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88 Cards in this Set
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What are the physical findings of lung consolidation?
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- Thorax expansion is reduced on affected side on inspiration
- Vocal fremitus is increased on side with consolidation - Percussion is dull on side with consolidation - Breath sounds are bronchial - Crackles - Vocal resonance is increased |
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What are the physical findings of pleural effusion?
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- Decreased movement of the chest on affected side
- Dullness to percussion over the fluid - Diminished breath sounds - Decreased vocal resonance - Decreased fremitus - Pleural friction rub |
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What are the physical findings of pneumothorax?
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- Diminished breath sounds on affected side
- Percussion is hyperresonant - Vocal resonance is decreased - Fremitus is decreased |
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What are the physical findings of right-sided congestive heart failure?
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- Peripheral pitting edema
- Ascites - Hepatomegaly - JVD - Hepatojugular reflex |
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What are the extra-cardiac manifestations bacterial endocarditis?
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- Fever
- Roth spots: retinal hemorrhages - Osler's nodes: small, tender nodules on finger and two pads - Murmur - Janeway lesions: painless hemorrhagic cutaneous lesions on palms and soles - Anemia - Nail-bed (splinter) hemorrhages - Emboli |
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What are the physical findings in chronic liver disease?
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- Clubbing
- Palmar erythema - Spider nevi - Gynecomastia - Testicular atrophy - Feminine hair distribution - Small shrunken liver - Anemia - Caput medusae |
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What are the differences between aortic stenosis and mitral regurgitation?
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Symptoms
- AS: angina to syncope to CHF to death (usually within 5 years) - MR: dyspnea, orthopnea, and fatigue Exam - AS: Pulsus parvus et tardus (weak, dilated carotid upstroke), single or paradoxically split S2 sound; systolic murmur radiating to carotids - MR: Holosystolic murmur radiating to axillae Diagnosis - AS: echo - MR: echo, demonstrating regurgitant flow; angiography can assess severity of disease Treatment - AS: valve replacement; balloon valvuloplasty - MR: antiarrhythmics (for AF); nitrates and diuretics to decrease preload |
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What is the murmur of mitral stenosis?
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Opening snap and mid-diastolic murmur at apex
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What are the differences between peripheral and central facial palsy?
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Peripheral (Bell's) palsy: Weakness in all muscles concerned with facial expression. Corner of mouth droops, forehead is unfurrowed, eyelids will not close.
Central (Supranuclear) palsy: Frontalis and orbicularis oculi muscles (forehead) involved less than the lower parts of face. Dissociation of emotional and voluntary facial movements, often some degree of paralysis of the arm and leg, or an aphasia is present. |
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What are the cardinal manifestations of Parkinson disease?
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- Bradykinesia
- Rest tremor - Muscular rigidity - Shuffling gait - Flexed posture |
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What are the differences between the clinical manifestations of rheumatoid arthritis and osteoarthritis?
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RA:
- Morning stiffness for > 1 hour - Painful, warm swelling of multiple symmetric joints (wrists, MCP joints, ankles, knees, shoulders, hips, elbows) for > 6 weeks - Hyperextension of the PIP joints, compensatory flexion of DIP joints (Swan neck deformity) - Flexion contracture of the PIP joints and extension of the DIP joints (Boutonniere deformity) OA: - Crepitus - Decreased range of motion - Pain that worsens with activity and weight bearing - Morning stiffness lasts for <30 minutes. - DIP, PIP, first metatarsal phalangeal joint (MTP) are affected in the hand |
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What are the differences in physical findings between gastroenteritis and appendicitis?
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Gastroenteritis:
- Nausea and vomiting - Diarrhea - Dehydration - Fever - Abnormal flatulence - Abdominal cramps - Bloody stools (bacterial) - Heartburn Appendicitis: - Migrating pain from periumbilical region (visceral) initially to right lower quadrant (somatic) - Anorexia - Nausea and vomiting - Fever - Rebound tenderness |
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What are the physical findings in cirrhosis of the liver?
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- Esophageal varices
- Ascites - Asterixis - Fetor hepaticus - Spider angiomas - Palmar erythema - Gynecomastia - Testicular atrophy |
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What are the classical physical findings of hypothyroidism?
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- Fatigue, weakness, lethargy
- Slight weight gain - Cold intolerance - Constipation - Muscle weakness, arthralgias - Dry skin, coarse hair - Hoarseness - Non-pitting edema - Carpal tunnel syndrome - Slow relaxation of deep tendon reflexes - Goiter |
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What is the management of acute diabetic ketoacidosis?
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Insulin:
- Give insulin immediately after diagnosis - Give a priming dose of 0.1 units/kg of regular insulin (IV) followed by an infusion of 0.1 units/kg per hour. Be certain that the patient is not hypokalemic before giving insulin. - Continue the insulin until the anion gap closes and metabolic acidosis is corrected, then begin to decrease the insulin. Give SC insulin when patient starts to eat. Fluid replacement (Normal Saline) - Give fluids immediately after diagnosis - Add 5% glucose once the blood glucose reaches 250 mg/dL to prevent hypoglycemia Replace potassium with IV fluids - Initiate within 1 to 2 hours of starting insulin - Ensure adequate renal function (urine output) before administering - Monitor potassium, magnesium, and phosphate levels very closely are replace as necessary HCO3 - Controversial - Not necessary in most cases |
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How do you prevent or slow the development of diabetic nephropathy?
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- Strict glycemic control
- Control HTN aggressively - Initiate ACE inhibitors immediately - Screen for microalbuminuria - Once diabetic nephropathy has progressed to the stage of proteinuria or early renal failure, glycemic control does not significantly influence its course. ACE inhibitors and dietary restriction of protein are recommended. |
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How do you treat thyrotoxic storm and myxedema coma?
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Thyroid Storm
- Provide supportive therapy with IV fluids, cooling blankets, and glucose - Give antithyroid agents (PTU every 2 hours). Follow with iodine to inhibit thyroid hormone release. - Administer beta-blocker for control of heart rate. Give dexamethasone to impair peripheral generation of T3 from T4 and to provide adrenal support. Myxedema Coma - Provide supportive therapy to maintain BP and respiration - Give IV thyroxine and hydrocortisone while carefully monitoring the hemodynamic state. |
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How do you rule out a diagnosis of Cushing disease in an obese, hypertensive patient?
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High-dose dexamethasone suppression test
- In Cushing's disease (pituitary adenoma), the result is a decrease in cortisol levels (greater than 50% suppression occurs) CRH stimulation test - If ACTH/cortisol levels increase, Cushing's disease is the diagnosis |
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How is adrenal insufficiency diagnosed in a hyponatremic patient?
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1. Decreased plasma cortisol level
2. Plasma ACTH level: if low, this implies a secondary adrenal insufficiency (ACTH-dependent cause) 3. Standard ACTH test (definitive): give an IV infusion of ACTH, and measure plasma cortisol at the end of infusion. - In primary adrenal insufficiency, cortisol does not increase sufficiently - In secondary, cortisol fails to respond to ACTH infusion, but after repeating for 4-5 days, adrenals respond. 4. Perform imaging tests (MRI of brain-pituitary/hypothalamus) if secondary or tertiary adrenal insufficiency is diagnosed. |
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What are the criteria for diagnosing SIADH, and what are its causes?
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Characteristics of SIADH:
a. Hyponatremia b. Volume expansion without edema c. Natriuresis d. Hypouricemia and low BUN e. Normal or reduced serum creatinine level because of dilution f. Normal thyroid and adrenal function Diagnosis of exclusion: 1. Support diagnosis a. Hyponatremia and inappropriately concentrated urine; plasma osmolality <270 mmol/kg b. Low serum uric acid level c. Low BUN and creatinine d. Normal thyroid and adrenal function, as well as renal, cardiac, and liver function e. Measurement of plasma and urine ADH level f. Absence of significant hypervolemia 2. Water-load test: patient drinks water load, and urine output is measured hourly. In SIADH, patients excrete <40% of water-load after 5 hours. Normal patients excrete >65% in 4 hours. Causes: - Neoplasms (in lung, pancreas, prostate, bladder), lymphomas, leukemia - CNS disorders (stroke, head trauma, infection) - Pulmonary disorders (pneumonia, tuberculosis) - Ventilators with positive pressure - Medication (vincristine, SSRIs, chlorpropamide, oxytocin, morphine, desmopressin) - Postoperative state |
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What is the differential diagnosis of hypercalcemia and the treatment of hypercalcemic crisis?
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Differential Diagnosis:
1. Endocrinopathies - Hyperparathyroidism - Renal failure (secondary hyperparathyroidism) - Paget's disease of bone - Acromegaly, Addison's disease 2. Malignancies - Metastatic cancer to bone - Multiple myeloma - Tumors that release PTH-like hormone (lung cancer) 3. Pharmacologic - Vitamin D intoxication - Milk-alkali syndrome - Drugs (thiazides, lithium) 4. Other - Sarcoidosis - Familial hypercalciuric hypercalcemia - Ca ingestion Treatment of hypercalcemic crisis (Ca > 14): - IV fluids - Calcitonin - Bisphosphonates - Furosemide |
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What is the presentation of prolactinoma and the treatment?
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Men:
- Hypogonadism, decreased libido, infertility, impotence - Galactorrhea or gynecomastia - Parasellar signs and symptoms (visual field defects and headaches) Women: - Premenopausal: menstrual irregularities, oligomenorrhea or amenorrhea, anovulation and infertility, decreased libido, dyspareunia, vaginal dryness, risk of osteoporosis, galactorrhea - Postmenopausal: parasellar signs and symptoms Treatment: - Bromocriptine (dopamine agonist) or Cabergoline for 2 years - Surgical intervention |
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What is the etiology of hypocalcemia?
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1. Hypoparathyroidism: usually from surgery on thyroid gland
2. Acute pancreatitis: deposition of Ca 3. Renal insufficiency: decreased production of Vitamin D 4. Hyperphosphatemia: PO4 precipitates with Ca, resulting in calcium phosphate deposition 5. Pseudohypoparathyroidism: AR disease causing congenital end-organ resistance to PTH (PTH is elevated) 6. Hypomagnesemia: results in decreased PTH secretion 7. Vitamin D deficiency 8. Malabsorption: short bowel syndrome 9. Blood transfusion: calcium binds with citrate found in blood 10. Osteoblastic metastases 11. Hypoalbuminemia |
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How would you make a clinical diagnosis of Kleinfelter syndrome? What would you see in laboratory tests?
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Clinical:
- Small testes - Infertility - Gynecomastia - Tall stature - Decreased facial or axillary hair Laboratory tests: - Increased LH and FSH - Decreased testosterone - Increased estradiol - Azoospermia - XXY chromosomal analysis |
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What are some causes of osteoporosis? How can it be treated?
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Causes:
- Estrogen depletion - Female gender - Calcium / Vitamin D deficiency - Decreased peak bone mass - Decreased physical activity - Hypogonadism in men - Hyperthyroidism - Smoking and alcohol abuse - Medications: corticosteroids, prolonged heparin use Treatment: - Bisphosphonates - Calcium and Vitamin D supplements - Calcitonin - Weight bearing exercises - Prevention: estrogen replacement therapy, raloxifene |
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Discuss the diagnostic criteria of rheumatoid arthritis.
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A patient has RA if four or more of these seven criteria are present at any time:
1. Morning stiffness for at least 6 weeks 2. Arthritis of three or more joints lasting at least 6 weeks - MCP, PIP, wrist, elbow, knee, ankle, MTP joints 3. Symmetric arthritis for at least 6 weeks 4. Arthritis of hand joints for at least 6 weeks - PIP, MCP, or wrist joint 5. Rheumatoid nodules 6. Serum Rheumatoid Factor 7. Radiographic changes consistent with RA (erosions and periarticular decalcification) Note: RA can involve every joint in the body except the DIP joints. Lab findings: - RF - Elevated ESR, CRP - Normocytic normchromic anemia Radiographs: - Loss of juxtaarticular bone mass near finger joints - Narrowing of the joint space - Bony erosions Synovial fluid analysis: Cloudy yellow, > 5000 WBC/mm3, 50-70% PMNs |
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Discuss the disease-modifying drugs used in treating rheumatoid arthritis.
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Disease-modifying drugs
Methotrexate: 80% experience symptomatic benefit; SE are GI upset, oral ulcers (stomatitis), mild alopecia, bone marrow suppression, hepatocellular injury, and idiosyncratic interstitial pneumonitis leading to pulmonary fibrosis; closely monitor liver and renal function; supplement with folate. Hydroxychloroquine: not as effective as MTX; requires eye examination every 6 months Sulfasalazine Gold compounds, penicillamine, azathioprine, and cyclosporine are second-line agents. |
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What is the CREST syndrome?
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A form of limited scleroderma.
Calcinosis of the digits Raynaud's phenomenon Esophogeal motility dysfunction Sclerodactyly of the fingers Telangiectases (over the digits and under the nails) |
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Discuss the treatment of acute gout.
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Bed rest: early ambulation may precipitate a recurrence
NSAIDs: usually indomethacin; treatment of choice Colchicine: alternative for patients who cannot take or respond to NSAIDs; SE are nausea/vomiting, abdominal cramps, severe diarrhea; contraindicated in renal insufficiency and cytopenia. Corticosteroids: Oral prednisone if patient cannot tolerate or respond to NSAIDs or colchicine. |
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What is the APLA syndrome?
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APLA syndrome is an autoimmune, hypercoagulable state caused by antibodies against cell-membrane phospholipids that provokes blood clots in both arteries and veins as well as pregnancy-related complications such as miscarriage, stillbirth, or severe preeclampsia.
Diagnosis: Lupus anticoagulant Anticardiolipin antibodies Treatment: Aspiring Warfarin or Heparin (for pregnancy) |
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How should a patient suspected of having temporal arteritis be managed?
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Diagnosis:
1. ESR is elevated (although normal ESR does not rule out) 2. Biopsy of temporal artery (sensitivity of 90%). Treatment: 1. High-dose steroids early to prevent blindness: treat immediately, even if TA is only suspected. Do not wait for biopsy results. If visual loss is present, start on IV prednisone; otherwise use oral prednisone. After diagnosis is confirmed, continue treatment for 4 weeks, then slowly taper off over 2-3 years. 2. Follow up on ESR levels to monitor treatment |
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What are the causes of monoarthritis?
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Septic arthritis
Gout Pseudogout Osteoarthritis Monoarthritic form of Chronic Juvenile Arthritis (CJA) Seonegative spondyloarthropathy Traumatic arthritis Psoriatic arthritis Hemarthrosis Hemophilia Monoarticular presentation of polyarticular disease |
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How should a patient with osteoarthritis be treated?
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1. Nonpharmacologic treatment: avoid activities that involve excessive joint use; weight loss; physical therapy; canes
2. Pharmacologic treatment: Acetominophen (first line), NSAIDs, intra-articular injections of steroids, viscosupplementation 3. Surgery for serious disability: total joint replacement, spine surgery 4. Nutritional products: glucosamine and chondroitin sulfate |
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What are the complications of long-standing SLE?
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Cardiac: pericarditis, endocarditis (Libman-Sacks), myocarditis
Pulmonary: pleuritis (most common lung finding), pleural effusion, pneumonitis (may lead to fibrosis), pulmonary HTN Hematologic: hemolytic anemia with anemia or reticulocytosis of chronic disease, leukopenia, lymphopenia, thrombocytopenia Renal: proteinuria > 0.5 g/day, cellular casts, GN (may have hematuria), azotemia, pyuria, uremia, HTN Immunologic: impaired immune response CNS: seizures, psychosis, depression, TIA, CVA Other: conjunctivitis, increased incidence of Raynaud's phenomenon and Sjogren's syndrome. |
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Describe the organ systems affected in a patient with scleroderma.
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Skin:
- Raynaud's phenomenon - Cutaneous fibrosis GI: - Dysphagia/Reflux from esophogeal dysmotility - Delayed gastric emptying - Constipation/Diarrhea - Abdominal distention Pulmonary: Most common cause of death - Interstitial fibrosis and/or pulmonary HTN Cardiac: - Pericardial effusions - Myocardial involvement leading to CHF - Arrhythmias Renal: - Renal crisis (rapid malignant hypertension) |
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Describe the typical presentation of Wegener's disease. How is it diagnosed and treated?
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Clinical Features:
- Upper respiratory symptoms (e.g. sinusitis); purulent or bloody nasal discharge - Oral ulcers - Pulmonary symptoms (cough, hemoptysis, dyspnea) - Renal: GN - Eye disease (conjunctivitis, scleritis) - Musculoskeletal (arthralgias, myalgias) - Tracheal stenosis - Constitutional findings (e.g. fever, weight loss) Diagnosis: - Chest radiograph is abnormal (nodules or infiltrates) - Laboratory findings: elevated ESR; anemia (normochromic normocytic); hematuria - Positive c-ANCA in 90% - Thrombocytopenia may be present - Open lung biopsy is confirmative Treatment: Prognosis is poor, most patients die within 1 year after diagnosed - Cyclophosphamide and corticosteroids can induce remissions, but relapses occur at any time - Consider renal transplantation if patient has ESRD. |
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What are the etiologies of hyperkalemia? How is it treated acutely
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1. Increased total body potassium
- Renal failure - Addison's disease - Potassium-sparing diuretics - Hyporeninemic hypoaldosteronism - ACE inhibitors - Iatrogenic overdose - Blood transfusion 2. Redistribution: translocation of potassium from intracellular to extracellular space - Acidosis - Tissue/cell breakdown: rhabdomyolysis, hemolysis, burns - GI bleeding - Insulin deficiency: insulin stimulates the Na-K ATPase and causes K to shift into cells. Insulin deficiency and hypertonicity (high glucose) promote K shifts from ICF to ECF - Rapid administration of beta-blocker 3. Pseudohyperkalemia - Artificially elevated plasma K concentration due to K movement out of cells during venipuncture. - Leukocytosis, hemolysis, and thrombocytosis Treatment: 1. If hyperkalemia is severe, first give IV calcium. - Calcium stabilizes the resting membrane potential - Be wary of giving Calcium to patients on digoxin 2. Shift potassium into intracellular compartment - Glucose and insulin - Sodium bicarbonate: increases pH level 3. Remove potassium from body - Kayexalate: absorbs K in the colon, passing it in stool - Hemodialysis: most rapid and effective way of lowering plasma K; reserved for intractable hyperkalemia - Diuretics (furosemide) |
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How do you differentiate between acute and chronic renal failure?
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Favors Chronic:
- History of kidney disease, HTN, abnormal urinalysis, edema - Small kidney size on renal US - Hyperkalemia, acidemia, hyperphosphatemia, anemia - Urinalysis with broad casts (>2-3 WBCs in diameter) Favors Acute: - Return of renal function to normal with time - Hyperkalemia, acidemia, hyperphosphatemia, anemia - Urine output < 500 mL/day without uremic symptoms ARF: - A rapid decline in renal function, with an increase in serum creatinine level (a relative increase of 50% or an absolute increase of 0.5 to 1.0 mg/dL) - Characterized by azotemia (elevated BUN and creatinine) - Most common cause of death is infection (75%) followed by cardiorespiratory complications CRF: - Occurs over a period of months to years - Diabetes is the most common cause (30%), followed by HTN (25%) and chronic GN (15%) When a patient comes in with elevated Cr levels, the first thing to do is determine the patient's baseline Cr level. This helps determine whether the patient has ARF or CRF. |
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What is contrast media nephropathy? How can it be prevented?
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Acute renal failure induced by a contrast agent.
Risk factors: - Systolic blood pressure < 80 - Intraarterial balloon pump - CHF (class III or IV or history of pulmonary edema) - Age > 75 - Hematocrit < 39% (men) or < 35% (women) - Diabetes - Contrast media volume - Renal insufficiency: Serum Cr > 1.5 or GFR < 60 Prevention: - Hydration with sodium bicarbonate - Limit the total contrast volume |
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How do you treat a patient with essential hypertension?
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1. Lifestyle changes
- Reduce salt intake - Lose weight - Avoid excessive alcohol - Exercise regularly - Follow a low-saturated-fat diet rich in fruits and veggies - Stop unnecessary medications that contribute to HTN - Manage stress 2. Pharmacological treatment - Thiazide diuretics - beta-blockers - ACE inhibitors or ARBs - CCBs - alpha-blockers - Vasodilators (hydralazine and minoxidil) General principles: - BP should be lowered to <140/90 - In diabetics or patients with renal insufficiency, BP must be lowered to <135/85 - Ideal goal is to lower BP to <120/80 - The most common initial choices are beta-blockers and thiazides - ACE inhibitors are great in diabetics |
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What antihypertensive agent would you give to a diabetic patient with hypertension?
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Target goal for BP in diabetic patients: <135/85
ACE inhibitors or ARBs are first line treatment. Beta-blockers and thiazides are useful but can increase insulin resistance and negatively impact the lipid profile. |
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What is renovascular hypertension?
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AKA Renal artery stenosis
- Causes a decrease in blood flow to the juxtaglomerular apparatus, resulting in the activation of the renin-angiotensin-aldosterone system. This leads to HTN. - This is the most common cause of secondary HTN Causes - Atherosclerosis (66%) - Fibromuscular dysplasia |
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What are some causes of acute glomerulonephritis?
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Acute glomerulonephritis is a common complication of streptocoocal skin infection (impetigo, strep throat), for which it is known as poststreptococcal glomerulonephritis.
Other causes: - IgA nephropathy - Lupus nephritis - Type 1 MPGN - Bacterial endocarditis - Nephrotic syndrome |
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How do you treat pyelonephritis?
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- Usually caused by an ascending spread from the bladder to the kidney.
- Organisms: E. coli (most frequent cause), gram-negative (Proteus, Klebsiella, Enterobacter, Pseudomonas), gram-positive (Enterococcus faecalis, S. aureus) Treatment: 1. For uncomplicated pyelonephritis: - Outpatient if patient can take oral antibiotics. - TMP/SMX or a fluoroquinolone for 10-14 days is effective for most gram-negative rods - Amoxicillin is appropriate for gram-positive cocci - A single dose of ceftriaxone or gentamicin is given before starting oral treatment - Repeat urine culture 2-4 days after cessation of therapy. 2. If patient is very ill, elderly, pregnant, unable to take oral meds, or has significant comorbidities, hospitalize patient. - Give IV fluids - Treat with antibiotics, starting with broad-spectrum parenteral: ampicillin plus gentamicin or ciprofloxacin - If blood cultures are negative, treat with IV antibiotics until patient is afebrile for 24 hours, then give oral antibiotics to complete 14-21 day course. 3. For recurrent pyelonephritis - Due to same organism: treat for 6 weeks - Due to new organism: treat with appropriate therapy for 2 weeks |
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How does a patient with renal cell carcinoma present?
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Hematuria: 70% of patients
Abdominal or flank pain: 50% Abdominal mass: 40% Weight loss, fever Paraneoplastic syndromes: tumors ectopically secreting EPO (causing polycythemia), PTH-like hormone (causing hypercalcemia), renin (causing HTN), cortisol (Cushing's syndrome), or gonadotropins (feminization or masculinization) |
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What are some causes of secondary hypertension?
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Renal/renovascular disease: Renal artery stenosis, chronic renal failure, polycystic kidneys
Endocrine causes: hyperaldosteronism, thyroid or parathyroid disease, Cushing's syndrome, pheochromocytoma, hyperthyroidism, acromegaly Medications: oral contraceptives, decongestants, estrogen, appetite suppressants, chronic steroids, TCAs, NSAIDs - Coarctation of the aorta - Cocaine, other stimulants - Sleep apnea |
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What are some common causes of chronic renal failure? What is the treatment?
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Causes:
- Diabetes (most common cause at 30%) - HTN (25%) - Chronic GN (15%) - Interstitial nephritis, polycystic kidney disease, obstructive uropathy - Any of the causes of ARF may lead to CRF if prolonged and/or if treatment is delayed. Treatment: 1. Diet: low protein, low-salt, restrict potassium, phosphate, and magnesium 2. ACE inhibitors 3. Strict BP control (ACE inhibitors preferred drug) 4. Glycemic control if diabetic patient 5. Correction of electrolyte abnormalities - Hyperphosphatemia: use calcium citrate - Long-term oral calcium and vitamin D - Acidosis: oral bicarb replacement 6. Anemia: Treat with EPO 7. Pulmonary edema: use dialysis if diuresis doesn't work 8. Pruritis: Capsaicin cream or cholestyramine and UV light 9. Dialysis 10. Transplantation (only cure) |
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Why do patients with chronic renal failure have anemia? How is it treated?
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Normochromic normocytic anemia is secondary to erythropoietin deficiency. Treat with EPO.
Iron-deficiency anemia may result due to the increased erythrocyte production after EPO administration, so supplemental iron may be needed. |
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What are the indications for dialysis?
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1. Nonemergent indications
- Cr and BUn levels are not absolute indications - Symptoms of uremia: nausea and vomiting; lethargy/deterioration in mental status, encephalopathy, seizures; pericarditis 2. Emergent indications - Life-threatening manifestations of volume overload: pulmonary edema, hypertensive emergency - Severe, refractory electrolyte disturbances (e.g. hyperkalemia, hypermagnesemia) - Severe metabolic acidosis - Drug toxicity/ingestions: methanol, ethylene glycol, lithium, aspirin |
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What are the manifestations, lab values, and main causes of nephrotic syndrome?
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Proteinuria > 3.5 g/24 hours
Hypoalbuminemia < 3g/dL Edema Hyperlipidemia Lipiduria Hypercoagulability Causes: Minimal Change Disease Focal Segmental Glomerulosclerosis Membranous Glomerulonephritis Membranoproliferative Glomerulonephritis Diabetic nephropathy Amyloidosis |
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Describe the treatment of community-acquired and nosocomial pneumonia.
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Community-Acquired:
1. Decision to hospitalize: consider demographics (sex, nursing home resident), comorbid illness, physical exam, lab and x-ray findings 2. Antimicrobial therapy - For outpatients <60: macrolides or doxycycline (first-line), fluoroquinolones (alternative) - For outpatients >60 or with comorbidities: 2nd or 3rd generation cephalosporin (first-line), amoxicillin/clavulanic acid (alternative) - For hospitalized patients: fluoroquinolone (levofloxacin) alone or 3rd gen cephalosporin plus macrolide Nosocomial pneumonia: 1. non-MDR: treat with single agent: Ceftriaxone, moxifloxacin, ciproflaxacin, levofloxacin, ampicillin/sulbactam, or ertapenem 2. MDR: three antibiotics (two for P. aeruginosa, one at MRSA); beta-lactam (ceftazidime), gentamicin or tobramycin, Vancomycin or linezolid |
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Describe the major causes of fever of unknown origin.
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Classic FUO
1. Infections 2. Neoplasms 3. Connective tissue disease 4. Miscellaneous disorders (e.g. alcoholic hepatitis, granulomatous conditions) 5. Undiagnosed conditions Nosocomial Immune-deficient HIV-associated |
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Describe the treatment of strep viridans endocarditis.
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For all endocarditis:
1. Parenteral antibiotics based on culture results for extended periods (4-6 weeks) 2. If cultures are negative but there is high clinical suspicion, treat empirically with a penicillin (or vancomycin) plus an aminoglycoside until the organism can be isolated. For strep viridans: most strains are susceptible to penicillin, penicillin MIC must be determined. Penicillin G should be given IV for 4 weeks. Gentamycin may also be added. |
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Describe the differences in CSF findings between viral and bacterial meningitis.
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WBC count: Normal <5
B: > 1,000 (1,000-20,000) V: < 1,000 WBC differential: Normal all lymphocytes or monocytes, no PMNs B: mostly PMNs V: mostly lymphocytes and monocytes Glucose: Normal 50-75 mg/dL B: Low V: Normal Protein: Normal <60 B: High V: Moderate elevation |
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Describe common causes of infectious diarrhea.
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Acute viral gastroenteritis (rotavirus, Norwalk virus)
Salmonella Shigella Staphylococcus food poisoning Campylobacter jejuni Clostridium perfringens Enterotoxic E. coli E. coli 0157:H7 Giardiasis Vibrio cholera |
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Discuss the various types of drugs used to treat AIDS.
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1. Antiretrovial therapy:
- Triple drug regiments (HAART): two nucleoside reverse transcriptase inhibitors and either: a nonnucleoside reverse transcriptase inhibitor or a protease inhibitor 2. Opportunistic infection prophylaxis - P. carinii: TMP/SMX - TB: Isoniazid and pyridoxine - Atypical mycobateria: Clarithromycin and azithromycin - Toxoplasmosis: TMP/SMX 3. Vaccination (no live-virus vaccines!) - Pneumococcal polysaccharide vaccine (Pneumovax): every 5-6 years - Influenza vaccine: yearly - Hep B vaccine (if not already antibody-positive) |
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Describe the indications for vaccination with Pneumovax.
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- Adults > 65 years of age
- Patients with sickle cell disease or asplenia - Adults with chronic medical problems or immunodeficiencies - Women with high-risk pregnancies |
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Discuss the causes of pharyngitis and cervical adenopathy.
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Pharyngitis:
Viral: adenovirus (most common), orthomyxoviridae, mononucleosis, herpes simplex, measles, common cold Bacterial: Group A strep (most common), C. diphtheriae, Neisseria gonorrhoeae, Chlamydophila pneumoniae, Mycoplasma pneumoniae Cervical adenopathy: - Rubella - Cat scratch fever - Leukemia - Infectious mononucleosis - Lymphoma - Strep pharyngitis - Viral respiratory infection - Toxoplasmosis - TB - Rhabdomyosarcoma - Neuroblastoma - Lymphadenitis - Kawasaki disease |
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Discuss the treatment of uncomplicated UTI in women.
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Use empiric treatment with oral TMP/SMX (Bactrim) for 3 days. If resistant to TMP/SMX, use a fluoroquinolone (ciprofloxacin) for 3 days.
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Discuss the treatment of chemotherapy-induced neutropenia and fever.
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G-CSF (granulocyte-colony stimulating factor) such as filgrastim
Obtain: CXR, PAN culture (blood, urine, sputum, line tips, wond), CBC, complete metabolic pane. |
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How is Clostridium difficile diarrhea treated?
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1. Discontinue offending antibiotic.
2. Metronidazole is drug of choice 3. Oral vancomycin used if patient is resistant to metronidazole or cannot tolerate. 5. Cholestyramine may be used as an adjuvant to improve diarrhea. |
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Describe the physical findings in a patient with asthma.
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Shortness of breath
Wheezing Chest tightness Cough - Symptoms typically worse at night - Most common physical finding is wheezing (during both inspiration and expiration) |
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Discuss the causes of an elevated pCO2.
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Respiratory acidosis pCO2 > 40
- Primary pulmonary disease: COPD, airway obstruction, ARDS - Neuromuscular disease: myasthenia gravis, poliomyelitis, ALS - CNS malfunction: injury to brainstem - Drug induced hypoventilation: morphine, anesthetics, sedatives - Sleep apnea Metabolic alkalosis: body compensates by hypoventilating - ECF contraction and hypokalemia - Vomiting, nasogastric suction, diuretics, diarrhea with high chloride content - ECF expansion and hypertension: primary hyperaldosteronism, Cushing's syndrome, K deficiency, Bartter's syndrome, hypothyroidism, diuretics |
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What is sleep apnea? How should it be treated?
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- Intermittent obstruction of the air flow produces periods of apnea during sleep.
- Each apneic period lasts 20-30 seconds, and results in hypoxia, which arouses the patient from sleep. This occurs multiple times overnight. Treatment: 1. Mild to moderate OSA (<20 episodes) - Weight loss - Avoid alcohol, sedatives - Avoid supine position 2. Severe OSA (>20 episodes) - Nasal continuous positive airway pressure - Uvulopalatopharyngoplasty: removal of redundant tissue in oropharynx - Tracheostomy (last resort) |
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Discuss several causes of interstitial lung disease.
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1. Environmental lung disease
- Coal worker's pneumoconiosis - Silicosis - Asbestosis - Berylliosis 2. ILD associated with granulomas - Sarcoidosis - Histiocytosis X - Wegener's granulomatosis - Churg-Strauss syndrome 3. Alveolar filling disease - Goodpasture's syndrome - Idiopathic pulmonary hemosiderosis - Alveolar proteinosis 4. Hypersensitivity lung disease - Hypersensitivity pneumonitis - Eosinophilic pneumonitis 5. Drug-induced - Amiodarone - Nitrofurantoin - Bleomycin - Phenytoin 6. Miscellaneous - Idiopathic pulmonary fibrosis - Bronchiolitis obliterans organizing pneumonia (BOOP) - ILD a/w RA, scleroderma, SLE, mixed connective tissue disease - ARDS - Radiation pneumonitis |
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What should be done with an asymptomatic medical student found to have a 20mm response to a tuberculin skin test (Mantoux)?
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For Mantoux method, ≥15 mm is positive.
For a positive TB exposure and a positive PPD test (but no active disease), treatment is INH only. If the patient has active TB, multiagent therapy is indicated. - Isoniazid (INH), rifamipin, pyrazinamide, and ethambutol. |
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Discuss the major causes of hemoptysis.
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Bronchitis (50%)
Lung cancer (bronchogenic carcinoma) TB Bronchiectasis Pneumonia Idiopathic (30%) Goodpasture's syndrome PE with pulmonary infarction Aspergilloma within cavities Mitral stenosis (elevated pulmonary venous pressure) |
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Describe the causes and evaluation of pleural effusion.
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Causes
1. CHF 2. Pneumonia (bacterial) 3. Malignancies: lung (36%), breast (25%), lymphoma (10%) 4. Pulmonary embolism 5. Viral diseases 6. Cirrhosis with ascites Evaluation 1. CXR: look for blunting of costophrenic angle 2. CT scan 3. Thoracentesis: diagnosis, drainage |
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Describe the typical arterial blood gasses seen in a patient with pulmonary embolus.
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PaO2 and PaCO2 are low
pH is high (respiratory alkalosis) A-a gradient is elevated |
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Describe the major differences between obstructive and restrictive lung disease, as reflected by pulmonary function studies.
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Obstructive:
Increased lung volumes, except for vital capacity. Decreased FEV1, FVC, and FEV1/FVC ratio. Decreased FEF25-75 Decreased peak expiratory flow rate Restrictive: Decreased lung volumes (except for residual volume which can be low, normal, or high) Normal or slightly low FEV1 Normal or High FEV1/FVC Normal peak expiratory flow rate |
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How would you evaluate a patient suspected of having a pulmonary embolus?
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The following tests provide an adequate basis for treating PE with anticoagulation:
- Intraluminal filling defects in central, segmental, or lobular pulmonary arteries on helical CT - DVT diagnosed with ultrasound - Positive pulmonary angiogram (definite diagnosis) The following rules out PE: - Low-probability V/Q scan (or normal helical scan) - Negative pulmonary angiogram (definite) - Negative D-dimer assay For PE: - ABG levels are not diagnostic - CXR is usually normal - Venous duplex ultrasound at the lower extremities (helpful when positive) - V/Q (Ventilation-perfusion) scan: used if CT scan is contraindicated - Helical CT scan of chest: good sensitivity and specificity - Pulmonary angiography is gold standard, but is invasive - D-dimer |
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What are the causes of pulmonary hypertension? How are the various causes treated?
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Causes:
1. Passive type: resistance to venous drainage - mitral stenosis - LV failure - atrial myxoma 2. Hyperkinetic type: caused by high pulmonary blood flow (left-to-right cardiac shunts) - VSD, ASD, PDA 3. Obstructive type: resistance to flow through large pulmonary arteries - PE - Stenosis of pulmonary artery 4. Obliterative type: resistance to flow through small pulmonary vessels (arterioles) due to parenchymal inflammation that leads to fibrosis 5. Vasoconstrictive type: resistance to flow due to hypoxia-induced vasoconstriction - Anything that causes chronic hypoxemia - COPD - Obstructive sleep apnea 6. Increased intrathoracic pressure: increased pressure is transmitted to pulmonary vasculature - Mechanical ventilation with PEEP - COPD 7. Increased blood viscosity (i.e. polycythemia vera)\ Treatment PE: O2, UFH, LMWH, Warfarin (long term), streptokinase/TPA, IVC interruption COPD: bronchodilators, anticholinergic drugs, corticosteroids, O2 |
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Describe the general classifications of various forms of lung cancers. What is known of the etiologies of these cancers?
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Small cell lung cancer (SCLC) = 25%
Non-small cell (NSCLC) = 75% - Squamous cell carcinoma - Adenocarcinoma (35%, most common) - Large cell carcinoma - Bronchoalveolar cell carcinoma Risk factors: - Smoking in >85% of cases - Passive smoke - Asbestos - Radon - COPD Location: Central: Squamous, SCLC Peripheral: Adeno, Large cell |
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What are the signs of digoxin intoxication?
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GI: Nausea/vomiting, anorexia
Cardiac: ectopic (ventricular) beats, AV block, AFib CNS: visual disturbances (yellow or green halos), disorientation *Hypokalemia predisposes patients to digoxin toxicity, so always monitor K+ levels. *Diuretics can cause hypokalemia Treatment: digoxin immune Fab |
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How is paracetamol intoxication diagnosed and treated?
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Diagnosis:
Blood paracetamol level (with nomogram) taken after 4 hours RUQ tenderness Evidence of hepatic necrosis: elevated AST, ALT, bilirubin, prolonged coagulation times (especially PT) - If AST and ALT > 1000 IU/L, a diagnosis for paracetamol-induced hepatotoxicity may be made. Treatment: Gastric decontamination - Gastric lavage - Activated charcoal (within 30 min-2 hours) Acetylcysteine - AKA N-acetylcysteine (NAC) - Replenishes stores of antioxidant glutathione Liver transplant: in patients who develop fulminant hepatic failure |
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What are the side effects of ACE inhibitors?
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Hypotension
Cough: increases in bradykinin levels Hyperkalemia: Suppression of angiotensin II leads to decrease in aldosterone levels, which results in retention of potassium. Headache Dizziness Fatigue Nausea Renal impairment Angioedema: due to increased bradykinin levels Contraindications: Previous angioedema Renal artery stenosis Hypersensitivity Pregnancy Use with caution: Impaired renal function Aortic valve stenosis Hypovolemia or dehydration Hemodialysis |
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What can cause the INR to raise in a patient receiving a stable dose of warfarin (Coumadin)?
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Vitamin K: The maintenance dose of warfarin can fluctuate significantly depending on the amount of vitamin K in the diet. If you eat less vitamin K, it can raise INR.
Alcohol Herbal supplements? Antibiotics? Analgesics? Antidepressants? Diabetes drugs? |
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Why does grapefruit juice affect the metabolism of many drugs?
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Grapefruit juice is a potent inhibitor of cytochrome P450 enzyme, which can increase the bioavailability of many drugs.
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What is the difference in action of an ACE inhibitor and an Angiotensin-receptor blocker (ARB)?
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ACE inhibitors: block ACE that cleaves angiotensin I to form the potent vasoconstrictor angiotensin II. The converting enzyme is also responsible for the breakdown of bradykinin. ACE inhibitors decrease angiotensin II and increase bradykinin levels. This causes vasodilation by two mechanisms. Decreased levels of angiotensin II also decrease the secretion of aldosterone.
Angiotensin II-receptor blockers: these drugs block the AT1 receptors. They produce arteriolar and venous dilation and block aldosterone secretion, thus lowering blood pressure and decreasing salt and water retention. ARBs do not increase bradykinin levels. |
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Describe the treatment of acute hypertensive crisis.
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Hypertensive emergency:
* Systolic > 220 and/or Diastolic > 120 * End-organ damage: - eyes (papilledema) - CNS (altered mental state; intracranial hemorrhage; encephalopathy) - Kidneys: renal failure, hematuria - Heart - Lungs: pulmonary edema Treatment: 1. Reduce mean arterial pressure by 25% in 1 to 2 hours. The goal is not to immediately achieve normal BP, but get patient out of danger, then reduce BP gradually. 2. If sever (diastolic > 130) or if encephalopathy is present, IV agents such as nitroprusside, labetalol, or nitroglycerin are appropriate 3. In patients who are in less danger, use oral agents: captopril, clonidine, labetalol (oral), and diazoxide |
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Describe the treatment of acute pulmonary edema.
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Maintain adequate oxygenation
- High flow oxygen - CPAP/VPAP - Mechanical ventilation - PEEP In cardiac causes: - Loop diuretics - IV nitrates |
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Discuss the evaluation of a patient suspected of having a pulmonary embolus.
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- Intraluminal filling defects in central, segmental, or lobular pulmonary arteries on helical CT
- DVT diagnosed with ultrasound - Positive pulmonary angiogram (definitive) - D-dimer (negative rules out) |
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Discuss the causes and evaluation of a patient with syncope.
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Causes:
1. Seizure disorder 2. Cardiac - Arrhythmias (sick sinus, VT, AV block, SVT) - Obstruction of blood flow (AS, HOCM, pulmonary HTN, atrial myxoma) - Massive MI 3. Vasovagal syncope (most common cause) - emotion stress, pain, fear, fatigue, claustrophobia 4. Orthostatic hypotension: - ganglionic blocking agents - diabetes, old age 5. Severe cerebrovascular disease 6. Metabolic (hypoglycemia), hypovolemia, hypersensitivity, medications Diagnosis: 1. Rule out life-threatening conditions 2. Differentiate between cardiac and noncardiac etiologies 3. History: events before, during, and after episode 4. Physical exam 5. Tests: ECG, CBC, metabolic panel 6. Other: Tilt-table, CT or EEG (for seizures), echo |
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Discuss the general approach to a patient with a hemoglobin of 7.0 g/dL.
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If the Hb concentration is < 7 g/dL, transfusion is recommended.
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Discuss the treatment of a patient with hypotension and a temperature of 39 degrees.
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Management of hypotension:
1. Quickly assess mental status - how symptomatic is the patient? 2. Obtain a full set of vitals, including BP in both arms. Expect a compensatory tachycardia. Bradycardia may result in reduced cardiac output. 3. Determine baseline BP 4. Consider ECG, CXR, ABG, blood culture (if febrile), and CBC (if bleeding) 5. Treatment should be directed toward the cause. 6. If patient is symptomatic, the reverse trendelenburg position 7. Consider NS bolus (500 mL) - repeat this if BP does not improve 8. Discontinue or hold antihypertensive meds 9. Vasopressors may be needed if there is no response to IV fluids 10. If hypotension is profound or persists despite fluid therapy, consider transferring the patient to the ICU. 11. Put the patient on a cardiac monitor. |
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Discuss the evaluation of a patient with fever of unknown origin.
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1. Careful history and physical - pay attention to medications, travel, immune system competency, and review of systems.
2. Laboratory tests - CBC with differential - Urinalysis - Culture of blood, sputum, CSF, urine, and stool when indicated by clinical presentation - Analysis and culture of abnormal fluid collections (joint, pleural) - Complement assay - PPD when TB is on differential - Other laboratory values: LFTs, ESR, ANA, RF, TSH 3. Imaging studies - CXR, CT scan of chest and abdomen (to detect tumors and abscesses) - Tagged WBC scan - MRI, US, echo 4. Invasive diagnostic procedures: biopsy of lymph node, bone marrow, or other tissue 5. Observation is sometimes necessary to make diagnosis |
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Discuss the differential diagnosis of chest pain.
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Causes:
1. Heart/vascular: angina, MI, pericarditis, aortic dissection 2. GI: GERD, diffuse esophageal spasm, peptic ulcer disease, gallbladder disease, acute cholecystitis 3. Chest wall: costochondritis, rib fracture, muscle strain, herpes zoster 4. Psychiatric: anxiety, somatization 5. Pulmonary: PE, pneumothorax, pleuritis 6. Cocaine use: can cause angina or MI Management: 1. Check vitals: obtain 12-lead ECG and compare with old ECG. Get history of cardiac disease 2. Order cardiac enzymes (CK, CKMB, Troponin) X3, every 8 hours 3. Consider CXR (pneumothorax, widened mediastinum, pleural effusion), ABG or CT scan (or V/Q scan) if PE suspected. 4. If myocardial ischemia is suspected: - Oxygen, 2 L by NC, titrate up as needed - Nitroglycerin (sublingual) for pain - Keep systolic BP > 90 - Aspirin - Heparin: give a loading dose, then start a drip. Check PTT in 6 hours - Put patient on a cardiac monitor 5. Treat other suspected conditions |
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Discuss the evaluation of a jaundiced patient.
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1. History and physical exam
2. Labs (LFTs): ALT, AST, ALK-P, PT, bilirubin, albumin - If normal LFTs: check for conjugated hyperbilirubinemia (Dubin-Johnson syndrome, Rotor syndrome) or unconjugated hyperbilirubinemia (Gilbert's, hemolysis) 3. If abnormal LFTs: - Suspected intrahepatic disease: viral serology, AMA, ANA, SMA, ceruloplasmin, Fe/TIBC, A1AT - Suspected extrahepatic obstruction: noninvasive imaging (US/CT); if normal, do direct duct visualization (ERCP or PTC) |
