditis?

Back 1261

Left-sided lesions of the aortic and mitral valves are the most common.

Front 1262

What procedures are associated with infective endocarditis?

Back 1262

Invasive and dental procedures. Oral and upper respiratory tract surgery. GI procedures. GU surgery. Alimentation catheters. Pressure-monitoring catheters. IV drug use.

Front 1263

What is the most common cause of acute infective endocarditis?

Back 1263

S. aureus is the most common cause. Seed previously normal valves. IV drug use is the major risk factor.

Front 1264

What are the signs of acute infective endocarditis?

Back 1264

Rapid onset of fever and sepsis. Splenomegaly of invasion of myocardium and rapid valve destruction. Embolic complications.

Front 1265

What is the most common cause of subacute infective endocarditis?

Back 1265

4-5% have negative blood cultures. Viridans group streptococci is the most common organism; low virulence. Seed abnormal valves.

Front 1266

Which cardiac conditions are risk factors for infective endocarditis?

Back 1266

1) Ventricular septal defect, 2) stenosis, 3) prosthetic valves, 4) indwelling catheters, 5) bicuspid aortic valve, 6) mitral valve prolapse, and 7) Marfan syndrome

Front 1267

What are the clinical signs of subacute infective endocarditis?

Back 1267

Slow onset with vague symptoms of malaise, low-grade fever, weight loss; and survival 80-90% with treatment.

Front 1268

What are the complications of infective endocarditis?

Back 1268

CHF (most common cause of death). Septic infarctions and metastatic infections to brain; spleen; kidneys; coronary arteries. Glomerulonephritis with nephrotic syndrome or renal failure (immune complex).

Front 1269

How is infective endocarditis diagnosed?

Back 1269

Positive blood cultures; transesophageal echo is >90% sensitive.

Front 1270

What is the treatment of infective endocarditis?

Back 1270

Empiric therapy with antistaphylococcal drug (nafcillin), and streptococcal drug (ampicillin and gentamicin). Vancomycin and gentamicin are empiric treatment if MRSA suspected.

Front 1271

What is the prophylactic treatment of bacterial endocarditis?

Back 1271

Dental procedures: Amoxicillin. For penicillin-allergic patients: clindamycin or (azithromycin, or clarithromycin or cephalexin). Urinary or gastrointestinal procedures: no prophylaxis is required.

Front 1272

What cardiac conditions require prophylactic antibiotics?

Back 1272

Prosthetic cardiac valves. Previous bacterial endocarditis, even in the absence of heart disease. Congenital cardiac malformations.

Front 1273

What cardiac conditions do not require prophylactic therapy?

Back 1273

Rheumatic and other acquired valvular disease. Hypertrophic cardiomyopathy; mitral valve prolapse with valvular regurgitation; surgically repaired shunts or intracardiac defects.

Front 1274

What are the causes of pericarditis?

Back 1274

Viruses/bacteria/tuberculosis/fungal/spirochetes; viral is most common (Coxsackie, ECHO). Acute HIV, SLE; RA, scleroderma. Uremia; neoplasia adjacent heart; hypothyroidism; irradiation; rheumatic fever, trauma, Dressler.

Front 1275

What is the clinical presentation of pericarditis?

Back 1275

Sharp, pleuritic, chest pain that improves when sitting up and leaning forward. Pericardial rub. Best at the apex with the patient sitting up. Low fever.

Front 1276

What is pulsus paradoxus?

Back 1276

Tamponade causes 10-mm drop in BP with inspiration. Blood is drawn into the right heart. Heart is compressed by fluid around it, and the septum bulges into left. Distended neck veins, tachycardia, hypotension also.

Front 1277

What are the ECG signs of pericarditis?

Back 1277

ST segment elevation in almost every lead, except aVR. The ST elevation progresses to T-wave inversion. PR depression may occur. Electrical alternans. Echocardiogram demonstrates effusion.

Front 1278

What is the treatment for viral pericarditis?

Back 1278

Indomethacin, ibuprofen, or Naprosyn. Prednisone if there is no response, or for tuberculosis with antitubercular medications. Pericardiocentesis and pericardial window for large effusion tamponade.

Front 1279

What is myocarditis?

Back 1279

Infection or inflammation of heart muscle by viruses (Coxsackie B). Other causes: bacteria, Rickettsia, fungi, parasites (Chagas, toxoplasmosis), Lyme. Radiation, drugs, collagen-vascular, hyperthyroidism.

Front 1280

What are the signs of myocarditis?

Back 1280

Myocardial dysfunction, dyspnea and fatigue. Asymptomatic, subclinical infection or a rapid progression to chest pain, arrhythmia, and death. S-3 gallop and murmurs.

Front 1281

How is myocarditis diagnosed?

Back 1281

Nonspecific ST-T changes are most common. Heart block. CK-MB, LDH, troponin elevated. LV systolic dysfunction. Viruses from stool, saliva, nasopharynx. Ab to viruses. Biopsy rarely done.

Front 1282

What is the vector for Lyme disease?

Back 1282

Lyme disease is spread by the bite of the Ixodes scapularis tick.

Front 1283

What is the clinical presentation of lyme disease?

Back 1283

Rash 3-30 d after tick bite. 80% develop erythema migrans rash at bite (red patch, central clearing, "bull's-eye"). Rash resolves in several weeks. Flulike illness with fever, chills, myalgias.

Front 1284

What are the neurologic symptoms of lyme disease?

Back 1284

Neurologic symptoms in 10-20% of patients, most commonly paralysis of the seventh cranial nerve (facial paralysis), which may be bilateral. Meningitis, encephalitis, headache, and memory disturbance may develop.

Front 1285

What are the cardiovascular signs of lyme disease?

Back 1285

AV heart block, myocarditis, pericarditis, and various arrhythmias. Joint involvement may develop months to years later in up to 60%, most commonly a migratory polyarthritis.

Front 1286

What is the diagnostic criteria of Lyme disease?

Back 1286

Erythema migrans with 1 late manifestation and lab confirmation. Treat based on rash. Serology by ELISA and western blot does not distinguish current and previous infection. Early test is often negative.

Front 1287

What is the treatment of Lyme disease?

Back 1287

The rash, the facial palsy, and joint pain can be treated with oral doxycycline or amoxicillin. Heart block, meningitis, myocarditis, or encephalitis are treated with intravenous ceftriaxone.

Front 1288

Which cell is the primary target of HIV?

Back 1288

The primary mechanism of HIV is to infect a subset of T lymphocytes called CD4 cells, often just referred to as T cells.

Front 1289

What are the symptoms of pneumocystis jiroveci pneumonia?

Back 1289

CD4 count <200. Pneumonia; dyspnea on exertion, dry cough, fever, chest pain; usually subacute onset and progression.

Front 1290

What is the diagnostic test for PJP?

Back 1290

Bronchoscopy with bronchoalveolar lavage for direct identification of the organism. Chest x-ray reveals bilateral, interstitial infiltrates. PJP may occur with a normal chest x-ray. Serum LDH is usually elevated.

Front 1291

What is the treatment of pneumocystis jiroveci pneumonia?

Back 1291

Trimethoprim-sulfamethoxazole (TMP-SMZ) IV is the first-line therapy for mild-severe disease and may cause a rash.

Front 1292

What is the alternative treatments for PJP if TMP-SMZ is not tolerated?

Back 1292

For mild-moderate disease: dapsone and trimethoprim, or primaquine and clindamycin; or atovaquone, or trimetrexate (with leucovorin).

Front 1293

What are the adverse effects of pentamidine?

Back 1293

Pancreatitis, hyperglycemia, hypoglycemia.

Front 1294

What are the indications for steroids in PJP?

Back 1294

Steroids are used as adjunctive therapy for any patient with severe pneumonia. Severe is defined with a PaO2 of <70 mm Hg or an A-a gradient of >35 mm Hg.

Front 1295

How is cytomegalovirus diagnosed?

Back 1295

Funduscopy; colonoscopy with biopsy for diarrhea; or upper gastrointestinal endoscopy with biopsy of ulcers.

Front 1296

What is the treatment of cytomegalovirus retinitis and esophagitis?

Back 1296

Valganciclovir, an oral prodrug of ganciclovir; achieves levels comparable to IV ganciclovir. IV ganciclovir is reserved for serious CNS infections; foscarnet and cidofovir for ganciclovir resistance.

Front 1297

What are the side effects of ganciclovir?

Back 1297

Ganciclovir may cause neutropenia.

Front 1298

What is the prophylactic therapy for cytomegalovirus retinitis?

Back 1298

Valganciclovir can be used for maintenance therapy.

Front 1299

What is Mycobacterium avium complex?

Back 1299

Occurs in HIV infected with CD4 <50/mm. Atypical mycobacteria found in the environment; mode of infection is inhalation or ingestion. Fevers, night sweats, bacteremia, wasting, anemia, diarrhea.

Front 1300

What is the testing for Mycobacterium avium complex?

Back 1300

Blood culture, culture of bone marrow, liver, or other body tissue or fluid.

Front 1301

What is the treatment of Mycobacterium avium complex?

Back 1301

Clarithromycin, ethambutol, rifabutin. Prophylaxis is azithromycin once a week or clarithromycin bid; rifabutin is alternative. Prophylaxis discontinued if antiretrovirals raise CD4 >100 for several months.

Front 1302

At what level of CD4 cell count does toxoplasmosis occur?

Back 1302

Occurs in HIV infected patients with CD4 <100/mcL.

Front 1303

What are the signs of cerebral toxoplasmosis?

Back 1303

Brain mass lesion: Headache, confusion, seizures, and focal neurologic deficits

Front 1304

What tests are used to detect toxoplasmosis?

Back 1304

CT of head showing a "ring" (contrast enhancing) with edema and mass effect. Trial of anti-toxoplasmosis therapy is given for 2 weeks, and scan repeated. Shrinkage of lesion is diagnostic. Toxoplasmosis serology, CSF PCR.

Front 1305

What is the treatment of toxoplasmosis?

Back 1305

Pyrimethamine and sulfadiazine. Clindamycin can be substituted for sulfadiazine. Leucovorin prevents marrow suppression. Prophylaxis with TMP/SMZ or dapsone/pyrimethamine.

Front 1306

What is cryptococcosis?

Back 1306

Occurs in HIV infected persons with CD4 <100/mcL. Meningitis; fever, headache, and malaise

Front 1307

How is cryptococcosis diagnosed?

Back 1307

Lumbar puncture with India ink and cryptococcal antigen testing. Serum cryptococcal antigen testing.

Front 1308

What is the treatment of cryptococcosis?

Back 1308

Amphotericin intravenously for 10-14 days (with flucytosine), followed by fluconazole orally for suppressive therapy.

Front 1309

What is the normal CD4 cell count?

Back 1309

700-1,500/mcL.

Front 1310

What CD4 cell count is associated with oral thrush, Kaposi sarcoma, tuberculosis, zoster, lymphoma?

Back 1310

200-500/mcL

Front 1311

What CD4 cell count is associated with pneumocystis jiroveci pneumonia, dementia, progressive multifocal leukoencephalopathy, disseminated histoplasmosis and coccidiomycosis?

Back 1311

100-200/mcL

Front 1312

What opportunistic infections occur when the CD4 count is <100/mcL?

Back 1312

Toxoplasmosis, Cryptococcus, cryptosporidiosis, disseminated herpes simplex

Front 1313

What opportunistic infections occur when the CD4 count is <50/mcL?

Back 1313

Cytomegalovirus, Mycobacterium avium complex. Progressive, multifocal leukoencephalopathy, CNS lymphoma.

Front 1314

What test indicates an adequate response to antiretroviral therapy in HIV-infected persons?

Back 1314

The goal is complete suppression of viremia with <50 to 70 copies of HIV-RNA/mcL.

Front 1315

What are the indications for viral sensitivity testing?

Back 1315

Patient failing a combination of medications and a change in therapy is necessary. Any pregnant woman who has not been fully suppressed on the initial combination of medications.

Front 1316

What are the side effects of zidovudine?

Back 1316

Leukopenia, anemia, gastrointestinal

Front 1317

What are the side effects of didanosine (DDI)?

Back 1317

Pancreatitis, peripheral neuropathy.

Front 1318

What are the side effects of stavudine (D4T)?

Back 1318

Peripheral neuropathy

Front 1319

What are the side effects of lamivudine (3TC)?

Back 1319

No side effects have been reported in additional to placebo.

Front 1320

What are the side effects of emtricitabine?

Back 1320

Structurally related to lamivudine; few side effects.

Front 1321

What is the structure of tenofovir?

Back 1321

Tenofovir is a nucleotide analog as compared to the others that are nucleoside analogs.

Front 1322

What are the side effects of abacavir?

Back 1322

Hypersensitivity reaction in the first 6 weeks of therapy. Rash, fever, nausea/vomiting, muscle and joint aches, dyspnea. The drug should be stopped and never restarted.

Front 1323

What are the side effects of zalcitabine (DDC)?

Back 1323

Pancreatitis, peripheral neuropathy, lactic acidosis

Front 1324

What are the nucleoside reverse transcriptase inhibitors?

Back 1324

Zidovudine (ZDV or AZT), didanosine (DDI), stavudine (D4T), lamivudine (3TC), emtricitabine, abacavir, zalcitabine (DDC).

Front 1325

What are the side effects of protease inhibitors?

Back 1325

Hyperlipidemia, hyperglycemia, elevated liver enzymes; fat loss (lipoatrophy) from the face and extremities with redistribution of fat to the back of the neck and abdominal viscera.

Front 1326

What are the side effects of nelfinavir?

Back 1326

Nausea, diarrhea.

Front 1327

What are the side effects of indinavir?

Back 1327

Nephrolithiasis (4%), hyperbilirubinemia (10%).

Front 1328

What are the side effects of ritonavir?

Back 1328

Severe nausea, diarrhea.

Front 1329

What are the side effects of saquinavir?

Back 1329

Gastrointestinal effects.

Front 1330

What are the side effects of amprenavir?

Back 1330

Rash, headache, diarrhea, and nausea.

Front 1331

What are the side effects of the lopinavir/ritonavir combination?

Back 1331

Diarrhea

Front 1332

What are the side effects of atazanavir?

Back 1332

Diarrhea, asymptomatic hyperbilirubinemia.

Front 1333

What are the names of the protease inhibitors?

Back 1333

Nelfinavir, indinavir, ritonavir, saquinavir, amprenavir, atazanavir.

Front 1334

What are the names of non-nucleoside reverse transcriptase inhibitors?

Back 1334

Efavirenz, nevirapine, delavirdine.

Front 1335

What are the side effects of efavirenz?

Back 1335

Neurologic; somnolence, confusion, or psychiatric disturbance; non-nucleoside reverse transcriptase inhibitor.

Front 1336

What are the side effects of nevirapine?

Back 1336

Rash, hepatotoxicity.

Front 1337

What are the side effects of delavirdine?

Back 1337

Rash.

Front 1338

When should antiretroviral therapy be started in HIV infected patients?

Back 1338

Antiretroviral medication should be started when the CD4 count has dropped or the viral load has risen.>55,000 copies/mL of RNA.

Front 1339

What antiretrovirals should be started in HIV infected patients?

Back 1339

Use two nucleosides combined with a protease inhibitor or, Use two nucleosides combined with efavirenz or, Use two nucleosides combined with two protease inhibitors.

Front 1340

What is highly active antiretroviral therapy?

Back 1340

Uses medications with activity at different sites; 2 NRTIs (tenofovir/emtricitabine or ZDV/lamivudine) combined with NNRTI (efavirenz) or 2 PI (atazanavir/ritonavir, fosamprenavir/ritonavir, lopinavir/ritonavir).

Front 1341

What is "boosted protease inhibitor therapy"?

Back 1341

Practice of giving protease inhibitors in combination with a low dose of ritonavir (a PI). Ritonavir when given in a low dose with other PIs, decreases metabolism of the second PI and increases drug level.

Front 1342

What is considered adequate antiretroviral therapy?

Back 1342

Any regimen that increases the CD4 count and reduces the viral load to undetectable amounts or close to undetectable amounts. Drop of at least 50% of viral load in the first month indicates adequate therapy.

Front 1343

What percentage of children born to HIV positive mothers will be infected with HIV?

Back 1343

Without treatment, 30% of children born to HIV-positive mothers will be infected. All children at birth will carry the maternal antibody by ELISA testing.

Front 1344

What treatment should be given to pregnant HIV infected women?

Back 1344

Women with low CD4 or high viral load should receive triple antiretrovirals. ZDV, a second nucleoside and a protease inhibitor should begin in pregnant women at 14 weeks if not already on therapy.

Front 1345

What are the indications for cesarean section in pregnant HIV-infected women?

Back 1345

C-section is used routinely in those whose CD4 count is low or whose viral load >1000 copies.

Front 1346

Which antiretroviral in a known teratogen?

Back 1346

The only known teratogen is efavirenz in animal studies.

Front 1347

What treatment is recommended for HIV infected pregnant women?

Back 1347

If already on antiretrovirals, continue. If low CD4 or opportunistic infection, start immediately. If high CD4, combination therapy can begin at 14 weeks. Can deliver vaginally if the viral load <1000.

Front 1348

What is the effect of breastfeeding on transmission of HIV to the infant?

Back 1348

Breast feeding is associated with transmission of virus to the infant.

Front 1349

What postexposure prophylaxis for HIV after needlestick injury should be given?

Back 1349

Persons with serious exposure to blood of HIV-pos should receive ZDV, lamivudine, nelfinavir (or any other fully suppressive 3-drug combo) for 4 wks. ZDV alone will decrease the risk of transmission by 80%.

Front 1350

What is Q-Fever?

Back 1350

Coxiella burnetii infection, which is transmitted by inhalation; found in cattle, sheep, and goats.

Front 1351

What are the clinical signs of Q-fever?

Back 1351

Febrile illness, atypical pneumonia, hepatitis, and hepatomegaly, endocarditis. Treatment is doxycycline. Diagnosed by specific serology.

Front 1352

What is Rocky Mountain spotted fever?

Back 1352

R. rickettsi is transmitted by the wood tick from the mid-Atlantic coast, upper South, and Midwest. In spring and summer.

Front 1353

What is the triad of Rocky Mountain spotted fever?

Back 1353

Abrupt fever, headache and erythematous maculopapules. Rash starts wrist, ankles and spreads centripetally, palms and soles. Confusion, lethargy, dizziness, irritability, stiff neck, GI symptoms.

Front 1354

How is Rocky Mountain spotted fever diagnosed?

Back 1354

Specific serology; biopsy of skin lesion.

Front 1355

What is the treatment of Rocky Mountain fever?

Back 1355

Doxycycline

Front 1356

What is toxoplasmosis?

Back 1356

Intracellular parasite. 50% of the US population is antibody positive. Prevalence increases with age. Undercooked meat, especially pork and lamb. Also from domestic cat feces; transplacental infection.

Front 1357

What is the presentation of toxoplasmosis?

Back 1357

80-90% asymptomatic in the immunocompetent. In AIDS: chorioretinitis, CNS mass lesion, encephalitis. Headache, fever, nausea. The retinal lesion can cause visual complaints.

Front 1358

How is toxoplasmosis diagnosed?

Back 1358

Serology is the most common method used. The best test is to visualize the parasite in biopsy tissue.

Front 1359

What is the treatment of toxoplasmosis?

Back 1359

Pyrimethamine and sulfadiazine.

Front 1360

What is tetanus?

Back 1360

Infectious complication of wounds caused by the toxin of Clostridium tetani; takes 1-7 days to develop; spore forming, Gram-positive rod.

Front 1361

What are the clinical signs tetanus infection?

Back 1361

Tonic spasms of voluntary muscles, respiratory arrest, difficulty in swallowing (dysphagia), restlessness, irritability, stiff neck, arms, and legs; headache, lockjaw, high mortality.

Front 1362

What is the prophylaxis of tetanus?

Back 1362

Tetanus toxoid (boosters every 10 years). Débride wound. Antitoxin is tetanus immunoglobulin; penicillin 10-14 days.

Front 1363

What is aspergillosis?

Back 1363

Fungus widespread in environment; pulmonary disease in immunocompromised. 90 species, with A. fumigatus the most common in decaying organic matter, ceiling tile, ventilation systems.

Front 1364

What are the signs of aspergillosis?

Back 1364

Asthma with cough, fever, wheezing. Mycetoma, a "fungal ball": in a pre-existing cavity, with hemoptysis. Invasive pulmonary. Disseminates to any organ from lung.

Front 1365

What are the risk factors for aspergillosis?

Back 1365

Risks: 1) neutropenia <500, 2) steroids 3) cytotoxic drugs (e.g., azathioprine, cyclophosphamide).

Front 1366

How is aspergillosis diagnosed?

Back 1366

Abnormal chest x-ray and Aspergillus in sputum.

Front 1367

What are voriconazole and caspofungin?

Back 1367

Drugs used to treat aspergillosis and other fungal infections.

Front 1368

What is the treatment of aspergillosis?

Back 1368

Invasive disease is treated with voriconazole, a broad-spectrum azole. Itraconazole for very mild disease. Caspofungin is superior to amphotericin. Caspofungin is an echinocandin.

Front 1369

What is blastomycosis?

Back 1369

A fungus that is strongly associated with rotting organic material and soil. Occurs in southeast and central US. It has a 10:1 male:female ratio. Begins with inhalation of decaying wood and vegetation.

Front 1370

What are the signs of blastomycosis?

Back 1370

Fever, cough, chest pain, and weight loss. After inhalation, disseminates anywhere in body, but skin is by far the most common.

Front 1371

What is the treatment of blastomycosis?

Back 1371

Prolonged amphotericin for severe disease (8-12 weeks); itraconazole or ketoconazole for mild disease.

Front 1372

What is the cause of toxic shock syndrome?

Back 1372

Staphylococcus aureus toxin TSST-1. Infected tampons, sponges, and surgical wound infections.

Front 1373

What are the clinical signs of toxic shock syndrome?

Back 1373

Hypotension, fever, mucosal changes, desquamative rash on hands and feet. Gastrointestinal, renal, hepatic, and muscular symptoms.

Front 1374

What is the treatment of toxic shock syndrome?

Back 1374

Beta-lactamase stable penicillin (nafcillin or oxacillin). Restoration of hypovolemic shock, remove infected tissue, prosthesis, tampons, diaphragm.

Front 1375

What is acute renal failure?

Back 1375

Rapid rise in blood urea nitrogen or creatinine over a period of several hours to days. Decrease in glomerular filtration rate.

Front 1376

What is renal insufficiency?

Back 1376

Renal insufficiency is renal failure, but not to the point of needing dialysis. The term azotemia can be used interchangeably with the term renal insufficiency.

Front 1377

What is uremia?

Back 1377

Very severe renal failure requiring dialysis. Severe acidosis, mental status changes, hyper, fluid overload, anemia, hypocalcemia, pericarditis. Bleeding. Uremia is same as "end stage renal disease.?

Front 1378

What is blood urea nitrogen?

Back 1378

BUN becomes abnormally elevated in all forms of renal failure. BUN rises after a protein meal or from gastrointestinal bleeding. BUN is derived from protein waste products.

Front 1379

What is creatinine?

Back 1379

Creatinine is the closest approximation of glomerular filtration rate. Creatinine is a metabolic product of skeletal muscle. Creatinine can be falsely low just because of a decrease in muscle mass.

Front 1380

What is prerenal azotemia?

Back 1380

Renal insufficiency caused by diminished perfusion, hypovolemia (dehydration, burns, diuretic, vomiting, diarrhea, hemorrhage), hypotension (septic, cardiogenic, anaphylactic), third spacing in peritonitis.

Front 1381

What is the laboratory criteria for prerenal azotemia?

Back 1381

BUN:creatinine ratio of 20:1. There is also a low urine sodium and low fractional excretion of sodium (FeNa <1%). High urine osmolality with a high specific gravity (>1.010) and a high urine osmolality (>500).

Front 1382

What are the signs of renal artery stenosis?

Back 1382

High BUN and creatinine with a high BUN:creatinine ratio. HTN, prerenal azotemia. ACE inhibitors will markedly diminish renal perfusion in renal artery stenosis because of the high aldosterone.

Front 1383

What is hepatorenal syndrome?

Back 1383

Renal failure caused by hepatic failure secondary to intense vasoconstriction of afferent arteriole, resulting in decreased renal perfusion.

Front 1384

What are the laboratory abnormalities in hepatorenal syndrome?

Back 1384

Prerenal azotemia with a high BUN:creatinine ratio >20:1. Urine Na <10 and a fractional excretion of sodium <1%. No improvement in renal failure after 1.5 L saline is diagnostic of hepatorenal syndrome.

Front 1385

What is the effect of ACE inhibitors on the kidney?

Back 1385

Renal failure can be caused by vasodilation of the efferent arteriole. In elderly, diabetic, hypertensive, or renal disease such as from myeloma, an ACEI can result in a decreased renal function. Rise in BUN and creatinine.

Front 1386

What is the hepatopulmonary syndrome?

Back 1386

Pulmonary failure is caused by hepatic disease. The oxygen saturation drops when the patient sits up and there is an increase in the A-a gradient.

Front 1387

What is postrenal azotemia?

Back 1387

Bilateral blockage in outflow of urine. Small stone or clot in bladder. Bladder CA, prostate hypertrophy or CA, retroperitoneal fibrosis, neurogenic bladder. Creatinine will only begin to rise when 80% of renal function lost.

Front 1388

What are the laboratory abnormalities in postrenal azotemia?

Back 1388

BUN and creatinine will elevate in a ratio of 20:1 as with prerenal azotemia. Low fractional excretion of sodium and low urine sodium.

Front 1389

What are the consequences of prolonged postrenal obstruction?

Back 1389

Permanent damage occurs, and the kidney tubule cells die, then the BUN:creatinine ratio will lower to 10:1, such as that seen in acute tubular necrosis. Recovery is possible until 10 days of obstruction.

Front 1390

What are the clinical findings in postrenal azotemia?

Back 1390

Distended bladder, bilateral hydronephrosis on renal sonogram or CT, or large volumes of urine in bladder after passing Foley catheter. After voiding, there should be no more than 50 mL of residual.

Front 1391

What is acute tubular necrosis?

Back 1391

85% of acute renal failure is caused by intrinsic renal disease, such as ATN caused by either hypoperfusion of kidney or toxic injury (aminoglycoside). ATN is most common cause of ARF in hospitalized.

Front 1392

What are the urine microscopic findings in acute tubular necrosis?

Back 1392

Severe ischemia causes the tubular cells to necrose and slough off into the urine and become visible as granular, muddy brown, or pigmented casts. At the point of necrosis, the renal insufficiency can be permanent.

Front 1393

How is acute tubular necrosis diagnosed?

Back 1393

BUN:creatinine ratio 10:1. High urine sodium (>40), high fractional excretion of sodium (>1%), and low urine osm (<350). If tubular cells die of ischemia, then kidney can neither concentrate nor dilute the urine.

Front 1394

What is the treatment of acute tubular necrosis?

Back 1394

Underlying cause must be corrected. Hydration is given to exclude possibility of prerenal component. Furosemide does not reverse ATN. Dopamine at low doses does not increase renal perfusion. Dialysis.

Front 1395

What is allergic interstitial nephritis?

Back 1395

Allergic interstitial nephritis causes 10-15% of intrinsic renal; failure fever and rash, eosinophils in the urine. AIN is usually caused by an adverse effect of medications. Infections can also cause AIN.

Front 1396

What medications can cause allergic interstitial nephritis?

Back 1396

Penicillin, cephalosporins, sulfas, allopurinol, rifampin, quinolones. Calcium blockers. Sulfa drugs include thiazides, furosemide, acetazolamide.

Front 1397

What infections can cause allergic interstitial nephritis?

Back 1397

AIN is also caused by infections by viruses, bacteria, and fungi. Leptospirosis, legionella, CMV, rickettsia, and streptococci.

Front 1398

What autoimmune disorders can cause allergic interstitial nephritis?

Back 1398

Systemic lupus erythematosus (SLE), Sjögren syndrome, sarcoidosis, and cryoglobulins.

Front 1399

What laboratory abnormalities are associated with allergic interstitial nephritis?

Back 1399

Eosinophilia, eosinophiluria, hematuria, proteinuria, increased IgE. Best initial test is a urinalysis for white cells. Urine eosinophils on Wright stain. Kidney biopsy not necessary.

Front 1400

What is the treatment of allergic intestinal nephritis?

Back 1400

AIN resolves spontaneously after stopping the offending agent. Short course of steroids may be administered.

Front 1401

A 25-year-old man was exercising vigorously became very weak with painful muscles and dark urine. What is the most important test to do first?

Back 1401

Electrocardiogram

Front 1402

What are the causes of rhabdomyolysis?

Back 1402

Rhabdomyolysis is caused by sudden, severe crush injury, seizures, severe exertion, hypokalemia, hypophosphatemia, and medications such as statins.

Front 1403

What are the laboratory signs of rhabdomyolysis?

Back 1403

The most important test after a severe crush injury or seizure and rhabdomyolysis is an ECG or potassium level. UA is positive for blood but with no red cells because myoglobin reacts with the dipstick.

Front 1404

What action should be taken if peaked T-waves are present on an ECG?

Back 1404

Acidosis and hyperkalemia can cause arrhythmia. If there are peaked T-waves, an amp of calcium gluconate should be given.

Front 1405

How is rhabdomyolysis confirmed in the laboratory?

Back 1405

CPK skeletal muscle necrosis. Metabolic acidosis with a decreased serum bicarbonate, hyperphosphatemia, hypocalcemia. Severe hyperuricemia. Rapidly rising creatinine.

Front 1406

What is the treatment for rhabdomyolysis?

Back 1406

If there are ECG abnormalities from the hyperkalemia, therapy is calcium chloride or gluconate. Hydration, mannitol. Alkalinize urine with bicarbonate to prevent precipitation of pigment in tubule.

Front 1407

What is the most common cause of hyperoxaluria resulting in acute renal failure?

Back 1407

Ethylene glycol overdose from antifreeze. An intoxicated person with a metabolic acidosis with an elevated anion gap and renal insufficiency. Oxalate crystals on UA. Oxalate crystals are shaped like envelopes.

Front 1408

What is the treatment of acute ethylene glycol overdose?

Back 1408

Fomepizole infusion to prevent the formation of the toxic metabolite of ethylene glycol (oxalic acid). Dialysis to then remove the ethylene glycol. Sodium bicarbonate to correct acidosis.

Front 1409

What renal complication occurs in patients being given chemotherapy?

Back 1409

Acute renal failure from uric acid toxicity occurs in the setting of tumor lysis syndrome. Vigorous hydration and allopurinol should be given before chemotherapy.

Front 1410

What is the effect of hypercalcemia on the kidneys?

Back 1410

Calcium precipitates in tubule, forming stones. Hypercalcemia can lead to distal RTA and nephrogenic diabetes insipidus. Most common cause of hypercalcemia is primary hyperparathyroidism.

Front 1411

Which drugs are toxic to the kidneys?

Back 1411

NSAIDs, aminoglycosides, cephalosporins, contrast agents, amphotericin, cisplatin, radiation effect, lead, mercury, or gold, and cyclosporine.

Front 1412

What method of administration of aminoglycosides reduces the risk of toxicity?

Back 1412

Ability of antibiotics to kill is associated with peak level, but toxicity is associated with the trough level. Once-a-day dosing allows high bactericidal levels and very low trough levels, which reduce toxicity.

Front 1413

What is the affect of amphotericin B on the kidneys?

Back 1413

Renal insufficiency and distal renal tubular acidosis. After several weeks of amphotericin, the patient will develop high creatinine and decreased magnesium.

Front 1414

How does atheroembolic disease affect the kidneys?

Back 1414

Vascular procedures (angioplasty) cause renal failure several days later. Atheroemboli are associated with eosinophilia, low complement, bluish discoloration of fingers, toes, livedo reticularis.

Front 1415

What are the common nephrotoxic medications?

Back 1415

Radiocontrast for CT can result in renal failure 12 hours after. Pentamidine is associated with renal failure and pancreatitis. Vancomycin, aminoglycosides, cyclosporine, and lithium.

Front 1416

Which antiretroviral is associated with renal failure?

Back 1416

Indinavir results in renal failure from the drug precipitating in the kidney tubules. Indinavir stones require contrast to be visualized on a spiral CT scan.

Front 1417

Which persons are at risk for analgesic nephropathy?

Back 1417

NSAIDs are a frequent cause of renal failure. A rise in creatine occurs in persons with significant impairment such as the elderly or those with hypertension or diabetes.

Front 1418

What are the causes of acute papillary necrosis?

Back 1418

Acute papillary necrosis occurs in sickle cell disease, diabetes, urinary obstruction, chronic pyelonephritis, and NSAIDs.

Front 1419

What is the presentation of acute papillary necrosis?

Back 1419

Sudden flank pain, hematuria, pyuria, fever. Similar to pyelonephritis. Necrotic material in urine. Papillary necrosis will have a negative culture. The best test for papillary necrosis is CT.

Front 1420

What is glomerulonephritis?

Back 1420

Glomerulonephritis is inflammation of the glomerulus caused by autoimmunity, antibodies, or vasculitis.

Front 1421

What is the presentation of glomerulonephritis?

Back 1421

Edema, hematuria, red cell casts, and hypertension. The urine red cells are dysmorphic.

Front 1422

What are the physical signs of glomerulonephritis?

Back 1422

Edema of GN initially appears in areas of low tissue tension, such as periorbital or scrotum. Edema can be diffuse. Salt and water retention leads to edema and hypertension.

Front 1423

What amount of proteinuria is associated with glomerulonephritis?

Back 1423

Modest amounts of protein appear in the urine with the daily total being <2 grams per 24 hours. When the proteinuria rises to >3.5 grams per 24 hours the patient has nephrotic syndrome.

Front 1424

What are the laboratory signs of glomerulonephritis?

Back 1424

Low urine Na with a fractional excretion of Na <1%.Many forms of GN are associated with a positive ANCA, basement membrane antibodies, ANA, or antistreptolysin. The most important test is renal biopsy.

Front 1425

What is Wegener granulomatosis?

Back 1425

Vasculitis of kidney, lung, upper respiratory, sinuses, middle ear. Chronic upper/lower respiratory illness, not responding to antibiotics, with renal disease suggests WG. Involves skin, joints, eyes, GI; neuropathy.

Front 1426

What are the laboratory abnormalities associated with Wegener granulomatosis?

Back 1426

Elevated ESR, anemia, leukocytosis. Rheumatoid factor in 50%. The best initial test that is specific for WG is the cytoplasmic antineutrophil cytoplasmic antibody. Complement levels are normal.

Front 1427

What is the most accurate test for Wegener granulomatosis?

Back 1427

The most accurate test for WG is a biopsy of the kidney or lung looking for granulomas. Biopsy of the nasal septum is less sensitive and has more false negative results.

Front 1428

What is the treatment of Wegener's granulomatosis?

Back 1428

Cyclophosphamide and steroids.

Front 1429

What is Churg-Strauss syndrome?

Back 1429

Characterized by lung involvement, neuropathy, skin lesions, GI, cardiac, and renal involvement.

Front 1430

What is the presentation of Churg-Strauss syndrome?

Back 1430

Fever, weight loss, malaise. Asthma, eosinophilia, atopic diseases. Elevated eosinophil, positive P-ANCA or antimyeloperoxidase. Most accurate test is lung biopsy: granulomas, eosinophils.

Front 1431

What is the treatment of Churg-Strauss syndrome?

Back 1431

Glucocorticoids and cyclophosphamide.

Front 1432

What is Goodpasture syndrome?

Back 1432

Idiopathic disorder of renal and lung disease characterized by a unique anti-basement membrane antibody. GP does not affect multiple organs or sites in the body other than the lung and the kidney.

Front 1433

What are the clinical signs of Goodpasture syndrome?

Back 1433

Hematuria, proteinuria, hemoptysis, cough, dyspnea. Best test is anti-basement membrane Ab to type IV collagen. Lung or kidney biopsy shows hemosiderin macrophages and linear deposits.

Front 1434

What is the treatment of Goodpasture syndrome?

Back 1434

Plasmapheresis and steroids. Cyclophosphamide.

Front 1435

What is polyarteritis nodosa?

Back 1435

Systemic vasculitis of small and medium arteries of every organ exception lung. Renal involvement manifests as HTN, renal insufficiency, and hemorrhage due to microaneurysms. Biopsy.

Front 1436

What is the treatment of polyarteritis nodosa?

Back 1436

Cyclophosphamide and steroids.

Front 1437

What are the symptoms of polyarteritis nodosa?

Back 1437

Fever, weight loss, malaise. Involvement of skin, eyes, muscles, GI, heart, kidneys, and neurologic system. Abdominal pain and joint pain. Anemia and an elevated sedimentation rate.

Front 1438

What is the treatment of polyarteritis nodosa?

Back 1438

Steroids and cyclophosphamide.

Front 1439

What is Henoch-Schönlein purpura?

Back 1439

Systemic deposition of IgA, resulting in renal insufficiency, skin lesions, GI symptoms.

Front 1440

What is the tetrad of Henoch-Schönlein purpura?

Back 1440

Tetrad of palpable purpura, arthralgias, abdominal pain, and renal disease. IgA deposited in walls of blood vessels. Biopsy is usually not performed. HSP most often resolves spontaneously.

Front 1441

What is the treatment of Henoch-Schönlein purpura?

Back 1441

Treatment is supportive. Steroids can be used.

Front 1442

What is IgA nephropathy (Berger disease)?

Back 1442

IgA nephropathy with mild hematuria that resolves spontaneously in 30%. About 40-50% of patients progress to end stage renal disease. Deposition of IgA only in kidney.

Front 1443

What are the signs of Berger disease?

Back 1443

HTN. Usually an Asian patient under 35 years of age who has had a recent viral illness or pharyngitis, then develops hematuria 1-2 days later.

Front 1444

How is Berger disease diagnosed?

Back 1444

The diagnosis is based on finding IgA deposited in the kidney on biopsy.

Front 1445

What is the treatment of Berger disease?

Back 1445

Proteinuria is treated with ACE inhibitors or angiotensin receptor blockers (ARB).

Front 1446

What are the causes of postinfectious glomerulonephritis?

Back 1446

Group A beta-hemolytic streptococci (S pyogenes) and other infections can cause postinfectious glomerulonephritis. Any infectious agent, including hepatitis B and C, CMV, staph endocarditis.

Front 1447

What type of infection can cause post-streptococcal glomerulonephritis?

Back 1447

Poststreptococcal glomerulonephritis can occur with throat or skin infection with S pyogenes. Rheumatic fever only occurs after pharyngitis in 10-15% of patients with GABS pharyngitis.

Front 1448

What are the signs of postinfectious glomerulonephritis?

Back 1448

Smoky, cola urine from hematuria, red cell casts, proteinuria. Periorbital edema and HTN. The best initial test is antistreptolysin (ASO) and the antihyaluronic acid. Complement low. Renal biopsy rarely.

Front 1449

What is the treatment of postinfectious glomerulonephritis?

Back 1449

Treatment is management of fluid overload and HTN with diuretics. Resolves spontaneously. Antibiotics should be given to eradicate the organism from the pharynx.

Front 1450

What are thrombotic thrombocytopenic purpura and hemolytic uremic syndrome?

Back 1450

TTP and HUS are two different varieties of the same disease of hemolytic anemia, uremia, and thrombocytopenia.

Front 1451

What are the causes of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome?

Back 1451

TTP is associated with HIV, but it is most often idiopathic. HUS is more common in children and with E. coli 0157:H7 food poisoning.

Front 1452

What is the triad of hemolytic uremic syndrome?

Back 1452

HUS is a triad of hemolytic anemia, uremia, and thrombocytopenia.

Front 1453

What are the signs of thrombotic thrombocytopenic purpura?

Back 1453

TTP has anemia, uremia, and thrombocytopenia, and is also associated with fever and headache, confusion, seizures, focal deficit.

Front 1454

What are the laboratory findings in hemolytic uremic syndrome and thrombotic thrombocytopenic purpura?

Back 1454

Anemia is intravascular, and the blood smear shows schistocytes, helmet cells, fragmented red cells. LDH and reticulocyte count will be elevated and the haptoglobin decreased.

Front 1455

What is the treatment of thrombotic thrombocytopenic purpura and hemolytic uremic syndrome?

Back 1455

Plasmapheresis. Dipyridamole may preventing platelet aggregation in TTP. Antibiotics contraindicated in HUS; organism releases toxins. Administering platelets will worsen CNS and renal.

Front 1456

What is Alport syndrome?

Back 1456

Glomerular disease with anterior lenti conus (lens protrusion), and sensorineural hearing loss.

Front 1457

What is idiopathic rapidly progressive glomerulonephritis?

Back 1457

RPGN may occur with any glomerular disease. Idiopathic form is associated with crescent formation in the kidney, which is ANCA negative. Diagnosis is with renal biopsy.

Front 1458

What us the treatment of idiopathic rapidly progressive glomerulonephritis?

Back 1458

Treatment is with steroids and cyclophosphamide.

Front 1459

What is amyloid?

Back 1459

Amyloid is a proteinaceous material associated with chronic infectious or inflammatory conditions, such as rheumatoid arthritis, inflammatory bowel disease, or myeloma.

Front 1460

How does amyloidosis affect the organs?

Back 1460

Amyloid builds up in kidney, causing glomerulonephritis, accumulates in GI, nerves, muscles. Restrictive cardiomyopathy, rhythm disorders, heart block. Macroglossia, carpal tunnel, malabsorption.

Front 1461

How is amyloidosis diagnosed?

Back 1461

Biopsy of the involved organ, such as the kidney. Congo red testing shows green birefringence. Amyloidosis treatment consists of controlling the underlying disease. Melphalan and prednisone.

Front 1462

What is nephrotic syndrome?

Back 1462

Renal disease sufficient to cause proteinuria >3.5 gm/24 h, hyperlipidemia, edema, and a low serum albumin.

Front 1463

What are the causes of nephrotic syndrome?

Back 1463

1/3 nephrotic syndrome associated diabetes, HTN, myeloma. Glomerulonephritis becomes nephrotic syndrome if massive proteinuria, low albumin. Nephrotic syndrome describes severity, not etiology.

Front 1464

What are the signs of nephritic syndrome?

Back 1464

Hyperlipiduria with droplets in shape of Maltese crosses in urinalysis. Hypercoagulability from urinary loss of anticoagulant proteins. Arterial or venous thrombosis.

Front 1465

How is nephrotic syndrome diagnosed?

Back 1465

High protein in urine, low protein in blood, edema, hyperlipidemia. 24-hour urine protein >3.5 gm. A protein:creatinine ratio of >3.5 on a single urine. The most accurate test is a renal biopsy.

Front 1466

What is the treatment for nephrotic syndrome?

Back 1466

Control the underlying disease. Steroids, cyclophosphamide, mycophenolate, azathioprine. ACE inhibitors or ARBs are used for all patients with proteinuria.

Front 1467

What are the causes of proteinuria?

Back 1467

Microalbuminuria is 30-300 mg/24 h. Mild amounts of proteinuria <1 gm/d can be seen in 10%. Proteinuria can also occur from fever, CHF, exercise, standing (orthostatic). Dipstick only detects albumin.

Front 1468

What are the causes of hematuria?

Back 1468

Nephrolithiasis, cancer, bleeding disorders, trauma, cyclophosphamide (hemorrhagic cystitis). Cystitis or prostatitis. The red cells become dysmorphic in glomerular disease.

Front 1469

What is the cause of nitrites on urinalysis?

Back 1469

Gram-negative bacteria reduce nitrate to nitrite.

Front 1470

What is the significance of asymptomatic bacteriuria?

Back 1470

The isolated finding of bacteria in the urine in pregnant women should be treated. About 30% of pregnant women with bacteriuria progress to pyelonephritis.

Front 1471

What is the significance of hyaline casts in the urinalysis?

Back 1471

Dehydration. These casts develop as an accumulation of the normal amount of tubular protein. Hyaline casts may occur in normal persons.

Front 1472

What is the significance of red cell casts on the urinalysis?

Back 1472

Glomerulonephritis

Front 1473

What is the significance of broad, waxy casts in the urinalysis?

Back 1473

Chronic renal failure

Front 1474

What is the significance of granular casts in the urinalysis?

Back 1474

Also called "dirty" or "muddy." They are associated with acute tubular necrosis and represent accumulated epithelial cells.

Front 1475

What is the significance of white cell casts in the urinalysis?

Back 1475

Pyelonephritis, interstitial nephritis.

Front 1476

What are the most common causes of end stage renal disease that require dialysis?

Back 1476

Diabetes and HTN. Glomerulonephritis is the etiology of about 15%, with cystic disease and interstitial nephritis, causing 4-5% each.

Front 1477

What are the indications for dialysis?

Back 1477

Life-threatening abnormalities that cannot be corrected, such as fluid overload refractory to diuretics. Acidosis, pericarditis, encephalopathy, neuropathies, hyperkalemia, persistent nausea, vomiting, bleeding.

Front 1478

What type of dialysis is used most frequently?

Back 1478

Hemodialysis is used in 85% of patients and peritoneal dialysis in 15%. The most common complication of peritoneal dialysis is peritonitis.

Front 1479

What is the cause of anemia in end-stage renal disease?

Back 1479

Decreased erythropoietin from the kidney. Treated with replacement of erythropoietin. The anemia of ESRD is normochromic and normocytic.

Front 1480

What is the cause of hypocalcemia/hyperphosphatemia in end-stage renal disease?

Back 1480

Loss of 1,25-dihydroxyvitamin D. Hyperphosphatemia is from inability of kidneys to excrete PO4. High PO4 contributes to low Ca by precipitating out in tissues in combination with the calcium.

Front 1481

What is the treatment of hyperphosphatemia in renal disease?

Back 1481

High phosphate levels are treated with phosphate binders, such as calcium carbonate or calcium acetate.

Front 1482

What is the treatment of hyperphosphatemia with hypercalcemia?

Back 1482

Sevelamer and lanthanum are phosphate binders. Used when calcium is high because of vitamin D. Aluminum-containing binders should not be used because associated with dementia and bone abnormalities.

Front 1483

What is osteodystrophy of end-stage renal disease?

Back 1483

Osteitis fibrosa cystica occurs because kidneys fail to produce 1,25 vitamin D. Low Ca leads to hyperparathyroidism, which removes Ca from bones. Controlled by increasing calcium levels.

Front 1484

What is the treatment of hypermagnesemia in renal insufficiency?

Back 1484

Magnesium accumulates because of decreased renal excretion. Treatment is restriction of magnesium intake.

Front 1485

What is the effect of end-stage renal disease on the cardiovascular system?

Back 1485

HTN, accelerated atherosclerosis, coronary artery disease. This is the most common cause of death for patients on dialysis. Goal BP is <130/80 for those with renal impairment.

Front 1486

What is the effect of end-stage renal disease on the immune system?

Back 1486

Increased infection because WBCs do not function in uremia. Infection is the second most common cause of death in dialysis patients. Most common organism is Staphylococcus.

Front 1487

What is the effect of end-stage renal disease on the coagulation system?

Back 1487

Bleeding occurs because uremic platelet dysfunction. Bleeding treated with desmopressin, which releases subendothelial von Willebrand factor and factor VIII, which increases platelet adherence.

Front 1488

What is the dietary treatment for severe renal disease?

Back 1488

Diet restricted in potassium, sodium, protein, magnesium, and phosphate.

Front 1489

What is hyponatremia?

Back 1489

Hyponatremia is defined as a low serum sodium <135 mEq. This generally occurs from either increased free water retention or urinary sodium loss. About 85-90% of sodium is extracellular.

Front 1490

What is the formula for serum osmolality?

Back 1490

Serum osmolality is largely a function of the serum sodium level. Serum osmolality = (2 x sodium) + BUN/2.8 + glucose/18. When the glucose and BUN are normal, this equation becomes 2 x sodium + 10.

Front 1491

What is the presentation of hyponatremia?

Back 1491

Neurologic symptoms range from mild confusion and memory loss to disorientation and obtundation to seizure or coma, depending on the severity.

Front 1492

What factor is associated with hyponatremic seizures?

Back 1492

Symptoms depend on rate of decline. Acute 15-20 point drop can result in a seizure or coma. If the level drops gradually, the patient can sustain an extremely low sodium. There should be no symptoms unless below 125.

Front 1493

What is the treatment of mild hyponatremia?

Back 1493

Mild asymptomatic hyponatremia should resolve with fluid restriction.

Front 1494

What is the treatment of moderate hyponatremia?

Back 1494

Moderate hyponatremia can be managed with normal saline administration combined with a loop diuretic such as furosemide. The saline provides sodium, and the loop diuretic causes a net free water loss.

Front 1495

What is the treatment of severe hyponatremia?

Back 1495

3% hypertonic saline. Severe symptoms do not occur unless Na <120. Central pontine myelinolysis occurs if Na is corrected rapidly. Rate should not exceed 0.5-1 mEq/h. No more than a 12-point rise in a 12-h.

Front 1496

What is the maximum rate of correction of severe hyponatremia?

Back 1496

Hyponatremia can be corrected as rapidly as 2 mEq per hour if the patient is having seizures. Fludrocortisone is given for cerebral salt wasting disease.

Front 1497

What is pseudohyponatremia?

Back 1497

Na level is artificially low because of hyperglycemia. Na is decreased by 1.6 mEq/L for every 100 increase in glucose. Glucose load causes a transcellular shift of water. Hyperlipidemia causes low Na.

Front 1498

What hypervolemic states (increased ECF) are associated with hyponatremia?

Back 1498

There is a decrease in intravascular volume resulting in an increase in ADH secretion from the posterior pituitary in congestive heart failure; nephrotic syndrome and low albumin states; and cirrhosis

Front 1499

What is the cause of hyponatremia in renal insufficiency?

Back 1499

When renal failure becomes advanced, the impaired free water excretion will reduce the sodium level and result in hypervolemia.

Front 1500

What is the cause of hyponatremia in hypovolemic states?

Back 1500

Loss of sodium through body fluids and replacement with free water. Sweating and replacement only with free water causes the sodium level to drop.

Front 1501

What are the gastrointestinal causes of hyponatremia?

Back 1501

Vomiting, diarrhea, gastric suction; hypovolemia.

Front 1502

What are the causes of sodium loss through the skin?

Back 1502

Skin loss: burns, sweating with replacement with free water, cystic fibrosis.

Front 1503

How does renal failure cause renal sodium loss?

Back 1503

The kidney can lose the ability to reabsorb sodium in the proximal convoluted tubule as the kidney is damaged. Damaged tubules cannot reabsorb sodium and hypovolemia results.

Front 1504

How does adrenal insufficiency (Addison disease) cause hyponatremia?

Back 1504

Aldosterone reabsorbs sodium from the kidney. Without aldosterone, sodium is lost.

Front 1505

What are the causes of hypovolemic hyponatremia with a urine sodium <10?

Back 1505

Dehydration, vomiting, diarrhea, sweating

Front 1506

What are the causes of hypovolemic hyponatremia with a urine sodium >10?

Back 1506

Diuretics, ACE inhibitors, renal salt wasting, Addison disease, cerebral sodium wasting

Front 1507

What are the causes of euvolemic hyponatremia?

Back 1507

Psychogenic polydipsia with >15-20 liters/d. Hypothyroidism. Diuretics: can be both hypovolemic and euvolemic. ACE inhibitors. Endurance exercise. Syndrome of inappropriate secretion of ADH.

Front 1508

What are the causes of syndrome of inappropriate secretion of ADH (SIADH)?

Back 1508

CNS infections, stroke, tumor, trauma, vasculitis, pain, pneumonia, TB, PE, asthma. Lung CA, pancreas CA. SSRIs, tricyclics, haloperidol, cyclophosphamide, vincristine, carbamazepine.

Front 1509

How is syndrome of inappropriate secretin of antidiuretic hormone diagnosed?

Back 1509

Neurologic symptoms; elevated urine osmolality and elevated urine sodium. If the urine osmolality is >100 Osm/L in the presence of hyponatremia, the person has SIADH. Elevated ADH level.

Front 1510

What is the treatment of SIADH?

Back 1510

Restrict fluids. Give hypertonic saline for severe disease. Normal saline with a loop diuretic. For chronic disease, demeclocycline or lithium to inhibit the effect of ADH on the kidney tubule.

Front 1511

What are the insensible causes of hypernatremia?

Back 1511

Insensible losses: extrarenal loss of water without intake of hypotonic fluids; increased skin loss of water (sweating, burns, fever, exercise) or respiratory infections

Front 1512

What are the gastrointestinal causes of hypernatremia?

Back 1512

Osmotic diarrhea (e.g., lactulose, malabsorption), infectious diarrhea. Transcellular shift caused by Rhabdomyolysis or seizures can cause muscles to take up water and Na.

Front 1513

What are the renal causes of hypernatremia?

Back 1513

Nephrogenic diabetes insipidus (NDI), causing by renal disease, increased calcium, decreased potassium, lithium, demeclocycline, sickle cell disease, and others

Front 1514

What are the causes of central diabetes insipidus?

Back 1514

Idiopathic, trauma, infectious, tumor, granulomatous, hypoxic brain damage or neurosurgical brain injury. Idiopathic most common.

Front 1515

What types of osmotic diuresis can cause hypernatremia?

Back 1515

Osmotic diuresis: diabetic ketoacidosis (DKA), nonketotic hyperosmolar coma, mannitol, diuretics.

Front 1516

What are the signs of hypernatremia?

Back 1516

Lethargy, weakness, irritability, seizures, and coma are present with severe hypernatremia of any cause. Diabetes insipidus causes a dilute diuresis of 3-20 L per day.

Front 1517

How is central diabetes insipidus distinguished from nephrogenic diabetes insipidus?

Back 1517

Decrease in urine volume after administering ADH distinguishes central diabetes insipidus from NDI.

Front 1518

What is the treatment of acute hypernatremia?

Back 1518

IV isotonic saline. Correction should not be >1 mEq every 2 h or 12 mEq/d. 1 mEq/h is acceptable if the patient is having seizures.

Front 1519

What are the complications of overly rapid correction of hypernatremia?

Back 1519

Complications of overly rapid correction include cerebral edema, permanent neurologic damage, or seizures.

Front 1520

What is the treatment of central diabetes insipidus?

Back 1520

Correct the underlying cause. Give vasopressin (ADH) subcutaneously, intravenously, intramuscularly, or by nasal spray.

Front 1521

What is the treatment of nephrogenic diabetes insipidus?

Back 1521

Correct underlying cause if possible. Diuretic or NSAIDs. NSAIDs function by inhibiting prostaglandins, which impair concentrating ability. NSAIDs will increase the action of ADH at the kidney.

Front 1522

What are the gastrointestinal causes of hypokalemia?

Back 1522

Gastrointestinal losses can be from vomiting, diarrhea, or tube drainage.

Front 1523

What types of transcellular shift can cause hypokalemia?

Back 1523

Increased entry into cells can be from alkalosis, increased levels of insulin, beta adrenergic, and the replacement of B12. Trauma causes increased beta adrenergic activity.

Front 1524

What are the causes of urinary potassium losses?

Back 1524

Diuretics. Increased aldosterone states, such as Conn, licorice, Bartter, or Cushing. Aldosterone is the most important regulator of potassium. Renal artery stenosis. Hypomagnesemia will cause potassium loss.

Front 1525

What is the presentation of hypokalemia?

Back 1525

Affects muscles and the heart. Weakness, paralysis, fatal arrhythmias, rhabdomyolysis. Potassium is necessary for ADH effect on the kidney, and hypokalemia causes nephrogenic diabetes insipidus.

Front 1526

What are the ECG signs of hypokalemia?

Back 1526

T-wave flattening and U-waves. A U-wave is an extra wave after the T-wave caused by Purkinje fiber repolarization.

Front 1527

What is the treatment of hypokalemia?

Back 1527

Correct the underlying cause. IV potassium maximum 10-20 mEq/h; do not use dextrose containing fluids, because dextrose causes increase insulin release and lower potassium.

Front 1528

What are the complications of excessively rapid repletion of potassium?

Back 1528

Fatal arrhythmia. Idioventricular rhythm, asystole.

Front 1529

How many mEq of potassium is needed to raise the potassium level by one point?

Back 1529

Very large amounts of potassium may be necessary to raise the body potassium level by 1 or 2 points. The total body requirement is to give 4-5 mEq per kg per point.

Front 1530

What are the causes of hyperkalemia related to movement of K+ from cells to extracellular fluid?

Back 1530

Pseudohyperkalemia: venipuncture, platelets >1,000,000, WBC >100,000. Acidosis. Insulin deficiency. Rhabdomyolysis, tumor lysis, seizures, exercise. Periodic paralysis: weakness, hyperK, family history.

Front 1531

What is the relationship between pH and potassium level?

Back 1531

H+ moves into cells, K+ out. For every 0.1-point decrease in the pH, the potassium level will increase by 0.7 points because of the transcellular shift.

Front 1532

What are the renal causes of hyperkalemia?

Back 1532

Renal failure. Hypoaldosteronism: ACE inhibitors, type IV RTA, adrenal enzyme deficiency; heparin. Primary adrenal insufficiency (Addison) or adrenalectomy. K-sparing diuretics. NSAIDs.

Front 1533

What is the presentation of hyperkalemia?

Back 1533

Muscular weakness can begin usually with K+ levels >6.5.Abnormal cardiac conduction is the most common cause of death, hypoventilation.

Front 1534

How is hyperkalemia diagnosed?

Back 1534

ECG findings: peaked T waves, widened QRS, short QT, or prolonged PR interval.

Front 1535

What is the acute treatment of hyperkalemia?

Back 1535

Calcium chloride one ampule for membrane stabilization. Effect is immediate and short lived. Bicarbonate one ampule. Do not give in same IV line as calcium. Glucose one ampule and insulin, takes 30 min.

Front 1536

What is the non-acute treatment of hyperkalemia?

Back 1536

Furosemide, beta agonists. Cation exchange resin (Kayexalate) absorbs 1 mEq K+/gm. Given with sorbitol. Kayexalate can also be given as a retention enema. Dialysis.

Front 1537

What are the causes of distal renal tubular acidosis (type I)?

Back 1537

Sporadic. Also caused by Sjögren, SLE. Amphotericin, lithium, analgesics, cyclophosphamide. Nephrocalcinosis, sickle cell, chronic infection. Familial, chronic hepatitis.

Front 1538

What is the presentation of distal renal tubular acidosis (type I)?

Back 1538

Inability to concentrate H+ in urine. Urine pH is >5.4. Secondary hyperaldosteronism and hypokalemia. Nephrocalcinosis and nephrolithiasis.

Front 1539

How is distal renal tubular acidosis (type I) diagnosed?

Back 1539

Acid load test; give ammonium, which should lower urine pH. With type I RTA, urine pH remains elevated. Bicarbonate <10. Hypokalemia because of inability to secrete hydrogen ions. Kidney excretes K+.

Front 1540

What is the treatment of distal renal tubular acidosis (type I)?

Back 1540

Oral bicarbonate is the treatment because bicarbonate reabsorption in the proximal tubule remains intact; potassium replacement.

Front 1541

What are the causes proximal (type II) renal tubular acidosis?

Back 1541

Fanconi, Wilson, amyloidosis, myeloma, acetazolamide, vitamin D deficiency, secondary hyperparathyroidism, hypocalcemia, heavy metals, hepatitis, SLE and Sjögren syndrome.

Front 1542

What is the presentation of proximal (type II) renal tubular acidosis?

Back 1542

Inability to absorb bicarbonate. Urine pH is basic. Hypokalemia and bicarbonate of 18-20, and malabsorption of glucose, phosphate, urate, amino acids. Bone lesions (osteomalacia and rickets).

Front 1543

How is proximal (type II) renal tubular acidosis diagnosed?

Back 1543

Patients are have a basic urine in the presence of acidemia.

Front 1544

What is the treatment of proximal (type II) renal tubular acidosis?

Back 1544

Give potassium; mild volume depletion will enhance proximal bicarbonate reabsorption. Thiazide diuretics and very large amounts of bicarbonates.

Front 1545

What are the causes of hyporeninemic/hypoaldosteronism (type IV renal tubular acidosis)?

Back 1545

An aldosterone deficiency of any cause or adrenal insensitivity to angiotensin II, diabetes (50%), Addison disease, sickle cell disease, renal insufficiency.

Front 1546

What is the presentation of hyporeninemic/hypoaldosteronism (type IV renal tubular acidosis)?

Back 1546

Usually asymptomatic hyperkalemia. Mild to moderate renal insufficiency. Hyperchloremic metabolic acidosis (nonanion gap).

Front 1547

How is hyporeninemic/hypoaldosteronism (type IV) diagnosed?

Back 1547

Presence of high urine sodium with oral salt restriction establishes the diagnosis.

Front 1548

What is the treatment of hyporeninemic/hypoaldosteronism (type IV)?

Back 1548

Administration of fludrocortisone. Fludrocortisone has a high degree of mineralocorticoid effect and is similar to administering aldosterone.

Front 1549

What is the relationship of serum bicarbonate and pCO2?

Back 1549

For every 1-point increase in the level of serum bicarbonate, there is a 0.7-point increase in pCO2. Dehydration results in increased aldosterone, which leads to metabolic alkalosis.

Front 1550

What are the causes of alkalosis from H+ ion loss?

Back 1550

Exogenous steroids. GI loss (vomiting, nasogastric suction). Renal loss (Conn syndrome, Cushing, ACTH overproduction, licorice, Bartter syndrome). Decreased chloride intake. Diuretics.

Front 1551

What are the causes of alkalosis from HCO3 retention?

Back 1551

Bicarbonate administration. Contraction alkalosis. Milk-alkali syndrome?

Front 1552

What is the cause of alkalosis from H+ movement into cells?

Back 1552

Hypokalemia.

Front 1553

What are the respiratory causes of alkalosis?

Back 1553

Hyperventilation, pulmonary embolus, sarcoid, anxiety, pain. Progesterone, catecholamines, hypoxia, cirrhosis, pregnancy, and salicylates.

Front 1554

What are the causes of acidosis (low pH) with a low anion gap?

Back 1554

Myeloma, low albumin level, lithium.

Front 1555

What is the formula for anion gap?

Back 1555

Anion gap = (Na + K) - (HCO3 + Cl) Normal: 8-14. Na+ and cations = HCO3- and Cl- and anions

Front 1556

What are the causes of a normal anion gap acidosis?

Back 1556

Diarrhea, renal tubular acidosis, ureterosigmoidostomy.

Front 1557

What are the causes of an increased anion gap acidosis?

Back 1557

Lactate (sepsis, ischemia). Aspirin. Methanol. Uremia. Diabetic ketoacidosis. Paraldehyde, Propylene glycol. Isopropyl alcohol, INH. Ethylene glycol (antifreeze), low calcium.

Front 1558

What are the causes of respiratory acidosis?

Back 1558

Hypoventilation, chronic obstructive pulmonary disease (COPD), Pickwickian, obesity, suffocation, opiates, sleep apnea, kyphoscoliosis, myopathies, neuropathy, effusion, aspiration.

Front 1559

What are the causes of nephrolithiasis?

Back 1559

1-5% of the population. Calcium oxalate stones in 70%. Calcium phosphate in 10%. Mg/Aluminum/phosphate (Struvite) 5%. Uric acid 5%. Cysteine 1%. Indinavir.

Front 1560

What are the causes of hypercalciuria?

Back 1560

Vitamin D intoxication with sarcoid and granulomatous disease. Familial. Idiopathic renal hypercalciuria. Hyperparathyroidism (10%). Multiple myeloma, metastatic disease to bone, hypercalcemia of malignancy.

Front 1561

What are the causes of hyperoxaluria?

Back 1561

Primary familial, enteric hyperoxaluria (chronic diarrhea causes excessive absorption of oxalate).

Front 1562

What complication may result from hypocitraturia?

Back 1562

Citrate binds calcium and prevents calcium absorption. Low citrate leads to increase in calcium absorption and kidney stones. Causes of hypocitraturia: renal tubular acidosis; chronic diarrhea, thiazides.

Front 1563

What are the causes of uric acid stones?

Back 1563

Uric acid stones are associated with diseases like gout, hematologic malignancies, and Crohn disease. Radiolucent on x-rays.

Front 1564

Infection with which organisms can cause struvite kidney stones?

Back 1564

Urinary infection with urease-producing organisms like Proteus, Staphylococcus, Pseudomonas, and Klebsiella causes a highly alkaline urine that produces struvite stones.

Front 1565

What is the presentation of nephrolithiasis?

Back 1565

Constant flank pain (not colicky), hematuria, and pain radiating to groin. Stones <5 mm should pass spontaneously

Front 1566

How is nephrolithiasis diagnosed?

Back 1566

Ultrasound. Strain the urine. Serum and urine calcium. Helical (spiral) CT scan is the best test. No contrast needed for stones. Plain x-ray (80% yield) is rarely used. Intravenous pyelogram is not done.

Front 1567

What is the treatment of nephrolithiasis?

Back 1567

Analgesia, hydration, and bed rest. Shockwave lithotripsy for stones <2 cm. The fragments may cause obstruction. Ureteroscopy. Percutaneous removal.

Front 1568

What is the presentation of adult polycystic kidney disease?

Back 1568

Flank pain, hematuria (micro and gross), infections, and calculi. Genetic. Hepatic cysts (40-60%), colonic diverticula, HTN (50%), intracranial aneurysm (10-20%), mitral valve prolapse (25%).

Front 1569

How is adult polycystic kidney disease diagnosed?

Back 1569

Ultrasound and CT scan.

Front 1570

What is the treatment of adult polycystic kidney disease?

Back 1570

Management of complications (UTI, calculi, and hypertension).

Front 1571

What are simple renal cysts?

Back 1571

Very common; if smooth-walled with no debris in cyst, no treatment necessary. Cysts with irregular walls or debris inside should be aspirated to exclude malignancy. Dialysis causes cysts.

Front 1572

What is essential hypertension?

Back 1572

A systolic blood pressure of 140 mm Hg or a diastolic >90 on multiple readings in the absence of a specific, identifiable underlying cause.

Front 1573

What is the criteria for hypertension in patients with diabetes or renal disease?

Back 1573

Any blood pressure above 130/80 mm Hg is defined as hypertension.

Front 1574

What is the treatment of stage 2 hypertension?

Back 1574

Patients with stage 2 hypertension (blood pressure >160/100 mm Hg), should receive initial therapy with two medications.

Front 1575

What is the criteria for normal BP?

Back 1575

120/80 mm Hg.

Front 1576

What is the criteria for pre-hypertension?

Back 1576

Systolic 120-139. Diastolic 80-89 mm Hg.

Front 1577

What is the criteria for stage 1 hypertension?

Back 1577

Systolic 140-159. Diastolic 90-99 mm Hg?

Front 1578

What is the criteria for stage 2 hypertension?

Back 1578

Systolic >160. Diastolic >100 mm Hg.

Front 1579

What is a hypertensive emergency?

Back 1579

HTN with stroke, subarachnoid hemorrhage, encephalopathy, myocardial ischemia, retinopathy. Requires substantial reduction of blood pressure within one hour.

Front 1580

What are the symptoms of a hypertensive emergency?

Back 1580

Headache, dizziness, chest pain, dyspnea, blurred vision, and palpitations. Malignant HTN is defined as encephalopathy or nephropathy.

Front 1581

What are the long-term cardiac complications of hypertension?

Back 1581

Myocardial ischemia or infarction, congestive heart failure, left ventricular hypertrophy, aortic aneurysm, and dissection. S4 gallop, accentuated A2 heart sound, and prominent left ventricular impulse.

Front 1582

What are the long-term cerebrovascular complications of hypertension?

Back 1582

Transient ischemic attack (TIA) and stroke.

Front 1583

What are the long-term renal complications of hypertension?

Back 1583

Proteinuria, microscopic hematuria, and elevation of BUN/creatinine.

Front 1584

What are the long-term ocular complications of hypertension?

Back 1584

Retinopathy: Hemorrhages, exudates, arteriolar narrowing, and papilledema. Blurred vision, scotomata, and blindness.

Front 1585

What are the signs of secondary hypertension?

Back 1585

<5% secondary. Renovascular: bruit; Cushing: weight gain, moon-face, striae, ecchymoses; pheochromocytoma: episodic HTN with headache, palpitations, sweating; aldosteronism: polyuria/ polydipsia, hypoK.

Front 1586

How is hypertension diagnosed?

Back 1586

Allow the patient to sit 5 min before BP measured. Should not diagnose HTN after only a single reading. Repeat the reading 3-6 times over several months before confirming diagnosis and initiating therapy.

Front 1587

What basic studies are obtained in the evaluation of hypertension?

Back 1587

Urinalysis for protein, glucose, and red blood cells. Hematocrit. Potassium to exclude hyperaldosteronism. Serum creatinine and BUN. ECG to evaluate for left ventricular hypertrophy. Glucose and lipid analysis.

Front 1588

What is the lifestyle modification for essential hypertension?

Back 1588

Weight reduction, sodium restriction, aerobic exercise, avoid alcohol. Low-fat, increased fiber. Severe HTN (diastolic >100 mm Hg) should be start drug therapy with 2 medications.

Front 1589

What is the drug treatment of essential hypertension?

Back 1589

If DBP >90 despite a 3-months nonpharmacologic, start antihypertensive. Diuretics are initial treatment. For stage 2 HTN, BP >160/100, use a diuretic with an ACE/ARB/calcium-blocker or beta-blocker.

Front 1590

What medication should be added if a diuretic dose not control the patient's blood pressure?

Back 1590

If diuretics do not control BP, then add a beta-blocker, calcium-blocker, ACE inhibitor, or angiotensin-receptor blocker. beta-Blockers avoided in asthma, COPD, heart block, or depression.

Front 1591

What is the initial antihypertensive for diabetics?

Back 1591

Diabetics should be treated with ACEI or ARBs, which prevent nephropathy. BP goal in a diabetic is lower, at <130/80; also lower with renal insufficiency, CHF, retinopathy, stroke. Microalbuminuria receive ACEI.

Front 1592

What is the initial antihypertensive for patients who have ischemic heart disease?

Back 1592

After a myocardial infarction (ischemic heart disease), beta-blockers should be started.

Front 1593

What is the initial antihypertensive for patients with decreased left-ventricular systolic function?

Back 1593

Decreased left-ventricular systolic function (congestive heart failure or postmyocardial infarction) should receive ACE inhibitors and beta blockers.

Front 1594

Which antihypertensive should be avoided in African American patients?

Back 1594

African American patients are least effectively treated with ACE inhibitors.

Front 1595

What are the initial antihypertensive choices for pregnant patients?

Back 1595

Alpha-methyldopa, labetalol, hydralazine, or calcium blockers. ACE inhibitors and angiotensin-receptor blockers are contraindicated in pregnancy. Diuretics are relatively contraindicated.

Front 1596

What is a hypertensive emergency?

Back 1596

The acute onset of severe hypertension with severe and rapidly worsening symptoms of end-organ damage. This usually happens with a diastolic pressure >120-130 mm Hg.

Front 1597

What are the neurologic manifestations of hypertensive emergencies?

Back 1597

Encephalopathy, headache, confusion, seizures, and subarachnoid or intracerebral hemorrhage.

Front 1598

What are the cardiac manifestations of hypertensive emergencies?

Back 1598

Chest pain, myocardial infarction, palpitations, dyspnea, pulmonary edema, jugular venous distension, and gallops.

Front 1599

What are the renal manifestations of hypertensive emergencies?

Back 1599

Nephropathy: Acutely progressive hematuria, proteinuria, and renal dysfunction.

Front 1600

What are the retinal manifestations of hypertensive emergencies?

Back 1600

Retinopathy: Papilledema, hemorrhages, and blurred vision.

Front 1601

What is the laboratory evaluation for hypertensive emergencies?

Back 1601

The laboratory evaluation is the same as with essential hypertension. CT scan of the head to exclude hemorrhage. ECG is as an initial test to exclude myocardial infarction.

Front 1602

What is the treatment of hypertensive emergencies?

Back 1602

Intravenous nitroprusside and labetalol are the two best agents. Nitroglycerin if myocardial ischemia. Enalaprilat is IV ACEI. Initial goal is to reduce BP by no more than 25% within the first 1 to 2 hours.

Front 1603

What is secondary hypertension?

Back 1603

HTN with underlying cause. 5% of cases of HTN are caused by an identifiable underlying cause. Renal artery stenosis is the most common of these causes.

Front 1604

Which patients should be screened for secondary hypertension?

Back 1604

Hypertension in the very young or very old (<25 or >55)

Front 1605

What is the cause of renal artery stenosis?

Back 1605

Caused by arthrosclerotic disease in elderly persons and fibromuscular dysplasia in young women. Upper abdominal bruit is present in 50-70% of patients.

Front 1606

How is renal artery stenosis diagnosed?

Back 1606

Screening ultrasound. Captopril renogram measures the uptake of radioisotope before and after captopril. Positive test is decreased uptake (decreased GFR) after captopril. Arteriogram is the best method of diagnosis.

Front 1607

What is the treatment of renal artery stenosis?

Back 1607

Percutaneous transluminal angioplasty. If stenosis recurs, then the procedure should be repeated. If angioplasty fails, surgical resection. ACE inhibitors if angioplasty or surgery is not possible.

Front 1608

What is the cause of primary hyperaldosteronism (Conn Syndrome)?

Back 1608

Conn Syndrome is most commonly due to a unilateral adrenal adenoma. Bilateral adrenal hyperplasia is less common. Cancer is rare as a cause of hyperaldosteronism.

Front 1609

What are the symptoms of primary hyperadosteronism?

Back 1609

Hypertension in association with hypokalemia. Symptoms of hypokalemia such as muscular weakness and polyuria and/or polydipsia from a nephrogenic diabetes insipidus.

Front 1610

How is primary hyperaldosteronism diagnosed?

Back 1610

Elevated aldosterone levels in urine and blood.

Front 1611

What is the treatment of Conn syndrome?

Back 1611

Surgical resection of adenoma. Potassium sparing diuretics such as spironolactone in adrenal hyperplasia.

Front 1612

What is pheochromocytoma?

Back 1612

Pheochromocytoma is most often due to a benign tumor of the adrenal gland; 10% are bilateral, 10% are malignant, and 10% are extra-adrenal.

Front 1613

What is the presentation of pheochromocytoma?

Back 1613

Episodic hypertension with headaches, sweating, palpitations, and tachycardia. Pallor or flushing may also occur.

Front 1614

How is pheochromocytoma diagnosed?

Back 1614

Initial test is urinary vanillylmandelic acid (VMA), metanephrines, and free urinary catecholamines. Plasma catecholamine evaluation. CT and MRI scanning is used to localize tumor.

Front 1615

What is the treatment of pheochromocytoma?

Back 1615

Alpha-adrenergic blockade with phentolamine or phenoxybenzamine, followed by surgical removal.

Front 1616

What is the most common cause of Cushing disease?

Back 1616

Cushing Disease is commonly caused by ACTH hypersecretion by a pituitary adenoma. HTN in association with cushingoid truncal obesity, buffalo hump, menstrual abnormalities, striae.

Front 1617

How is Cushing disease diagnosed?

Back 1617

Dexamethasone suppression testing and 24-hour urine cortisol are the best initial tests.

Front 1618

What is the treatment of Cushing disease?

Back 1618

Surgical resection of the pituitary adenoma.

Front 1619

What is the clinical sign of coarctation of the aorta?

Back 1619

Hypertension greater in the upper extremities compared with the lower extremities.

Front 1620

What are the endocrinologic and renal causes of secondary hypertension?

Back 1620

Oral contraceptives, acromegaly, congenital adrenal enzyme deficiencies, glomerulonephritis, polycystic disease, diabetic nephropathy, pyelonephritis.

Front 1621

What are the commonly used thiazide diuretics?

Back 1621

Hydrochlorothiazide, chlorthalidone, metolazone, indapamide.

Front 1622

What are the names of the potassium sparing diuretics?

Back 1622

Spironolactone, amiloride, triamterene.

Front 1623

What are the indications for diuretics in hypertension?

Back 1623

Congestive heart failure, edematous states, African-American patients; least expensive.

Front 1624

What are the major side effects of diuretics?

Back 1624

Decreases in potassium and magnesium; increases in calcium, uric acid, glucose, LDL-cholesterol; gynecomastia.

Front 1625

What are the relative contraindications to diuretics?

Back 1625

Diabetes, gout, hyperlipidemia.

Front 1626

What are the two most commonly used beta-blockers for hypertension?

Back 1626

Metoprolol and atenolol are the most commonly used.

Front 1627

What are the specific indications for beta-blockers in hypertension?

Back 1627

Myocardial infarction or ischemic heart disease, supraventricular arrhythmias, migraine headaches, glaucoma, anxiety (resting tachycardia), congestive failure from diastolic dysfunction.

Front 1628

What are the major side effects of beta-blockers?

Back 1628

Bronchospasm, heart block, bradycardia, Raynaud phenomenon, depression, impotence, fatigue, decreased HDL, increased triglycerides, hyperglycemia.

Front 1629

What are the relative contraindications to beta blockers?

Back 1629

Asthma, COPD, atrioventricular conduction defects, congestive heart failure from systolic dysfunction; diabetes because of masking signs of hypoglycemia.

Front 1630

What are the names of the angiotensin converting enzyme (ACE) inhibitors?

Back 1630

Benazepril, captopril, enalapril, fosinopril, lisinopril, quinapril, ramipril, moexipril, enalaprilat (only IV form).

Front 1631

What are the specific indications for ACE inhibitors?

Back 1631

Diabetics with HTN to prevent nephropathy; BP goal in a diabetic is <130/80. Congestive heart failure as afterload reduction. Postmyocardial infarction with left ventricular impairment.

Front 1632

What are the major side effects of ACE inhibitors?

Back 1632

Cough, angioneurotic edema, neutropenia, hyperkalemia, taste disturbances, anaphylactoid reactions. Less effective in African-American patients.

Front 1633

What are the absolute contraindications to ACE inhibitors?

Back 1633

Bilateral renal artery stenosis, pregnancy.

Front 1634

What are the names of the calcium channel blockers?

Back 1634

Amlodipine, diltiazem, felodipine, isradipine, nicardipine, nifedipine, verapamil.

Front 1635

What are the specific indications for calcium channel blockers?

Back 1635

Angina pectoris, supraventricular arrhythmia, migraine, Raynaud phenomenon, esophageal spasm.

Front 1636

What are the side effects of calcium-channel blockers?

Back 1636

Peripheral edema, constipation, heart block, reflex tachycardia.

Front 1637

What are the relative contraindications to calcium channel blockers?

Back 1637

Atrioventricular conduction defects, congestive heart failure from systolic dysfunction.

Front 1638

What are the angiotensin receptor antagonists?

Back 1638

Losartan, valsartan, irbesartan, candesartan, telmisartan

Front 1639

What are the indications for angiotensin receptor antagonists?

Back 1639

Patients who are intolerant to ACE inhibitors (because of cough).

Front 1640

What are the names of the central-acting sympatholytics?

Back 1640

Clonidine, guanabenz, guanfacine, methyldopa.

Front 1641

What are the side effects of central-acting sympatholytics?

Back 1641

Depression, fatigue, dry mouth, impotence, bradycardia, heart block, memory loss. Methyldopa causes hepatitis and Coombs-positive hemolytic anemia.

Front 1642

What is the criteria for an abnormal pulmonary flow rate?

Back 1642

<80% of predicted in any lung volume or flow rate is abnormal; lung volume >120% of predicted is consistent with air trapping.

Front 1643

What is vital capacity?

Back 1643

The volume of gas exhaled with maximal forced expiration.

Front 1644

What is total lung capacity?

Back 1644

Volume of gas in the lungs after maximal inspiration.

Front 1645

What is residual volume?

Back 1645

Volume of gas remaining in the lungs after forced maximal expiration (unused space).

Front 1646

What is the formula for total lung capacity?

Back 1646

TLC = RV + VC or VC = TLC - RV

Front 1647

What is the purpose of measuring forced expiratory volumes (FEVs)?

Back 1647

FEVs determine degree of obstruction by comparing forced volume expired at 1 sec to the forced vital capacity. 80% of predicted is normal. It is decreased in patients with COPD or asthma. FEVs normal in restrictive.

Front 1648

What is the purpose of measuring carbon monoxide diffusing capacity (DLco)?

Back 1648

Lung diffusion testing determines how well oxygen passes from the alveolar space into blood. Diffusing capacity is reduced by emphysema, edema, consolidation, or fibrosis.

Front 1649

If pulmonary function tests show an obstructive pattern and decreased DLco, what is the diagnosis?

Back 1649

Emphysema.

Front 1650

If pulmonary function tests show a restrictive pattern and decreased DLco, what is the diagnosis?

Back 1650

Interstitial lung disease (intrapulmonary restriction) or mild left heart failure. Increased DLco may be seen in pulmonary hemorrhage caused by Goodpasture syndrome.

Front 1651

What is the methacholine challenge test?

Back 1651

Bronchoprovocation with methacholine is done to evaluate patients with cough or wheezing and who have a normal PFT; tests for asthma (bronchial reactivity).

Front 1652

What is the formula for oxygen delivery?

Back 1652

The most important factor in gas exchange is oxygen delivery (Do2) to the vital organs. Do2 = Cardiac Output x (1.34 x Hb x HbSat) + 0.0031 x PaO2

Front 1653

What are the two most important factors in maintaining the delivery of oxygen to the vital organs?

Back 1653

The two most important factors in the delivery of oxygen to the vital organs are the cardiac output and hemoglobin. In a critically ill patient, the hemoglobin and cardiac output should be kept near normal.

Front 1654

What is the formula for alveolar-arterial O2 gradient?

Back 1654

PAO2-PaO2 gradient is an assessment of oxygenation. The A-a gradient is valid on room air and increases with age. PAO2-PaO2 gradient = (150 -1.25) x pCO2 -PaO2orA - a = [150 - (1.25 x PaCO2) - PaO2]

Front 1655

What is the normal alveolar-arterial O2 gradient?

Back 1655

The normal gradient is between 5 and 15 mm Hg. It increases with all causes of hypoxemia except hypoventilation and high altitude.

Front 1656

What percentage of solitary pulmonary nodules are malignant?

Back 1656

One third of all solitary nodules are malignant. Calcification indicates benign. Popcorn calcifications are caused by hamartomas. Bull's-eye calcifications are caused by granulomas.

Front 1657

What is the first step in the evaluation of a solitary pulmonary nodule?

Back 1657

The first step in the evaluation of a pulmonary nodule is to look for a prior x-ray. Finding the same pulmonary nodule on an x-ray done years ago eliminates the need for further evaluation.

Front 1658

What is the approach to evaluation of a solitary pulmonary nodule if no prior x-ray is available and the patient is low-risk?

Back 1658

Low risk patients are <35 and nonsmokers with calcified nodules, which may be followed with chest x-rays or chest CTs every 3 months for 2 years. Follow-up may be discontinued after 2 years if no growth.

Front 1659

What is the approach to the evaluation of a solitary pulmonary nodule if no prior x-ray is available and the patient is high risk?

Back 1659

High-risk patients: >50 smokers with a nodule, are likely to have bronchogenic cancer. Diagnostic procedure is open-lung biopsy and removal.

Front 1660

What are the causes of exudative effusions?

Back 1660

Pneumonia, cancer, and tuberculosis. An exudative effusion will cause unilateral effusions. Exudative effusions need further investigation.

Front 1661

What are the causes of transudative pleural effusions?

Back 1661

Heart failure, nephrotic syndrome, liver disease, pulmonary embolism, atelectasis.

Front 1662

What are the causes of exudative pleural effusions?

Back 1662

Parapneumonic effusions (pneumonia), malignancy (lung, breast, lymphoma), tuberculosis, pulmonary embolism, collagen vascular disease (RA, SLE), drug-induced, pancreatitis.

Front 1663

What is the diagnostic approach to pleural effusions?

Back 1663

Thoracentesis should be performed for new and unexplained pleural effusions when sufficient fluid is present. Observe pleural effusions when there is CHF, viral pleurisy, or recent thoracic or abdominal surgery.

Front 1664

What is the laboratory testing for thoracentesis fluid?

Back 1664

Lactate dehydrogenase (LDH) and protein. Measure serum LDH and protein. Calculate the ratios of effusion to serum for these measurements.

Front 1665

What is the Light criteria for exudative pleural effusion?

Back 1665

LDH of effusion >200 IU/mL, LDH effusion/serum ratio >0.6, and protein effusion/serum ratio >0.5. If one criteria is met, it is an exudative effusion, and further evaluation is required.

Front 1666

What is the Light criteria for transudative pleural effusion?

Back 1666

All three are required: LDH of effusion <200 IU/mL, LDH effusion/serum ratio <0.6, and protein effusion/serum ratio <0.5.

Front 1667

What kind of pleural effusion is associated with pulmonary embolism?

Back 1667

Pulmonary embolism can cause a transudate or exudate. A patient with a transudative effusion but no apparent cause may have a PE.

Front 1668

What is the management of parapneumonic effusions?

Back 1668

Thoracentesis to rule out an empyema (pus in the pleural space), which needs chest-tube drainage. Uncomplicated parapneumonic effusions respond to antibiotics alone.

Front 1669

What are the most common causes of malignant pleural effusion?

Back 1669

Lung cancer, breast cancer, and lymphoma. Cytologic examination is diagnostic.

Front 1670

What are the causes of hemorrhagic pleural effusions?

Back 1670

Hemorrhagic pleural effusion may be seen in mesothelioma (a pleural-based cancer associated with asbestos), metastatic lung or breast cancer, pulmonary thromboembolism (with infarction), and trauma.

Front 1671

What are the causes of lymphocytic predominant, exudative pleural effusions?

Back 1671

Caused by tuberculosis. Adenosine deaminase is elevated, and the PCR for tuberculous DNA is positive. Acid-fast stain and culture for Tb are positive in less than 30%. Pleural biopsy confirms diagnosis.

Front 1672

What amount of fluid is required for thoracentesis to be done safely?

Back 1672

If decubitus chest x-ray detects 1 cm or more of free-flowing fluid, the thoracentesis can be performed. If non-free fluid (loculated) an ultrasound-guided thoracentesis should be done.

Front 1673

What are the causes of respiratory compromise?

Back 1673

Airway obstruction (asthma, COPD, foreign object), parenchymal lung disease (bacterial or viral pneumonia, lung injury), heart failure, pulmonary embolism, opiates, myasthenia gravis.

Front 1674

What are the steps in treating respiratory compromise?

Back 1674

The first task is to ensure that the patient's airway is patent and that breathing is adequate. Administer supplemental oxygen.

Front 1675

What are the clinical manifestations of respiratory compromise?

Back 1675

Acute cough, fever, sputum suggest infection. Sudden dyspnea without fever suggests airway obstruction, cardiac disease, or thromboembolism. Chronic dyspnea is usually CHF, interstitial disease, COPD.

Front 1676

What are the physical signs of respiratory compromise?

Back 1676

Resp >30 is severe respiratory compromise. Wheezing indicates asthma, COPD. Localized wheezing: foreign object, mass. Rales indicate pneumonia, interstitial disease, CHF. Consolidation: pneumonia, atelectasis.

Front 1677

What disorders are associated with respiratory compromise with a normal lung exam?

Back 1677

Normal lung examination may be seen in thromboembolic disease, Pneumocystis jiroveci, and disorders of central respiratory drive.

Front 1678

What are the most important laboratory tests in the evaluation of acute respiratory compromise?

Back 1678

An arterial blood-gas measurement is the most important initial laboratory test in determining the presence and severity of respiratory compromise.

Front 1679

What are the laboratory signs of acute respiratory failure?

Back 1679

Rise in pCO2 accompanied by a drop in pH. The bicarbonate level will decrease over 24 hours with renal compensation. Metabolic acidosis (lactic acidosis) in the presence of hypercapnia is an indication for ventilation.

Front 1680

What is the target O2 saturation in COPD exacerbations?

Back 1680

In the setting of acute-on-chronic respiratory failure, the administration of supplemental oxygen is often accompanied by a rise in PaCO2. The target range should be oxygen saturation 88-92%.

Front 1681

What is the significance of an elevated B-type natriuretic peptide?

Back 1681

An elevated BNP is seen in patients with left heart failure. Cor pulmonale and acute right ventricular failure (thromboembolism) may also cause a rise in the BNP.

Front 1682

What are the causes of respiratory failure with a clear chest x-ray?

Back 1682

Chest x-ray without parenchymal infiltrates accompanies respiratory failure due to thromboembolism, central respiratory depression, neuromuscular disease, and upper airway obstruction.

Front 1683

What are the chest x-ray findings in asthma and COPD?

Back 1683

Hyperinflation (hyperlucency). Focal infiltrates suggest bacterial, viral, or fungal pneumonia, aspiration, or pulmonary hemorrhage. Heart failure and ARDS present with diffuse edema.

Front 1684

What blood gas results indicate the need for mechanical ventilation in patients with an asthma exacerbation?

Back 1684

Respiratory acidosis and hypercapnia with asthma exacerbation requires ventilation. Indications for intubation include upper-airway injury, airway compromise, neurologic depression.

Front 1685

What are the signs of pulmonary embolism in ICU patients?

Back 1685

Dyspnea, tachypnea, hypoxemia.

Front 1686

What complication may result from gastric aspiration?

Back 1686

Aspiration, which may precipitate respiratory failure directly or through the development of pneumonia or acute respiratory distress syndrome.

Front 1687

What are the risk factors for aspiration?

Back 1687

The risk factors for aspiration include impaired consciousness and upper airway instrumentation (nasogastric tubes). Respiratory depression from opiates.

Front 1688

What is acute respiratory distress syndrome?

Back 1688

Diffuse inflammatory response of lungs within 24 hours of the onset of severe illness or injury. Tachypnea and hypoxemia. Diffuse pulmonary infiltrates of noncardiogenic pulmonary edema.

Front 1689

22-year-old with asthma, wheezing after URI. Resp 28, pulse 120; afebrile. Oxygen by nasal cannula is administered. What should be the next treatment?

Back 1689

Beta-Agonist (albuterol) by nebulizer.

Front 1690

What is asthma?

Back 1690

Inflammatory hyperreactivity of the respiratory tree, resulting in reversible airway obstruction. Mucosal inflammation, bronchial musculature constriction, excessive mucus; episodic pattern.

Front 1691

What factors precipitate attacks in intrinsic asthma?

Back 1691

Occurs in 50% of asthmatics who are nonallergic. Attacks are precipitated by infections, irritants, cold air, exercise, emotional upset. Prognosis is poor.

Front 1692

What is the pathophysiology of extrinsic asthma?

Back 1692

Extrinsic (allergic, atopic) asthma results from sensitization. IgE elevated. Family history. Precipitated by allergens and accounts for 20% of asthma. Allergic rhinitis, urticaria, eczema. Prognosis good.

Front 1693

What are the most common stimuli that cause asthma exacerbations?

Back 1693

Respiratory infections with respiratory syncytial virus in young children, rhinoviruses in adults. Aspirin, coloring agents such as tartrazine, and beta-adrenergic antagonists.

Front 1694

What are the signs of asthma?

Back 1694

Tachypnea, tachycardia, prolonged expirations, diffuse wheezing. Use of accessory muscles, diminished breath sounds, hyperresonance, intercostal retraction.

Front 1695

What are the signs of poor prognosis in asthma?

Back 1695

Poor prognostic factors include fatigue, diaphoresis, pulsus paradoxus, inaudible breath sounds, decreased wheezing, cyanosis, bradycardia.

Front 1696

What are the arterial blood gas findings in acute asthma?

Back 1696

In the acute phase, PaCO2, increase in pH, and normal or low PaCO2. In severe asthma or status asthmaticus there will be a decreased PaCO2, increased PaCO2, and decreased pH.

Front 1697

What is the significance of a normal PaCO2 in acute asthma?

Back 1697

A normal PaCO2 may indicate respiratory muscle fatigue in acute asthma.

Front 1698

What are the chest x-ray findings in asthma?

Back 1698

Chest x-ray shows hyperinflation. Acute infection may be visible as the cause of an acute attack.

Front 1699

What are the pulmonary function test abnormalities in asthma?

Back 1699

PFTs show obstructive pattern that reverses with bronchodilation. PFTs may be normal because asthma is episodic; in this case a provocative challenge may be performed with methacholine or cold air.

Front 1700

What is the treatment of acute exacerbations of asthma?

Back 1700

beta-Adrenergic agonist inhalers (albuterol, terbutaline). Inhaled beta-adrenergic agonists are preferred. Side effect is tremor. beta-Adrenergic agonists terminate 70% of asthmatic attacks.

Front 1701

What are the indications for salmeterol?

Back 1701

Salmeterol is a long-lasting (12 h) type of albuterol that is effective in nocturnal cough variant and exercise-induced asthma. Salmeterol has no benefit in acute episodes.

Front 1702

What diseases may be adversely affected by beta-agonists?

Back 1702

beta-Adrenergic agonists must be used with caution in cardiovascular disorders, hypothyroidism, diabetes mellitus, hypertension, and coronary insufficiency.

Front 1703

What is the role of theophylline in the treatment of asthma?

Back 1703

Aminophylline and theophylline are only modest bronchodilators. Sometimes of benefit for nocturnal cough. Improve contractility of diaphragm. Not routinely used in asthma because no added benefit.

Front 1704

What are the indications for ipratropium and tiotropium in the treatment of asthma?

Back 1704

Anticholinergics (ipratropium, tiotropium) are especially beneficial with heart disease when beta-adrenergic agonists may be dangerous. Slow to achieve bronchodilation (>90 min), medium potency.

Front 1705

What is the role of supplemental oxygen in the treatment of acute asthma exacerbations?

Back 1705

Supplemental oxygen, by nasal cannula or mask, should be given immediately for acute asthma exacerbation. Always maintain an oxygen saturation above 90%.

Front 1706

When should antibiotics be given to patients with an exacerbation of asthma?

Back 1706

Antibiotic treatment should be considered in patients with purulent sputum and chest x-ray infiltrates consistent with bacterial pneumonia.

Front 1707

What medication is used for long-term control of asthma?

Back 1707

Corticosteroids reduce airway inflammation. Used in acute exacerbations in short bursts for 10-14 days, along with bronchodilators.

Front 1708

What are the side effects of systemic corticosteroids?

Back 1708

Oral candidiasis, weight gain, HTN, glaucoma, cataracts, diabetes, muscle weakness, and osteoporosis.

Front 1709

What is the role of mast cell stabilizers in the treatment of asthma?

Back 1709

Cromolyn and nedocromil. Used for prophylaxis, and exercise and allergic asthma. Adults will benefit less than children. Cromolyn is first-line chronic treatment in children.

Front 1710

What is the mechanism of the leukotriene modifiers?

Back 1710

Inhibit 5-lipoxygenase, the enzyme of leukotriene production, or competitively antagonize LTD4. Zileuton is the only leukotriene inhibitor. The LTD4 receptor antagonists are zafirlukast and montelukast.

Front 1711

What is the role of leukotriene modifiers in the treatment of asthma?

Back 1711

This group of drugs is approved for severe asthma resistant to maximal doses of inhaled steroids. Leukotriene modifiers are not first-line drugs.

Front 1712

What is the treatment of mild asthma?

Back 1712

Mild asthma: Inhaled, short-acting bronchodilators as needed (albuterol inhaler).

Front 1713

What is the treatment of moderate asthma?

Back 1713

Inhaled steroids. Children with mild symptoms benefit from cromolyn, along with inhaled beta-agonists as needed. Nocturnal symptoms, despite short-acting beta agonists, will benefit from salmeterol.

Front 1714

What is the treatment of severe asthma?

Back 1714

Inhaled steroids daily, inhaled long-acting beta agonists (salmeterol), inhaled short-acting agonists for breakthrough symptoms, along with antileukotriene drugs (montelukast) and oral steroids.

Front 1715

What is the most common cause of chronic obstructive pulmonary disease?

Back 1715

Cigarette smoking; 10-15% of smokers develop COPD. 90% of COPD patients are cigarette smokers. COPD symptoms usually begin after at least 20 pack-years of tobacco exposure.

Front 1716

What is alpha-1 antitrypsin deficiency?

Back 1716

Rare hereditary autosomal recessive disease which can cause emphysema and liver abnormalities.

Front 1717

What are the physical signs of emphysema?

Back 1717

Distant breath sounds will be heard on auscultation.

Front 1718

What are the physical signs of chronic bronchitis?

Back 1718

Rhonchi and wheezes. Right heart failure (cor pulmonale) and clubbing.

Front 1719

What are the chest x-ray findings in chronic bronchitis?

Back 1719

Increased pulmonary markings can be seen?

Front 1720

What are the chest x-ray findings in emphysema?

Back 1720

Hyperinflation with diaphragm flattening, small heart size, and increase in retrosternal space. Cor pulmonale in COPD is caused by chronic pulmonary HTN.

Front 1721

How is COPD diagnosed?

Back 1721

Reduction in FEV1/FVC ratio and FEF 25. RV and TLC are increased. Emphysema will has decreased DLco; chronic bronchitis has normal DLco. After a bronchodilator the FEV1/FVC increase.

Front 1722

What are the complications of chronic obstructive pulmonary disease?

Back 1722

Hypoxemia with nocturnal desaturation. Erythrocytosis. Pulmonary HTN, cor pulmonale and right HF. Ventilatory failure and CO2 retention in early chronic bronchitis and end-stage emphysema.

Front 1723

What is the treatment of chronic obstructive pulmonary disease?

Back 1723

Anticholinergic agents (ipratropium bromide and tiotropium) are the first-line drugs in COPD via MDI. Anticholinergic agents can be used synergistically with beta2-adrenergic agonists in COPD.

Front 1724

What medication is given if chronic obstructive pulmonary disease remains symptomatic after treatment with ipratropium?

Back 1724

beta2 agonists (albuterol) are used after anticholinergic. Beta-agonists are not first-line agents in COPD because many have heart disease. Inhaled corticosteroids are not used routinely in COPD.

Front 1725

What is the role of theophylline in the treatment of COPD?

Back 1725

Theophylline is used if beta2 adrenergics and anticholinergics are not effective.

Front 1726

What medications interact with theophylline?

Back 1726

Increased theophylline clearance is seen in smokers, rifampin, phenytoin, phenobarbital. Decreased theophylline clearance is seen with erythromycin, ciprofloxacin, or H2-blockers (cimetidine, ranitidine).

Front 1727

What are the indications for home oxygen in patients with COPD?

Back 1727

Home O2 is given to patients with hypoxemia (PaO2 <55 mm Hg or saturation <88%); goal is O2 saturation >90%. Cor pulmonale will benefit from home oxygen when PaO2 <59 mm Hg.

Front 1728

What immunizations should be given to patients with chronic bronchitis or emphysema?

Back 1728

All patients with COPD should receive the pneumococcal vaccine (Pneumovax) every 5 years and the influenza vaccine yearly. H. influenzae vaccine if they were not previously immunized.

Front 1729

What are the most common causes of COPD exacerbations?

Back 1729

Viral lung infections. Other: bacterial infections, heart failure, myocardial ischemia, pulmonary embolism, lung cancer, esophageal reflux disease, and beta-blockers.

Front 1730

What is the initial management of COPD exacerbation?

Back 1730

Measure O2 saturation. Arterial blood gas determination of hypercapnia and hypoxia. Chest x-ray to identify pulmonary infiltrates pneumonia. Pulmonary edema indicates heart failure.

Front 1731

What is the laboratory evaluation of COPD exacerbations?

Back 1731

Check theophylline levels. CBC for elevated WBCs and polycythemia; ECG may reveal atrial fibrillation, that may precipitate heart failure and exacerbate COPD.

Front 1732

What are the indications for mechanical ventilation in COPD?

Back 1732

Intubation and mechanical ventilation for decreased consciousness, cyanosis, or hemodynamic instability, persistent hypoxemia.

Front 1733

What is the role of antibiotics in patients with COPD exacerbations?

Back 1733

Beneficial in exacerbations. Second-gen macrolides (clarithromycin, azithromycin), extended-spectrum fluoroquinolones (levofloxacin, moxifloxacin), cephalosporins (2nd/3rd gen), amoxicillin-clavulanate.

Front 1734

What medications are used to treat exacerbations of COPD?

Back 1734

O2 supplementation titrated to >90% saturation. Inhaled bronchodilators are the most effective. In acute COPD exacerbations, use albuterol and anticholinergics (ipratropium) simultaneously.

Front 1735

What medications should be avoided in patients with COPD?

Back 1735

There is no benefit to intravenous aminophylline. Avoid opiates and sedatives that may suppress respiratory system.

Front 1736

What is the role of corticosteroids in the treatment of COPD?

Back 1736

Corticosteroids may be given intravenously or orally because the efficacy is similar. 60 mg prednisone is continued for 2 weeks. Severe exacerbation is treated with IV methylprednisolone.

Front 1737

What is bronchiectasis?

Back 1737

Permanent dilation of small- and medium-sized bronchi from destruction of bronchial elastic and muscle. Can be caused by tuberculosis, fungal infections, abscess, cystic fibrosis, immotile cilia syndrome.

Front 1738

What are the clinical signs of bronchiectasis?

Back 1738

Chronic cough, hemoptysis, copious, foul-smelling sputum, sinusitis, immune deficiencies. Wheezes, crackles. Recurrent pneumonias with gram-negative bacteria, especially Pseudomonas. Polycythemia.

Front 1739

How is bronchiectasis diagnosed?

Back 1739

Chest x-ray: advanced cases may show 1- to 2-cm cysts and crowding of the bronchi (tram-tracking). High- resolution CT scan of the chest detects bronchiectasis.

Front 1740

What is the treatment for bronchiectasis?

Back 1740

Bronchodilators, chest physical therapy, postural drainage. TMP-SMZ, amoxicillin, amoxicillin/clavulanate when sputum production increases. A different antibiotic each time.

Front 1741

What bacterial coverage is required in the treatment of bronchiectasis?

Back 1741

Symptoms should be treated IV for gram-negative bacteria (quinolones, ceftazidime, aminoglycosides. Surgical therapy with localized bronchiectasis or massive hemoptysis.

Front 1742

What vaccines are indicated for patients with bronchiectasis?

Back 1742

Yearly vaccination for influenza and vaccination for pneumococcal infection with a single booster at 5 years.

Front 1743

What are the complications of bronchiectasis?

Back 1743

Complications hemoptysis, amyloidosis, cor pulmonale, and visceral abscesses.

Front 1744

What is interstitial lung disease?

Back 1744

Group of heterogeneous diseases of chronic inflammation and fibrosis of interstitium and lung parenchyma. The worst prognosis is with idiopathic pulmonary fibrosis and interstitial pneumonitis.

Front 1745

What is the pathophysiology of interstitial lung disease?

Back 1745

Inflammation and scarring of the interstitium that disrupts normal gas exchange the area in and around the small blood vessels and alveoli.

Front 1746

What are the clinical signs of interstitial lung disease?

Back 1746

Exertional dyspnea and nonproductive cough. Coarse crackles, pulmonary HTN (increased pulmonic sound, right heart failure), and clubbing.

Front 1747

What are the chest x-ray findings in interstitial lung disease?

Back 1747

Reticular (branching) or reticulonodular pattern ("ground-glass" appearance). PFTs show intrapulmonary restrictive pattern.

Front 1748

What are the causes of interstitial lung disease?

Back 1748

Idiopathic pulmonary fibrosis, sarcoidosis, pneumoconiosis, occupational; autoimmune; hypersensitivity pneumonitis; eosinophilic, Wegener, hemosiderosis, bronchiolitis obliterans, lymphangioleiomyomatosis.

Front 1749

What is the diagnostic evaluation of interstitial lung disease?

Back 1749

High-resolution CT scan and, eventually, biopsy via bronchoscopy or open lung biopsy.

Front 1750

55-year-old man with exercise intolerance. Dyspnea on exertion; nonsmoker. Resp 25, JVD, crackles, clubbing, pedal edema. Diffuse reticular disease. What is the diagnosis?

Back 1750

Idiopathic pulmonary fibrosis.

Front 1751

What is idiopathic pulmonary fibrosis?

Back 1751

Inflammatory lung disease of unknown origin that causes lung fibrosis and restrictive lung disease. Only the lung and has no extrapulmonary manifestations except clubbing.

Front 1752

What is the age of onset of idiopathic pulmonary fibrosis?

Back 1752

IPF occurs in patients in the fifth decade of life, with an equal distribution between men and women.

Front 1753

What are the clinical signs of idiopathic pulmonary fibrosis?

Back 1753

Progressive exercise intolerance and dyspnea. Coarse dry crackles.

Front 1754

What are the radiographic findings in idiopathic pulmonary fibrosis?

Back 1754

Reticular or reticulonodular disease. CT shows ground-glass appearance. A restrictive intrapulmonary process on PFTs. Bronchoalveolar lavage will show increased macrophages.

Front 1755

What is the treatment for idiopathic pulmonary fibrosis?

Back 1755

Treatment with steroids with or without azathioprine will benefit 20% of patients; 80% progress to fatal lung fibrosis. There is a 20 to 40% five-year survival.

Front 1756

A 29-year-old woman, painful erythematous papules. Joint swelling, pain. Fever, symmetric swelling of knees, PIP and MCP joints, and 3 cm papules over the anterior legs. What is the diagnosis?

Back 1756

Sarcoidosis

Front 1757

What is sarcoidosis?

Back 1757

Systemic disease, characterized by noncaseating granulomas in the lung and other organs. Increased incidence of sarcoidosis among blacks and patients 20-40 years.

Front 1758

What are the clinical signs of sarcoidosis?

Back 1758

Sarcoidosis can involve any organ system. Hilar adenopathy in an asymptomatic patient. Erythema nodosum, arthritis. Fever, parotid enlargement, uveitis, facial palsy. Lung involvement in 90%.

Front 1759

What are the chest x-ray findings in sarcoidosis?

Back 1759

Hilar adenopathy, reticulonodular parenchyma, or honeycombing with fibrosis.

Front 1760

What are the laboratory findings in sarcoidosis?

Back 1760

Hypercalcemia or hypercalciuria caused by vitamin D produced by macrophages. Elevation in ACE in 60%. Increased LFTs in 30%. Skin anergy; PFT restrictive pattern. Uveitis and conjunctivitis in >25%.

Front 1761

How is sarcoidosis diagnosed?

Back 1761

Lung biopsy shows noncaseating granulomas.

Front 1762

What is the prognosis in sarcoidosis?

Back 1762

Eighty percent of patients with lung involvement from sarcoidosis remain stable, or the disease resolves. Twenty percent of patients develop progressive disease with end-organ compromise.

Front 1763

What is the treatment for sarcoidosis?

Back 1763

Trial of steroids. Mandatory for uveitis, sarcoidosis involving the CNS, and hypercalcemia.

Front 1764

What are the pneumoconioses?

Back 1764

Occupational lung diseases in which inhalation of fibers initiate an inflammatory process that leads to fibrosis. Appears 20-30 years after exposure to mining of gold, silver, lead, copper.

Front 1765

What is the pathology of pneumoconioses?

Back 1765

Macrophages engulf offending agents, causing inflammation and fibrosis of the lung. Respiratory insufficiency.

Front 1766

What are the signs of pneumoconioses?

Back 1766

Dyspnea, shortness of breath, cough, sputum production, cor pulmonale, and clubbing. PFTs show a restrictive pattern with a decreased DLco. Hypoxemia with an increased PAO2-PaO2 gradient.

Front 1767

What are the chest x-ray finding in pneumoconiosis?

Back 1767

Small irregular opacities, interstitial densities, ground glass appearance, and honeycombing.

Front 1768

What is asbestosis?

Back 1768

Lung disease caused by inhalation of asbestos fiber in mining, milling, foundry work, shipyards, or the application of asbestos to pipes, brake linings, insulation, and boilers.

Front 1769

What are the signs of asbestosis?

Back 1769

Exertional dyspnea and reduced exercise tolerance, cough and wheezing, chest wall pain, and respiratory failure.

Front 1770

What are the chest x-ray findings in asbestosis?

Back 1770

Pleural thickening, pleural plaques, and calcifications of the diaphragm. Pleural effusions and the interstitial lung process associated with asbestosis usually involves the lower lung fields.

Front 1771

What cancer is most commonly associated with asbestosis?

Back 1771

The most common cancer associated with asbestosis is bronchogenic carcinoma (adenocarcinoma or squamous cell). Mesotheliomas are also associated with asbestos.

Front 1772

How is asbestosis diagnosed?

Back 1772

Lung biopsy shows barbell-shaped asbestos fiber.

Front 1773

What is silicosis?

Back 1773

Lung disease caused by inhalation of silica dust during mining, quarrying, tunneling, glass and pottery making, and sandblasting.

Front 1774

What are the signs of silicosis?

Back 1774

Exertional dyspnea, cough, wheezing.

Front 1775

What are the chest x-ray findings in silicosis?

Back 1775

Nodules (1-10 mm) throughout the lungs, most prominent in the upper lobes. Eggshell calcifications.

Front 1776

What percentage of miners contract coal miner's lung/coal worker's pneumoconiosis?

Back 1776

12% of all miners.

Front 1777

What is the presentation of coal worker's pneumoconiosis?

Back 1777

Coal worker's pneumoconiosis presents with exertional dyspnea, cough, wheezing.

Front 1778

What are the chest x-ray findings in coal worker's pneumoconiosis?

Back 1778

Small round densities in parenchyma, upper half of the lungs.

Front 1779

What are the laboratory abnormalities associated with coal worker's pneumoconiosis?

Back 1779

Increased IgA, IgG, C3, antinuclear antibodies, and rheumatoid factor are seen in coal worker's pneumoconiosis.

Front 1780

38-year-old woman with sudden onset of shortness of breath and pleuritic chest pain; oral contraceptives. Respirations 28, pulse 110. Mild hypoxemia (7.52/70/25/90%). Chest x-ray is normal. What is the diagnosis?

Back 1780

Pulmonary embolism

Front 1781

What are the high-risk factors for embolism and DVTs?

Back 1781

Surgery, cancer, CHF, travel. Lupus anticoagulant, nephrotic syndrome (loss of antithrombin III), OCPs (smoker). Factor V Leiden mutation; protein C, S, antithrombin III deficiency. Pregnancy.

Front 1782

What are the symptoms and signs of pulmonary embolism and deep vein thrombosis?

Back 1782

Sudden onset of dyspnea (shortness of breath) and tachypnea. Thigh or calf swelling. Pleuritic chest pain, hemoptysis. Increased respiratory rate with tachycardia; increased pulmonic sound (P2).

Front 1783

What patients are considered to be high-risk for pulmonary embolism?

Back 1783

Patients with one risk factor and consistent symptoms and no alternative diagnosis. Low-risk patients have no risk factors, atypical symptoms, and an alternative diagnosis (eg, pneumonia).

Front 1784

What are the arterial blood gas findings in pulmonary embolism?

Back 1784

Hypoxemia with an elevated A-a gradient. The A-a gradient may be normal.

Front 1785

What are chest x-ray findings in pulmonary embolism?

Back 1785

Usually normal. Other nonspecific findings include atelectasis and pleural effusion. Westermark sign is the loss of vascular markings. Hampton hump is a wedge-shaped infiltrate caused by pulmonary infarction.

Front 1786

What diagnosis should be considered in all patients with dyspnea and normal chest x-ray?

Back 1786

Pulmonary embolus should be considered in all patients with dyspnea and normal chest radiography.

Front 1787

What are the ECG signs of pulmonary embolism?

Back 1787

Right heart strain: large S wave in lead I and deep Q in lead III with T-wave inversion in the same lead. The most common finding is sinus tachycardia. The ECG excludes acute pericarditis and myocardial ischemia.

Front 1788

What diagnostic tests are used to diagnose pulmonary embolism?

Back 1788

Spiral CT is initial test for PE. Ventilation-perfusion scan is a nuclear test. Pulmonary embolus will cause perfusion defects. Angiogram is most accurate test, but risk of pulmonary artery rupture is 1%.

Front 1789

What diagnostic tests are used to diagnose deep vein thrombosis?

Back 1789

Compression or duplex ultrasound. Venogram is rarely done. MRI.

Front 1790

What is the role of D-dimer testing in evaluating thromboembolic disease?

Back 1790

D-dimer is the most sensitive test for PE. Indicates fibrin degradation from thromboembolism, surgery, infection, trauma, pregnancy, DIC. Normal test means no thrombus; only be used to rule out PE.

Front 1791

What is the diagnostic approach to suspected pulmonary embolism?

Back 1791

CXR, then spiral CT. Normal CT and normal D-dimer in low-risk excludes PE. Normal CT and normal Doppler ultrasound in low-risk excludes PE. If tests are negative, but high risk, angiogram is done.

Front 1792

What treatment should begin to patients suspected of having a pulmonary embolism or deep vein thrombosis?

Back 1792

All patients should be on anticoagulation while completing diagnostic evaluations. Heparin should always be started before sending that patient for CT or V/Q scan.

Front 1793

What is the treatment of pulmonary embolism?

Back 1793

Give oxygen and start heparin immediately while the diagnostic evaluation is being completed. LMWH or unfractionated heparin for 7-10 d. Warfarin should be started with heparin and continued for 6 mo.

Front 1794

What is the mechanism of action of low molecular weight heparin?

Back 1794

LMWH inactivates factor Xa but has no effect on thrombin (no need PTT). Dosing is based on weight QD or bid. LMWH is equal to unfractionated heparin in DVT and PE.

Front 1795

What are the advantages of low molecular weight heparin over unfractionated heparin?

Back 1795

Less hemorrhage or heparin-induced thrombocytopenia.

Front 1796

What is heparin-induced thrombocytopenia?

Back 1796

Heparin-induced thrombocytopenia (HIT) is a common complication of heparin 5 days after starting in 5%. Associated more with thrombotic events than bleeding. Stop heparin when platelets decrease.

Front 1797

What is the cause of recurrent pulmonary embolism despite treatment with heparin?

Back 1797

Consider heparin-induced thrombocytopenia in a patient with recurrent pulmonary embolism or DVT despite heparin.

Front 1798

What is the treatment of heparin-induced thrombocytopenia?

Back 1798

HIT is treated with the new anticoagulants (argatroban, lepirudin).

Front 1799

What are argatroban and lepirudin?

Back 1799

Anticoagulants that are used in patients who can not use heparin.

Front 1800

What is the mechanism of warfarin?

Back 1800

Warfarin inhibits the vitamin K-dependent factors (II, VII, IX, and X). Factor VII has the shortest half-life of all the affected factors.

Front 1801

What test is used to assess the anticoagulant effect of warfarin?

Back 1801

PT is monitored to assess the warfarin anticoagulant effect. INR is used to control for variability in PT. Warfarin should be titrated to an INR of 2-3.

Front 1802

What complication occurs when warfarin is given to patients with protein C deficiency?

Back 1802

Rare procoagulant effect that occurs in preexisting protein C deficiency. Warfarin causes transient hypercoagulable state and diffuse thrombosis. Risk reduced by starting heparin and warfarin simultaneously.

Front 1803

What are the contraindications to anticoagulation?

Back 1803

Anticoagulation is contraindicated in patients with recent neurosurgery or eye surgery.

Front 1804

What is the anticoagulant treatment of patients who have had recent neurosurgery or eye surgery?

Back 1804

An inferior vena cava filter (Greenfield filter) should be used to prevent further embolism in these patients.

Front 1805

Want is the anticoagulation method for pregnant patients with deep vein thrombosis?

Back 1805

Warfarin is contraindicated in pregnant patients. LMWH for 6 months is the best alternative with injections once or twice a day.

Front 1806

What is the indication for thrombolytics in patients with pulmonary embolism?

Back 1806

Thrombolytics (tPA) for hemodynamically unstable (hypotension, right heart failure) or for massive DVT to prevent the postphlebitic syndrome.

Front 1807

What is postthrombotic syndrome?

Back 1807

Most common complication of DVT, occurring in up to two-thirds. Destruction of the valves. Pain, edema, hyperpigmentation, and skin ulceration. Compression stockings prevent the postthrombotic syndrome.

Front 1808

What is the duration of anticoagulation for noncomplicated proximal deep vein thrombosis?

Back 1808

6 months. In patients with thrombophilias (hypercoagulable states), lifelong anticoagulation is with warfarin if there have been two or more episodes of thrombosis.

Front 1809

Why should protein C or protein S levels not be checked during acute thrombosis?

Back 1809

Both warfarin and acute clot formation cause lower protein C and S.

Front 1810

What disorders should be suspected in patients who develop recurrent thrombosis while on anticoagulants?

Back 1810

Heparin-induced thrombocytopenia or cancer-related thrombosis. Place an inferior vena cava filter or use the hirudin derivative anticoagulants. IVC filters are associated with clot formation around the filter site.

Front 1811

What is the management of distal deep vein thromboses?

Back 1811

Below-the-knee DVT is not a cause of pulmonary embolism unless extend to proximal veins. Monitor for extension to the proximal veins by serial ultrasound or anticoagulation for 3 mo.

Front 1812

What is fat embolism syndrome?

Back 1812

Fat embolism is a rare type of embolism that occurs 3 days after long bone fracture (femur fracture). It may rarely occur after CPR. Acute dyspnea, petechiae (neck and axilla), and confusion.

Front 1813

What is the treatment of fat embolism syndrome?

Back 1813

The treatment is supportive (no anticoagulation).

Front 1814

A 50-year-old man with gram-negative sepsis severe dyspnea. Crackles; ABG shows hypoxemia and hypercarbia. Diffuse alveolar densities. What is the diagnosis?

Back 1814

Acute respiratory distress syndrome

Front 1815

What is acute respiratory distress syndrome?

Back 1815

Increased permeability of alveolar-capillary membrane, edema, hypoxemia caused by sepsis, trauma, DIC, drug overdose, inhalation of toxins, Goodpasture, SLE, drowning, bypass surgery.

Front 1816

What are the signs and symptoms of acute respiratory distress syndrome?

Back 1816

Dyspnea, increased respiratory rate, diffuse crackles, and rhonchi.

Front 1817

What are the chest x-ray findings in acute respiratory distress syndrome?

Back 1817

Diffuse interstitial or alveolar infiltrates; whiteout of both lung fields.

Front 1818

What are the blood gas findings in acute respiratory distress syndrome?

Back 1818

Decreased PaO2 and increased or normal PaCO2. Swan-Ganz catheter findings will reveal normal cardiac output and normal capillary wedge pressure, but increased pulmonary artery pressure.

Front 1819

What is the treatment for acute respiratory distress syndrome?

Back 1819

Mechanical support with increased positive end-expiratory pressure and permissive hypercapnia. Mortality rate 70%.

Front 1820

What is sleep apnea?

Back 1820

Cessation of airflow (>10 seconds) that occurs at least 10-15 times per hour during sleep. Oxygen saturation decreases. Daytime somnolence. Systemic HTN. Pulmonary HTN and cor pulmonary.

Front 1821

What is obstructive sleep apnea?

Back 1821

Airway closure despite adequate ventilatory effort. Usually obese and have abnormal airways. Treatment is weight loss and nasal continuous positive airway pressure.

Front 1822

What is the central sleep apnea?

Back 1822

Central sleep apnea occurs in <5% with sleep apnea; caused by inadequate ventilatory drive. Treatment is acetazolamide, progesterone, and O2.

Front 1823

How is sleep apnea diagnosed?

Back 1823

Polysomnography (sleep studies).

Front 1824

64-year-old man with headache and blurry vision. Neck vein distension and darker coloration over his face and neck. Confusion. Right upper lobe lung mass. Hypercalcemia. What is the diagnosis?

Back 1824

Bronchogenic carcinoma

Front 1825

What is the leading cause of cancer death in men and women?

Back 1825

Bronchogenic carcinoma is the leading cause of cancer death in men and women. 5-year survival rate for small cell cancer is 5% and non-small cell cancer is 8%.

Front 1826

What is the most common cause of bronchogenic carcinoma?

Back 1826

90% of bronchogenic carcinoma are directly related to smoking. 2 most common bronchogenic lung cancers are adenocarcinoma (40%) and squamous cell carcinoma.

Front 1827

What are the characteristics of squamous cell carcinoma?

Back 1827

Squamous cell carcinoma is centrally located. Cavitary lesions. Usually metastasizes by direct extension to hilar node and mediastinum. Hypercalcemia from the secretion of a PTH-like substance.

Front 1828

What are the characteristics of small cell carcinoma?

Back 1828

Central, rapidly growing, early metastasis to liver, adrenals, brain, bone. Associated with Eaton-Lambert syndrome (weakness), and paraneoplastic syndromes. Most common cause of venocaval obstruction syndrome.

Front 1829

What are the characteristics of large-cell carcinoma?

Back 1829

Peripherally located. Metastasize late in the course of disease.

Front 1830

What are the characteristics of adenocarcinoma?

Back 1830

Peripheral lesion metastasizes to liver, adrenals, brain, bone. Bronchioalveolar carcinoma is a subtype of adenocarcinoma; low-grade, may be caused by asbestos.

Front 1831

What are the symptoms of lung cancer?

Back 1831

Cough (74%), weight loss (68%), dyspnea (58%). Hemoptysis, chest wall pain, and post-obstructive pneumonia. Hoarseness indicates a nonresectable bronchogenic carcinoma.

Front 1832

How is lung cancer diagnosed?

Back 1832

Sputum cytology. Bronchoscopy for centrally located lesions. If there is a high degree of suspicion for carcinoma and the bronchoscopy results are nonspecific, a biopsy must be done.

Front 1833

What is the clinical evaluation of benign solitary pulmonary nodules?

Back 1833

75% of solitary nodules are benign. Benign nodules <35 years, nonsmokers, <2 cm, smooth distinct margins, calcification, nodule that has not changed size.

Front 1834

What is the management of solitary pulmonary nodules in low-risk persons?

Back 1834

If a patient is at low-risk for carcinoma, follow-up CT scans are indicated. In a high-risk patient the lesion should be removed.

Front 1835

What is the significance of bull's-eye lesions and popcorn bull lesions on chest x-ray?

Back 1835

Bull's-eye lesions are seen in granulomas, popcorn ball lesions are seen in hamartomas.

Front 1836

What are the symptoms that suggest an unresectable lesion?

Back 1836

Wt loss >10%, bone pain, extrathoracic metastases, CNS, superior vena cava syndrome, hoarseness, mediastinal adenopathy, TV <800, tumor class M1, tracheal, esophagus, pericardium, chest wall.

Front 1837

What is the treatment of small cell carcinoma?

Back 1837

Resectable lesions are treated with VP16 (etoposide, platinum). Non-small cell lesions are treated with chemotherapy and radiation therapy or cyclophosphamide, Adriamycin, and platinum. Effusions can be sclerosed.

Front 1838

67-year-old man dyspneic after cholecystectomy. Resp 24, pulse 100. Fever and decreased breath sounds in left lower lobe. Leukocytosis of 27,000. What is the diagnosis?

Back 1838

Atelectasis

Front 1839

What is atelectasis?

Back 1839

Collapse of part or the entire lung. Most commonly postoperative; caused by poor inspiration or lack of coughing, mucous plug, tumor, or foreign body.

Front 1840

What are signs of atelectasis?

Back 1840

Tachycardia, dyspnea, fever, hypoxemia. Tracheal deviation caused by volume loss. Diaphragm elevation . Mediastinal shift. Lobe will appear to be densely consolidated and smaller.

Front 1841

What is the treatment for atelectasis?

Back 1841

Induce deep breathing and stimulate coughing. Incentive spirometry and pulmonary toilet. Bronchoscopy with subsequent removal of mucous plugs.

Front 1842

After determining that the unresponsive patient is truly unresponsive, what is the next step?

Back 1842

Call for help. After calling for help, position the patient on a firm, flat surface, and roll the patient so that he is face up. Open the airway by performing the chin lift or jaw-thrust maneuver.

Front 1843

After opening the airway of an unresponsive patient, what is the next step?

Back 1843

After opening the airway, assess the patient's breathing by looking, listening, and feeling for air movement. If there is no air movement, then perform two rescue breaths with about two seconds per breath.

Front 1844

After delivering two rescue breaths to a non-breathing patient, what is the next step?

Back 1844

Check to see if there is a pulse by feeling for at least 5-10 seconds at the carotid artery.

Front 1845

If a patient has no pulse, what is the next action that should be taken?

Back 1845

If no pulse, perform chest compressions at a rate of 100 per minute, "push hard and push fast:" Provide 30 compressions and then two ventilations, regardless of whether one or two rescuers is present in adults.

Front 1846

What is the compression to ventilation ratio for CPR on a child?

Back 1846

In children, perform 30 compressions and 2 ventilations if one rescuer is present, and give 15 compressions and 2 ventilations if two rescuers are present.

Front 1847

What are the causes of asystole?

Back 1847

Ischemia and severe underlying cardiac disease. Metabolic derangements, drug overdose, trauma.

Front 1848

How is asystole diagnosed?

Back 1848

Asystole should always be confirmed by observing the rhythm in more than one lead on the ECG.

Front 1849

What is the treatment for asystole?

Back 1849

1 mg epinephrine IV q3-5min. Atropine 1 mg IV q 3-5min (max 0.04 mg/kg). Bicarbonate if cause of asystole is acidosis, or if the cause is tricyclic or aspirin overdose, hyperkalemia, or DKA. Pacing for very slow bradycardia.

Front 1850

What are the "H's and T's" of the causes of arrhythmias?

Back 1850

Hypoxia, Hyper/Hypokalemia, Hypothermia, Hypoglycemia, Hypovolemia, Trauma, Toxins (overdose), Tamponade, Tension pneumothorax, Thrombosis (coronary and pulmonary)

Front 1851

What are the ECG signs of ventricular tachycardia?

Back 1851

Ventricular tachycardia (VT) is a wide complex tachycardia with an organized, uniform sawtooth pattern on the ECG. There are no P-waves visible.

Front 1852

What are the causes of ventricular tachycardia?

Back 1852

Ischemia, MI, anatomic cardiac disease. Quinidine, tricyclics, phenothiazines. Long QT syndromes. The dysrhythmia originates from an ectopic focus in the myocardium or from the AV node.

Front 1853

What are the ECG characteristics of ventricular tachycardia?

Back 1853

The slowness of the conduction produces the slower and wider complexes on the ECG. The rate varies between 160-240 beats per minute.

Front 1854

What is the ECG appearance of torsade de pointes VT?

Back 1854

Torsade is a form of VT in which the morphology varies with an undulating amplitude, making it seem to "twist around a point." Associated with hypomagnesemia.

Front 1855

What is the treatment of torsade de pointes VT?

Back 1855

Magnesium is most useful for torsade.

Front 1856

What is the presentation of ventricular tachycardia?

Back 1856

VT lasting more than 30 seconds is referred to as sustained VT. Symptoms include lightheadedness, hypotension, congestive heart failure, syncope, and death.

Front 1857

What is the treatment for unstable ventricular tachycardia?

Back 1857

Requires immediate synchronized cardioversion if hypotension, chest pain, altered mental, or CHF. A lower dose of electricity, starting at 100 J, can be used at first for monomorphic VT. Synchronized.

Front 1858

What is the management of ventricular tachycardia without a pulse?

Back 1858

Immediate synchronized cardioversion. VT without serious hemodynamic compromise can be treated with amiodarone. If there is no response, then lidocaine or electrical cardioversion is used.

Front 1859

What is the long-term therapy for ventricular tachycardia?

Back 1859

Long-term therapy is most effective with beta-blockers. VT producing sudden death or VT that is sustained through initial drug therapy requires placement of an implantable cardiac defibrillator.

Front 1860

What is pulseless electrical activity?

Back 1860

Loss of pulse with some type of electrical activity. Caused by hypovolemia, tamponade, tension pneumothorax, PE, MI, hypoxia, hypothermia, potassium disorders, acidosis, tricyclics, digoxin, beta-blockers, Ca-blockers.

Front 1861

What is the treatment for pulseless electrical activity?

Back 1861

CPR while determining the cause. Epinephrine. Atropine if there is bradycardia. Bicarbonate is useful if a known acidosis caused the arrest or in a prolonged resuscitation, or hyperkalemia.

Front 1862

What are the atrial dysrhythmias?

Back 1862

Atrial fibrillation, flutter, supraventricular tachycardia. Ectopic focus in atrium or re-entry at AV. Atrial dysrhythmias have normal conduction in ventricles. QRS normal and narrow. A normal P is not present.

Front 1863

What are the causes of supraventricular tachycardia?

Back 1863

Re-entrant around AV node. A-fib is most commonly caused by HTN, enlarged atria. Hyperthyroidism, pheochromocytoma, caffeine, theophylline, alcohol, cocaine, digoxin, pericarditis, PE, surgery, trauma, ischemia.

Front 1864

What percentage of cardiac output is attributable to the atria?

Back 1864

In normal heart, only 10% of cardiac output is from atria. In a person with a dilated or postinfarction heart, or in significant valvular disease, the contribution is 30-40%, in which case more severe symptoms arise.

Front 1865

What are the symptoms of supraventricular tachycardia?

Back 1865

Asymptomatic to palpitations, lightheadedness, hypotension, disorientation, CHF, syncope. Rate-related symptoms are unlikely if the heart rate is <150.

Front 1866

How is supraventricular tachycardia diagnosed?

Back 1866

ECG and may need a 24-72 hour Holter monitor to detect brief paroxysms of the dysrhythmia not seen on the ECG.

Front 1867

What is the origin of narrow complex tachycardias?

Back 1867

Narrow complex tachycardia is always atrial in origin (QRS <0.12). Wide complex tachycardia can be either atrial or ventricular in origin.

Front 1868

What is the treatment for supraventricular tachycardia?

Back 1868

Hypotension, confusion, CHF, chest pain require synchronized cardioversion. If stable, use vagal maneuvers such as carotid sinus massage, Valsalva, ice water. If vagal maneuvers are not effective, give IV adenosine.

Front 1869

What drugs are used to slow the ventricular rate in supraventricular tachycardias?

Back 1869

For atrial fibrillation, atrial flutter, and in SVT after the failure of adenosine, slow the heart rate with calcium-channel blockers (such as diltiazem or verapamil), beta-blockers, or digoxin.

Front 1870

What are the contraindications for verapamil?

Back 1870

Severe left ventricular dysfunction and low EJECTION FRACTION. Beta-blockers are contraindicated in reactive airway disease.

Front 1871

What is the best treatment approach for atrial fibrillation?

Back 1871

Rate control to <100 with anticoagulation with warfarin to an INR of 2-3 is superior to converting into sinus rhythm. Return to a normal sinus rhythm can prevent in embolic stroke in 5% per year.

Front 1872

What are the medications that convert atrial fibrillation to sinus rhythm?

Back 1872

Procainamide, amiodarone, ibutilide, sotalol, quinidine, propafenone, and dofetilide can convert a minority to sinus. Elective cardioversions should be preceded and followed by several weeks of Coumadin.

Front 1873

What is the treatment of atrial fibrillation that cannot be converted with antiarrhythmics?

Back 1873

If medications can not convert to sinus, then attempt electrical cardioversion. Preceded and followed by several weeks of anticoagulation if AF present >48 h. Transesophageal echo can exclude a clot.

Front 1874

What is bradycardia?

Back 1874

Heart rate <60 bpm. Degeneration of the node. Serious bradycardias are Mobitz-type II second-degree block and 3rd-degree block. Caused by ischemic damage to AV node, myocarditis, amyloidosis, sarcoidosis.

Front 1875

What is the presentation of bradycardia?

Back 1875

Hypotension and decreased cardiac output. Mobitz-type I second-degree block is characterized by progressive P-R lengthening, whereas in Mobitz-type II, the P-R interval remains constant.

Front 1876

What is the treatment for asymptomatic bradycardia?

Back 1876

Asymptomatic bradycardia, first-degree block, Mobitz-type I (Wenckebach) second-degree block need no therapy.

Front 1877

What is the treatment for symptomatic bradycardia?

Back 1877

Symptomatic bradycardia is treated with atropine and pacemaker. Mobitz-type II second-degree block and third-degree block pacemaker. Dopamine or epinephrine if hypotension.

Front 1878

Which toxins cause miosis?

Back 1878

Clonidine, barbiturates, opiates, cholinergics, and pontine stroke.

Front 1879

Which toxins may cause mydriasis?

Back 1879

Sympathomimetics and anticholinergics.

Front 1880

Which toxins may cause dry skin?

Back 1880

Anticholinergics

Front 1881

Which toxins may cause profuse sweating?

Back 1881

Cholinergics, sympathomimetics.

Front 1882

What are the indications for gastric lavage?

Back 1882

Lavage is only useful within first hour after ingestion (usually not done). Contraindicated with acids or alkalis. If altered mental, lavage should be preceded by intubation. Large bore oropharyngeal hose (eg, an Ewald tube).

Front 1883

What are the indications for activated charcoal administration?

Back 1883

The main therapy for toxin ingestion is activated charcoal administration every 2-4 h to block absorption and accelerate the removal of toxins. Not effective for hydrocarbon or for metals such as iron.

Front 1884

What are the indications for whole bowel irrigation?

Back 1884

Large-volume pill ingestions in which the pills can be seen on x-ray. Gastric tube is placed and 1-2 L/h of GoLYTELY (polyethylene glycol) until the bowel movements run clear.

Front 1885

What medications should be given first to any patient with altered mental status or coma?

Back 1885

Naloxone, dextrose, and thiamine should be given first to any altered mental status or coma. Naloxone has no adverse effects and is immediately effective. Dextrose prevents permanent brain damage from hypoglycemia.

Front 1886

What are the substances or drugs that may require dialysis for removal?

Back 1886

Ethylene glycol poisoning, lithium overdose, methanol poisoning, aspirin overdose, theophylline overdose.

Front 1887

What amount of acetaminophen will cause serious toxicity?

Back 1887

140 mg per kg of acetaminophen causes serious toxicity. For a 70-kg person, 7-10 grams will cause toxicity. Fatalities can occur above 12-15 grams.

Front 1888

What is the presentation of acetaminophen overdose?

Back 1888

Nausea, vomiting from gastritis. At 24-48 h, there is subclinical elevation transaminases, bilirubin. At 48-72 h, liver damage, nausea, jaundice, abdominal pain, encephalopathy, renal failure, death.

Front 1889

What is the treatment of acetaminophen overdose?

Back 1889

Large acetaminophen ingestions warrant - acetyl cysteine. Nomogram based on drug level is necessary to determine risk of toxicity. Elevated AST is more common than ALT. Bilirubin, PT indicate hepatic necrosis.

Front 1890

What elimination measures are used for acetaminophen overdose?

Back 1890

Gastric emptying should not be used because it will delay NAC as a. Activated charcoal is given in repeated doses. When more than 24 hours have elapsed since ingestion, there is no therapy that can prevent toxicity.

Front 1891

What are the common causes of methanol ingestion?

Back 1891

Methanol paint thinner, Sterno, solvents, and windshield washer solution.

Front 1892

What is the most common source of ethylene glycol ingestion?

Back 1892

Ethylene glycol is most often found in antifreeze.

Front 1893

What is the pathophysiology of alcohol toxicity?

Back 1893

All alcohols are metabolized by alcohol dehydrogenase, which metabolizes methanol to formaldehyde and formic acid. Ethylene glycol is metabolized partially to oxalic acid and oxalate, which leads to kidney damage.

Front 1894

What is the presentation of ethanol, methanol, ethylene glycol, and isopropyl alcohol toxicity?

Back 1894

Methanol causes visual disturbances, including blindness. Ethylene glycol causes renal failure, oxalate crystals, stones. Isopropyl alcohol can only be distinguished by drug level or by non-anion gap acidosis.

Front 1895

What are the laboratory signs of isopropyl alcohol ingestion?

Back 1895

Isopropyl alcohol results in ketonuria and ketonemia with little to no metabolic acidosis (without evidence of an increased anion gap).

Front 1896

How is toxicity from the alcohols diagnosed?

Back 1896

Specific levels. Ethylene glycol has oxalate crystals in urine, increasing BUN/creatinine, hypocalcemia. Ethylene glycol and methanol cause metabolic acidosis with anion gap.

Front 1897

What is the treatment for ethylene glycol and methanol intoxication?

Back 1897

Fomepizole (Antizol) is an IV alcohol dehydrogenase inhibitor. Fomepizole inhibits the production of toxic metabolites without leading to intoxication.

Front 1898

What are the symptoms of carbon monoxide poisoning?

Back 1898

Dyspnea, tachypnea, and shortness of breath. Headache, nausea, and dizziness occur early. Confusion, syncope. Chest pain, arrhythmia, and hypotension.

Front 1899

What is the laboratory evaluation of carbon monoxide poisoning?

Back 1899

Carboxyhemoglobin levels. Metabolic acidosis is caused by the failure of carboxyhemoglobin to release oxygen to tissues. The pO2 will be normal. CPK is elevated. Pulse oximetry is not helpful.

Front 1900

What is the treatment of carbon monoxide poisoning?

Back 1900

100% oxygen administration. Hyperbaric oxygen in severe cases with CNS abnormalities or chest pain.

Front 1901

What are the common sources of acid ingestions?

Back 1901

Toilet, drain, swimming pool, and metal cleaners. Common alkali ingestions are lye, dishwasher detergents, hair relaxers, and oven cleaners.

Front 1902

What is the presentation of acid or alkali ingestion?

Back 1902

Oral pain, drooling, odynophagia, abdominal pain. Esophageal injury with subsequent stricture formation from acid or alkali ingestion. Gastric perforation. Alkali is more destructive than acid.

Front 1903

What is the treatment of acid or alkali ingestion?

Back 1903

Wash out the mouth with large volumes of cold water. Irrigate ocular exposures with saline or water. Do not induce emesis with either acids or alkaline ingestion because emesis can worsen the injury.

Front 1904

What conditions predispose to digoxin toxicity?

Back 1904

Poisoning is more common with renal failure. Hypokalemia predisposes to toxicity because potassium and digoxin bind to the same site on the sodium-potassium ATPase pump.

Front 1905

What is the presentation of digoxin toxicity?

Back 1905

Nausea, vomiting, diarrhea, anorexia, blurred vision, color vision, hallucinations. Bradycardia, PVCs, VT, arrhythmias. Paroxysmal atrial tachycardia is most common. HyperK from inhibition of Na+/K+ ATPase. Digoxin level.

Front 1906

What is the treatment of digoxin toxicity?

Back 1906

Repeated charcoal. Digoxin-antibodies (Digibind) for arrhythmias. Potassium correction. Phenytoin, lidocaine for ventricular arrhythmias. Pacemaker for bradycardia or block refractory to atropine.

Front 1907

What are the signs of opiate intoxication?

Back 1907

Death from acute respiratory acidosis. Analgesic and euphoric effects, pupillary constriction, constipation, bradycardia, hypothermia, hypotension. Opiates can be rapidly reversed by naloxone.

Front 1908

What is the mechanism of cocaine?

Back 1908

Cocaine blocks the re-uptake of norepinephrine at synapse.

Front 1909

What is the presentation of cocaine toxicity?

Back 1909

Alpha-adrenergic stimulation, HTN, hemorrhagic stroke, subarachnoid hemorrhage, MI, arrhythmia, seizures, death. Metabolic acidosis, rhabdomyolysis, hyperthermia. Pulmonary edema.

Front 1910

What is the treatment for cocaine toxicity?

Back 1910

Benzodiazepines control agitation. Alpha/beta agents, such as labetalol, or alpha-blockers, such phentolamine, for HTN. Pure beta-blockers, propranolol, should be avoided.

Front 1911

What are the signs of benzodiazepine overdose?

Back 1911

Somnolence, dysarthria, ataxia, stupor. Rarely cause death from respiratory depression. Most deaths from benzodiazepine are co-ingestion with ethanol or barbiturate. Flumazenil is not used because seizures.

Front 1912

What are the signs of barbiturate overdose?

Back 1912

Death from respiratory, CNS depression. Hypothermia, loss of tendon reflexes, corneal reflexes, coma, flat EEG. Withdrawal may result in seizures. Bicarbonate can increase the urinary excretion of phenobarbital.

Front 1913

What are the signs of hallucinogen ingestion?

Back 1913

Marijuana, LSD, mescaline, peyote, psilocybin can cause delirium, bizarre behavior, flushed skin, dry mouth, dilated pupils, urinary retention. PCP may cause seizures. Treatment is benzodiazepines.

Front 1914

What are the symptoms of lead toxicity?

Back 1914

Adults: Abdominal pain, anemia, renal disease, headache, memory loss. Children: Abdominal pain, anemia, lethargy, seizures, coma; mental retardation.

Front 1915

What are the laboratory signs of lead toxicity?

Back 1915

Blood lead levels >10 mcg/dL. "Lead lines" are densities seen at the metaphyseal plate of the bones of children. Anemia and azotemia.

Front 1916

What is the treatment of lead overdose?

Back 1916

Chelation with calcium EDTA, dimercaprol (BAL), penicillamine, or succimer.

Front 1917

What are the signs of mercury toxicity?

Back 1917

Interstitial pneumonitis; tremors, excitability, memory loss, delirium, insomnia; nausea, vomiting, pain, bleeding.

Front 1918

What is the treatment of mercury toxicity?

Back 1918

Organic mercury is in paints and cosmetics. Treatment is oral chelation with succimer or dimercaprol.

Front 1919

What is the presentation of salicylate overdose?

Back 1919

Nausea, vomiting, gastritis, tinnitus. Stimulate respiratory centers to hyperventilation; salicylates directly toxic to lungs, causing edema. Hyperthermia, confusion, coma, seizures, encephalopathy.

Front 1920

What are the laboratory abnormalities in salicylate overdose?

Back 1920

Salicylates interfere with Krebs cycle and lead to metabolic acidosis. Salicylates cause lactic acid production with metabolic acidosis, an elevated anion gap and compensatory respiratory alkalosis.

Front 1921

How is salicylate overdose diagnosed?

Back 1921

Aspirin level. Elevated anion gap metabolic acidosis. Respiratory alkalosis early. An elevated prothrombin time and hypoglycemia.

Front 1922

What is the treatment for salicylate overdose?

Back 1922

Within the first hour after ingestion, gastric decontamination may be attempted. Charcoal and increase alkalization of the urine along with aggressive fluid resuscitation.

Front 1923

What is the pathophysiology of tricyclic antidepressant overdose?

Back 1923

Tricyclic antidepressants have anticholinergic and sodium channel blocker effects. Cardiac and CNS toxicities.

Front 1924

What is the presentation of tricyclic antidepressant overdose?

Back 1924

Anticholinergic dry mouth, tachycardia, dilated pupils, and flushed skin. Dysrhythmia, widening QRS, resulting in VT, and first-degree conduction blocks; confusion, seizures.

Front 1925

How is tricyclic antidepressant overdose diagnosed?

Back 1925

Serum drug levels, ECG: sinus tachycardia; prolongation of PR, QRS and QT.

Front 1926

What is the treatment for tricyclic antidepressant overdose?

Back 1926

Charcoal is the primary treatment in the acute setting. Any sign of cardiac toxicity should lead to the immediate use of bicarbonate, which protects the heart.

Front 1927

How is head trauma imaged?

Back 1927

CT of head. Contrast is not necessary because blood does not enhance. Hemorrhage should be visible. Skull x-rays are not useful. A concussion is a loss of consciousness plus a negative CT.

Front 1928

What is the CT-scan appearance of subdural hematomas?

Back 1928

Subdural hematomas are crescent-shaped and epidural hematomas are lens-shaped.

Front 1929

What are the indications for cervical spine x-rays after head trauma?

Back 1929

Cervical spine x-rays should be obtained in head trauma if there are focal findings consistent with a cervical radiculopathy or if spinal tenderness is present.

Front 1930

What is the treatment for severe intracranial hemorrhage?

Back 1930

Lowering intracranial pressure with hyperventilation to pCO2 of 30-35, mannitol, elevation of head of bed. Surgical evacuation. Maintain the SBP 110-160. Slight degree of HTN maintains cerebral perfusion.

Front 1931

A 50-year-old woman with sudden loss of consciousness, severe headache, nuchal rigidity, photophobia, and a temperature of 38.5 C (101.3 F). What is the diagnosis?

Back 1931

Subarachnoid hemorrhage

Front 1932

What is subarachnoid hemorrhage?

Back 1932

Bleeding into caused by aneurysm. Around the circle of Willis. Association with polycystic kidney disease, Ehlers-Danlos syndrome. Occurs spontaneously. Head trauma is a rare cause.

Front 1933

What is the presentation of subarachnoid hemorrhage?

Back 1933

Sudden, severe headache, loss consciousness 50%. Focal neurologic symptoms 30% from compression of occulomotor nerve. Nuchal rigidity, photophobia, headache, papilledema. Seizures.

Front 1934

What are the long-term outcome of subarachnoid hemorrhage?

Back 1934

One-year mortality 50%, with half of the people dying immediately. Longer-term manifestations include focal deficits, seizures, rebleeding, hydrocephalus.

Front 1935

How is subarachnoid hemorrhage diagnosed?

Back 1935

CT of head without contrast has 95% sensitivity. If CT is normal and SAH is suspected, lumbar puncture is done. Lumbar puncture is most sensitive. The absence of red cells in CSF excludes SAH.

Front 1936

What is the treatment for subarachnoid hemorrhage?

Back 1936

Maintain SBP 110-160. Seizure prophylaxis with phenytoin. Nimodipine is a calcium-channel antagonist that lowers risk of blood vessel spasm.

Front 1937

What test should be done after subarachnoid hemorrhage has been diagnosed?

Back 1937

Angiography to determine the site of the bleeding. Surgical clipping of the AVM should occur before rebleeding develops.

Front 1938

What is the management of hydrocephalus after subarachnoid hemorrhage?

Back 1938

If hydrocephalus occurs, then shunting should be done.

Front 1939

What is the treatment for spinal headache after lumbar puncture?

Back 1939

A spinal headache is treated with a blood patch.

Front 1940

What are the signs of respiratory injury in burn injuries?

Back 1940

Soot in the mouth or nose, stridor, wheezing, altered mental status, burned nasal hairs, and burns involving closed spaces are signs of impending pulmonary and laryngeal edema.

Front 1941

What are the signs of carbon monoxide overdose?

Back 1941

Altered mental status, dyspnea, headache, and chest pain are clues to severe carbon monoxide poisoning.

Front 1942

What are the signs of pulmonary thermal injury?

Back 1942

Laryngeal edema can result in stridor, hoarseness, and dyspnea. Soot in the nose and mouth can imply impending airway compromise.

Front 1943

How is the extent of skin burn injury assessed?

Back 1943

"Rule of Nines". The head and arms are 9% each. Chest, back, and legs are 18% each. Patchy burns can be estimated by using one hand's width as 1% of body surface area burned.

Front 1944

How is the severity of burn injury assessed?

Back 1944

Carboxyhemoglobin elevated in severe burns. Severe burns are defined as combined second- and third-degree burns >20% in adults or >10% in the old or very young or third-degree burns >5% of body surface area.

Front 1945

What is the management of severe respiratory injury?

Back 1945

If there are signs of severe respiratory injury, intubate the patient. If the carboxyhemoglobin level is significantly elevated (>5-10%), give 100% oxygen.

Front 1946

How is the fluid resuscitation requirement determined for burns?

Back 1946

Fluid resuscitation over first 24 hours is 4 ml per % BSA/kg. Ringer's to provide half fluid in first 8 h, with 1/4 in second 8 h, and 1/4 in final 8 h (Parkland formula). Maintain a urine output >0.5-1 mL/kg/h.

Front 1947

What is the treatment for burns?

Back 1947

Stress ulcer prophylaxis with H2 blockers. Silver sulfadiazine. Do not break blisters. Escharotomy for circumferential burns. Skin grafting.

Front 1948

What are heat cramps?

Back 1948

Mild fluid and electrolyte depletion. Painful muscular contractions lasting a few minutes. Body temperature normal. Treatment is oral rehydration and salt replacement.

Front 1949

What is heat exhaustion?

Back 1949

Weakness; body temperature slightly elevated; headache, anxiety. The patient is still able to sweat. Treatment with oral fluid and electrolyte replacement; may need intravenous hydration.

Front 1950

What is heat stroke?

Back 1950

Loss of ability to lose heat, inability to sweat. T >40 C, confusion, disorientation, nausea, blurred vision, seizures; hemoconcentration, rhabdomyolysis, elevation BUN, creatinine, WBC. Anuria, DIC, lactic acidosis.

Front 1951

What is the treatment of heat stroke?

Back 1951

Treatment with intravenous fluid replacement and rapid cooling. The body should be sprayed with water. Chlorpromazine and diazepam to control shivering.

Front 1952

What is malignant hyperthermia?

Back 1952

Nonexertional idiosyncratic heat reaction of rhabdomyolysis caused by anesthetic agents such as halothane or succinylcholine. Treatment is dantrolene.

Front 1953

What is neuroleptic malignant syndrome?

Back 1953

Idiosyncratic reaction to phenothiazines or butyrophenones, such as haloperidol. Muscular rigidity and rhabdomyolysis.

Front 1954

What is the treatment of neuroleptic malignant syndrome?

Back 1954

Treatment is bromocriptine or dantrolene.

Front 1955

What is hypothermia?

Back 1955

Core body temperature below 35 C (normal 37 C). Severe hypothermia is a core temperature below 30 C. Hypothermia often occurs with alcohol intoxication.

Front 1956

What is the presentation of hypothermia?

Back 1956

Lethargy, confusion, and weakness. Death from arrhythmia. Ventricular fibrillation or ventricular tachycardia. J-wave elevation may mimic ST segment elevation.

Front 1957

What is the effect of ionizing radiation on the body?

Back 1957

Ionizing radiation destroys DNA molecules. Lethal and can cause cancer. Nonionizing radiation includes infrared, ultraviolet, microwave radiation, which are less destructive and causes burns.

Front 1958

What are the symptoms of radiation exposure?

Back 1958

Nausea and vomiting early; intestinal ulceration, bleeding, infection later. Injury to skin, salivary glands, respiratory epithelium, thyroid, bone marrow.

Front 1959

What is the treatment of radiation exposure?

Back 1959

Antiemetics, platelets and RBC transfusions. Colony-stimulating factors (G-CSF, GM-CSF) to restore marrow. Bone marrow transplantation.

Front 1960

What is the presentation of near drowning?

Back 1960

Agitation, coma, cyanosis, coughing, and pulmonary edema, tachypnea, tachycardia, and blood-tinged sputum. Rales and rhonchi. Hypothermia. Hypoxia, hypercarbia, metabolic acidosis, hyperkalemia, hemolysis.

Front 1961

What is the presentation of anaphylaxis?

Back 1961

Urticaria, dyspnea, stridor, tachycardia, hypotension, and hemodynamic collapse.

Front 1962

What is the treatment of anaphylaxis?

Back 1962

Antihistamine (diphenhydramine), epinephrine injections, intravenous fluids, H2 blockers, and systemic corticosteroids.

Front 1963

What is the bacteriology of cat and dog bites?

Back 1963

Infections are most often polymicrobial. Cat bites are associated with Pasteurella multocida; dog bites are associated with Pasteurella, Eikenella, and Capnocytophaga canimorsus.

Front 1964

What is the treatment of cat and dog bites?

Back 1964

Wound care. Prophylactic antibiotic is amoxicillin/clavulanate (clindamycin and either ciprofloxacin or trimethoprim/ sulfamethoxazole or azithromycin if penicillin allergic).

Front 1965

What is the bacteriology of human bites?

Back 1965

Human bites carry an infection rate of 15%. Anaerobic and aerobic bacteria. Hepatitis B and HIV can also be transmitted through bites.

Front 1966

What is the treatment for human bite wounds?

Back 1966

Irrigate wound; cultures are not useful. If the bite is <12 hours old, close loosely. Tetanus and hepatitis B, prophylaxis. 5 to 7 day course of antibiotics.

Front 1967

Which animals carry rabies?

Back 1967

Raccoons, rats, wild dogs, woodchucks, skunks, foxes. 100% fatal. Less than 10 persons per year are infected in the US.

Front 1968

What is the presentation of rabies?

Back 1968

Incubation period up to one year. Prodrome of 2-10 days of fever and paresthesias at the bite site. Aphasia, paralysis, hypersalivation, and myoclonus.

Front 1969

How is rabies diagnosed?

Back 1969

Viral cultures from saliva, CSF, or serum

Front 1970

What is the treatment for rabies infection?

Back 1970

Ribavirin. Prophylaxis with human rabies immunoglobin provides immediate passive immunity. Human diploid cell vaccine should be given at 0, 3, 7, 14, and 28 days (5 shots total).

Front 1971

How many deaths per year are caused by snake bites?

Back 1971

<5-10 deaths per year, with rattlesnakes accounting for almost all fatalities. Snake venom contains hemolysis toxin, cardiotoxin, neurotoxin, and proteolytic enzymes.

Front 1972

What is the treatment of snake bites?

Back 1972

Decrease the spread of venom with compression bandages. Antivenin may cause anaphylactic reactions. Hypotension is managed with fluids. Ventilatory support for laryngeal edema.

Front 1973

What are the causes of spinal cord compression?

Back 1973

Commonly caused by lymphoma, multiple myeloma, carcinomas of prostate, lung, breast, kidney, or colon; herniated disk, epidural abscess, hematoma, or trauma.

Front 1974

What is the presentation of spinal cord compression?

Back 1974

Sensory loss, lower extremity weakness; sphincter dysfunction or sexual dysfunction. History of cancer, fever, and bowel or bladder incontinence or retention.

Front 1975

How is spinal cord compression diagnosed?

Back 1975

Plain x-rays are abnormal. The diagnostic test of choice is an MRI of the spine.

Front 1976

What is the treatment for spinal cord compression?

Back 1976

High-dose dexamethasone immediately, then MRI. For lymphoma or multiple myeloma, radiation therapy should be started. Surgical decompression for a herniated disk, epidural abscess, or hematoma.

Front 1977

What is syringomyelia?

Back 1977

Cavitation of spinal cord. Communicating with CSF or noncommunicating. Associated with congenital Arnold Chiari; caused by trauma, tumors.

Front 1978

What are the signs of syringomyelia?

Back 1978

Impaired pain, temperature; intact sensation to light touch. Loss of pain and temperature occurs in a cape-like distribution. Sparing of tactile sensation, position, and vibratory sense. Areflexia.

Front 1979

What is subacute combined degeneration?

Back 1979

B12 deficiency. Distal paresthesias and weakness of extremities followed by spastic paresis and ataxia. Deficit of vibration and proprioception with pyramidal signs (plantar extension, hyperreflexia). Low B12.

Front 1980

What is the presentation of anterior spinal artery infarct?

Back 1980

Flaccid paralysis, spastic paresis. Loss pain, temperature; sparing vibration and position. Motor, sensory, autonomic is lost below the level of the infarction with retained vibration and position. Treatment is supportive.

Front 1981

What is the Brown-Sequard syndrome?

Back 1981

Hemisection of the cord with ipsilateral spastic paresis. Ipsilateral loss of joint position sense, tactile discrimination, and vibratory sensations. Contralateral loss of pain and temperature.

Front 1982

A 60-year-old woman with sudden onset of right upper extremity weakness, aphasia, pronator drift and right facial nerve palsy. What is the most likely cause?

Back 1982

Ischemic stroke

Front 1983

What is a stroke?

Back 1983

Sudden onset of a focal neurologic deficit.

Front 1984

What are the mechanisms of strokes?

Back 1984

Large artery thrombosis, small artery thrombosis (lacunar), embolic (cardiogenic or artery-to-artery), vascular dissection, systemic hypotension, intracranial bleeding.

Front 1985

What is the presentation of ischemic stroke?

Back 1985

Acute onset of a focal neurologic deficit.

Front 1986

What is the blood supply to the brain?

Back 1986

Two major systems: carotid (anterior) circulation, and vertebrobasilar (posterior) circulation. The anterior circulation include the anterior cerebral artery and middle cerebral artery.

Front 1987

What are the signs of occlusion of the anterior cerebral artery?

Back 1987

Contralateral weakness in arm and sensory loss in leg more than in the upper extremity. Urinary incontinence, confusion, behavioral disturbances. Lower extremity weakness exceeds upper extremity.

Front 1988

What are the signs of occlusions of the middle cerebral artery?

Back 1988

Contralateral hemiplegia, hemisensory loss, homonymous hemianopia, eyes deviated toward lesion. Dominant results in aphasia. Nondominant results preserved speech, comprehension with confusion, apraxia.

Front 1989

What parts of the brain are supplied by the posterior circulation?

Back 1989

Cerebellum, brain stem, occipital lobe of the cortex, and pons. The major blood vessels of the posterior circulation are the posterior cerebral artery, basilar artery, and vertebral arteries.

Front 1990

What are the signs of posterior cerebral artery occlusion?

Back 1990

Contralateral homonymous hemianopia, hallucinations, agnosias. Occlusion of the penetrating branches of the PCA can result in CN III palsy with contralateral hemiplegia (Weber syndrome) or CN III palsy.

Front 1991

What is the "locked- in syndrome"?

Back 1991

Occlusion of the paramedian branches of the basilar artery, presenting as quadriparesis with intact vertical eye movements.

Front 1992

What is Wallenberg syndrome?

Back 1992

Occlusion of posterior inferior cerebellar artery, which presents as ipsilateral facial sensory loss, contralateral body sensory loss, vertigo, ataxia, dysarthria, dysphagia, and Horner syndrome (ptosis).

Front 1993

What are the signs of occlusion of the major cerebellar arteries?

Back 1993

Vertigo, vomiting, nystagmus, and ipsilateral limb ataxia.

Front 1994

How is stroke diagnosed?

Back 1994

Noncontrast CT to distinguish between hemorrhagic and ischemic stroke. CT often negative for ischemia within the first 48 hours. Diffusion-weighted MRI is the most accurate test for cerebral ischemia.

Front 1995

What tests will find the embolic source after an acute ischemic stroke?

Back 1995

Echocardiogram, carotid duplex, and 24-hour Holter monitor. Evaluation for inherited hypercoagulability.

Front 1996

What is the treatment for ischemic stroke?

Back 1996

Tissue plasminogen activator if within 4.5 hours of symptom onset.

Front 1997

What are the contraindications to tissue plasminogen activator for ischemic stroke?

Back 1997

Stroke or head trauma within 3 mo, hemorrhage (GI, GU), surgery within 14 d, intracranial hemorrhage, arterial puncture within 7 d, BP > 185/110, anticoagulants; platelets <100,000, PT >15 sec).

Front 1998

What is the prognosis for patients who receive tissue plasminogen activator?

Back 1998

39% of all patients treated with tPA have a good functional outcome. Only 26% of untreated have a good outcome. Intracranial hemorrhage occurs in 5.8%. The fatality rate after intracranial hemorrhage is 45%.

Front 1999

What is the secondary prevention of ischemic stroke?

Back 1999

Started 24 hours after TPA. When patients have allergy to aspirin or continue to have recurrent cerebrovascular events on aspirin, dipyridamole may be added or the patient may be switched to clopidogrel.

Front 2000

When should heparin be given to patients with ischemic stroke?

Back 2000

Heparin in acute ischemic stroke is limited to patients with atrial fibrillation, basilar artery thrombosis, or stroke in evolution.

Front 2001

What is the treatment of subarachnoid hemorrhage?

Back 2001

Nimodipine to reduce the risk of ischemic stroke. Early surgical clipping of the aneurysm or embolization of the vessel. Aspirin is contraindicated.

Front 2002

What is the management of intracranial aneurysms that are found incidentally?

Back 2002

Unruptured aneurysms found incidentally should be repaired if they exceed 10 mm.

Front 2003

What are the indications for carotid endarterectomy?

Back 2003

Carotid endarterectomy for occlusion > 70% and the lesion is symptomatic. Endarterectomy may benefit those who are asymptomatic if there is >60% stenosis in men who are <60 years old.

Front 2004

What is a seizure?

Back 2004

Paroxysmal event caused by abnormally discharging central nervous system neurons. Epilepsy is a condition of recurrent seizures due to a chronic underlying process.

Front 2005

What are the causes of seizures?

Back 2005

Stroke, bleed, AV malformation; meningitis, abscess, encephalitis, trauma, vasculitis, hypoNa, hypoCa, hypoMg, hypoglycemia, hypoxia, drug overdose/withdrawal, idiopathic, neoplasm, psychiatric.

Front 2006

What is the presentation of a seizure?

Back 2006

Paroxysmal, involuntary, abnormal movement or change of consciousness. Sudden onset, with or without an aura. Disorientation, sleepiness, muscle aches. Incontinence, tongue biting, headache.

Front 2007

How is syncope different from a seizure?

Back 2007

Patients with syncope will not complain of significant postictal symptoms. Syncope patients will recover consciousness within several minutes of the event, and will not have incontinence or tongue biting.

Front 2008

How are seizures classified?

Back 2008

Partial or generalized and complex or simple.

Front 2009

What are partial seizures?

Back 2009

Partial seizures affect discrete portions of the brain, such as causing involuntary jerking of a finger or hand.

Front 2010

What is a simple partial seizure?

Back 2010

Consciousness is maintained for the duration of a simple seizure, and the seizure affects a discrete portion of brain. When there is a change in consciousness, the seizure is termed a complex partial seizure.

Front 2011

What are generalized seizures?

Back 2011

Arise from both cerebral hemisphere. Generalized tonic-clonic seizures are tonic contraction of muscles throughout the body followed by intermittent relaxation (clonic phase).

Front 2012

What are absence seizures?

Back 2012

Sudden, brief loss of consciousness without loss of postural tone. The ECG shows a generalized, symmetric 3-Hz spike-and-wave discharge pattern.

Front 2013

What are atonic seizures?

Back 2013

Atonic seizures are characterized by sudden loss of postural tone, lasting 1 to 2 seconds.

Front 2014

What are myoclonic seizures?

Back 2014

Myoclonic seizures are characterized by a sudden, brief muscle contraction.

Front 2015

What is status epilepticus?

Back 2015

Recurrent or continuous seizures lasting at least 5-30 min.

Front 2016

How are seizures diagnosed?

Back 2016

Electroencephalogram, serum electrolytes, glucose, toxicology, and arterial blood gas to exclude hypoxia. A CT scan or MRI of the head is indicated to exclude a structural lesion as the cause of seizure.

Front 2017

What is the treatment for status epilepticus?

Back 2017

Secure airway, breathing, circulation. Evaluate and treat causes. Lorazepam, which potentiates GABA receptor. If seizure continues, phenytoin or fosphenytoin to add phenobarbital.

Front 2018

What are the side effects of phenytoin?

Back 2018

Diplopia, dizziness, ataxia. Gum hyperplasia, lymphadenopathy, hirsutism, and rash.

Front 2019

What are the side effects of phenobarbital?

Back 2019

Sedation, ataxia, and rash.

Front 2020

What drug should be given if patients continue to seize after administration of lorazepam, phenytoin and Phenobarbital?

Back 2020

Midazolam or propofol anesthesia.

Front 2021

When should anticonvulsant therapy be started in patients with a first-time seizure?

Back 2021

Anticonvulsants should be started only if the patients has an abnormal neurologic exam, presented with status epilepticus, has a strong family history of seizure, or has an abnormal EEG.

Front 2022

What is the treatment for primary generalized tonic-clonic seizures?

Back 2022

Valproic acid. Valproic acid increases the availability of GABA. Lamotrigine, carbamazepine, or phenytoin are alternatives.

Front 2023

What are the side effects of valproic acid?

Back 2023

Side effects include ataxia, tremor, hepatotoxicity, thrombocytopenia, gastrointestinal irritation, and hyponatremia.

Front 2024

What is the mechanism of action of lamotrigine?

Back 2024

Lamotrigine decreases glutamate release. Side effects: Stevens-Johnson syndrome.

Front 2025

What is the treatment of absence seizures?

Back 2025

Ethosuximide. Valproic acid is an acceptable option.

Front 2026

What is the treatment for myoclonic and atonic seizures?

Back 2026

Valproic acid.

Front 2027

What is the treatment for partial seizures?

Back 2027

Carbamazepine and phenytoin are first-line therapy. Valproic acid, lamotrigine, and levetiracetam are alternatives.

Front 2028

What is vertigo?

Back 2028

False sensation of movement.

Front 2029

What are the causes of vertigo?

Back 2029

Mèniére, labyrinthitis, positional vertigo, traumatic, perilymphatic fistula, cervical vertigo. Brain stem disease, AV malformations, tumor, multiple sclerosis, drug overdose, vertebrobasilar migraine.

Front 2030

What are the characteristics of central vertigo?

Back 2030

No tinnitus or hearing loss is present. There are is often diplopia, cortical blindness, dysarthria, extremity weakness or numbness. Nystagmus is pure, vertical, does not suppress with fixation, and multidirectional.

Front 2031

What are the characteristics of peripheral vertigo?

Back 2031

Tinnitus and hearing loss. Absence of diplopia, cortical blindness, dysarthria, extremity weakness or numbness. Nystagmus is mixed, horizontal, suppresses with fixation, and unidirectional.

Front 2032

What are the signs of Mèniére disease?

Back 2032

Tinnitus, hearing loss, episodic vertigo of 1 to 8 h. Symptoms wax and wane as the endolymphatic pressure rises and falls. Most common causes of Mèniére disease are syphilis and head trauma.

Front 2033

What are the signs of labyrinthitis?

Back 2033

Sudden onset of severe vertigo that lasts for several days with hearing loss and tinnitus. Occurs with an upper respiratory tract infection.

Front 2034

What are the signs of benign paroxysmal positional vertigo?

Back 2034

Peripheral vertigo that characteristically is exacerbated by head movement or change in head position. Episodes occur in clusters that persist for several days. The vertigo usually lasts 10 to 60 seconds.

Front 2035

What are the causes of perilymphatic fistula?

Back 2035

Form of peripheral vertigo related temporally to head trauma (slap to the ear) or extreme barotrauma during air flight, scuba diving, or vigorous Valsalva maneuver.

Front 2036

What are the causes of central vertigo?

Back 2036

Caused by cerebellar or brain-stem tumor, bleed, or ischemia. Drug toxicity or overdoses. In young patient with unexplained central vertigo, consider multiple sclerosis.

Front 2037

What is the treatment of peripheral vertigo?

Back 2037

Meclizine or diazepam.

Front 2038

What is the treatment of Mèniére disease?

Back 2038

Low-salt diet and diuretics. Surgical decompression.

Front 2039

What is the treatment of benign paroxysmal positional vertigo?

Back 2039

Positional maneuvers that attempt to move the otolith out of the circular canals (e.g., Dix Hallpike and Barany maneuvers).

Front 2040

What is the treatment of vertigo caused by labyrinthitis?

Back 2040

Meclizine and diazepam.

Front 2041

28-year-old woman with throbbing, right-side headache; nausea; worsened by walking, loud noise, bright light. What is the diagnosis?

Back 2041

Migraine

Front 2042

What are the primary headache syndromes?

Back 2042

Migraine, cluster, and tension headache. Migraine affects 15% of the population.

Front 2043

What are the secondary causes of headache?

Back 2043

Intracranial hemorrhage, brain tumor, meningitis, temporal arteritis, and glaucoma.

Front 2044

What type of headache is characterized by fever and nuchal rigidity?

Back 2044

Meningitis.

Front 2045

"The worst headache of my life" or a "thunderclap" at onset with nuchal rigidity without fever, suggests what type of headache?

Back 2045

Intracranial hemorrhage.

Front 2046

What are the clinical symptoms of brain tumors?

Back 2046

Deep, dull, aching pain that disturbs sleep. Vomiting before the onset of headache, or a history of headache induced by coughing, lifting or bending is typical of posterior fossa brain tumors.

Front 2047

What are the characteristics of temporal arteritis?

Back 2047

Unilateral pounding headache with visual changes; dull and boring with lancinating pains. Polymyalgia rheumatica, jaw claudication, fever, weight loss, scalp tenderness; elderly.

Front 2048

What are the laboratory abnormalities associated with temporal arteritis?

Back 2048

Increased sedimentation rate; diagnosed with biopsy of the temporal artery. Initiate therapy with steroid immediately.

Front 2049

What cause of headache syndrome is associated with eye pain?

Back 2049

Glaucoma

Front 2050

What are the characteristics of migraine headaches?

Back 2050

Benign and recurrent syndrome of headache, nausea, vomiting, and focal neurologic deficits. Pulsatile, throbbing, unilateral, aggravated by movement. Photophobia, phonophobia.

Front 2051

What are the triggers of migraine?

Back 2051

Alcohol, chocolate, cheeses, monosodium glutamate, hunger, or irregular sleep patterns.

Front 2052

What is migraine without aura?

Back 2052

Migraine without a preceding focal neurologic deficit. Migraine with aura is a migraine headache that is accompanied by a preceding motor, sensory, or visual symptoms. Focal neurologic symptoms.

Front 2053

What is the pathognomonic aura for migraine?

Back 2053

Scintillating scotoma. Only 20% of migraine has aura. Stars, sparks, and flashes of light. Migraine equivalent is defined as focal neurologic symptoms without headache.

Front 2054

What are complicated migraines?

Back 2054

Migraines with severe neurologic deficits that persist after the resolution of pain.

Front 2055

What are basilar migraines?

Back 2055

Migraine headaches associated with vertigo, diplopia, ataxia, or dysarthria.

Front 2056

What are the characteristics of tension-type headaches?

Back 2056

Tension-type headaches are tight, band-like headaches are bilateral.

Front 2057

What are the characteristics of cluster headaches?

Back 2057

Excruciating, unilateral, periorbital headache without warning 30 min-3 hrs; 1-3 times a day for 4-week period. Red eye, lacrimation, nasal stuffiness, nausea, sensitivity to alcohol. Horner syndrome (ptosis).

Front 2058

How is migraine headache diagnosed?

Back 2058

Severe, sudden onset of a first-time headache with signs of an underlying cause should have a CT scan of the head.

Front 2059

What is the treatment of migraine headache?

Back 2059

Abortive sumatriptan, which is a serotonin receptor agonist. Dihydroergotamine is an alternative. The triptans are contraindicated in cardiovascular disease. Almotriptan, naratriptan, zolmitriptan, and eletriptan.

Front 2060

What is the prophylactic treatment for migraine?

Back 2060

Prophylactic treatment for migraine should be initiated when acute migraine headaches occur more than three to four times per month. Propranolol, timolol, valproic acid, and topiramate. Verapamil and tricyclics.

Front 2061

What is the treatment of cluster headaches?

Back 2061

The most effective treatment is 100% oxygen. Cluster headaches are treated with prednisone, lithium, ergotamine, and verapamil. Sumatriptan.

Front 2062

What is pseudotumor cerebri?

Back 2062

Idiopathic increase in intracranial pressure. 8-10 times more common in women. Association with obesity, chronic lung disease, Addison disease, oral contraceptives, tetracycline, and vitamin A toxicity.

Front 2063

What is the presentation of pseudotumor cerebri?

Back 2063

Headache, diplopia, and 6th cranial nerve (abducens) palsy. Papilledema, blind spot on visual field testing. The CT and MRI are normal, CSF is normal except for an increase in pressure.

Front 2064

What is the treatment for pseudotumor cerebri?

Back 2064

Weight loss, discontinue oral contraceptives, acetazolamide, furosemide, prednisone. Repeated lumbar punctures; placement of ventriculoperitoneal shunt.

Front 2065

What is trigeminal neuralgia?

Back 2065

Idiopathic, sudden, severe, sharp pain side of the mouth and progressing to ear, eye, or nostril. Triggered by touch or movement; pain lasts a few seconds. Compression of the trigeminal nerve root by a vessel, MS, tumor.

Front 2066

What is the treatment of trigeminal neuralgia?

Back 2066

Carbamazepine. Phenytoin, baclofen, or gabapentin. Surgery or alcohol injection into the affected nerve.

Front 2067

16-year-old boy with leg weakness. 3 weeks ago had diarrhea. Bilateral lower-extremity weakness and a loss of reflexes. What is the diagnosis?

Back 2067

Guillain-Barre syndrome

Front 2068

What is Guillain-Barre syndrome?

Back 2068

Acute, often severe polyradiculopathy caused by autoimmune destruction of myelin by an immune response.

Front 2069

What is the presentation of Guillain-Barre syndrome?

Back 2069

Sudden weakness begins lower extremities and moves upward. Loss of reflexes. Legs are more affected than arms and face. Pain, tingling. Loss of large sensory fibers, loss of reflexes and proprioception.

Front 2070

What autonomic instabilities are associated with Guillain-Barre syndrome?

Back 2070

Profuse sweating, postural hypotension, labile blood pressure, cardiac dysrhythmia occurs in severe GBS.

Front 2071

What is the etiology of Guillain-Barre syndrome?

Back 2071

75% have history of infection 1-3 weeks prior; respiratory or GI © jejuni). GBS may be preceded by HSV, CMV, EBV. Influenza vaccine associated with one case per million. HIV, SLE, lymphoma.

Front 2072

How is Guillain-Barre syndrome diagnosed?

Back 2072

A lumbar puncture has an elevated protein without an associated rise in the cell count. Electromyography will show demyelination of the peripheral nerves.

Front 2073

What is the treatment for Guillain-Barre syndrome?

Back 2073

Intravenous immunoglobulin or plasmapheresis; monitor the vital capacity and initiate early respiratory support if respiratory weakness.

Front 2074

A 32-year-old woman with double vision, difficulty chewing. Symptoms improve following sleep. Snarling appearance when asked to smile, nasal tone in voice; weakness in the upper extremities. What is the diagnosis?

Back 2074

Myasthenia gravis.

Front 2075

What is myasthenia gravis?

Back 2075

Disease of the neuromuscular junction characterized by weakness and fatigability. Acetylcholine-receptor antibodies leads to a decreased acetylcholine receptors at the postsynaptic membrane.

Front 2076

What is the presentation of myasthenia gravis?

Back 2076

Weakness, fatigability. Initially, diplopia, ptosis, dysphagia. Speech nasal; "snarling." Asymmetric proximal muscle weakness. Normal reflexes, pupillary responses, sensory. Impaired respiration.

Front 2077

What is Eaton-Lambert myasthenic syndrome?

Back 2077

Eaton-Lambert myasthenic syndrome is characterized by weakness with increasing muscle strength on repetitive contraction; caused by a malignancy, especially small-cell carcinoma of the lung.

Front 2078

What are the signs of botulism?

Back 2078

Botulism may cause myasthenic-like weakness, but pupils are usually dilated and repetitive nerve stimulation shows an incremental increase in muscular fiber contraction (opposite of myasthenia).

Front 2079

How is myasthenia gravis diagnosed?

Back 2079

Initial test for myasthenia is acetylcholine-receptor Ab, 80-90% positive. Most accurate test is EMG. Edrophonium (Tension) test is sensitive but not specific. CT performed to detect a thymoma;10%.

Front 2080

What is the treatment of myasthenia gravis?

Back 2080

Anticholinesterase (pyridostigmine, neostigmine). If glucocorticoids fail, azathioprine used. Mycophenolate. Plasmapheresis, IV Ig rapidly improve myasthenic crisis with respiratory failure.

Front 2081

What are the indications for thymectomy in myasthenia gravis?

Back 2081

Thymectomy is indicated in postpubertal patients and in those younger than 60 before initiation of immunosuppressive therapy. Aminoglycosides exacerbate myasthenia gravis.

Front 2082

What is amyotrophic lateral sclerosis?

Back 2082

Idiopathic weakness with upper and lower motor neuron loss, CN palsies, respiratory involvement; preserved bowel, bladder sensory, cognitive, sexual.

Front 2083

What are the signs of amyotrophic lateral sclerosis?

Back 2083

Cranial nerve or bulbar palsies result in dysphagia, difficulty chewing, decreased gag, dysarthria; respiratory weakness; aspiration pneumonia is most common cause of death. Weak cough; head ptosis.

Front 2084

What is the presentation of amyotrophic lateral sclerosis?

Back 2084

Fully mentally alert patient loses nearly all motor control while still being able to think and perceive.

Front 2085

What are the upper motor neuron manifestations of amyotrophic lateral sclerosis?

Back 2085

Weakness with spasticity and hyperreflexia. Lower motor neuron manifestations are weakness with muscle wasting, atrophy, fasciculations. Upper and lower motor neuron weakness is unique to ALS.

Front 2086

What is the confirmatory test for amyotrophic lateral sclerosis?

Back 2086

Confirmatory test is the electromyogram. Cerebrospinal fluid and MRI are normal.

Front 2087

What is the treatment of amyotrophic lateral sclerosis?

Back 2087

Riluzole shows progression by inhibiting glutamate release. Spasticity is treated with baclofen and tizanidine. Death in 3-5 years.

Front 2088

What is the presentation of multiple sclerosis?

Back 2088

Weakness, numbness, tingling, or unsteadiness of a limb. Urinary urgency or retention, blurry vision, double vision. Symptoms persist for weeks; may resolve spontaneously.

Front 2089

How is multiple sclerosis diagnosed?

Back 2089

MRI of the brain is the most accurate test (sensitivity 95%); demyelinated plaques in the cerebrum and spine. Enhancement with gadolinium. Mild pleocytosis (< 50 cells/mcL), total protein mildly elevated.

Front 2090

What is the treatment for the spasticity of multiple sclerosis?

Back 2090

Baclofen; tizanidine and diazepam for nocturnal spasticity. Pain caused by trigeminal neuralgia and dysesthesias responds to carbamazepine, gabapentin, phenytoin, pregabalin, tricyclic.

Front 2091

What is the treatment of bladder hyperactivity in multiple sclerosis?

Back 2091

Bladder hyperactivity is treated with oxybutynin; urinary retention is treated with bethanechol.

Front 2092

What is dementia?

Back 2092

Loss of memory with impairment of any other cognitive function (aphasia, agnosia, apraxia, executive) sufficient to interfere with social or occupational functioning.

Front 2093

What are the reversible causes of dementia?

Back 2093

Hypothyroidism, B12 deficiency, hepatic or uremic encephalopathy, vasculitis, syphilis, abscess, tumor, anticholinergics, sleep apnea, trauma, subdural hematoma, normal pressure hydrocephalus, depression.

Front 2094

What are the irreversible causes of dementia?

Back 2094

Progressive multifocal leukoencephalopathy, Alzheimer, Lewy bodies, Pick disease, multi-infarct dementia, Binswanger disease, Creutzfeldt-Jakob disease. Alzheimer accounts for 80%.

Front 2095

What is the prevalence of dementia?

Back 2095

1-5% between ages 65-69; 45% by age 100. Only 5% of Alzheimer disease is inherited.

Front 2096

What is the presentation of frontotemporal dementia?

Back 2096

Pick disease presents with personality changes early, with relative sparing of visuospatial function. Social, interpersonal, emotional abnormalities. Frontotemporal dementia lacks insight.

Front 2097

What is the presentation of dementia with Lewy bodies?

Back 2097

Dementia with Lewy bodies is characterized by fluctuating cognitive impairment. Dementia caused by Parkinson disease should be accompanied by recurrent visual hallucinations are also characteristic.

Front 2098

What are the characteristics of dementia caused by Creutzfeldt-Jakob disease?

Back 2098

Short, aggressive course over weeks. Dementia, myoclonus, ataxia, and 14-3-3 protein in CSF. Variant CJD is bovine spongiform encephalopathy from ingestion of prions from cattle.

Front 2099

What are the characteristics of multi-infarct dementia?

Back 2099

Stepwise progression associated with discrete cerebrovascular events. Binswanger disease involves the subcortical white matter and presents with a slowly progressive course.

Front 2100

What are the characteristics of normal pressure hydrocephalus?

Back 2100

Prominent gait abnormalities before the onset of cognitive impairment, urinary incontinence.

Front 2101

What is the diagnostic evaluation for dementia?

Back 2101

Rule out reversible causes of the dementia. CBC, electrolytes, calcium, creatinine, LFTs, glucose, TSH, v B12, RPR, HIV. MRI or CT with contrast.

Front 2102

What is the treatment for dementia?

Back 2102

Memantine is a disease-modifying drug used in advanced disease either alone or with a cholinesterase inhibitor. Memantine is neuroprotective and reduces the rate of progression.

Front 2103

A 35-year-old man with spontaneous movements, grimacing with grunting. Father died at the age of 41 from dementia. What is the diagnosis?

Back 2103

Huntington disease

Front 2104

What is the cause of Huntington disease?

Back 2104

Degenerative brain disorder. HD gene contains a CAG trinucleotide repeat that codes for huntingtin. Abnormal cleavage of huntingtin protein interferes with nuclear mechanisms, cell death; autosomal dominant.

Front 2105

What is the presentation of Huntington disease?

Back 2105

Chorea in 4th-5th decade. Irritability, anger, paranoia, depression. Antisocial. Fidgeting that progresses to sudden movements of the trunk or limbs. Choreic gait. Memory is preserved until late.

Front 2106

How is Huntington disease diagnosed?

Back 2106

Genetic testing. CT scanning shows cerebral atrophy or atrophy of caudate nucleus.

Front 2107

What is the treatment for Huntington disease?

Back 2107

Haloperidol or clozapine control behavioral changes. Death occurs 15-20 years after diagnosis. Children should receive genetic testing.)

Front 2108

58-year-old man with resting tremor; slow moving. Stooped forward, small steps. Cogwheel rigidity in arms; positive Myerson sign. What is the diagnosis?

Back 2108

Parkinson disease

Front 2109

What is Parkinson disease?

Back 2109

Neurologic syndrome resulting from the deficiency of the neurotransmitter dopamine; degenerative, vascular, or inflammatory changes in the basal ganglia.

Front 2110

What are the causes of Parkinson disease?

Back 2110

Neuroleptics (haloperidol, chlorpromazine), metoclopramide, alpha-methyldopa, reserpine. MPTP, carbon monoxide, cyanide, manganese. Encephalitis. Basal ganglia lesions.

Front 2111

What is the presentation of Parkinson disease?

Back 2111

Bradykinesia (mask facies, reduction of automatic movements), cogwheel rigidity, postural instability, resting tremor. Myerson sign is inability to resist blinking when trapped on the glabella.

Front 2112

What is Shy-Drager syndrome?

Back 2112

Parkinsonism with prominent orthostatic hypotension.

Front 2113

How is Shy-Drager syndrome diagnosed?

Back 2113

Diagnosis of Parkinson disease is clinical. Identify any secondary causes of Parkinsonism that are reversible. There is no diagnostic test that can identify Parkinson disease.

Front 2114

What is the treatment for Parkinson disease?

Back 2114

Parkinson disease is caused by low dopaminergic and excessive cholinergic tone on the basal ganglia. Medical treatment increases dopaminergic tone or decreases cholinergic tone on the basal ganglia.

Front 2115

What medications are used to stimulate dopamine receptors in patients with Parkinson disease?

Back 2115

Carbidopa/levodopa, dopamine agonists, indirectly increase the amount of dopamine (COMT inhibitors, selegiline, amantadine).

Front 2116

Which medications block acetylcholine stimulation of the basal ganglia?

Back 2116

Benztropine and trihexyphenidyl.

Front 2117

What direct-acting dopamine agonists are used to treat Parkinson disease?

Back 2117

Pramipexole or ropinirole alone as initial therapy or with levodopa/carbidopa. Other dopamine agonists are bromocriptine, pergolide, tolcapone, entacapone.

Front 2118

How does the efficacy of pramipexole and ropinirole compare to levodopa for the treatment of Parkinson disease?

Back 2118

Dopamine agonists are less efficacious than levodopa. Dopamine agonists have less dyskinetic side effects.

Front 2119

What is the mechanism of the catechol-O-methyl transferase inhibitors?

Back 2119

COMT inhibitors decrease the metabolism of the levodopa. They are an adjunct to levodopa for the treatment of Parkinson disease.

Front 2120

What is the role of selegiline in Parkinson disease?

Back 2120

Selegiline can be used in those with a declining or fluctuating response to levodopa. Selegiline offers mild symptomatic benefit in early disease. Rasagiline is a newer version.

Front 2121

What is benign essential tremor?

Back 2121

Idiopathic disorder of isolated tremor of the hands, head. Worsened by caffeine or beta agonists. Interferes with ability to write. Improvement with the use of alcohol.

Front 2122

What is the treatment of benign essential tremor?

Back 2122

Propranolol. Alternatives are primidone, alprazolam, and clozapine. If no medical therapy is effective, thalamotomy is indicated.

Front 2123

What is restless leg syndrome?

Back 2123

Idiopathic sensation of creeping and crawling dysesthesia within legs; involuntary movements during sleep; familial; exacerbated by sleep deprivation, caffeine, pregnancy.

Front 2124

What is the treatment of restless leg syndrome?

Back 2124

Treatment is with dopamine agonists, such as pramipexole or ropinirole; levodopa/carbidopa, benzodiazepines.

Front 2125

What is pemphigus vulgaris?

Back 2125

Autoimmune disease of allergy to own skin. Pemphigus vulgaris is most often idiopathic, but ACE inhibitors or penicillamine can cause it.

Front 2126

What is the presentation of pemphigus vulgaris?

Back 2126

Vulgaris occurs in thirties and forties, whereas bullous pemphigoid occurs in those in their seventies and eighties. Pemphigus vulgaris is a potentially life-threatening disease. Vulgaris has oral erosions.

Front 2127

What is Nikolsky sign?

Back 2127

Removal of skin by a little pressure from the examiner's finger, pulling skin off like a sheet in pemphigus vulgaris, staph scalded skin syndrome, toxic epidermal necrolysis. Lesions of pemphigus vulgaris are painful.

Front 2128

How is pemphigus vulgaris diagnosed?

Back 2128

Biopsy the skin with immunofluorescent stains.

Front 2129

What is the treatment for pemphigus vulgaris?

Back 2129

Systemic glucocorticoids, such as prednisone; azathioprine, mycophenolate, or cyclophosphamide. Rituximab and IVIg are also effective.

Front 2130

What is pemphigus foliaceus?

Back 2130

Blistering disease often associated with other autoimmune diseases, or it can be induced by ACE inhibitors or NSAIDs.

Front 2131

What is the presentation of pemphigus foliaceus?

Back 2131

Foliaceus is much more superficial, and intact bullae are not seen because they break. There are no oral lesions. Treatment of pemphigus foliaceus is steroids.

Front 2132

What is bullous pemphigoid?

Back 2132

Pemphigoid is twice as common as pemphigus vulgaris and occurs in elderly persons in their seventies and eighties. May be induced with sulfa drugs, furosemide; penicillamine.

Front 2133

How is bullous pemphigoid diagnosed?

Back 2133

Biopsy with immunofluorescent antibodies.

Front 2134

What is the treatment of bullous pemphigoid?

Back 2134

Systemic steroids, such as prednisone; topical steroids only if no oral lesions.

Front 2135

What is porphyria cutanea tarda?

Back 2135

Deficiency of uroporphyrinogen decarboxylase results in accumulation of porphyrins, which leads to photosensitivity; HIV, alcoholism, liver disease, hepatitis C, oral contraceptives.

Front 2136

What is the presentation of porphyria cutanea tarda?

Back 2136

Fragile, nonhealing blisters on sun-exposed backs of the hands and the face. Hyperpigmentation of the skin and hypertrichosis of face.

Front 2137

How is porphyria cutanea tarda diagnosed?

Back 2137

Uroporphyrins are elevated two to five times above the coproporphyrins.

Front 2138

What is the treatment for porphyria cutanea tarda?

Back 2138

Stop alcohol and discontinue estrogen, and iron. Chloroquine increases the excretion of porphyrins.

Front 2139

What is acute urticaria?

Back 2139

Hypersensitivity reaction with IgE, mast cell activation; wheals, hives, without hypotension.

Front 2140

What are the causes of acute urticaria?

Back 2140

Allergic reaction to insect bites, foods, emotions, aspirin, NSAIDs, morphine, codeine, penicillin, phenytoin, quinolones, ACEI. peanuts, shellfish, tomatoes, strawberries, latex.

Front 2141

What is the presentation of acute urticaria?

Back 2141

Lasts <6 weeks and self-limited: onset of wheals and hives within 30 min, lasts for <24 h. Itching. Chronic urticaria lasts >6 weeks and is associated with pressure on the skin, cold, or vibration.

Front 2142

What is the treatment of acute urticaria?

Back 2142

H1 antihistamines. Severe, urticaria is treated with diphenhydramine, hydroxyzine, or cyproheptadine. H2 antihistamines, systemic steroids. Chronic therapy is with nonsedating antihistamines, such as loratadine.

Front 2143

What is a morbilliform rash?

Back 2143

Milder hypersensitivity reaction than urticaria. Typical type of drug reaction and lymphocyte mediated.

Front 2144

What is the presentation of morbilliform rash?

Back 2144

Usually caused by medications allergy, such as penicillin, sulfa drugs, allopurinol, or phenytoin. Generalized, maculopapular eruption that blanches with pressure.

Front 2145

What is the treatment of morbilliform rash?

Back 2145

Antihistamines and steroids.

Front 2146

What is erythema multiforme?

Back 2146

Caused by penicillins, phenytoin, NSAIDs, sulfa drugs. Majority of cases follow infection with herpes simplex or Mycoplasma.

Front 2147

What is the presentation of erythema multiforme?

Back 2147

Target-like lesions that occur on the palms and soles. Bullae are not found, and it does not involve mucous membranes. Treatment is antihistamines.

Front 2148

What is Stevens-Johnson syndrome?

Back 2148

Stevens-Johnson syndrome is erythema multiforme major. SJS and toxic epidermal necrolysis are considered to be degrees of same disorder. Penicillin, sulfa drugs, NSAIDs, phenytoin or phenobarbital.

Front 2149

What is the presentation of Stevens-Johnson syndrome?

Back 2149

SJS involves <10-15% of the total body surface area; the overall mortality rate is <5-10%. Mucous-membrane involvement of oral and conjunctivae, respiratory tract.

Front 2150

What is the treatment for Stevens-Johnson syndrome?

Back 2150

Admission to a burn unit, withdrawal of offending drug, mechanical ventilation. Death occurs from infection, dehydration, malnutrition. No benefit from steroids.

Front 2151

What is toxic epidermal necrolysis?

Back 2151

Toxic epidermal necrolysis is the most serious cutaneous hypersensitivity reaction. Mortality 40-50%.

Front 2152

What is the presentation of toxic epidermal necrolysis?

Back 2152

Skin sloughing involving a body surface area (BSA) 30 to 100%. Nikolsky sign, and the skin easily sloughs off. TEN is drug induced.

Front 2153

How is toxic epidermal necrolysis diagnosed?

Back 2153

Skin biopsy reveal full thickness epidermal necrosis in which the epidermis separates from the dermis. A skin biopsy is usually not necessary.

Front 2154

What is the treatment for toxic epidermal necrolysis?

Back 2154

Topical anesthetics, cover denuded skin with saline or Burow solution compresses. Sepsis is the most common cause of death. Systemic steroids are not effective.

Front 2155

What is a fixed drug reaction?

Back 2155

Recurrent localized allergic reaction to aspirin, NSAIDs, tetracycline, barbiturates. Round, sharply demarcated, and leave a hyperpigmented spot. Treated with topical steroids.

Front 2156

What is erythema nodosum?

Back 2156

Localized inflammatory condition, occurring after infections inflammatory conditions, pregnancy, strep infections, coccidioidomycoses, histoplasmosis, sarcoidosis, IBD, syphilis, hepatitis, Yersinia.

Front 2157

What is the presentation of erythema nodosum?

Back 2157

Multiple painful, red, raised nodules on anterior lower extremities; tender, do not ulcerate, last 6 weeks. ASLO titers can reveal a streptococcal infection.

Front 2158

What is the treatment for erythema nodosum?

Back 2158

Analgesics and NSAIDs. Potassium iodide solution; usually self-limiting.

Front 2159

What are the superficial fungal infections?

Back 2159

Tinea pedis, cruris, corporis, versicolor, capitis, and onychomycosis

Front 2160

What is the appearance of tinea versicolor on KOH?

Back 2160

Malassezia furfur organism appears as "spaghetti and meatballs" on KOH. The most accurate test is fungus culture, but this is not practical because dermatophytes take up to 6 weeks to grow.

Front 2161

What is the treatment for onychomycosis or hair infection (tinea capitis)?

Back 2161

Terbinafine or itraconazole for 6 weeks for fingernails and 12 weeks for toenails. Terbinafine is hepatotoxic. Griseofulvin must be used for 6-12 months and has much less antifungal efficacy than terbinafine.

Front 2162

What is the treatment of dermatophyte infection of the hair?

Back 2162

Griseofulvin for 6-8 weeks for tinea capitis. Terbinafine for 2-4 weeks.

Front 2163

What is the treatment of fungal infections of the skin that do not involve the hair or nails?

Back 2163

Topical ketoconazole, clotrimazole, econazole, terbinafine, miconazole, sertaconazole, sulconazole, tolnaftate, or naftifine.

Front 2164

What is tinea versicolor?

Back 2164

Tan to pink lesions. KOH and fungal culture reveals dermatophytes. Topical selenium sulfide every 2 to 3 weeks or oral therapy with itraconazole or fluconazole.

Front 2165

What are the most common bacterial organisms that cause skin infections?

Back 2165

Staphylococcus and Streptococcus.

Front 2166

What antibiotics are used to treat Staphylococcus?

Back 2166

Dicloxacillin, cephalexin, cefadroxil, cefazolin, nafcillin, oxacillin. If allergic to penicillin was a rash, then cephalosporins can be safely used. <5% cross-reactivity between penicillin and cephalosporins.

Front 2167

What is the treatment of staphylococcal skin infections if the patient is allergic to penicillin?

Back 2167

Cephalosporins cannot be used if anaphylaxis. Alternatives for skin are macrolides, or extended fluoroquinolones (levofloxacin, gatifloxacin, moxifloxacin). Ciprofloxacin will not cover skin.

Front 2168

What is impetigo?

Back 2168

Superficial bacterial infection of the skin; usually caused by Staphylococcus, but is sometimes caused by Streptococcus pyogenes.

Front 2169

What is the presentation of impetigo?

Back 2169

Weeping, oozing, honey colored crusts; warm, humid conditions. Contagious and autoinoculable. Impetigo may cause glomerulonephritis, but not fever.

Front 2170

What is the treatment of impetigo?

Back 2170

Topical mupirocin or retapamulin; antistaphylococcal oral antibiotics, such as dicloxacillin or cephalexin (Keflex).

Front 2171

What is erysipelas?

Back 2171

Dermis and epidermis infection by group A Streptococcus (pyogenes). Fever, chills, and bacteremia; involves the face, giving a bright-red, swollen appearance.

Front 2172

What is the treatment for erysipelas?

Back 2172

Oral dicloxacillin or intravenous nafcillin or cefazolin.

Front 2173

What is cellulitis?

Back 2173

Bacterial infection of the dermis and subcutaneous tissues with Staphylococcus and Streptococcus.

Front 2174

What is the presentation of cellulitis?

Back 2174

Redness, swelling, and warmth and tenderness of the skin; no oozing, crusting, weeping, or draining.

Front 2175

What is the treatment for cellulitis?

Back 2175

Dicloxacillin or intravenous oxacillin, nafcillin, or cefazolin.

Front 2176

What are folliculitis, furuncles, and carbuncles?

Back 2176

Folliculitis, furuncles, and carbuncles represent three different degrees of severity of staphylococcal infections occurring around hair follicle. Folliculitis can be caused by Pseudomonas from a whirlpool or hot tub.

Front 2177

What is the presentation of a folliculus?

Back 2177

Folliculitis starts as a superficial infection around a hair follicle progressing to a small collection of infected material known as a furuncle. Several furuncles merge into a single carbuncle, which is a skin abscess.

Front 2178

What is the treatment for folliculitis?

Back 2178

Warm compresses; mupirocin. Furuncles and carbuncles require systemic antistaphylococcal antibiotics. Carbuncles require dicloxacillin or cefadroxil or IV nafcillin and surgical drainage.

Front 2179

What is necrotizing fasciitis?

Back 2179

Severe, life-threatening infection that starts as a cellulitis that dissects into the fascial planes of the skin. Streptococcus and Clostridium produce a toxin. Diabetes increases risk of fasciitis.

Front 2180

What is the presentation of necrotizing fasciitis?

Back 2180

High fever, portal of entry into the skin, pain, bullae, palpable crepitus.

Front 2181

How is necrotizing fasciitis diagnosed?

Back 2181

Elevated creatine phosphokinase; x-ray, CT scan or MRI show air in the tissue or necrosis.

Front 2182

What is the treatment for necrotizing fasciitis?

Back 2182

Surgery. beta-Lactam/beta-lactamase combination medications, such as ampicillin/sulbactam (Unasyn), ticarcillin/clavulanate (Timentin), or piperacillin/tazobactam (Zosyn).

Front 2183

What is paronychia?

Back 2183

Infection under the skin surrounding a nail.

Front 2184

What is the treatment of paronychia?

Back 2184

Treatment: drainage, dicloxacillin, cefadroxil or cephalexin orally, or oxacillin, nafcillin, or cefazolin intravenously.

Front 2185

What is herpes simplex?

Back 2185

Infection of the genitals, multiple, painful vesicles. Most accurate diagnostic test is a viral culture, which will grow in 24 to 48 hours. Serology is not useful.

Front 2186

What is the treatment for herpes simplex?

Back 2186

Acyclovir, famciclovir, or valacyclovir. Topical acyclovir has little efficacy in primary lesions and will not prevent recurrent lesions. Acyclovir-resistant herpes is treated with foscarnet.

Front 2187

What are the complications of varicella?

Back 2187

Pneumonia, hepatitis, dissemination. Dermatomal herpes zoster occur more frequently in elderly and with immune defects. The vesicles are 2 to 3 mm in size on an erythematous base.

Front 2188

How is varicella diagnosed?

Back 2188

Tzanck prep and viral culture

Front 2189

What is the treatment for varicella?

Back 2189

If immunocompromised child or primary infection in adult, then acyclovir, valacyclovir, or famciclovir.

Front 2190

What is the treatment of zoster?

Back 2190

Acyclovir decreases risk of postherpetic neuralgia. Steroids in elderly with zoster. Postherpetic neuralgia is treated with gabapentin.

Front 2191

What is human papilloma virus?

Back 2191

Responsible for sexually transmitted anogenital and oral warts (condylomata acuminata). Lesions, are translucent, white, or flesh, and are located on skin and mucosal surfaces.

Front 2192

What is the treatment for condyloma acuminata?

Back 2192

Cryotherapy with liquid nitrogen, laser removal, and trichloroacetic acid or podophyllin (teratogenic). Imiquimod is a local immunostimulant that takes 14 weeks to result in sloughing off of the wart.

Front 2193

What is the presentation of primary syphilis?

Back 2193

The chancre of primary syphilis is an ulceration with heaped-up, indurated edges that is painless. Causative organism is Treponema pallidum.

Front 2194

What is secondary syphilis?

Back 2194

Generalized copper-colored, maculopapular rash that is more intense on the palms and soles of the feet. The other manifestations of secondary syphilis are mucous patch, alopecia areata, and condylomata lata.

Front 2195

How is primary syphilis diagnosed?

Back 2195

Initial test darkfield. False-neg rate 25% for VDRL/RPR. Serologic tests need several weeks to become positive, and only 75% sensitive in primary. For secondary syphilis, VDRL/RPR tests are 100% sensitive.

Front 2196

What is the treatment of syphilis?

Back 2196

Primary and secondary syphilis are treated with a single, intramuscular dose of penicillin; penicillin allergic patients are treated with doxycycline orally for 2 weeks.

Front 2197

What is scabies?

Back 2197

Vesicular eruptions resulting from Sarcoptes scabiei (hominis) mites burrowing into the skin.

Front 2198

What is the presentation of scabies?

Back 2198

Web spaces of hands, feet, pruritic lesions around penis, breasts. Itching, burrows and excoriations around small pruritic vesicles. Spares head. Patients with HIV have severe crusting, known as Norwegian scabies.

Front 2199

How is scabies diagnosed?

Back 2199

Scraping out the organism after mineral oil is applied to a burrow (not routinely done).

Front 2200

What is the treatment for scabies?

Back 2200

Permethrin. Lindane has equal efficacy, but greater toxicity. Norwegian scabies can be treated with ivermectin orally.

Front 2201

What is pediculosis?

Back 2201

Pediculosis (lice and crabs from the genus Pediculus) tends to involve the head. Both P. humanus (lice) and P. pubis (crabs) can be sexually transmitted.

Front 2202

What is the treatment for pediculosis?

Back 2202

Over-the-counter pyrethrins, Lindane.

Front 2203

What is the cause of Lyme disease?

Back 2203

Borrelia burgdorferi spirochete, transmitted by the deer tick (Ixodes scapularis).

Front 2204

What is the presentation of Lyme disease?

Back 2204

Erythematous with central clearing at least 5 cm in diameter. 7 to 10 days after the tick bite.

Front 2205

How is Lyme disease diagnosed?

Back 2205

This rash is more important than serologic testing for diagnosis.

Front 2206

What is the treatment for Lyme disease?

Back 2206

Doxycycline, amoxicillin, or cefuroxime. Without therapy, two-thirds develop joint disease. Some develop neurologic or cardiac disorders.

Front 2207

What is toxic shock syndrome?

Back 2207

Systemic reaction to a toxin produced by Staphylococci in a tampon, vaginal packing, nasal packing, retained sutures, or other surgical material.

Front 2208

What is the clinical presentation of toxic shock syndrome?

Back 2208

Presence of 3 or more or of the following: fever >102, SBP <90, desquamative rash, vomiting, involvement of mucous membranes of the eyes, mouth, or genitals, elevated bilirubin, platelets <100,000.

Front 2209

What is the treatment for toxic shock syndrome?

Back 2209

Remove the source of the infection; fluid resuscitation, dopamine, and clindamycin plus vancomycin.

Front 2210

What is staphylococcal scalded skin syndrome?

Back 2210

Occurs in infants and young children and in the immunocompromised. Mediated by a toxin from Staphylococcus, loss of the superficial layers of the epidermis in sheets.

Front 2211

What is the treatment for staphylococcal scalded skin syndrome?

Back 2211

Managed in a burn unit and nafcillin.

Front 2212

What is anthrax?

Back 2212

Bacillus anthracis cutaneous infection acquired from contact with infected livestock; woolsorters, bioterrorism.

Front 2213

What is the presentation of anthrax?

Back 2213

Papule appears that later becomes inflamed and develops with central necrosis, which is black in color.

Front 2214

How is anthrax diagnosed?

Back 2214

Gram stain and culture.

Front 2215

What is the treatment of anthrax?

Back 2215

In lesions due to occupational exposure, penicillin V or doxycycline. Bioterrorism: ciprofloxacin.

Front 2216

What are the characteristics of benign skin lesions?

Back 2216

Benign lesions do not grow in size and have smooth, regular borders with a diameter usually <1 cm. Homogenous in color.

Front 2217

What is seborrheic keratosis?

Back 2217

Benign hyperpigmented lesions in the elderly with a "stuck on" appearance; most common on the face shoulders, chest, and back.

Front 2218

What is the treatment for seborrheic keratosis?

Back 2218

Liquid nitrogen or curettage.

Front 2219

What are actinic keratoses?

Back 2219

Precancerous lesion on sun-exposed areas of the body in older persons. 1:1,000 progresses to squamous cell cancer. Light in color. Removed with cryotherapy, 5FU, imiquimod.

Front 2220

What is the presentation of melanoma?

Back 2220

Grow in size, irregular borders shape, inconsistent color.

Front 2221

What is lentigo maligna melanoma?

Back 2221

Lentigo maligna melanoma arises on sun-exposed body parts in the elderly. Acral-lentiginous melanoma arises on the palms, soles of feet, and nail beds.

Front 2222

What is the treatment for melanoma?

Back 2222

Melanoma is removed by excision. Interferon reduces the recurrence rates of melanoma.

Front 2223

What is squamous cell carcinoma?

Back 2223

Develops on sun-exposed skin surfaces in elderly patients. Ulceration. Metastases are rare.

Front 2224

What is basal cell carcinoma?

Back 2224

Sixty-five to eighty percent of all skin cancers are basal cell. Shiny or "pearly" appearance. Rate of metastases is <0.1%.

Front 2225

What is the treatment of basal cell carcinoma?

Back 2225

Mohs microsurgery. 5-FU for superficial lesions.

Front 2226

What is Kaposi sarcoma?

Back 2226

Purplish lesions found on the skin predominantly of patients with HIV and CD4 counts <100/mm3. Human herpes virus 8 is the causative organism.

Front 2227

What is the treatment for Kaposi sarcoma?

Back 2227

Antiretroviral therapy to raise the CD4 count. Cryotherapy liposomal doxorubicin hydrochloride or vinblastine.

Front 2228

What is the presentation of psoriasis?

Back 2228

Silvery scales on extensor surfaces. Local or extensive. Nail pitting. Koebner phenomenon.

Front 2229

What is the treatment for psoriasis?

Back 2229

Salicylic acid, coal tar or anthralin derivatives. Biologic agents, such alefacept, efalizumab, etanercept, and infliximab, which are monoclonal antibodies.

Front 2230

What is atopic dermatitis?

Back 2230

Pruritic disorder with high IgE levels. Red, itchy plaques appear on the flexor surfaces, cheeks, lichenification.

Front 2231

What is the treatment for atopic dermatitis?

Back 2231

Emollients, avoid hot water and drying soaps; wear cotton clothes. Topical steroids, antihistamines, coal tars, phototherapy. Antistaphylococcal antibiotics. Topical doxepin.

Front 2232

What is seborrheic dermatitis?

Back 2232

Oversecretion of sebaceous material and a hypersensitivity reaction to a superficial fungus, Pityrosporum ovale. Scaly, greasy, flaky skin is found on a red base on the scalp, eyebrows, and in the nasolabial fold.

Front 2233

What is the treatment for seborrheic dermatitis?

Back 2233

Low-potency hydrocortisone, or topical antifungals in the form of shampoos, such as ketoconazole or sulfide.

Front 2234

What is contact dermatitis?

Back 2234

Hypersensitivity reaction to soaps, detergents, latex, sunscreens, or neomycin, jewelry, nickel.

Front 2235

What is the presentation of contact dermatitis?

Back 2235

Linear, vesicles, particularly when it is from poison ivy.

Front 2236

What is the treatment of contact dermatitis?

Back 2236

Antihistamines and topical steroids.

Front 2237

What is pityriasis rosea?

Back 2237

Pruritic eruption that begins with a "herald patch". Mild, self-limited, and usually resolves in 8 weeks without scarring.

Front 2238

What is the presentation of pityriasis rosea?

Back 2238

Salmon colored patches that are similar to secondary syphilis, except spares the palms and soles and has a herald patch. Lesions on the back appear in a pattern like a Christmas tree. VDRL negative.

Front 2239

What is alopecia areata?

Back 2239

Autoimmune disease in which antibodies attack the hair follicles.

Front 2240

What is telogen effluvium?

Back 2240

Loss of hair in response to physiologic stress, such as cancer or malnutrition.

Front 2241

What is the treatment for acne?

Back 2241

Topical clindamycin or erythromycin. Benzoyl peroxide. Retinoids: tazarotene, tretinoin, and adapalene. Severe cystic acne is treated with minocycline, tetracycline, clindamycin, oral isotretinoin (teratogenic).

Front 2242

What are the steps in assessing the technical quality of a chest x-ray?

Back 2242

Determine if rotated by determining if trachea and spinous apophysis are midway between the clavicles. Ten ribs visible. Underexposed film appear too white. Overexposure is too dark.

Front 2243

What are the chest x-ray signs of chronic obstructive pulmonary disease and emphysema?

Back 2243

Hyperinflation of the lung causes darkening of the lung fields; flat the diaphragm and tubular-shaped heart. Increased anterior/posterior diameter, or "barrel chest," bullae are thin, white lines.

Front 2244

What are the chest x-ray signs of pneumonia?

Back 2244

Whitening of lobe. "Silhouette" sign: border between the affected lobe and a structure is obscured. Lower lobe pneumonia causes a silhouette of diaphragm. Right middle-lobe pneumonia obscures right heart border.

Front 2245

What are the signs of interstitial pneumonia?

Back 2245

Disease of the lung in the interstitial space produces a fine, lacy appearance visible in most of the lobes.

Front 2246

What disorders cause interstitial infiltrates?

Back 2246

Pneumocystis pneumonia, Mycoplasma, viruses, Chlamydia, pulmonary fibrosis caused by silicosis, asbestosis, mercury poisoning, berylliosis, idiopathic pulmonary fibrosis.

Front 2247

What are the chest x-ray signs of congestive heart failure?

Back 2247

Fluid overload causes the blood vessels toward the apices become fuller, which is pulmonary vascular congestion, or "cephalization" of flow. Cardiomegaly, pleural effusions, and Kerley B lines.

Front 2248

What are Kerley B lines?

Back 2248

Kerley B lines are small, horizontal lines at the bases that represent fluid in the interlobular septa.

Front 2249

What is the proper position of the tip of an endotracheal tube on a chest x-ray?

Back 2249

1 to 2 cm above the carina.

Front 2250

What is the correct position of a central line on a chest x-ray?

Back 2250

Tip at junction of the superior vena cava and the right atrium, at right main stem bronchus. The tip of the line should not be inside the atrium because it can irritate the heart and provoke an arrhythmia.

Front 2251

What conditions can cause air under the diaphragm on a chest x-ray?

Back 2251

Perforation of esophagus or ulcer. In the upright position. Air is also visible after surgery or laparoscopy.

Front 2252

What are the indications for high resolution CT scan?

Back 2252

Symptomatic patients with a normal chest x-ray to detect metastatic lesions, solitary nodules, bullae, bronchiectasis, and diffuse parenchymal disease. CT is used as a guide to determine the site of biopsy.

Front 2253

What conditions are detected by abdominal x-rays?

Back 2253

Abdominal x-rays are useful only in the detection of an abdominal obstruction, such as an ileus or a volvulus.

Front 2254

What is the best method of detecting mass lesions of the abdomen?

Back 2254

Mass lesions in all abdominal organs are best detected with CT scanning or an MRI of the abdomen. Polyps are detected by colonoscopy. Ascites is visualized by ultrasound or CT scanning.

Front 2255

What is the best test for detecting inflammatory bowel disease, diverticulitis, or colon cancer?

Back 2255

Inflammatory bowel disease, diverticulosis, and cancer are detected by either endoscopy or barium studies of the bowel.

Front 2256

What are the best tests for detecting kidney stones?

Back 2256

Kidney stones are best detected by sonography or CT scanning.

Front 2257

What are the best tests for detecting gallstones?

Back 2257

Only 10 to 15% of gallstones can be detected on an abdominal film; the best tests for gallstones are sonography and CT scanning.

Front 2258

What is the role of sonography in detecting abdominal lithiasis?

Back 2258

Sonograms should be used first for evaluation of the biliary tract for cholelithiasis. Nephrolithiasis is visible by sonography, although there is less accuracy because retroperitoneal location.

Front 2259

What is the role of sonography in evaluating the abdomen?

Back 2259

Sonography is useful in the evaluation of masses in the liver, spleen, pancreas, pelvis, and for evaluating the presence of ascites. CT has a greater sensitivity and specificity for the abdomen and pelvis.

Front 2260

What is endoscopic retrograde cholangiopancreatography?

Back 2260

Contrast is injected to visualize the biliary tract and pancreatic structures for detecting strictures, stones, and neoplasms. ERCP can remove stones and dilate strictures and biopsy.

Front 2261

What is capsule endoscopy?

Back 2261

Allows direct visualization of the small bowel by swallowing a camera. If a patient has serious bleeding and both upper and lower endoscopy do not reveal the source, capsule endoscopy is indicated.

Front 2262

What is HIDA scanning?

Back 2262

Nuclear scan useful only in the detection of acute cholecystitis. Useful in patients in whom the diagnosis of cholecystitis is not clear. An abnormal or positive test is lack of visualization of the gallbladder.

Front 2263

What is positron emission tomography?

Back 2263

Useful to determine if lesions are malignant or benign. Cancer is associated with increased uptake of fluorodeoxyglucose. Used after chemotherapy to assess the presence of residual cancer.

Front 2264

What is the most accurate test for evaluating central nervous system lesions?

Back 2264

Magnetic resonance imaging is superior for the detection of stroke, cancer, multiple sclerosis, infections, and in the evaluation of the posterior fossa, such as the cerebellum and brainstem.

Front 2265

What is the sensitivity of MRI in detecting ischemic strokes?

Back 2265

>90% within the 24 h after onset, whereas the CT needs 3 days before >90% of ischemic strokes are visible. CT is superior to MRI in detection of blood. CT is the best for trauma and to exclude hemorrhagic stroke.

Front 2266

What are the indications for using contrast during a head CT scan?

Back 2266

Contrast is indicated for the detection of cancers and infection. When an abscess or neoplastic process is present, extravasation of contrast is visible as "ring"-enhancing lesion.

Front 2267

What tests are useful for diagnosing osteomyelitis?

Back 2267

X-ray is done first. Plain x-rays lack sensitivity; the specificity for osteomyelitis is excellent. Earliest finding of osteomyelitis is elevation of the periosteum. The MRI has high sensitivity (95%) and specificity (95%).

Front 2268

What is diabetic retinopathy?

Back 2268

Caused by damage to the endothelial lining of small blood vessels, leading to occlusion. The earliest form is nonproliferative retinopathy, characterized by dilation of veins, microaneurysms, edema, hemorrhages.

Front 2269

What is proliferative retinopathy?

Back 2269

Proliferative retinopathy progresses rapidly to blindness. "Neovascularization," or new blood vessel formation leads to new vessel formation. Intravitreal hemorrhages. Treatment is laser photocoagulation.

Front 2270

What are the predisposing factors to retinal detachment?

Back 2270

Spontaneous, but may result from trauma. Predisposing factors are myopia and surgical extraction of cataracts; proliferative retinopathy, retinal vein occlusion, and age-related macular degeneration.

Front 2271

What is the presentation of retinal detachment?

Back 2271

Blurry vision developing in one eye without pain or redness. Floaters, flashes, "curtain coming down."

Front 2272

What are the causes of central retinal artery occlusion?

Back 2272

Carotid artery embolic disease, temporal arteritis, cardiac thrombi or myxoma, or thrombophilia, such as factor V Leiden mutation.

Front 2273

What is the presentation of retinal artery occlusion?

Back 2273

Sudden, painless, unilateral loss of vision. No redness. Pale retina, with diminished perfusion and a "cherry- red" spot at the fovea.

Front 2274

What is the treatment of central retinal artery occlusion?

Back 2274

Lay the patient flat and give oxygen; ocular massage in an attempt to unobstruct the vessel. Acetazolamide and thrombolytics.

Front 2275

What is the presentation of central retinal vein occlusion?

Back 2275

Sudden loss of vision without pain, redness, or abnormality in pupillary dilation. Ocular examination by funduscopy reveals disk swelling, venous dilation, tortuosity, and retinal hemorrhages.

Front 2276

What medications can cause acute angle-closure glaucoma?

Back 2276

Precipitated by anticholinergic medications, such as ipratropium bromide or tricyclic antidepressants.

Front 2277

How is open-angle glaucoma diagnosed?

Back 2277

Cup-to-disk ratio of >0.3; confirmed by an elevation in intraocular pressure by tonometry. This disorder accounts for >90% of cases of glaucoma; asymptomatic.

Front 2278

What medications are useful for decreasing the production of the aqueous humor in glaucoma?

Back 2278

Beta-blockers (timolol, betaxolol, levobunolol), alpha-adrenergic agonists (apraclonidine, brimonidine), and carbonic anhydrase inhibitors (dorzolamide and brinzolamide).

Front 2279

What treatments increase the outflow of aqueous humor in the treatment of glaucoma?

Back 2279

Prostaglandin analogs, such as latanoprost, travoprost, bimatoprost. Can change the color of the eyes and darken eyelid. Pilocarpine is a miotic agent that increases outflow of aqueous humor. Laser trabeculoplasty or surgical trabeculectomy.

Front 2280

What is the presentation of closed-angle glaucoma?

Back 2280

Eye is red, painful, hard, fixed midpoint pupil. The cornea has a hazy cloudiness, diminished visual acuity. Precipitated by anticholinergic medications.

Front 2281

What is the treatment of closed-angle glaucoma?

Back 2281

IV acetazolamide, urea, osmotic diuretics (mannitol or glycerol). Pilocarpine can be used to open the canal of Schlemm; beta-blockers decrease humor production. Laser trabeculoplasty.

Front 2282

What are the causes of infectious conjunctivitis?

Back 2282

Bacteria, viruses, and fungi.

Front 2283

What is the presentation of bacterial conjunctivitis?

Back 2283

Unilateral, purulent discharge. Crusting overnight. Less itching compared with viral conjunctivitis. Red eye, normally reactive pupil, normal ocular pressure, and no visual impairment.

Front 2284

What is the presentation of viral conjunctivitis?

Back 2284

Viral conjunctivitis is more often bilateral in nature, with much more severe ocular itching and enlarged preauricular adenopathy. The eyes are also red, the pupil reacts normally, and there is no photophobia.

Front 2285

What is the treatment of bacterial conjunctivitis?

Back 2285

Erythromycin ointment, sulfacetamide drops, or topical fluoroquinolones.

Front 2286

What is the treatment of viral conjunctivitis?

Back 2286

Topical antihistamine and decongestants.

Front 2287

What is subconjunctival hemorrhage?

Back 2287

Most commonly caused by trauma. The hematoma stops at the limbus, which is the junction between the conjunctiva and the cornea. There is no impairment of vision.

Front 2288

What is keratitis?

Back 2288

Any infection or inflammation of the cornea.

Front 2289

What is the presentation of herpes simplex keratitis?

Back 2289

Severe pain in the eye and a foreign body sensation under the eyelid.

Front 2290

How is herpes simplex keratitis diagnosed?

Back 2290

Characteristic dendritic pattern over the cornea on fluorescein staining of the eye under a blue light.

Front 2291

What is the treatment for herpes simplex keratitis?

Back 2291

Oral acyclovir, famciclovir, or valacyclovir and topical trifluridine 1% solution or idoxuridine.

Front 2292

What is periorbital cellulitis?

Back 2292

Cellulitis caused by Staphylococcus aureus or Streptococcus infecting the dermis and subcutaneous tissues surrounding the eye.

Front 2293

What is the treatment for periorbital cellulitis?

Back 2293

Antistaphylococcal penicillins, such as oxacillin or nafcillin. If there is an allergic rash to penicillins, then first-generation cephalosporins can be used (cefazolin).

Front 2294

What is uveitis?

Back 2294

Uveitis is inflammation of the iris, ciliary body, and choroid. Uveitis is caused by psoriasis, sarcoidosis, syphilis, reactive arthritis, and inflammatory bowel disease.

Front 2295

What is the presentation of uveitis?

Back 2295

Painful, red eye with photophobia. Pain also occurs when shining a light in the unaffected eye.

Front 2296

How is uveitis diagnosed?

Back 2296

Slit lamp examination. Inflammation of the iris, ciliary body, and choroid.

Front 2297

What is the treatment for uveitis?

Back 2297

Topical or systemic steroids.