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813 Cards in this Set
- Front
- Back
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What are the three cancers for which regular screening is recommended?
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Cancers of the colon, breast, and cervix.
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When should screening for colon cancer begin in the patient with no family history of colon cancer?
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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.
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What are the screening mammography recommendations for breast cancer?
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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.
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What is the prophylaxis for hepatitis A for travelers?
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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.
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What is the most common cause of hepatitis A?
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Hepatitis A is the most common vaccine-preventable disease in travelers; from fecal contamination of food or water.
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Which travelers should receive hepatitis B vaccine?
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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.
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What is the recommended prophylaxis for malaria for travelers?
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Traveling to Mexico, Central America (except Panama), or Caribbean, chloroquine is prophylaxis for malaria. For travelers to areas where chloroquine resistance common, mefloquine recommended.
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What is the recommended prophylaxis for malaria for travelers?
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Rabies vaccination is recommended for patients traveling to areas where rabies is common (India, Asia, Mexico).
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What is the vaccination recommendation for yellow fever for travelers?
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Yellow fever vaccine is required for travel to sub-Saharan Africa and South American countries.
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What are the vaccination recommendations for meningococcal meningitis?
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Persons traveling to Nepal, sub-Saharan Africa, northern India should be immunized with the polysaccharide vaccine. Saudi Arabia requires immunization for pilgrims to Mecca.
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At what age is meningococcal vaccine usually given?
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Meningococcal is routinely given at age 11.
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What are the recommendations for prevention of traveler's diarrhea?
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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.
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What are the recommendations for tetanus and diphtheria vaccination in adults who were never vaccinated?
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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.
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What are the recommendations for influenza vaccination?
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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.
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What are the indications for pneumococcal vaccination?
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Adults >65; sickle-cell, splenectomy, cardiopulmonary disease, alcoholism, cirrhosis, Alaskan natives, Native Americans; immunocomp (heme malignancies, CRF, nephrotic, HIV; immunosuppressives).
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What are the indications for hepatitis B vaccination?
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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.
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What are the recommendations for hepatitis A vaccine?
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Hepatitis A vaccine is recommended for travelers to endemic areas, day-care employees, homosexual men, and chronic liver disease.
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What are the indications for varicella vaccine?
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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.
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What are the recommendations for measles, mumps, rubella vaccine?
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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.
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What are the recommendations for osteoporosis screening?
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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.
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What are the recommendations for screening for abdominal aortic aneurysm?
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Ultrasound should be given once in male smokers older than age 65.
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What are the recommendations for cholesterol screening?
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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.
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What are the recommendations for screening for diabetes?
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Obesity, impaired fasting glucose, African-Americans, native Americans and/or positive family history.
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What is the criteria for the diagnosis of diabetes?
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Diabetes mellitus is diagnosed when two fasting are greater than 126 mg/dL, or when a random glucose is >200 mg/dL.
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What clinical test should be used to screen for alcohol abuse?
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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.?
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What pathological conditions are associated with hyperprolactinemia?
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Excess of prolactin occurs with prolactinomas (most common functioning pituitary adenomas, 60% of pituitary tumors.
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What medications cause hyperprolactinemia?
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Decreased inhibitory action of dopamine caused by drugs that block dopamine synthesis (phenothiazines, metoclopramide) and dopamine-depleting agents (alpha-methyldopa).
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What is the presentation of hyperprolactinemia?
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Women have galactorrhea, amenorrhea/oligomenorrhea, osteoporosis, infertility, gynecomastia; men have hypogonadism, erectile dysfunction, decreased libido, gynecomastia and infertility.
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How is hyperprolactinemia diagnosed?
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Always exclude pregnancy, lactation, hypothyroidism and medications before starting the evaluation of hyperprolactinemia. Prolactin levels >100 ng/mL suggest probable pituitary adenoma.
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What is the management of hyperprolactinemia?
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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.
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What is acromegaly?
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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.
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How is acromegaly diagnosed?
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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.
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What is the management of acromegaly?
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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.
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What are the causes of hypopituitarism?
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Tumors, cysts, sarcoidosis, Tb, syphilis, eosinophilic granuloma, Hashimoto, gastric atrophy. Trauma, radiation, surgery, infections, hypoxia. Sheehan postpartum necrosis, hemochromatosis, amyloidosis.
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What are the signs of hypopituitarism?
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Amenorrhea, genital atrophy, loss pubic hair. Growth fail. Thyrotropin deficiency: hypothyroidism. Adrenocorticotropin def: fatigue, anorexia, wt loss, decreased skin pigment, hypotension, hypoNa.
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How is hypopituitarism diagnosed?
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Measure GH, TSH, LH, and insulin-like-GF1.
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How is ACTH deficiency diagnosed?
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Insulin tolerance test: give insulin and measure serum cortisol. Metyrapone tests for decreased ACTH production. Metyrapone blocks cortisol production, which should increase ACTH levels.
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How is gonadotropin deficiency diagnosed?
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To diagnose gonadotropin deficiency in women, measure LH, FSH, and estrogen. In males, gonadotropin deficiency is detected by measuring LH, FSH, and testosterone.
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How is thyroid stimulating hormone deficiency diagnosed?
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To diagnose TSH deficiency, measure serum thyroxine (T4), and free triiodothyronine (T3), which are low, with a normal to low TSH.
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What is central diabetes insipidus?
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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.
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What are the causes of central diabetes insipidus?
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Adenomas, craniopharyngiomas; leukemias, sarcoid histocytosis. Pituitary/hypothalamic surgery, radiotherapy, severe head injuries, anoxia, hypertension, and meningitis. Idiopathic; encephalitis, TB, and syphilis.
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What are the causes of nephrogenic diabetes insipidus?
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Nephrogenic DL: idiopathic or caused by hyperCa, hypoK, sickle cell, amyloidosis, myeloma, pyelonephritis, sarcoidosis, Sjögren syndrome, lithium, demeclocycline, colchicine.
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What are the clinical signs of diabetes insipidus?
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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.
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How is diabetes insipidus diagnosed?
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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.
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How is nephrogenic diabetes insipidus differentiated from central diabetes insipidus?
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ADH levels will be low in central DL and high in nephrogenic DL.
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What is the differential diagnosis of diabetes insipidus?
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Psychogenic polydipsia, drug-induced polydipsia from chlorpromazine, anticholinergic drugs, or thioridazine, and hypothalamic diseases.
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What is the management of central diabetes insipidus?
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Hormone replacement with vasopressin. For nephrogenic DL, HCTZ or amiloride increase the reabsorption of fluid from the proximal tubule.
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What are the causes of syndrome of inappropriate secretion of ADH?
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Small cell CA, pancreas CA, ectopic ADH; TB, pneumonia, lung abscess; head injury, stroke, encephalitis; chlorpropamide, clofibrate, vincristine, vinblastine, cyclophosphamide, carbamazepine.
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What are the clinical signs of syndrome of inappropriate ADH?
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Water retention and ECF expansion without edema or hypertension. Hyponatremia. Hyponatremia and concentrated urine (Uosm >300 mOsm), no edema or dehydration.
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What are the CNS signs of SIADH?
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Cerebral edema from hyponatremia causes irritability, confusion, seizures, coma.
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What are the laboratory findings in syndrome of inappropriate secretion of ADH?
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Hyponatremia <130 mEq/L, and Posm <270 mOsm/kg. Urine Na >20 mEq/L (inappropriate natriuresis). Low BUN, low creatinine, low urate, low albumin.
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What is the management of SIADH?
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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.
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What is the most sensitive test for thyroid diseases?
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The most sensitive test in thyroid diseases is the TSH. If the TSH is normal, then the patient is euthyroid.
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What are the effects of thyroid binding globulin levels on the thyroxine levels?
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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.
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What are the signs of thyrotoxicosis?
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Graves disease, diffuse goiter, exophthalmos, dermopathy. More in women in the fourth decade.
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What is the cause of Grave disease?
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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.
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What are the causes of transient hyperthyroidism?
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Subacute thyroiditis (painful) and lymphocytic thyroiditis (painless, postpartum). Thyrotoxicosis factitia and ectopic thyroid tissue (struma ovarii, functioning follicular carcinoma).
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What are the cardiovascular signs of Graves disease?
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Anxiety, insomnia; atrial fibrillation, tremors, frequent bowel movements, excessive sweating, heat intolerance. Weight loss, increased appetite, weakness. Dyspnea, palpitations, angina, or cardiac failure.
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What are the dermatologic signs of Grave disease?
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Skin is warm and moist, palmar erythema; fine, silky hair. Staring, infrequent blinking, oligomenorrhea; osteoporosis and hypercalcemia.
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What are the laboratory findings in Graves disease?
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Low TSH; increased serum free T4 and T. RIAU is increased. Antithyroglobulin and antimicrosomal antibodies are elevated in Graves disease and autoimmune thyroiditis.
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What is the treatment of hyperthyroidism?
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Popranolol, propylthiouracil (safe in preg) or methimazole. Both can cause agranulocytosis. Ablation with radioactive iodine. Subtotal thyroidectomy only in pregnancy and children.
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What is a thyroid storm?
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Thyrotoxicosis precipitated by stress, infection, surgery, or trauma. Extreme irritability, delirium, coma, tachycardia, restlessness, vomiting, jaundice, diarrhea, hypotension, dehydration, and fever.
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What is the treatment for thyroid storm?
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Glucose, hydration, glucocorticoids, oxygen, cooling blanket. Propylthiouracil, beta-blockers, and iodine inhibit hormone release.
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What is the affect of antithyroid drugs on uptake of radioactive iodine?
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Antithyroid drugs should be stopped several days before radioactive iodine treatment because the antithyroid medications block the uptake of the radioactive iodine.
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What are the causes of primary hypothyroidism?
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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.
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What is the most common cause of goitrous hypothyroidism?
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Hashimoto disease is most common cause of goitrous hypothyroidism.
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What are the clinical signs in congenital hypothyroidism?
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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.
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What are the signs and symptoms of hypothyroidism in the adult?
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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.
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What is the treatment of hypothyroidism?
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Levothyroxine (T4) should be administered with monitoring of TSH/T3 levels (6 weeks to steady state after dosing changes).
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What is myxedema coma?
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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.
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What are the causes of subacute thyroiditis?
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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.
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What are the laboratory findings in subacute thyroiditis?
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Elevated erythrocyte sedimentation rate (ESR), decreased radioactive iodine uptake, initial elevation in T4 and T3, followed by hypothyroidism.
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What is the treatment of subacute thyroiditis?
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Aspirin, prednisone, and Popranolol.
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What is Hashimoto thyroiditis?
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Chronic autoimmune inflammatory process with lymphocytic infiltration. Common disorder most frequently in middle-aged women; most common cause of sporadic goiter in children.
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What are the clinical signs of Hashimoto thyroiditis?
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Goiter that is painless, rubbery and hypothyroidism.
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How is Hashimoto thyroiditis diagnosed?
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TSH increases, and T4 and T decrease. Antimicrosomal and antithyroperoxidase antibodies.
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What is the management of Hashimoto thyroiditis?
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Replacement with L-thyroxine (T4).
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What is chronic lymphocytic thyroiditis?
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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.
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What is Reidel thyroiditis?
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Fibrosis of the thyroid and mediastinal and retroperitoneal fibrosis.
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What is papillary carcinoma?
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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.
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What is follicular carcinoma of the thyroid?
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Follicular carcinoma accounts for 15% of thyroid cancers. Elderly women. More malignant than papillary carcinoma. Spreads hematogenously.
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What is the treatment of follicular thyroid cancer?
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Treatment is near-total thyroidectomy with postoperative radioiodine ablation.
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What is anaplastic thyroid carcinoma?
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10% of all thyroid cancer. Elderly women. Highly malignant, painful enlargement. Eighty percent of patients die.
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What is medullary thyroid carcinoma?
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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.
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What is the treatment of medullary thyroid cancer?
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Treatment is thyroidectomy. Calcitonin levels can also be increased from cancer of the lung, pancreas, breast, and colon.
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What are the clinical signs of thyroid carcinoma?
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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.
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What is the significance of psammoma bodies in the thyroid?
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Calcifications such as psammoma bodies suggest papillary carcinoma; increased density is associated with medullary carcinoma.
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What is the significance of finding hyperthyroidism in association with a thyroid nodule?
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Hyperthyroidism is never associated with cancer.
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What is the diagnostic approach to solitary nonfunctioning nodule?
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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.
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What is the function of parathyroid hormone?
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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.
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What is the effect of parathyroid hormone on the bones?
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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.
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What is the most common cause of hypercalcemia?
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Primary hyperparathyroidism. Hypercalcemia of malignancy caused by PTH-like protein. Sarcoidosis, Tb, berylliosis, histoplasmosis, coccidioidomycosis increase vitamin D.
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What are the rare causes of hypercalcemia?
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Rare causes: vitamin D, thiazides, lithium, Paget, immobilization, hyperthyroidism.
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What are the signs of hypercalcemia?
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Lethargy, confusion, constipation, anorexia, nausea, vomiting. Pancreatitis because of precipitation of Ca pancreas. Polyuria, polydipsia. Ca precipitates kidney, resulting in nephrolithiasis. HTN in 50%.
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What are the ECG signs of hypercalcemia?
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ECG shows short QT.
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What is the treatment for hypercalcemia?
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Saline or half-normal and furosemide, which promote calcium loss. Bisphosphonates such as alendronate, zoledronate, risedronate, pamidronate inhibit osteoclasts and stimulate osteoblasts. Calcitonin.
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What are the causes of primary hyperparathyroidism?
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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.
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What the effects of hyperparathyroidism on bone?
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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.
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How is primary hyperparathyroidism diagnosed?
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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).
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What is the management of primary hyperparathyroidism?
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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.
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What are the causes of hypocalcemia?
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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.
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What are the signs of hypocalcemia?
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Hypocalcemia results in neural hyperexcitability, seizures, tetany, circumoral numbness, and tingling. Cataracts.
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What are the ECG signs of hypocalcemia?
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Arrhythmias may develop because of a prolonged QT.
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What is the most common cause of hypoparathyroidism?
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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.
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What are the neurologic signs of hypoparathyroidism?
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Neuromuscular irritability, tetany, laryngospasm, cramps, seizures, impaired memory. Chvostek sign: percussion of facial nerve contraction face. Trousseau: inflation of cuff elicits flexion metacarpophalangeal.
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What are the cardiovascular signs of hypocalcemia?
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QT prolongation, CHF, and/or hypotension. Circumoral tingling and tingling of the hands and feet.
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How is hypoparathyroidism diagnosed?
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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.
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What are the causes of a low calcium with low phosphorous?
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Low calcium with low phosphorous is caused by low vitamin D.
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What is the management of hypoparathyroidism?
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Calcium gluconate IV. Maintenance oral calcium 2-4 g/d, vitamin D, and if there is hyperphosphatemia, diet restriction and phosphate binders (CaCO3).
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What is the usual age of onset of type 1 diabetes?
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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.
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What is the usual age of onset of type 2 diabetes?
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Usually >40; males > females. >20% of first-degree relatives are affected with 90-100% occurrence in identical twins. Obese.
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What is the cause of type 2 diabetes?
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90% of diabetes is type 2, caused by abnormal insulin secretion and resistance to insulin.
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What are the clinical signs of diabetes?
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Hyperglycemia causes polyuria, polydipsia, polyphagia, coma (ketoacidosis for type I diabetes and hyperosmolar coma for type 2 diabetes).
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How is diabetes diagnosed?
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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.
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What is glycosylated hemoglobin A1c?
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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.
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What is the glycosylated hemoglobin A1c goal?
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The goal of therapy is to have an HgA1c <7%.
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What is the management of type 2 diabetes?
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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.
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What is the dosage for insulin in type 2 diabetes?
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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.
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What is the dosage for glargine insulin?
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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.
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What is the acute complication of uncontrolled type 1 diabetes mellitus?
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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.
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What are the clinical signs of diabetic ketoacidosis?
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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.
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What is the treatment of diabetic ketoacidosis?
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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.
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What acid-base disorder is associated with uncontrolled diabetes?
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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)].
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What is hyperosmolar nonketotic coma?
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HONK occurs in type 2 diabetes; severe hyperglycemia without ketosis. Precipitated by noncompliance plus inability to drink. Elderly, infections, strokes, steroids, immunosuppressants, diuretics.
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What is the presentation of hyperosmolar nonketotic coma?
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Profound dehydration results from hyperglycemic diuresis. Weakness, polyuria, polydipsia, lethargy, confusion, convulsions, and coma.
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What are the laboratory findings in hyperosmolar nonketotic coma?
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Elevated blood glucose (>1,000 mg/dL) and extremely high serum osmolality.
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What is the treatment of hyperosmolar non-ketotic coma?
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High-volume fluid and electrolyte replacement and insulin.
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What are the chronic ocular complications of diabetes?
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Retinopathy is the leading cause of blindness; background or proliferative (microaneurysms, hemorrhages, exudates, retinal edema).
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What are the ophthalmic screening recommendations for diabetes?
|
Diabetics should be screened for retinopathy once a year. Proliferative retinopathy is treated with laser photocoagulation.
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What are the renal complications of diabetes?
|
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.
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What is the treatment of diabetic nephropathy?
|
Management of nephropathy involves strict control of diabetes, angiotensin-converting enzyme inhibitors, and dialysis or renal transplantation.
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What are the screening recommendations for proteinuria in diabetics?
|
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.
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What are the cardiovascular complications of diabetes?
|
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.
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What is the lipid management of diabetes?
|
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.
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What is the management of diabetic retinopathy?
|
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.
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What is the treatment of diabetic gastroparesis?
|
Metoclopramide or erythromycin.
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|
What is the treatment of diabetic erectile dysfunction?
|
Occurs in 50% of patients after 10 years of diabetes. Treatment is sildenafil.
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What is the screening for diabetic peripheral neuropathy?
|
Podiatric examination annually. Neuropathy leads to increased injury. Diabetes is responsible for 50% of all nontraumatic amputations.
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What are the characteristics of diabetic peripheral neuropathy?
|
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.
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What are the signs of diabetic autonomic neuropathy?
|
Difficulty swallowing, delayed gastric emptying (gastroparesis), constipation, or diarrhea. Bladder dysfunction or paralysis.
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What is the treatment for peripheral neuropathy?
|
Analgesics, gabapentin, pregabalin, amitriptyline, and carbamazepine
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What is the Somogyi effect?
|
Rebound hyperglycemia in the morning because of counterregulatory hormone release after hypoglycemia at night.
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What is the dawn phenomenon?
|
Early morning rise in plasma glucose, requiring increased amounts of insulin to maintain euglycemia.
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What are the symptoms of hypoglycemia?
|
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.
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What are the causes of hypoglycemia?
|
Panhypopituitarism, adrenal insufficiency, enzyme defects, malnutrition, pregnancy, liver disease, alcohol, Popranolol, salicylates. Insulinoma, exogenous insulin, sulfonylureas, quinine, endotoxic shock, insulin receptor Ab.
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What are the clinical signs of insulinoma?
|
Insulinoma (pancreatic B-cell tumor) can cause hypoglycemia. Benign symptoms of hypoglycemia are blurred vision, headache, feelings of detachment, slurred speech, and weakness.
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How is insulinoma diagnosed?
|
Serum insulin level of >8 mg/mL in the presence of blood glucose values <40 mg/dL.
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What are the causes of factitious hyperinsulinism?
|
Administration of insulin or ingestion of Equal or oral sulfonylureas. It is common.
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What are the laboratory abnormalities in factitious hyperinsulinism?
|
Hypoglycemia, high insulin and suppressed plasma C peptide is pathognomonic of exogenous insulin. Ethanol-hypoglycemia with starvation.
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What is Cushing syndrome?
|
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
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|
What is Cushing disease?
|
Pituitary adenoma that secretes ACTH, causing hypercortisolism.
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What percentage of Cushing syndrome is caused by ACTH-producing pituitary adenomas?
|
ACTH-producing pituitary adenomas cause 40% of Cushing cases.
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|
What types of cancers can cause adrenal hyperplasia by producing ACTH?
|
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.
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What are the clinical signs of Cushing syndrome?
|
Moon face, buffalo hump, truncal obesity; HTN, weakness, osteoporosis; striae, bruises. Acne, hirsutism, oligomenorrhea. Depression, psychosis. Hyperglycemia, delayed healing, nephrolith; glaucoma, polyuria, infections.
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What are the laboratory signs of Cushing syndrome?
|
Cushing's is associated with hypokalemia and leukocytosis. Hypokalemia occurs because of the mineralocorticoid effect of steroids.
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How is Cushing syndrome diagnosed?
|
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.
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What is the 1-mg overnight dexamethasone suppression test?
|
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.
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How is the etiology of the Cushing syndrome established?
|
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.
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|
When there is a high ACTH level, how is the precise etiology of Cushing syndrome determined?
|
MRI of the pituitary for an adenoma or a CT scan of the chest looking for an ectopic focus.
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What is hyperaldosteronism?
|
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.
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What are the causes of primary hyperaldosteronism?
|
Unilateral adrenal adenoma (70%). Bilateral hyperplasia accounts for 25-30%. Excessive licorice ingestion (licorice has aldosterone-like qualities).
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How is primary hyperaldosteronism diagnosed?
|
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.
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|
What is the treatment of bilateral adrenal hyperplasia?
|
Bilateral adrenal hyperplasia is treated with spironolactone, which blocks aldosterone.
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What is Bartter syndrome?
|
Secondary hyperaldosteronism without edema or hypertension; defect in the loop of Henle; severe hypokalemic alkalosis, defect in renal conservation of sodium or chloride.
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What is congenital adrenal hyperplasia?
|
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.
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What are the common enzymatic defects associated with congenital adrenal hyperplasia?
|
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.
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|
What are the signs of congenital adrenal hyperplasia?
|
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.
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How is congenital adrenal hyperplasia diagnosed?
|
Failure to thrive, adrenal insufficiency, salt wasting, HTN. Decreased testosterone, androstenedione, dehydroepiandrosterone, 17-hydroxy-progesterone, urinary 17-ketosteroid,, pregnanetriol.
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|
What is the management of congenital adrenal hyperplasia?
|
Glucocorticoid (hydrocortisone) replacement.
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|
What are the two types of adrenal deficiency disorders?
|
Adrenal insufficiency is divided into primary adrenocorticoid deficiency (Addison disease) and secondary failure in elaboration of ACTH. Primary adrenocortical insufficiency results from adrenal hypofunction.
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What are the causes of Addison disease?
|
Caused by destruction of gland. Autoimmune destruction accounts for 80%. Destruction by surgical removal, Tb, fungal, CMV, Mycobacterium avium complex, hemorrhagic, trauma, metastatic invasion.
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What are the clinical signs of Addison disease?
|
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.
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How is primary adrenocortical insufficiency diagnosed?
|
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.
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|
What is the cosyntropin or ACTH stimulation test?
|
A cortisol level is obtained before and after administering ACTH. A normal person should show a rise in cortisol level after ACTH administration.
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|
What is the management of Addison disease?
|
Glucocorticoid, mineralocorticoid, and sodium chloride replacement.
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|
What is an adrenal crisis?
|
Fever, vomiting, abdominal pain, altered mental, vascular collapse. Previously undiagnosed adrenal insufficiency after surgery, serious infection, stress; bilateral adrenal infarction/hemorrhage, withdrawal from glucocorticoids.
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|
What is the treatment of adrenal crisis?
|
Measure cortisol level, then rapidly administer fluids and IV hydrocortisone.
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|
What is pheochromocytoma?
|
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.
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What substances are secreted by pheochromocytomas?
|
Epinephrine secretion causes tachycardia, sweating, flushing, and hypertension. Norepinephrine is secreted by all extraadrenal pheochromocytomas.
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What are the clinical signs of pheochromocytoma?
|
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.
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|
How is pheochromocytoma diagnosed?
|
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.
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|
What is the management of pheochromocytomas?
|
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.
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|
What are the causes of primary hypogonadism?
|
Primary hypogonadism (hypergonadotropic: increased LH, FSH) from Klinefelter syndrome (small testes, eunuchoid, XXY), anorchia, castration or radiotherapy, mumps, TB, leprosy, or chemotherapeutic agents.
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What are the causes of secondary hypogonadism?
|
Secondary hypogonadism (low LH, FSH) can result from hypopituitarism caused by idiopathic, tumors, hypothalamic lesions, Kallmann syndrome (hypergonadotrophic hypogonadism, decreased smell).
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|
What are the clinical signs of prepubertal hypogonadism?
|
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.
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|
What are the laboratory abnormalities in hypogonadism?
|
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.
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|
|
What are the causes of postpubertal hypogonadism?
|
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.
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|
What is Klinefelter syndrome?
|
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.
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|
What are the laboratory abnormalities in Klinefelter syndrome?
|
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.
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|
|
What are the basic synovial fluid tests?
|
Cell count, crystals, cultures, and Gram stain.
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|
|
What are the synovial fluid cell count in osteoarthritis?
|
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.
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|
What are antinuclear antibodies?
|
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.
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|
How is the ANA test performed?
|
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.
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|
|
What subsets of ANAs are associated with systemic lupus erythematosus?
|
Anti ds-DNA and anti-SM antibodies are found in patients with SLE; anti-histone antibodies are found in patients with drug-induced lupus.
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|
What is the significance of a positive ANA test?
|
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.
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|
What are rheumatoid factors?
|
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.
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|
What is the significance of a positive cyclic citrullinated peptide?
|
Cyclic citrullinated peptide is associated with rheumatoid arthritis.
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|
|
What are antineutrophil cytoplasmic antibodies?
|
ANCAs are antibodies directed against cytoplasm of neutrophils in Wegener granulomatosis. Perinuclear ANCA is found in polyarteritis nodosa and Churg-Strauss syndrome.
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|
What is antiphospholipid antibody syndrome?
|
Hypercoagulable state with Ab against phospholipids or cardiolipins (lupus anticoagulant or anticardiolipin antibodies). Elevated PTT, false-positive VDRL.
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|
|
What is the presentation of antiphospholipid antibody syndrome?
|
Presents with spontaneous abortions or thromboembolism. If two first-trimester spontaneous abortions occur, antiphosolipid antibodies should be checked.
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|
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?
|
Rheumatoid arthritis.
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|
|
What is rheumatoid arthritis?
|
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.
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|
What is the diagnostic criteria for rheumatoid arthritis?
|
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.
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|
|
Which joints are never involved in rheumatoid arthritis?
|
Distal interphalangeal joints and joints of the lower back.
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|
|
What are the systemic symptoms of rheumatoid arthritis?
|
Two-thirds of the patients present with fatigue, anorexia, weight loss, generalized weakness before the onset of the arthritis.
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|
|
What are the extraarticular manifestations of rheumatoid arthritis?
|
Damage to the ligaments and tendons. Radial deviation of the wrist with ulnar deviation of the digits. Boutonniere deformity. Swan-neck deformity. Rheumatoid nodules.
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|
|
What are the laboratory findings in rheumatoid arthritis?
|
Rheumatoid factor, anemia, increased ESR, X-rays erosions.
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|
|
What is the initial treatment for rheumatoid arthritis?
|
Nonsteroidal antiinflammatory drugs (NSAIDs) have fewer side effects than aspirin.
|
|
|
What is the mechanism of selective COX-2 inhibitors?
|
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.
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|
|
What is the mechanism of action of nonselective NSAIDS?
|
Nonselective of NSAIDs block both COX-2 and COX-1, which can lead to increased risk for gastrointestinal side effects (bleeding).
|
|
|
What is the beneficial effect of selective NSAID COX-2 inhibitors?
|
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.
|
|
|
What is the treatment of rheumatoid arthritis that does not respond to NSAIDs?
|
Glucocorticoids. Disease-modifying agents: antimalarials, gold, sulfasalazine, methotrexate, and tumor necrosis factor receptor inhibitors: infliximab (Remicade), adalimumab (Humira), etanercept (Enbrel)
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|
|
What is atlantoaxial subluxation?
|
Occurs in rheumatoid arthritis when there is excessive movement between atlas (Cl) and axis (C2). Neck pain, C2 radicular pain (hands), myelopathy, paraplegia, quadriplegia.
|
|
|
What is a ruptured Baker cyst?
|
Extension of inflamed synovium into the popliteal space; swollen, painful calf.
|
|
|
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?
|
Systemic lupus erythematosus.
|
|
|
What is systemic lupus erythematosus?
|
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.
|
|
|
What is the diagnostic criteria for systemic lupus erythematosus?
|
4 required: malar/discoid rash, photosensitivity, oral ulcers, arthritis, serositis, renal; neurologic (seizures, psychosis); hematologic (hemolysis, leukopenia); immunologic (ANA).
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|
|
What are the skin manifestations of systemic lupus erythematosus?
|
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.
|
|
|
What are the joint manifestations of systemic lupus erythematosus?
|
Arthritis is systemic, non-erosive of wrists, MCPs, PIPs.
|
|
|
What are the psychiatric manifestations of systemic lupus erythematosus?
|
Change in personality and psychosis with CNS lupus. Libman-Sacks endocarditis is noninfectious endocarditis that is rare in lupus
|
|
|
What are the laboratory findings in lupus?
|
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.
|
|
|
What is the treatment for systemic lupus?
|
NSAIDs for arthritis, pleurisy. Corticosteroid for rashes. Hydroxychloroquine and corticosteroids for arthritis. Cytotoxics (azathioprine, cyclophosphamide) for nephritis, carditis, pleuritis. Sunscreen.
|
|
|
What drugs cause drug-induced lupus?
|
Hydralazine, isoniazid, procainamide, quinidine.
|
|
|
What is the presentation of drug-induced lupus?
|
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.
|
|
|
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?
|
Scleroderma.
|
|
|
What is systemic sclerosis?
|
Thickening of the skin caused by accumulation of connective tissue; involvement of GI, lungs, kidneys. All scleroderma patients have Raynaud phenomenon.
|
|
|
What are the gastrointestinal signs of systemic sclerosis?
|
Esophageal dysmotility and achalasia, hypomotility of the small intestine with bacterial overgrowth and malabsorption, and dilatation of the large intestine with diverticula.
|
|
|
What are the pulmonary manifestations of scleroderma?
|
Pulmonary fibrosis with restrictive lung disease and cor pulmonale.
|
|
|
What are the renal manifestations of scleroderma?
|
Renal crisis in which malignant hypertension acute renal failure. Treated with angiotensin-converting enzyme inhibitors.
|
|
|
What is limited scleroderma (CREST syndrome)?
|
Variant of scleroderma: Calcinosis, Raynaud, Esophageal dysfunction, Sclerodactyly, Telangiectasias. Calcium deposits in fingers, knees, elbows, ulcerate. Sclerodactyly is skin thickening of fingers, toes.
|
|
|
What are the laboratory findings in limited scleroderma?
|
Limited scleroderma has positive ANA test. Antibodies to Sc-70 are negative in limited scleroderma and positive in diffuse scleroderma.
|
|
|
What is Raynaud phenomenon?
|
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.
|
|
|
What is the treatment for systemic sclerosis?
|
No cure. D-penicillamine may be used. Raynaud phenomenon: use calcium-channel blockers; for hypertension use angiotensin-converting enzyme inhibitors.
|
|
|
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?
|
Sjögren syndrome.
|
|
|
What is Sjögren syndrome?
|
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.
|
|
|
What is the presentation of Sjögren syndrome?
|
Itchy eyes, sandy feeling under their eyes destruction of the corneal epithelium (keratoconjunctivitis sicca), and dysphagia.
|
|
|
What are diagnostic tests for Sjögren syndrome?
|
Schirmer's test shows decreased tear production. ANA positive; anti-Ro (SSA) and anti-La (SSB) are positive. Treatment is artificial tears.
|
|
|
Which autoimmune diseases have arthritis plus multiple organ involvement?
|
SLE, systemic sclerosis (scleroderma), and Sjögren syndrome.
|
|
|
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?
|
Ankylosing spondylitis.
|
|
|
What allele is associated with the spondyloarthropathies?
|
B-27 allele.
|
|
|
What is ankylosing spondylitis?
|
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.
|
|
|
What is the presentation of ankylosing spondylitis?
|
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.
|
|
|
What are the x-ray abnormalities in ankylosing spondylitis?
|
Sacroiliitis and fusing of the sacroiliac joint. Bamboo spine and squaring of the vertebral bodies.
|
|
|
What is the treatment for ankylosing spondylitis?
|
NSAIDs, physical therapy, exercise. TNF blockers (infliximab, adalimumab, etanercept).
|
|
|
What is reactive arthritis?
|
Seronegative arthropathy after infection, non-gonococcal urethritis. Keratoderma blennorrhagica (waxy, palms/soles), circinate balanitis, oral/genital ulcers, conjunctivitis, arthritis. Campylobacter, Salmonella.
|
|
|
What is the treatment for reactive arthritis?
|
Severe form of reactive arthritis in HIV patients improves with antiretroviral medications. NSAIDS, tumor necrosis factor blockers.
|
|
|
What is psoriatic arthritis?
|
Arthritis involves the DIP joints and associated with psoriatic nail disease (pitting of the nails); sausage-shaped digit.
|
|
|
What is enteropathic arthropathy?
|
Joint arthropathy with ulcerative colitis or Crohn disease; associated with pyoderma gangrenosum and erythema nodosum.
|
|
|
A 66-year-old man with knee pain and pain in distal interphalangeal joints. Knee crepitations. What is the diagnosis?
|
Osteoarthritis
|
|
|
What is osteoarthritis?
|
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.
|
|
|
What are the major risk factors for osteoarthritis?
|
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.
|
|
|
What is the presentation of osteoarthritis?
|
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.
|
|
|
What X-ray findings are associated with osteoarthritis?
|
Osteophytes and unequal joint space PIP osteophytes are called Bouchard's nodes, in the DIP are called Heberden's nodes.
|
|
|
What is the treatment of osteoarthritis?
|
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).
|
|
|
What are the crystal-induced arthropathies?
|
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.
|
|
|
What is gout?
|
Gout affects middle-aged men and presents with acute monoarthritis. Deposition of urate crystals in connective tissue (tophi) and kidneys.
|
|
|
What is the presentation of acute gout?
|
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.
|
|
|
What are the factors that can precipitate gout?
|
Excessive alcohol, trauma, surgery, infection, steroid withdrawal, hydrochlorothiazide, furosemide; pyrazinamide and ethambutol, and serious medical illnesses.
|
|
|
How is gout diagnosed?
|
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.
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What is the treatment of acute gouty arthritis?
|
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.
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|
What is the treatment of recurrent gouty attacks?
|
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.
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What is pseudogout?
|
Calcium pyrophosphate crystal deposition is more common in the elderly population and preexisting joint damage. Hyperparathyroidism, hemochromatosis, hypophosphatemia, hypomagnesemia.
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|
What are the clinical signs of pseudogout?
|
The knee is the most commonly affected joint; other joints are the wrist, shoulder, and ankle.
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How is pseudogout diagnosed?
|
Rhomboid, positive birefringent crystals on synovial fluid evaluation. Linear radiodense deposits in joint menisci or articular cartilage (chondrocalcinosis).
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What is the treatment for calcium pyrophosphate crystal deposition disease?
|
NSAIDS, colchicine, corticosteroid. Prevent frequent recurrences with low doses of colchicine.
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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?
|
Perform arthrocentesis
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|
What is the most common cause of infectious arthritis in patients younger than 40 years old?
|
Gonorrhea, which accounts for 70% of episodes in patients younger than 40 years old.
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|
What is the most common cause of infectious arthritis in older patients?
|
Staphylococcus aureus is most common cause of infectious arthritis and occurs in preexisting joint destruction from other rheumatic diseases. RA is highest risk.
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|
What are the synovial fluid findings in gonococcal infectious arthritis?
|
Infected joints with gonococci will not have positive cultures, and the Gram stain will be negative.
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What treatment should be prescribed for a young woman with acute monoarticular arthritis with >50,000 WBCs in synovial fluid without crystals?
|
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.
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What treatment should be ordered for an elderly man with RA and acute monoarticular arthritis and >50,000 WBCS in synovial fluid?
|
An elderly man with infectious arthritis should be treated with IV nafcillin or vancomycin.
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|
What is Wegener granulomatosis?
|
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%.
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|
How is Wegener granulomatosis diagnosed?
|
Associated with antineutrophil cytoplasmic antibodies (C-ANCA). Confirm diagnosis by biopsy of an involved organ (nasal septum), vasculitis and granulomas.
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|
What is the treatment of Wegener granulomatosis?
|
Glucocorticoid and immunosuppressive agent (cyclophosphamide).
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|
What is polyarteritis nodosa?
|
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.
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|
What is the presentation of polyarteritis nodosa?
|
Peripheral neuropathies. abdominal pain and gastrointestinal bleeding. Biopsy of skin, symptomatic nerves, or muscles medium-size arteritis.
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|
What is the treatment of polyarteritis nodosa?
|
Corticosteroids, immunosuppressive drugs (cyclophosphamide).
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|
What is Churg-Strauss syndrome?
|
Vasculitis can involve any organ; asthma, eosinophilia, lung involvement.
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|
What is the presentation of Churg-Strauss syndrome?
|
Middle aged individual with new-onset asthma, mononeuropathy, transient pulmonary infiltrates, paranasal sinus abnormalities, nasal polyps, allergic rhinitis.
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|
What are the biopsy findings in Churg-Strauss syndrome?
|
Biopsy: medium arteritis. Treatment is prednisone and cytotoxic agent.
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|
What is temporal arteritis?
|
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.
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|
What is the presentation of temporal arteritis?
|
Headache, pain in temples. Scalp tenderness, jaw claudication, decreased vision, tongue numbness, sudden loss of vision. 25% also have polymyalgia rheumatica.
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|
How is temporal arteritis diagnosed?
|
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).
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|
A 73-year-old woman with new right-sided headache, fever, decreased vision. What is the first step?
|
Check the ESR; if elevated, start prednisone 60 mg daily.
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|
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?
|
Dermatomyositis
|
|
|
What are the inflammatory myopathies?
|
Inflammatory muscle diseases with progressive muscle weakness. Polymyositis, dermatomyositis, and inclusion body myositis.
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|
|
What are the clinical signs of inflammatory myopathies?
|
Proximal muscle weakness: lifting objects, combing hair, rising from chair. Ocular muscles never involved, which differentiates inflammatory myopathies from myasthenia.
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|
What is the presentation of dermatomyositis?
|
Dermatomyositis will have weakness with heliotrope rash, which is a purple-lilac discoloration of the face, eyelids, and sun-exposed areas of body.
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|
What are the laboratory findings in inflammatory myopathies?
|
Inflammatory destruction of muscles causes an elevation of the muscle enzymes creatine kinase and aldolase. EMG shows of myopathic potentials; confirmed by biopsy.
|
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|
What is the treatment for polymyositis and dermatomyositis?
|
Steroids are useful in polymyositis and dermatomyositis.
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|
|
What is achalasia?
|
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.
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|
|
What is the presentation of achalasia?
|
Achalasia presents with progressive dysphagia to both solids and liquids; regurgitation.
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|
How is achalasia diagnosed?
|
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.
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|
A 65-year-old man with difficulty swallowing solids, weight loss. reflux esophagitis, smoking, enlarged left supraclavicular lymph node. What is the diagnosis?
|
Esophageal cancer.
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|
|
What are the causes of esophageal cancer?
|
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.
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|
|
What is the presentation of esophageal cancer?
|
Progressive dysphagia first for solid food, then liquids, weight loss. Halitosis, regurgitation, hoarseness, and hypercalcemia.
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|
|
How is esophageal cancer diagnosed?
|
Barium swallow first; endoscopy is mandatory for biopsy. CT scan assesses local spread; bronchoscopy detects spread into the bronchi. Endoscopic ultrasound for staging.
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|
|
What is the presentation of esophageal spasm?
|
Intermittent chest pain, dysphagia, with no relationship to exertion or eating. The pain is precipitated by drinking cold liquids.
|
|
|
How is esophageal spasm diagnosed?
|
Barium studies show a "corkscrew" pattern. The most accurate test is manometric studies.
|
|
|
What is the treatment of esophageal spasm?
|
Nifedipine and nitrates.
|
|
|
What is Schatzki's ring?
|
Schatzki's rings are thin, epithelial membranes; intermittent dysphagia; painless. More distal and located at the squamocolumnar junction proximal to the lower esophageal sphincter.
|
|
|
What is Plummer-Vinson syndrome?
|
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.
|
|
|
How is Plummer-Vinson syndrome diagnosed?
|
Diagnosed with a barium swallow.
|
|
|
What is the treatment of Plummer-Vinson syndrome?
|
May respond to treatment of iron deficiency. Dilation procedures are used.
|
|
|
What is the most common infectious cause of esophagitis?
|
Candida albicans. HIV positive with a CD4 <200/mm3. Diabetes mellitus is the second most common risk. Herpes simplex, cytomegalovirus, aphthous ulcers.
|
|
|
What is the treatment of esophagitis?
|
If the patient is HIV positive, empiric treatment is with fluconazole.
|
|
|
What medications are associated with esophagitis?
|
Pills that cause esophagitis are alendronate, quinine, risedronate, vitamin C, potassium chloride, doxycycline, NSAIDs, and iron sulfate.
|
|
|
What is a Zenker diverticulum?
|
Outpocketing of posterior pharynx. Older patients have bad breath and difficulty initiating swallowing. Repeated clearing of throat; regurgitation of food eaten several days ago.
|
|
|
How is Zenker diverticulum diagnosed?
|
The diagnosis is made by barium studies. Treated with surgical resection.
|
|
|
What is Mallory-Weiss syndrome?
|
Tear of the lower esophagus caused by retching and vomiting. Painless upper gastrointestinal bleeding. Melena or hematemesis. Diagnosed by upper endoscopy.
|
|
|
What is the treatment for Mallory-Weiss tears?
|
Resolve spontaneously. Injection of the tear with epinephrine or cauterization.
|
|
|
What are the causes of epigastric pain?
|
Ulcer disease, pancreatitis, gastroesophageal reflux disease, gastritis, and gastric cancer.
|
|
|
What organism causes gastric ulcers, duodenal ulcers, and gastritis?
|
Helicobacter pylori is most strongly associated with the development of duodenal ulcers, gastric ulcers, and gastritis.
|
|
|
What is the most common cause of epigastric tenderness?
|
Pancreatitis is the most common cause for epigastric tenderness and pain. Ulcer disease is associated with epigastric tenderness in <20% of patients.
|
|
|
What is the most common cause of epigastric pain?
|
The most common etiology of epigastric pain is nonulcer dyspepsia, a functional disorder of persistent pain with normal tests.
|
|
|
How is Helicobacter pylori disease diagnosed?
|
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.
|
|
|
When is endoscopy indicated for patients with ulcer disease?
|
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.
|
|
|
What is the treatment of Helicobacter pylori disease?
|
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.
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|
|
What is the cause of gastroesophageal reflux disease?
|
Abnormal flow of the acid gastric contents backward from the stomach up into the esophagus through the lower esophageal sphincter.
|
|
|
What factors decrease tone of the lower esophageal sphincter?
|
Nicotine, alcohol, caffeine, peppermint, chocolate, anticholinergics, calcium-channel blocking agents, and nitrates.
|
|
|
What is the clinical presentation of GERD?
|
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.
|
|
|
What is the treatment for GERD?
|
PP-inhibitors: omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole increase pH. Avoid nicotine, alcohol, caffeine, chocolate, late meals. Elevate bed. 5% require Nissen fundoplication.
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|
|
What is Barrett esophagus?
|
Complication of long-standing reflux disease where epithelium of lower esophagus changes from normal squamous epithelium to columnar epithelium. Treatment is proton-pump inhibitors.
|
|
|
What are the causes of peptic ulcer disease?
|
Ulcers are caused by NSAIDs, H pylori, stomach CA, Zollinger-Ellison, Crohn, burns, head trauma, mechanical ventilation. Ulcers not caused by smoking, alcohol, steroids.
|
|
|
What is the pathophysiology of peptic ulcer disease?
|
Prostaglandins stimulate mucous production that forms a protective barrier. Prostaglandins are inhibited by NSAIDs. Parietal cells produce acid.
|
|
|
What hormones stimulate acid production?
|
Stimulants of acid production are gastrin, acetylcholine, histamine. Histamine is released by stomach cells and stimulates acid release.
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|
|
What is the mechanism of action of H2 blockers?
|
H2 blockers, such as cimetidine, famotidine, and ranitidine, inhibit acid release by blocking histamine effect on parietal cells.
|
|
|
What is Zollinger-Ellison syndrome?
|
Zollinger-Ellison syndrome is the excessive production and release of gastrin from G cells.
|
|
|
What is the most common cause of ulcer disease?
|
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.
|
|
|
How is ulcer disease diagnosed?
|
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.
|
|
|
How is H. pylori disease diagnosed?
|
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.
|
|
|
What is the advantage of breath testing for H pylori over serology?
|
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.
|
|
|
What is the treatment of H pylori ulcer disease?
|
PPI, clarithromycin and amoxicillin. Omeprazole, lansoprazole, pantoprazole, rabeprazole, and esomeprazole are all equal. PPI/clarithromycin/amoxicillin is >90% effective. Therapy 10-14 d.
|
|
|
What is the approach to patients who fail therapy for H pylori?
|
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.
|
|
|
What is gastritis?
|
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.
|
|
|
What is the presentation of gastritis?
|
Most patients with gastritis present with asymptomatic bleeding. Other patients have epigastric pain, nausea and vomiting, hematemesis or melena.
|
|
|
How is gastritis diagnosed?
|
The diagnosis of H. pylori is based on either serology, urea breath testing, stool antigen testing, or biopsy with histology.
|
|
|
When should endoscopy be performed in patients with gastritis?
|
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.
|
|
|
How is gastritis treated?
|
PPI combined with clarithromycin and amoxicillin. Omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole are equal. Duration of therapy is 10 to 14 days.
|
|
|
How is pernicious anemia diagnosed?
|
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.
|
|
|
What is Zollinger-Ellison syndrome?
|
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.
|
|
|
What is the presentation of Zollinger-Ellison syndrome?
|
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.
|
|
|
How is Zollinger-Ellison syndrome diagnosed?
|
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.
|
|
|
What is gastroparesis?
|
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.
|
|
|
What is the treatment for gastroparesis?
|
Increase motility of the stomach with erythromycin or metoclopramide.
|
|
|
What are the symptoms of inflammatory bowel disease?
|
Fever, diarrhea, weight loss, and abdominal pain and bleeding. Episcleritis, scleritis and iritis, sclerosing cholangitis, joint pains, and pyoderma gangrenosum or erythema nodosum.
|
|
|
What are skip lesions in inflammatory bowel disease?
|
"Skip lesions" are areas of normal tissue in between the areas of disease; associated with Crohn disease.
|
|
|
What are the characteristics of ulcerative colitis?
|
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.
|
|
|
Which type of inflammatory bowel disease can lead to colon cancer?
|
Both forms of IBD can lead to colon cancer after 8 to 10 years of involvement of the colon.
|
|
|
What are the complications of Crohn disease?
|
Complications of Crohn disease are calcium oxalate kidney stones, diarrhea, and cholesterol gallstones.
|
|
|
How is inflammatory bowel disease diagnosed?
|
Colonoscopy. Antineutrophil cytoplasmic antibody is associated with UC.
|
|
|
What laboratory abnormalities are associated with Crohn disease?
|
B12, calcium, vitamin K, iron deficiencies because malabsorption. Anti-saccharomyces cerevisiae antibodies. PT increased because vitamin K malabsorption. Kidney stones because increased absorption oxalate.
|
|
|
What is the treatment of inflammatory bowel disease?
|
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.
|
|
|
What is the treatment of exacerbations of inflammatory bowel disease?
|
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.
|
|
|
What is the treatment of Crohn perianal disease?
|
Ciprofloxacin and metronidazole are used for CD with perianal disease. Infliximab is used for CD fistulae or refractory disease.
|
|
|
What is the role of surgery in inflammatory bowel disease?
|
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.
|
|
|
What is the laboratory evaluation of inflammatory bowel disease?
|
Stool should be evaluated for fecal leukocytes, culture, and ova and parasite examination. Clostridium difficile toxin and stool Giardia-antigen testing.
|
|
|
What are the most common causes of infectious diarrhea?
|
Campylobacter and Salmonella.
|
|
|
What is the presentation of Bacillus cereus diarrhea?
|
Ingestion of refried Chinese food. Short incubation period (1-6 hours). Vomiting is prominent. Blood is never present.
|
|
|
What type of diarrhea is associated with reactive arthritis and Guillain-Barre syndrome?
|
Campylobacter
|
|
|
What type of diarrhea occurs in HIV-positive patients with <100/mm3 CD4 cells?
|
Cryptosporidium and Isospora.
|
|
|
What type of food is associated with E. coli 0157:H7?
|
Hamburger meat. Shiga toxin may cause hemolytic uremic syndrome when organism dies; therefore, antibiotics are contraindicated. Platelet transfusions exacerbate the disease.
|
|
|
What type of ingestion is associated with Giardia diarrhea?
|
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.
|
|
|
What type if diarrhea is associated with ingestion of chicken and eggs, dairy products?
|
Salmonella
|
|
|
What type of ingestion is associated with scombroid poisoning?
|
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.
|
|
|
What is the presentation of Yersinia diarrhea?
|
Yersinia can mimic appendicitis. Also common in people with iron overload, e.g., hemochromatosis.
|
|
|
What type of ingestion is associated with Vibrio parahaemolyticus?
|
Ingestion of raw shellfish, such as mussels, oysters, and clams.
|
|
|
What type of ingestion is associated with Vibrio vulnificus?
|
Raw shellfish; high incidence in people with underlying liver disease or disorders of iron metabolism. Associated with the development of skin bullae.
|
|
|
What population is predisposed to viral diarrhea?
|
Children in day-care centers; absence of blood and white cells
|
|
|
Ingestion of what type of foods is associated with Staphylococcus aureus gastroenteritis?
|
Ingestion of dairy products, eggs, salads. Short incubation period (1-6 hours); nausea/vomiting predominate; rarely diarrhea.
|
|
|
Ingestion of what type of food is associated with ciguatera-toxin?
|
2-6 hours after ingestion of grouper fish, red snapper, and barracuda. Neurological symptoms include paresthesia, weakness, and reversal of heat and cold.
|
|
|
How is acute diarrhea diagnosed?
|
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.
|
|
|
What are the invasive organisms that cause infectious diarrhea?
|
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.
|
|
|
How is cryptosporidiosis diagnosed?
|
Cryptosporidiosis is diagnosed with a modified acid-fast test.
|
|
|
How is giardia diagnosed?
|
Giardia is diagnosed with an ELISA stool antigen test. 90% sensitivity.
|
|
|
What is the treatment of acute infectious diarrhea?
|
Antibiotics are used if there is abdominal pain, blood in the stool, and fever. Empiric therapy for infectious diarrhea is ciprofloxacin.
|
|
|
What is the treatment for scombroid poisoning?
|
Scombroid poisoning is treated with diphenhydramine.
|
|
|
What is the treatment of Giardia?
|
Giardia is treated with metronidazole. A newer agent for Giardia is tinidazole, which is effective in a single dose.
|
|
|
What is the treatment of Cryptosporidiosis?
|
Cryptosporidiosis is treated with paromomycin and raise the CD4 count to >100/mm3 with antiretrovirals.
|
|
|
What is antibiotic-associated diarrhea?
|
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.
|
|
|
What is the treatment for antibiotic-associated diarrhea?
|
Metronidazole. Oral vancomycin only if not resolve with metronidazole.
|
|
|
What is the presentation of lactose intolerance?
|
Diarrhea with gas and bloating; never has blood or leukocytes. Weight loss does not occur. High prevalence. Increased stool osmolality and increased osmolar gap.
|
|
|
How is lactase deficiency diagnosed?
|
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.
|
|
|
What is irritable bowel syndrome?
|
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.
|
|
|
How is irritable bowel syndrome diagnosed?
|
No specific diagnostic test. Exclude lactose intolerance, inflammatory bowel disease, celiac disease, carcinoid, Giardia infection, and anatomic defects of the bowel.
|
|
|
What is the Rome criteria for irritable bowel syndrome?
|
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.
|
|
|
What is the treatment for irritable bowel syndrome?
|
High-fiber, loperamide, diphenoxylate. Antispasmodics: hyoscyamine, dicyclomine, belladonna. Tricyclics. Tegaserod in constipation-predominant; may cause diarrhea. Alosetron reduces diarrhea.
|
|
|
What is carcinoid syndrome?
|
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.
|
|
|
What is the presentation of carcinoid syndrome?
|
Diarrhea, flushing, tachycardia, hypotension. Tricuspid insufficiency and pulmonic stenosis.
|
|
|
How is carcinoid syndrome diagnosed?
|
Urinary 5-hydroxyindolacetic acid level (5-HIAA).
|
|
|
What is the treatment of carcinoid syndrome?
|
Control diarrhea with octreotide (somatostatin analog). Very few carcinoids are localized enough for surgical resection.
|
|
|
What are causes of fat malabsorption?
|
Celiac disease and chronic pancreatitis; tropical sprue and Whipple disease are extremely rare causes.
|
|
|
What is the presentation of fat malabsorption?
|
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.
|
|
|
What type of malabsorption causes Vitamin B12 deficiency?
|
Vitamin B12 malabsorption occurs from damage or loss of the mucosal surface of the terminal ileum from celiac disease.
|
|
|
What is the most common presentation of celiac disease?
|
Iron deficiency anemia. Dermatitis herpetiformis is a vesicular skin rash on the extensor surfaces of the body in 10%.
|
|
|
What is the most common cause of fat malabsorption?
|
Celiac disease is the most likely cause of fat malabsorption because it is the most common.
|
|
|
What is the presentation of malabsorption caused by chronic pancreatitis?
|
Patients with chronic pancreatitis will give a history steatorrhea with repeated episodes of pancreatitis from alcohol or gallstones.
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What type of malabsorption is associated with travel to a tropical country?
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Tropical sprue is suspected when there is a history of being in a tropical country.
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What is the presentation of Whipple disease?
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Whipple disease is the rarest cause of fat malabsorption; dementia (10%), arthralgias (80%), and ophthalmoplegia. Caused by the bacterium Tropheryma whipplei.
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How is celiac disease diagnosed?
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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.
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What is the presentation of chronic pancreatitis?
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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.
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How is tropical sprue diagnosed?
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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.
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What is the treatment of malabsorption?
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Chronic pancreatitis can be managed by orally replacing, amylase, lipase, trypsin. Tropical sprue is treated with sulfamethoxazole/trimethoprim or doxycycline.
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What is the treatment of Whipple disease?
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Whipple disease is treated with sulfamethoxazole/trimethoprim or doxycycline or ceftriaxone for 1 year.
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What is diverticulosis?
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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.
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What is the presentation of diverticulosis?
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Asymptomatic. Left lower quadrant abdominal pain that can be colicky in nature.
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How is diverticulosis diagnosed?
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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.
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What is the treatment for diverticulosis?
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Dietary fiber in bran, or bulking agents, such as psyllium husks.
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What is the presentation of diverticulitis?
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Fever, tenderness, pain, and elevation of white blood cell count.
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How is diverticulitis diagnosed?
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CT scanning. Barium studies and endoscopy are relatively contraindicated in diverticulitis.
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What is the treatment for diverticulitis?
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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.
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What are the causes of constipation?
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Lack of fiber; calcium-channel blockers, oral ferrous sulfate, hypothyroidism, opiate analgesics, anticholinergics, and tricyclic antidepressants.
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What is the lifetime risk of colon cancer?
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>6%. Most cases occur sporadically. Diets that are high in red meat, fat and smoking increase the risk.
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What is the presentation of colon cancer?
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Heme-positive, brown stool; chronic anemia when the cancer in right side of colon. Left-sided lesions cause obstruction and decreased stool caliber.
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What type of cancer is associated with endocarditis caused by Streptococcus bovis?
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Colon cancer is associated with endocarditis by Streptococcus bovis and Clostridium septicum.
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What is the treatment for colon cancer?
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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.
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What is the screening for colon cancer?
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Annual fecal occult blood testing, colonoscopy every 10 years, and sigmoidoscopy every 5 years. Screening should occur after the age of 50 years.
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What are the causes of a false-positive stool guaiac test?
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False-positive stool guaiac tests can be caused by aspirin, NSAIDs, red meat, and poultry. False-negative tests can be caused by vitamin C.
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What is hereditary polyposis colorectal cancer syndrome?
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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.
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What is familial adenomatous polyposis?
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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.
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What is the colon cancer risk in juvenile polyposis syndrome?
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Juvenile polyposis syndrome has 10% risk of colon cancer. Hamartomas have very little risk of developing into cancer.
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What is Gardner syndrome?
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Gardner syndrome is colon cancer with multiple, osteomas, lipomas, cysts, and fibrosarcomas. The osteomas have predilection for the mandible.
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What is Peutz-Jeghers syndrome?
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Hamartomatous polyps in the large and small intestine with hyperpigmented spots. Melanotic spots on lips, buccal, skin. Risk of cancer increased. Intussusception, obstruction.
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What is the usual outcome of gastrointestinal bleeding?
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80% of cases of gastrointestinal bleeding will resolve spontaneously with supportive management, irrespective of etiology.
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What is the initial management of gastrointestinal bleeding?
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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.
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What medications should be given to patients with gastrointestinal bleeding?
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Patients with gastritis or ulcer disease should be treated with PPIs empirically. H2 blockers have no efficacy in acute gastrointestinal bleeding.
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What medication reduces portal hypertension in patients with cirrhosis of the liver and gastrointestinal bleeding?
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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.
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What are the indications for transfusion in acute bleeding?
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Hematocrit should be maintained >30% in older patients or CAD. Younger patients do not need to be transfused, unless their hematocrit is <20%.
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What is the treatment of bleeding esophageal varices?
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Octreotide to lower portal pressure. If ineffective, endoscopy to place bands. If banding is not effective, then transjugular intrahepatic portosystemic shunting.
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What is transjugular intrahepatic portosystemic shunting?
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Creates shunt between the systemic circulation of hepatic vein and portal circulation of portal vein.
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What is the primary complication of TIPS?
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Complication of transjugular intrahepatic portosystemic shunting is worsening of encephalopathy.
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What are the indications for a Blakemore tube?
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A Blakemore tube tamponades the site of bleeding in the stomach or esophagus; rarely used and is only a temporary bridge to surgery.
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What medication reduces risk of bleeding in portal hypertension?
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Propranolol is a nonselective beta-blocker that used in the long-term management of portal hypertension to decrease the frequency of bleeding.
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What are the most common causes of upper gastrointestinal bleeding?
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Ulcers, gastritis, Mallory-Weiss, esophagitis, gastric cancer. Variceal bleeding is common in portal hypertension from cirrhosis.
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What is the anatomic definition of upper gastrointestinal bleeding?
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Upper gastrointestinal bleeding is defined as bleeding proximal to the ligament of Treitz.
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What are the causes of lower gastrointestinal bleeding?
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Diverticulosis, angiodysplasia, hemorrhoids, cancer, and inflammatory bowel disease.
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What is the clinical presentation of lower gastrointestinal bleeding?
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Red blood in stools; upper gastrointestinal bleeding presents with black stool or melena.
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What degree of blood loss is indicated by the finding of orthostasis?
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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.
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If the resting pulse is >100 bpm, what amount of blood loss has occurred?
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Pulse above 100/min or a systolic blood pressure under 100 indicates >30% blood loss.
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How is lower gastrointestinal bleeding diagnosed?
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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.
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What are the causes of acute pancreatitis?
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Majority from alcoholism/gallstones. Pentamidine, didanosine, azathioprine, sulfas (sulfamethoxazole/trimethoprim thiazides). Hypercalcemia, hypertriglyceridemia. ERCP, trauma, mumps.
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What is the pathophysiology of pancreatitis?
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Premature activation of trypsinogen into trypsin while in the pancreas. Autodigestion of the pancreas.
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What is the clinical presentation of acute pancreatitis?
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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.
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How is acute pancreatitis diagnosed?
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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.
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What test determines the severity of pancreatitis?
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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
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What are the signs of severe necrotizing pancreatitis?
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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.
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What are the complications of pancreatitis?
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Ascites (high in amylase); pleural effusion (transudate, amylase); splenic vein thrombosis.
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What is the treatment of pancreatitis?
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Intravenous fluids, bowel rest, and pain medication. ERCP removes stone in the pancreatic duct or and to dilate a stricture.
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What as the management of pancreatic necrosis?
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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.
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What is the management of pancreatic pseudocysts?
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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.
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What is the pathophysiology of cirrhosis of the liver?
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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.
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What are the causes of cirrhosis of the liver?
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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.
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What are the signs of hepatic cirrhosis?
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Esophageal varices, ascites, edema; spider angiomata, palmar erythema, asterixis, encephalopathy, jaundice, low albumin. PT prolonged because of inability to make clotting factors.
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What is spontaneous bacterial peritonitis?
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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.
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What is the treatment of spontaneous bacterial peritonitis?
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Cefotaxime and ceftriaxone are the drugs of choice for SBP and albumin infusion decreases risk of hepatorenal syndrome.
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What is the serum-ascites albumin gradient?
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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.
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What is the treatment of cirrhotic edema?
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Edema and fluid overload in third spaces, such as ascites, are managed with spironolactone.
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What is the treatment of cirrhotic portal hypertension?
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Portal hypertension and varices are managed with propranolol to prevent bleeding. Encephalopathy is managed with neomycin or lactulose. Vitamin K is not effective.
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What is primary biliary cirrhosis?
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Idiopathic autoimmune disorder in middle-aged women. Bilirubin levels do not elevate until 5 years. Association with Sjögren syndrome, rheumatoid arthritis, and scleroderma.
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What is the presentation of primary biliary cirrhosis?
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Fatigue, pruritus. Asymptomatic with an elevated alkaline phos. Osteoporosis. Transaminases normal. GGTP, IgM elevated. Antimitochondrial Ab specific. Biopsy diagnostic.
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What is the treatment for primary biliary cirrhosis?
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Bile acid-binding medication, such as ursodeoxycholic acid and cholestyramine. Ultraviolet light. Liver transplant.
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What is the presentation of primary sclerosing cholangitis?
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Fatigue, pruritus; increased alkaline phos. Idiopathic disorder of biliary system associated more often ulcerative colitis, also with Crohn. Cancer of biliary system in 15%.
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How is primary sclerosing cholangitis diagnosed?
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Elevated alkaline phosphatase; the antimitochondrial antibody test is negative. The most specific test for primary sclerosing cholangitis is an ERCP or transhepatic cholangiogram.
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What is the treatment for primary sclerosing cholangitis?
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Bile acid-binding resins. Liver transplant.
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What is hemochromatosis?
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Common genetic disease of overabsorption of iron in duodenum. Hepatic inflammation, fibrosis, cirrhosis. Hepatocellular CA in 20%. Restrictive cardiomyopathy 15%. Arthralgias, skin hyperpigmentation, diabetes.
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What are the laboratory findings in hemochromatosis?
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Decreased iron-binding capacity. Ferritin is elevated. Liver biopsy.
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What is the treatment of hemochromatosis?
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Phlebotomy to remove iron.
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What is Wilson disease?
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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.
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How is Wilson disease diagnosed?
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Low ceruloplasmin level. High urinary copper level. Liver biopsy is most specific.
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What is the treatment for Wilson disease?
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Penicillamine is a copper chelator. Liver transplantation is curative.
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What is alpha-1 antitrypsin deficiency?
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Autosomal recessive disorder leading to deficient alpha-1 antitrypsin levels. Cirrhosis, emphysema developing at a young age in a nonsmoker.
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How is alpha-1 antitrypsin deficiency diagnosed?
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Low level of the enzyme in a person with COPD confirms diagnosis.
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What is the treatment of alpha-1 antitrypsin deficiency?
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Replacement of the enzyme and stop smoking.
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How is chronic hepatitis B and C diagnosed?
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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.
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What is the treatment for chronic hepatitis B?
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Chronic hepatitis B is treated with interferon, lamivudine, or adefovir.
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What is the treatment for chronic hepatitis C?
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Chronic hepatitis C is treated with the combination of pegylated interferon and ribavirin.
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What are the important aspects of the chest pain history?
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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."
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What is the clinical presentation of inferoposterior myocardial ischemia?
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Nausea and vomiting are sometimes the main symptoms in inferoposterior wall ischemia. In inferoposterior wall ischemia, vagal reflexes may cause bradycardia and hypotension.
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What are the characteristics of pain that is less likely to be caused by ischemia?
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"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.
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What is the usual amount of time that myocardial infarction pain is present?
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Myocardial infarction lasts more than 20-30 minutes.
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What etiology is suggested if pain is relieved by nitroglycerine?
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Relief of chest pain with nitroglycerin indicates ischemia or esophageal spasm. Chest pain that worsens with nitroglycerin occurs with gastroesophageal reflux disease.
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What is the presentation of acute coronary syndrome in women?
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Acute coronary syndromes in women present with atypical symptoms: dyspnea, shortness of breath, fatigue.
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What are the physical examination findings that suggest aortic dissection?
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Blood pressure a difference between arms of over 20 mm Hg systolic suggests aortic dissection.
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What etiologies of chest pain are suggested by hypotension?
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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.
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What etiology is suggested by wide splitting of the second heart sound?
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Wide physiologic splitting of the second heart sound (splitting wider with inspiration) can be found in right ventricular infarction.
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What is the significance of fourth heart sound in patients with chest pain?
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A new fourth heart sound can occur with angina or infarction. An S3 is may be caused by underlying heart failure.
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What etiology is suggested by the finding of a murmur of aortic regurgitation in patients with ischemic chest pain?
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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.
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What are the 12-lead ECG signs of an acute myocardial infarction?
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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).
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What is the role of creatine kinase MB isoenzyme in patients with an acute coronary syndrome?
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CK-MB isoenzyme is cardiac specific and is useful for early diagnosis of MI.
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At what time after an acute myocardial infarction does the CK-MB become elevated?
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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.
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What are cardiac troponins?
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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.
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What is the difference between troponin T and I?
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Unlike troponin I levels, troponin T levels may be elevated in patients with renal disease, polymyositis, or dermatomyositis.
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What is the significance of an elevated troponin level and a normal CK-MB in a patient with chest pain?
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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.
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How much time is required before cardiac troponins return to normal after an acute myocardial infarction?
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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.
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What is the role of the chest x-ray in patients with chest pain?
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Pneumothorax, pneumomediastinum, effusion, infiltrates. Aortic dissection can cause widening of mediastinum. Loss of lung volume or unilateral loss of vascular markings suggest PE.
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What are the symptoms of aortic dissection?
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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.
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What are the symptoms of pulmonary embolism?
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Dyspnea, tachycardia, hypoxemia; pleuritic pain.
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How is pulmonary embolism diagnosed?
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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.
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What are the symptoms of pericarditis?
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Pain is sharp, positional, pleuritic, and relieved by leaning forward; preceded by viral illness; pericardial rub.
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What are the ECG signs of acute pericarditis?
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Diffuse ST elevation occurs without evolution of Q waves; CK level usually normal.
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What are the symptoms of myocarditis?
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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.
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What are the musculoskeletal causes of chest pain?
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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.
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What are the gastrointestinal causes of chest pain?
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Esophageal reflux is worse with recumbency or meals; regurgitation; relieved by antacids, nitroglycerin. Ulcers, cholecystitis. Pancreatitis causes abdominal tenderness, with radiation to back, hyperamylasemia.
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What are the symptoms of pneumothorax?
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Onset abrupt with sharp pleuritic chest pain and dyspnea; breath sounds are absent, chest x-ray confirms.
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What are the symptoms of pleuritis?
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Pain is sharp and increases on inspiration; pleural friction rub; underlying pulmonary infection.
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What are the major modifiable risk factors for ischemic heart disease?
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Hypercholesterolemia, smoking hypertension, physical inactivity, obesity, diabetes.
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What subgroup of hypercholesterolemia is the most important risk factor for ischemic heart disease?
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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.
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What is the risk of myocardial infarction in smokers?
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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.
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What degree of hypertension is a risk factor for cardiovascular events?
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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.
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What percentage of patients with diabetes die of cardiovascular disease?
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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.
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What are the clinical signs of stable angina?
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Substernal pressure lasting 5-15 min; not affected by respiration/position. Stable angina occurs when myocardium becomes ischemic during exercise, hypotension, anemia.
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What is the most common ECG sign in patients with angina?
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Most commonly ST segment depression is seen. ST segment elevation typically occurs in variant angina (Prinzmetal angina) where coronary artery spasm is responsible.
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How is ischemic heart disease diagnosed?
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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.
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What is the criteria for a positive exercise stress test for myocardial ischemia?
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>2 mm ST-segment depressions or hypotension (a drop of more than 10 mm Hg in systolic pressure) occur either alone or in combination.
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What type of noninvasive test for ischemic heart disease is indicated for patients who are unable to exercise?
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Patients who are unable to exercise or walk should be considered for chemical stress testing, such as dipyridamole (Persantine) or dobutamine stress tests.
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What type of noninvasive test for ischemic heart disease is indicated for patients with bundle branch block?
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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.
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What is a nuclear stress test?
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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.
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What are the dobutamine and adenosine stress tests?
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This test is used in people who are unable to exercise. A drug is given to induce tachycardia.
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What is a stress echocardiogram?
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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.
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What are the indications for cardiac catheterization?
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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.
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What is the treatment of ischemic heart disease?
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Nitroglycerin SL alleviates pain. Long-acting nitrates, beta blockers. Aspirin and statins. All patients with stable angina need cardiac angiography or stress testing.
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What are the target goals for treatment of hyperlipidemic patients with coronary artery disease?
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LDL less than 100 mg/dL. HDL 40 mg/dL or greater. Triglycerides less than 150 mg/dL.
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What is the optimal LDL-cholesterol goal for patients at very high risk of coronary artery disease?
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<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.
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What are the indications for coronary bypass graft in ischemic heart disease?
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Left main coronary disease or three vessel disease and left ventricular (LV) dysfunction. More efficacious in diabetes. More beneficial in low ejection fraction.
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What are the types of acute coronary syndromes?
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Acute coronary syndromes (ACS) include a range of thrombotic coronary diseases, including unstable angina (UA), non-ST elevation myocardial infarction, and STEMI.
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What is a non ST-segment elevation myocardial infarction?
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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.
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What are the indications for thrombotic therapy in patients with acute coronary syndrome?
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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.
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What is unstable angina?
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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.
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What are the ECG findings in non-segment elevation MI?
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Dynamic ST-segment depression (>5 mm), or new T-wave inversion ( 2 mm), but the ECG may be normal or show minor changes.
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What are the high-risk features for patients with UA/NSTEMI?
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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.
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What is the general management of NSTEMI?
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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.
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What are the drugs that are used in NSTEMI?
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Aspirin, clopidogrel, heparin, tirofiban, metoprolol, nitroglycerine.
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What antiplatelet therapy should be given to patients with NSTEMI?
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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.
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What are the indications for anticoagulants in NSTEMI?
|
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.
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What is the mechanism of the glycoprotein (GP) Hb/IIIa inhibitors?
|
Inhibit platelet function by blocking a receptor involved in platelet aggregation, providing a more comprehensive platelet blockade than the combination of aspirin and heparin.
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What is the indication for tirofiban or eptifibatide in NSTEMI?
|
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.
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What are the indications for a beta-blocker in patients with NSTEMI?
|
A beta-blocker should be given unless contraindicated. Intravenous nitroglycerin is given for refractory pain.
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Which patients with NSTEMI should receive invasive management?
|
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.
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What are the clinical signs of ST elevation myocardial infarction?
|
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.
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What are the signs of STEMI in elderly and diabetic patients?
|
Elderly and diabetic patients are prone to atypical symptoms, such as nausea or dyspnea. 20% of MI are "silent".
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What are the physical signs of ST elevation myocardial infarction?
|
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
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What are the ECG criteria for STEMI?
|
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).
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What is the initial nonspecific management of acute coronary syndrome?
|
Initial nonspecific management for all patients with possible MI (chest pain) is oxygen therapy, aspirin (unless contraindicated), nitroglycerin and morphine.
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What is the management of STEMI in patients who present within 12 hours of the onset of ischemic symptoms?
|
Completely occluded coronary artery with thrombus at the site of a ruptured plaque. Reperfusion strategy with fibrinolytic therapy or percutaneous coronary intervention.
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Which ECG leads have ST elevation in an inferior myocardial infarction?
|
II, III, aVF
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Which coronary artery is occluded in an inferior myocardial infarction?
|
Right coronary.
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Which ECG leads have ST elevation in an anteroseptal myocardial infarction?
|
V1-V3
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Which coronary artery is occluded in an anteroseptal myocardial infarction?
|
Left anterior descending
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Which ECG leads have ST elevation in an anterior myocardial infarction?
|
V2-V4
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Which coronary artery is occluded in an anterior myocardial infarction?
|
Left anterior descending artery.
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Which ECG leads have ST elevation in a lateral myocardial infarction?
|
I, aVL, V4, V5, and V6
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Which coronary artery is occluded in an anterior myocardial infarction?
|
Left anterior descending or circumflex artery.
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Which ECG leads have ST elevation in a posterior MI?
|
V1-V2: Tall broad initial R wave, ST depression, tall upright T wave; usually occurs in association with inferior or lateral MI.
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Which coronary artery is occluded in a posterior myocardial infarction?
|
Posterior descending
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What is the time of onset of hyperacute T waves (tall, peaked T waves) after a myocardial infarction?
|
Immediately. Disappear in 6-24 hours.
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What is the time of onset of ST-segment elevations after a myocardial infarction?
|
Immediately
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At what time do ST-segment elevations disappear after a myocardial infarction?
|
1-6 weeks
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What is the time of onset of Q waves longer than 0.04 seconds after a myocardial infarction?
|
One to several days. 0.04 seconds is one small ECG box.
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At what time do Q waves longer than 0.04 seconds disappear after a myocardial infarction?
|
Years to never
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|
What is the time of onset of T wave inversions after a myocardial infarction?
|
6-24 hours
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|
At what time do T wave inversions disappear after a myocardial infarction?
|
Disappear months to years later.
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|
What is the best emergent reperfusion therapy?
|
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.
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|
What are the indications for thrombolytics?
|
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
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|
What are the contraindications to thrombolytic therapy?
|
Active bleeding or bleeding diathesis, head or facial trauma within 3 months, suspected aortic dissection, prior intracranial hemorrhage, ischemic stroke within 3 months.
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What are the relative contraindications to thrombolytic therapy?
|
Recent major surgery (<3 weeks); traumatic or prolonged cardiopulmonary resuscitation; recent internal bleeding; active peptic ulcer. Severe, poorly controlled HTN. Ischemic stroke.
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What are the indications for antiplatelet agents in STEMI?
|
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.
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What are the indications for antithrombin in STEMI?
|
With PCI: Antithrombin therapy should be used in conjunction with PCI. Enoxaparin in acute STEMI in conjunction with PCI is effective.
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What are the indications for enoxaparin with fibrinolysis?
|
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.
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What are the indications for glycoprotein IIb/IIIa inhibitors in STEMI?
|
Use abciximab with primary PCI in patients with STEMI.
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|
What are the recommended discharge medications after ACS?
|
Aspirin, clopidogrel, beta-blocker, statin, nitrates.
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What discharge antiplatelet therapy should be given to patients after ACS?
|
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.
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|
What are the indications for a beta-blocker after ACS?
|
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.
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What are the indications for ACE inhibitors after ACS?
|
ACE inhibitors should be given in patients with ACS in congestive heart failure, left ventricular dysfunction (ejection fraction 40%).
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What are the indications for statin therapy after ACS?
|
Statin therapy should be initiated in the hospital in all patients with ACS.
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What are the indications for nitrates after ACS?
|
All patients should be prescribed short-acting nitrates. Long-acting nitrates (isosorbide) are given if there is continuous and frequent chest pain.
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|
What are the indications for warfarin after ACS?
|
Warfarin is recommended after ACS only for those at high risk of systemic thromboembolism because of atrial fibrillation, mural thrombus, or congestive heart failure.
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|
What are the recommendations for exercise ECG testing after ACS?
|
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.
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|
What are the complications of ACS?
|
Pump dysfunction, ischemia, pericarditis (Dressler syndrome), thromboembolism, sudden cardiac death due to arrhythmia (most commonly ventricular fibrillation). Ventricular tachycardia.
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|
What is right ventricular infarction?
|
Accompanies 30% of inferior MIs. It is diagnosed with right side leads and treated with fluids.
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|
What is Prinzmetal angina?
|
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.
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|
What is the treatment of Prinzmetal angina?
|
Calcium channel blockers or nitrates.
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|
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?
|
Congestive heart failure
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|
What is systolic heart failure?
|
Systolic dysfunction is caused by a loss of contractile strength of the myocardium with ventricular dilatation. Ischemic cardiomyopathy and dilated cardiomyopathy.
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|
What is diastolic heart failure?
|
Filling of one or both ventricles is impaired while the emptying capacity is normal (the ejection fraction is normal). Infiltrative cardiomyopathies (amyloidosis).
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|
What are the causes of decompensated heart failure?
|
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.
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|
What are the causes of congestive heart failure?
|
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.
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|
What are the symptoms of left ventricular heart failure?
|
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, and weakness.
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|
What is the New York Heart Association Functional Classification of heart failure?
|
Class I: no limitation. Class II: slight, mild limitation of activity. Class III: marked limitation. Class IV: confined to bed or chair.
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|
What is the best test to confirm the diagnosis of heart failure?
|
Echocardiography is the test-of-choice for diagnosis and to classify the type (systolic vs. diastolic). Echocardiography measures ejection fraction.
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|
What are the chest x-ray findings in congestive heart failure?
|
The chest x-ray may show cardiomegaly, vascular redistribution, Kerley B-lines, and interstitial edema.
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|
What are the ECG findings in congestive heart failure?
|
Electrocardiogram identifies ventricular hypertrophy, ischemic heart disease, arrhythmias or conduction delays which may cause HF.
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|
What is B-type natriuretic peptide?
|
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.
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|
What are the beneficial effects of ACE inhibitors in congestive heart failure?
|
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).
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|
What are the side effects of captopril?
|
Rash, nonproductive cough, proteinuria, renal failure, taste disturbance, agranulocytosis, hypotension
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|
|
What are the side effects of enalapril?
|
Hypotension, angioedema, renal failure, laryngeal edema, cough.
|
|
|
What are the side effects of lisinopril?
|
Hypotension, proteinuria, renal insufficiency, rash, cough.
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|
|
What are the side effects of nitroprusside?
|
Thiocyanate toxicity, methemoglobinemia.
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|
|
What are the side effects of nitroglycerin?
|
Headache, postural hypotension, methemoglobinemia.
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|
|
What are the side effects of isosorbide dinitrate?
|
Headache, postural hypotension
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|
|
What are the side effects of hydralazine?
|
Headache, positive ANA, SLE-like syndrome (10-20%) drug fever, rash.
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|
|
What is the treatment of congestive symptoms in heart failure?
|
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.
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|
What is the mechanism of action of thiazides?
|
Inhibits NaCl cotransport; used mostly for treatment of hypertension; hydrochlorothiazide, chlorothiazide
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|
|
What are the side effects of thiazides?
|
HypoNa, hypoK, hyperlipidemia, hyperCa, metabolic alkalosis, hyperuricemia, reduced GFR, allergy, thrombocytopenia, agranulocytosis, leukopenia, anemia, pancreatitis, sexual dys, glucose intolerance.
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|
What are the side effects of indapamide?
|
Hypokalemia and lipid abnormalities are less common than with other thiazides. Hyponatremia, hypercalcemia, metabolic alkalosis, hyperuricemia, reduced glomerular filtration rate, allergy.
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|
What are the side effects of phthalimidine derivatives?
|
Similar to thiazides, but hypokalemia may be profound. Chlorthalidone, metolazone.
|
|
|
What is the mechanism of action of loop diuretics?
|
Inhibitors of Na/K/Cl cotransport; most commonly used diuretics in heart failure; furosemide, ethacrynic acid, bumetanide.
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|
|
What are the side effects of loop diuretics?
|
Hyponatremia, hypokalemia, hypocalcemia, metabolic alkalosis, hyperuricemia, interstitial nephritis, ototoxicity, thrombocytopenia, agranulocytosis, leukopenia, anemia.
|
|
|
What are the side effects of potassium-sparing diuretics?
|
Hyperkalemia, mental confusion, nausea, and gynecomastia (spironolactone only).
|
|
|
What is the initial therapy for congestive heart failure?
|
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.
|
|
|
What treatment is recommended for black patients with severe heart failure who have already been treated with the standard therapy?
|
Reduction in death and a decrease in hospitalization occurs with the combination of hydralazine and isosorbide.
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|
|
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)?
|
Addition of spironolactone significantly reduces death and hospitalizations.
|
|
|
What is the treatment of severe refractory heart failure?
|
Inotropic agents for severe heart failure improves symptoms, quality of life and reduces hospitalizations, but does not improve survival.
|
|
|
What is the mechanism of digitalis?
|
Inhibits Na+/K+ - ATPase pump which results in increased intracellular Na+ and decreased intracellular Ca. Increase in intracellular Ca results in improved cardiac contractility.
|
|
|
What is the effect of potassium levels on the effect of digitalis?
|
Hyperkalemia will decrease digitalis activity, whereas hypokalemia results in toxicity.
|
|
|
What conditions predispose to digitalis toxicity?
|
Renal insufficiency, hypokalemia, hypercalcemia, hypomagnesemia, advanced age, sinoatrial and atrioventricular block; hypothyroidism, hypoxic states, pulmonary disease; multiple drug therapy.
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|
|
What drug interaction occurs with digoxin and quinidine?
|
Decreases renal clearance of digoxin.
|
|
|
What drug interaction occurs with digoxin and verapamil/diltiazem?
|
Decreases renal clearance of digoxin.
|
|
|
What drug interaction occurs with digoxin and cholestyramine/colestipol?
|
Binds digoxin in gastrointestinal tract; interferes with enterohepatic circulation.
|
|
|
What drug interaction occurs with digoxin and spironolactone?
|
Inhibits tubular secretion of digoxin.
|
|
|
What drug interaction occurs with digoxin and thiazides/furosemide?
|
Diuretic-induced hypokalemia and/or bumetanide. Hypomagnesemia potentiates digitalis action.
|
|
|
What are the side effects of digoxin?
|
Nausea, vomiting, gynecomastia, blurred vision; yellow halo around objects; paroxysmal atrial tachycardia with block, PVCs, and bradycardia.
|
|
|
What is the treatment for digoxin toxicity?
|
Stop the drug. K+ administration if needed. Lidocaine and phenytoin. Digibind only for acute overdose.
|
|
|
What is the treatment of severe heart failure that does not respond to standard therapy?
|
Sympathomimetic amines (dopamine, dobutamine) and phosphodiesterase inhibitors (amrinone, milrinone) IV infusion. Other options: pacing, implantable defibrillator, heart transplantation.
|
|
|
What is the treatment of diastolic heart failure?
|
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.
|
|
|
What are the signs of pulmonary edema?
|
Increased respiratory rate, nocturnal dyspnea, cough with expectoration of pink frothy sputum, cyanosis, crackles, rhonchi, wheezing.
|
|
|
What are the chest x-ray findings in pulmonary edema?
|
Prominent pulmonary vasculature, enlarged cardiac silhouette, Kerley B lines, effusions.
|
|
|
What is the treatment of pulmonary edema?
|
Morphine sulfate. Furosemide reduces preload. Nitroglycerin reduces preload. Digoxin if atrial fibrillation. Intravenous ACE inhibitors.
|
|
|
What is mitral stenosis?
|
Thickened valve leaflets impede left ventricular filling; increased left atrial pressure causes pulmonary congestion; cardiac output reduced, secondary pulmonary vasoconstriction and RV failure occurs
|
|
|
What is the most common lesion caused by rheumatic fever?
|
Mitral stenosis is the most common lesion caused by rheumatic fever. Rarely congenital.
|
|
|
What are the early clinical signs of mitral stenosis?
|
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, wasting, hemoptysis (rupture of pulmonary vessels); systemic embolism from stasis of blood in an enlarged left atrium
|
|
|
What are the late clinical signs of severe mitral stenosis?
|
Hoarseness due to impingement of an enlarged left atrium on recurrent laryngeal nerve; right-sided heart failure; hepatomegaly, ascites; peripheral edema.
|
|
|
What are the physical signs of mitral stenosis?
|
Atrial fibrillation (irregular rhythm); pulmonary rales; decreased pulse pressure; loud S1, opening snap following S2, diastolic rumble, sternal lift (right ventricular enlargement).
|
|
|
What are the ECG findings in mitral stenosis?
|
Right ventricular hypertrophy; left and right atrial enlargement; atrial fibrillation may occur.
|
|
|
What are the chest x-ray findings in mitral stenosis?
|
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.
|
|
|
What is the treatment of mitral stenosis?
|
Diuretics and salt-restricted diet; digitalis, anticoagulants if atrial fibrillation; when symptomatic: mitral commissurotomy or valve replacement.
|
|
|
What are the hemodynamic findings in mitral regurgitation?
|
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.
|
|
|
What are the acute causes of mitral regurgitation?
|
Rupture chordae tendineae; papillary muscle rupture; endocarditis, trauma.
|
|
|
What are the chronic causes of mitral regurgitation?
|
Rheumatic heart disease, papillary muscle dysfunction, mitral prolapse/calcification, endocarditis; HCM; endocardial cushion defect, corrected transposition; endocardial fibroelastosis; LV dilatation.
|
|
|
What are the physical signs of mitral regurgitation?
|
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.
|
|
|
What are the ECG signs of mitral regurgitation?
|
Left ventricular hypertrophy and left atrial enlargement. Chest x-ray: cardiac enlargement vascular congestion.
|
|
|
What is the treatment of mitral regurgitation?
|
Digitalis, diuretics, arteriolar vasodilators (ACE inhibitors), warfarin; mitral valve replacement when symptoms.
|
|
|
What is mitral valve prolapse?
|
Most common congenital valvular abnormality; also in young women with connective tissue disease (e.g., Marfan or idiopathic).
|
|
|
What is the presentation of mitral valve prolapse?
|
Asymptomatic. Lightheadedness, palpitations, syncope, chest pain. Arrhythmias. Mid-to-late systolic click, late systolic murmur at apex which worsens with Valsalva; improves with squatting.
|
|
|
What are the complications of mitral valve prolapse?
|
Serious arrhythmias, sudden death, congestive heart failure, bacterial endocarditis, calcifications, transient cerebral ischemic attacks, mitral regurgitation.
|
|
|
What is the treatment of mitral valve prolapse?
|
Endocarditis prophylaxis only in severe cases. Beta-blocker for chest pain. Mitral valve replacement is rarely necessary.
|
|
|
What is aortic stenosis?
|
Calcification and degeneration; more common in elderly. Calcification and fibrosis of a congenitally bicuspid aortic valve. Rheumatic valvular disease.
|
|
|
What is the pathophysiology of aortic stenosis?
|
Elevation LV systolic pressure and LV hypertrophy. Noncompliant left ventricle causes a prominent S4 gallop. LV diastolic pressure increases; pulmonary congestion.
|
|
|
What are the clinical signs of aortic stenosis?
|
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.
|
|
|
What are the ECG signs of aortic stenosis?
|
Left ventricular hypertrophy. Chest x-ray: calcification, cardiomegaly, pulmonary congestion.
|
|
|
What is the treatment of aortic stenosis?
|
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.
|
|
|
What is aortic valve sclerosis of the elderly?
|
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.
|
|
|
What are the clinical signs of hypertrophic obstructive cardiomyopathy?
|
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).
|
|
|
What are the clinical sings of mitral regurgitation?
|
Murmur is holosystolic and radiates to axilla and not carotids. Carotid upstroke is normal; dilated left ventricle.
|
|
|
What are the clinical signs of pulmonic stenosis?
|
Murmur does not radiate into neck; loudest along the left sternal border; increases with inspiration.
|
|
|
What are the causes of aortic regurgitation?
|
Hypertension is the most common cause; infectious endocarditis, syphilis, ankylosing spondylitis; Marfan syndrome, rheumatic fever, aortic dissection, aortic trauma.
|
|
|
What is the pathophysiology of aortic regurgitation?
|
Aortic regurgitation results in a volume overload of the left ventricle.
|
|
|
What are the clinical signs of aortic regurgitation?
|
Dyspnea is most common. Diastolic decrescendo murmur. Systolic flow murmur. S3 in left ventricular failure, Austin-Flint murmur: low pitched, late diastolic apex murmur
|
|
|
How is aortic regurgitation diagnosed?
|
ECG: LV hypertrophy; chest x-ray: LV and aortic dilation; echocardiogram
|
|
|
What is the treatment of aortic regurgitation?
|
Endocarditis prophylaxis is not recommended. Salt restriction, diuretics, ACE inhibitors. Aortic valve replacement when symptoms worsen.
|
|
|
What is hypertrophic obstructive cardiomyopathy?
|
Marked hypertrophy of left ventricle; usually disproportionate hypertrophy of septum
|
|
|
What is restrictive cardiomyopathy?
|
Reduced ventricular compliance; usually caused by infiltration of myocardium (by amyloid, hemosiderin, or glycogen deposits).
|
|
|
What is obliterative cardiomyopathy?
|
Thickened endocardium or mural thrombi, or both, act as space-occupying lesions and reduce left ventricular filling.
|
|
|
What is dilated cardiomyopathy?
|
Characterized by diminished myocardial contractility, usually involving both ventricles; most common cause for heart transplants.
|
|
|
What are the causes of dilated cardiomyopathy?
|
Idiopathic, alcoholic, peripartum; viruses, parasites, mycobacteria, Rickettsiae; toxins (cobalt, lead, arsenic); doxorubicin cyclophosphamide, vincristine. Hypophosphatemia, hypoK, hypoCa, uremia.
|
|
|
What are the clinical signs of dilated cardiomyopathy?
|
Symptoms of left and right ventricular failure: dyspnea, orthopnea; peripheral edema.
|
|
|
What are the x-ray signs of dilated cardiomyopathy?
|
Cardiomegaly with pulmonary congestion. ECG: sinus tachycardia, arrhythmias, conduction disturbances.
|
|
|
What is the cause of hypertrophic obstructive cardiomyopathy?
|
Hypertrophic cardiomyopathy can develop sporadically; it is hereditary in 60%; autosomal dominant.
|
|
|
What is the pathophysiology of hypertrophic obstructive cardiomyopathy?
|
Thickening of interventricular septum. LV compliance reduced. Heart is hypercontractile. EJECTION FRACTION 80% (normal is 60%). Obstruction worsened by increased contractility.
|
|
|
What is the effect of digitalis glycosides on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of increased contractility.
|
|
|
What is the effect of beta-adrenergic stimulation (eg, isoproterenol, epinephrine) on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of increased contractility.
|
|
|
What is the effect of premature beats on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of increased contractility.
|
|
|
What is the effect of Valsalva maneuver on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of decreased preload.
|
|
|
What is the effect of decrease in intravascular volume (eg, hemorrhage, diuresis, gastrointestinal losses) on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of decreased preload.
|
|
|
What is the effect of standing on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of decreased preload.
|
|
|
What is the effect of nitroglycerin on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of decreased preload.
|
|
|
What is the effect of vasodilator drugs on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of decreased preload.
|
|
|
What is the effect of tachycardia on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of decreased preload and increased contractility.
|
|
|
What is the effect of hypovolemia on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of decreased afterload.
|
|
|
What is the effect of nitroglycerin and related drugs on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of decreased afterload.
|
|
|
What is the effect of vasodilator drugs on hypertrophic obstructive cardiomyopathy?
|
Increase obstruction because of decreased afterload.
|
|
|
What is the effect of beta-adrenergic blockade (eg, propranolol) on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of decreased contractility.
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What is the effect of heavy sedation and general anesthesia on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of decreased contractility.
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What is the effect of calcium channel blockers, disopyramide, and other drugs that depress myocardial function on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of decreased contractility.
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What is the effect of intravascular volume expansion on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of increased preload.
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What is the effect of squatting on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of increased preload.
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What is the effect of bradycardia on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of increased preload.
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What is the effect of beta-adrenergic blockade on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of increased preload.
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What is the effect of intravascular volume expansion on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of increased afterload.
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|
What is the effect of squatting on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of increased afterload.
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What is the effect of alpha-adrenergic stimulation (e.g., phenylephrine, mephentermine) on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of increased afterload.
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|
What is the effect of handgrip exercise on hypertrophic obstructive cardiomyopathy?
|
Decreased obstruction because of increased afterload.
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|
What are the symptoms of hypertrophic obstructive cardiomyopathy?
|
Dyspnea, angina, presyncope, syncope, and palpitations.
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|
What are the physical signs of hypertrophic obstructive cardiomyopathy?
|
Large jugular A wave, bifid carotid pulse, palpable S4 gallop, systolic murmur and thrill, mitral regurgitation murmur; sudden death.
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What are the ECG signs of hypertrophic obstructive cardiomyopathy?
|
Left ventricular hypertrophy, pseudo Q waves (V1-V3), ventricular arrhythmias.
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What is the treatment of hypertrophic obstructive cardiomyopathy?
|
Beta-blockers, calcium channel blockers, surgery.
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|
What is restrictive cardiomyopathy?
|
Least common cause of cardiomyopathy; rigid noncompliant ventricular walls.
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|
What are the causes of restrictive cardiomyopathy?
|
Sarcoidosis; amyloidosis, hemochromatosis, neoplasia, scleroderma, radiation
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|
What is the pathophysiology of restrictive cardiomyopathy?
|
Myocardium is rigid and noncompliant, impeding ventricular filling and raising cardiac filling pressures. Systolic performance reduced.
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What are the signs of restrictive cardiomyopathy?
|
Dyspnea, exercise intolerance, weakness. Elevated jugular venous pressure, edema, hepatomegaly, ascites, S4 and S3 gallop, Kussmaul sign.
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What are the x-ray signs of restrictive cardiomyopathy?
|
Mild cardiomegaly, pulmonary congestion. Echocardiogram is diagnostic.
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What is the treatment of restrictive cardiomyopathy?
|
Heart transplantation; death from congestive heart failure or arrhythmias.
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What are the causes of acute pericarditis and myopericarditis?
|
Idiopathic, infections (viral), vasculitis (connective tissue disease), disorders of metabolism, neoplasms, trauma, drug reactions.
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What are the clinical symptoms of acute pericarditis?
|
Chest pain at left of sternum, worsened by lying down, coughing, and deep inspiration, relieved by sitting up and leaning forward.
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What are the physical signs of acute pericarditis?
|
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.
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What are the ECG signs of acute pericarditis?
|
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.
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What is the treatment of acute pericarditis?
|
NSAIDs, aspirin, corticosteroids.
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What are the types of pericardial effusions?
|
Transudates, serosanguineous, blood.
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What are the causes of transudative pericardial effusions?
|
Transudates occur with congestive heart failure, overhydration, or hypoproteinemia. Exudates occur in the presence of pericardial injury.
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What are the causes of serosanguineous pericardial effusions?
|
Serosanguineous pericardial fluid is sign in tuberculosis and neoplastic diseases.
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What are the causes of bloody pericardial effusions?
|
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.
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How is pericardial effusion diagnosed?
|
Echocardiography. Chest x-ray may show a "water-bottle" cardiac silhouette.
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What is the treatment of pericardial effusion?
|
Pericardial fluid aspiration.
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|
What is cardiac tamponade?
|
A life-threatening condition in which a pericardial effusion compresses the heart.
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What are the causes of cardiac tamponade?
|
Neoplasia, idiopathic (viral) pericarditis, tuberculosis, suppurative, intrapericardial hemorrhage, central line extravasation, surgery, postpericardiotomy syndrome, uremia, radiation therapy, vasculitis.
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|
What are the clinical manifestations of pericardial tamponade?
|
Dyspnea, fatigue, orthopnea. Pulsus paradoxus (decrease in systolic blood more than 10 with inspiration or disappearance pulse with inspiration).
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|
What is the triad of pericardial tamponade?
|
Triad of neck vein distension with clear lung, hypotension, and muffled heart sounds.
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What is the treatment of cardiac tamponade?
|
Pericardiocentesis; subxiphoid surgical drainage.
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|
What is constrictive pericarditis?
|
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.
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|
What are the causes of constrictive pericarditis?
|
Idiopathic; following open-heart surgery; thoracic radiation; postviral infection.
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What are the clinical manifestations of constrictive pericarditis?
|
Dyspnea on exertion, orthopnea; ascites, edema, jaundice, hepatic tenderness, and hepatomegaly (right-side failure). Jugular venous distension that increases with inspiration (Kussmaul sign).
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|
How is constrictive pericarditis diagnosed?
|
CT: thickened pericardium; pericardial calcifications in tuberculous constriction. Left ventricular ejection fraction is decreased in restrictive cardiomyopathy, but not in constrictive pericarditis.
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|
|
What is the treatment of constrictive pericarditis?
|
Sodium restriction, diuretics, pericardiectomy.
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|
|
What is sinus bradycardia?
|
Ventricular complexes are normal width, evenly spaced, rate is <60/min.
|
|
|
What are the causes of sinus bradycardia?
|
Acute MI, carotid sinus pressure, vomiting, Valsalva maneuver, phenothiazines, digitalis glycosides, beta-adrenergic blocking agents, calcium blockers, marathoners and swimming, hypothyroidism, normal variant.
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|
|
What is the treatment of sinus bradycardia?
|
Atropine if symptoms. Pacemaker.
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|
What are the types of atrioventricular block?
|
The three classic clinical types are first-, second-, and third-degree (or complete) atrioventricular block.
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|
What is first-degree atrioventricular block?
|
PR interval greater than 0.20 s at a heart rate of 70 beats/min.
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|
What are the causes of first-degree heart block?
|
Digitalis; exaggerated vagal tone after tracheal suctioning; ischemia, inflammation (myocarditis, acute rheumatic fever), cardiomyopathies.
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|
What are the types of second-degree atrioventricular block?
|
Type I (Mobitz I, Wenckebach) and type II (Mobitz II).
|
|
|
What is type I atrioventricular block (Mobitz I, Wenckebach)?
|
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.
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|
What is type II (Mobitz II) atrioventricular block?
|
An intermittent blocked beat occurs suddenly and is not preceded by a change in the duration of the PR interval.
|
|
|
What is the site of the block in type I second-degree atrioventricular block?
|
Usually AV nodal (supra-Hisian)
|
|
|
What is the site of the block in type II second degree atrioventricular block?
|
Infranodal (infra- or infra-Hisian).
|
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|
What are the causes of type I second degree atrioventricular block?
|
Degenerative changes in AV node; diaphragmatic myocardial infarct; digitalis toxicity; myocarditis; rheumatic fever; increased vagal tone.
|
|
|
What are the causes of type II second degree AV block?
|
Extensive anterior myocardial infarct; degenerative changes in His-Purkinje system; calcification of mitral or aortic valve annulus.
|
|
|
What are the ECG findings in type I second degree AV block?
|
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.
|
|
|
What are the ECG findings in type II second degree AV block?
|
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.
|
|
|
What is third-degree atrioventricular block?
|
In 3rd degree block, all atrial beats are blocked, and ventricles are driven by an escape focus.
|
|
|
What are the most common causes of 3rd degree atrioventricular block?
|
Most common is fibrous degeneration of conduction system from aging; inferior/ posterior infarction; infection, inflammation, digitalis, ankylosing spondylitis, Adams-Stokes, heart failure.
|
|
|
What are Adams-Stoke attacks?
|
Sudden asystole or transient ventricular tachycardia or ventricular fibrillation.
|
|
|
What is the treatment of third degree AV block?
|
Pacing.
|
|
|
What is sinus tachycardia?
|
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.
|
|
|
What is paroxysmal supraventricular tachycardia?
|
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.
|
|
|
What are the ECG signs of paroxysmal supraventricular tachycardia?
|
Paroxysmal supraventricular tachycardia has an absolutely regular rhythm at a rate between 130 and 220 beats/min. P-wave is abnormal.
|
|
|
What is the treatment of paroxysmal supraventricular tachycardia?
|
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.
|
|
|
What are the ECG signs of multifocal atrial tachycardia?
|
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.
|
|
|
What are the causes of atrial flutter?
|
Chronic obstructive lung disease, pulmonary embolism, thyrotoxicosis, mitral valve disease, alcohol.
|
|
|
What are the ECG signs of atrial flutter?
|
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).
|
|
|
What is the initial treatment of atrial flutter?
|
Cardioversion if hemodynamically unstable (e.g., hypotension); digitalis, verapamil, diltiazem, beta-blockers.
|
|
|
What is the most common sustained cardiac rhythm disturbance?
|
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.
|
|
|
What are the ECG signs of atrial fibrillation?
|
No p waves. Fibrillatory waves with an irregular, rapid ventricular response (irregularly, irregular).
|
|
|
What is the sign of Wolf-Parkinson White syndrome with atrial fibrillation?
|
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.
|
|
|
What is the rate of ischemic stroke in atrial fibrillation?
|
The rate of ischemic stroke among patients with nonrheumatic atrial fibrillation averages 5% per year.
|
|
|
What are the signs of atrial fibrillation?
|
Elderly patients with shortness of breath, dizziness, or palpitations. Acute fatigue or exacerbation of congestive heart failure. Irregularly irregular pulse.
|
|
|
What is "lone atrial fibrillation"?
|
Atrial fibrillation with no evidence of structural heart disease.
|
|
|
What are the causes of atrial fibrillation?
|
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.
|
|
|
What tests are use in the evaluation of atrial fibrillation?
|
ECG: AF, left ventricular hypertrophy, pre-excitation, prior myocardial infarction. Echocardiogram: identifies LVH, valvular disease, atrial size, and left atrial thrombus. Thyroid function tests.
|
|
|
What drugs are effective for pharmacologic cardioversion of atrial fibrillation?
|
Amiodarone, dofetilide, flecainide, ibutilide, propafenone, and quinidine.
|
|
|
Which drugs are used to maintain sinus rhythm in patients with atrial fibrillation?
|
Drugs used to maintain sinus rhythm in patients with atrial fibrillation include amiodarone, disopyramide, dofetilide, flecainide, propafenone, and sotalol.
|
|
|
What is the first step in managing atrial fibrillation?
|
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.
|
|
|
What is the recommended treatment strategy for atrial fibrillation?
|
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.
|
|
|
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?
|
Electrical cardioversion.
|
|
|
What is Wolff-Parkinson-White syndrome?
|
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.
|
|
|
What is the treatment of Wolff-Parkinson-White syndrome?
|
If unstable, then synchronized cardioversion. If stable, then procainamide. Ablation.
|
|
|
What drugs should be avoided in Wolff-Parkinson-White syndrome?
|
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.
|
|
|
What is ventricular tachycardia?
|
VT is three or more consecutive beats of ventricular origin at a rate greater than 120 beats/min. QRS complexes are wide and bizarre.
|
|
|
What are the causes of ventricular tachycardia?
|
Ischemic heart disease after an acute MI; cardiomyopathies, hypokalemia, hypercalcemia, hypomagnesemia, hypoxia, digitalis toxicity and thioridazine drugs.
|
|
|
What are the clinical manifestations of ventricular tachycardia?
|
Hypotension, congestive heart failure, syncope, or cardiac arrest.
|
|
|
What are the ECG signs of torsade de pointes ventricular tachycardia?
|
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.
|
|
|
What are the causes of torsade de pointes ventricular tachycardia?
|
Antiarrhythmics that prolong ventricular repolarization (prolong QT); quinidine, procainamide, disopyramide, phenothiazines, thioridazine, tricyclics, lithium, hypoK hypoMg, intracerebral hemorrhage.
|
|
|
What is the treatment of torsade de pointes ventricular tachycardia?
|
Treat underlying electrolyte disorders. Magnesium and potassium are first-line therapies. Isoproterenol and short-acting beta-blockers. Overdrive pacing. If unstable, perform electrical cardioversion.
|
|
|
What are the indications for amiodarone?
|
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).
|
|
|
What are the side effects of amiodarone?
|
Cough, fever; painful breathing can be fatal. 20% neurotoxicity with imbalance, tremor, numbness, weakness. Hypothyroidism/ hyperthyroidism; blue-gray skin; halos, blurred vision; corneal deposits.
|
|
|
What are the indications for disopyramide?
|
Ventricular ectopic activity and atrial ectopic activity.
|
|
|
What are the adverse effects of disopyramide?
|
Anticholinergic effects; hypotension, heart failure, heart block, tachyarrhythmia.
|
|
|
What are the indications for lidocaine?
|
Ventricular ectopic activity
|
|
|
What are the adverse effects of lidocaine?
|
Drowsiness, agitation, seizures; rarely congestive heart failure or heart block.
|
|
|
What are the cardiac indications for phenytoin?
|
Ventricular ectopic activity.
|
|
|
What are the adverse effects of phenytoin?
|
Ataxia, nystagmus, drowsiness; hypotension and heart block with rapid IV injection
|
|
|
What are the indications for procainamide?
|
Ventricular ectopic activity, atrial ectopic activity
|
|
|
What are the adverse effects of procainamide?
|
Lupus-like syndrome; nausea/vomiting; insomnia; rash; hypotension; aggravation of arrhythmia; blood, dyscrasias
|
|
|
What are the indications for quinidine?
|
Ventricular ectopic activity, atrial ectopic activity
|
|
|
What are the adverse effects of quinidine?
|
Aggravation of arrhythmias; thrombocytopenia; fever, rash; cinchonism; nausea; digoxin-quinidine interaction (elevation of digoxin levels).
|
|
|
What are the antiarrhythmic indications for beta-adrenergic blocking agents?
|
Atrial ectopic activity, ventricular ectopic activity.
|
|
|
What are the adverse effects of beta-blockers?
|
Heart block, hypotension, heart failure, asthma, hypoglycemia, lethargy, impotence.
|
|
|
What are the antiarrhythmic indications for verapamil?
|
Atrial ectopic activity.
|
|
|
What are the adverse effects of verapamil?
|
Congestive heart failure, asystole, constipation
|
|
|
What are the indications for adenosine?
|
Ventricular tachycardia
|
|
|
What are the adverse effects of adenosine?
|
Transient dyspnea, noncardiac chest pain, rarely hypotension.
|
|
|
What are the indications for mexiletine?
|
Ventricular ectopic activity
|
|
|
What is mexiletine?
|
Lidocaine-like drug. Local anesthetic; half-life, 8-14 h.
|
|
|
What are the indications for tocainide?
|
Ventricular ectopic activity
|
|
|
What is tocainide?
|
Lidocaine-like drug. Half-life 14-16 h in patients with high-grade ventricular ectopic activity.
|
|
|
What are the indications for amiodarone?
|
Atrial ectopic activity (especially WPW), ventricular ectopic activity.
|
|
|
What are the adverse effects of amiodarone?
|
Very long half-life (20-40 d). May increase digoxin level. May worsen existing cardiac conduction disturbances. May prolong Coumadin effect.
|
|
|
What are the indications for encainide?
|
Ventricular tachycardia, Wolff-Parkinson-White syndrome.
|
|
|
What are the adverse effects of encainide?
|
Negative inotropism; QRS and PR prolongation. Hepatic metabolism to active metabolites.
|
|
|
What are the indications for flecainide?
|
Ventricular tachycardia, supraventricular tachycardia, Wolff-Parkinson-White syndrome.
|
|
|
What are the adverse effects of flecainide?
|
Negative inotropism, QRS, PR prolongation
|
|
|
What are the indications for propafenone?
|
Ventricular tachycardia, atrial fibrillation
|
|
|
What the adverse effect of propafenone?
|
Negative inotropism
|
|
|
What are the physiologic effects of low doses of nitrates?
|
In low doses, nitrates increase venous dilation and reduce preload.
|
|
|
What are the physiologic effects of medium doses of nitrates?
|
In medium doses, nitrates increase arteriolar dilatation and decrease afterload and preload.
|
|
|
What are the physiologic effects of high doses of nitrates?
|
In high doses, nitrates increase coronary artery dilatation and increase oxygen supply.
|
|
|
What are the side effects of nitrates?
|
Vasodilation can lead to orthostatic hypotension, reflex tachycardia, throbbing headache, and blushing.
|
|
|
What is the contraindication to nitrates?
|
Contraindicated if systolic blood pressure is <90 mm Hg.
|
|
|
What is the dosing pattern for nitrates?
|
Requires a window-free period of more than 8 hours with nitrate therapy to reduce tachyphylaxis.
|
|
|
What are the beneficial effects of beta-blockers?
|
Beta-blockers have been shown to improve survival after an acute myocardial infarction and in CHF.
|
|
|
What are the adverse effects of beta-blockers?
|
Fatigue, mental depression, insomnia, adverse effects on lipid panel; hallucinations, Raynaud phenomenon, bronchoconstriction, mask signs and symptoms of insulin-induced hypoglycemia, sexual dysfunction.
|
|
|
What are the adverse effects of nonselective beta-blockers?
|
Nonselective beta-blockers may mask hypoglycemic symptoms in insulin-dependent diabetics.
|
|
|
What is the contraindication to beta-blockers?
|
Contraindicated in severe asthma.
|
|
|
What are the physiologic effects of calcium-channel blockers?
|
Produces decreases in preload and afterload. May be harmful in postinfarction period, especially if left ventricular failure.
|
|
|
What are the adverse effects of calcium channel blockers?
|
Congestive heart failure, reflex tachycardia, hypotension, lightheadedness; flushing, headache, weakness, nausea, constipation, nasal congestion, wheezing, peripheral edema.
|
