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Posted Jun 17, 2008 10:14 PM
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* dr asher high yield
#161290
s786 - 02/13/07 11:57
USMLE Step 2 — Lesson 1: Strategy & Pulmonary
Internal Medicine - Part 2 Asher Kornbluth, MD LUNGS Lungs A 62-year-old plumber presents to your office complaining of 6 months of a progressive, non-productive cough. He has not smoked and has noted that he has limited exercise tolerance over the last several months. He has had no fevers or other associated symptoms. A CXR shows bilateral hazy infiltrates and calcification of the pleura. Occupational Lung Disease Asbestosis · Progressive pulmonary fibrosis in reaction to inhaled asbestos fibers · Symptoms o Dyspnea o Non-Productive cough o Pleuritic chest pain Occupational Lung Disease Asbestosis · CXR o Pleural plaques and thickening o Hazy infiltrate in lower lobe · PFTs – restrictive pattern · Increased risk of bronchogenic carcinoma and mesothelioma A 37-year-old woman presents to your office complaining of several episodes of coughing up bright red blood. She denies any recent travel. She works as a librarian and has had no other complaints. On physical examination, there are several scattered rhonchi throughout both lung fields; the remainder of the examination is normal. Lab results reveal that her serum Na, K, glucose, and HCO3 are normal, the BUN is 37 and the creatinine is 4.9. Urinalysis shows a lot of hematuria. MISCELLANEOUS INTERSTITIAL AND ALVEOLAR-FILLING LUNG DISEASES Goodpasture’s syndrome · Diffuse alveolar hemorrhage and glomerulonephritis with Ig deposition along alveoli and GBM (anti-GBM) MISCELLANEOUS INTERSTITIAL AND ALVEOLAR-FILLING LUNG DISEASES · Symptoms o Hemoptysis o Cough o Dyspnea o Hematuria o Renal insufficiency MISCELLANEOUS INTERSTITIAL AND ALVEOLAR-FILLING LUNG DISEASES Goodpasture’s syndrome · CXR – bilateral, symmetric, alveolar-filling · infiltrates o Therapy o Steroids o Cytotoxic drugs o Plasmapheresis Drug-Induced Lung Disease Cancer chemotherapy · Methotrexate · Bleomycin - may cause pneumonitis or fibrosis DRUG-INDUCED LUNG DISEASE Cardiac meds · Amiodarone - pneumonitis with bilateral interstitial or alveolar pattern · Beta blockers - bronchoconstriction · ACE inhibitors - non-productive cough · Hydralazine, procainamide, quinidine - pleurisy due to drug-induced lupus · Aspirin - rhinitis, nasal polyps, bronchospasm Drug-Induced Lung Disease Illicit drugs, ie, narcotics · Overdose --» non cardiogenic pulmonary edema · Interstitial lung disease due to talc · Septic emboli from right-heart endocarditis A 32-year-old African-American woman presents to you complaining of a non-productive cough over the last 6 months. She has no travel history. She has been otherwise healthy and is on no medications. On physical examination, vital signs are normal, she has scattered large nodes in the anterior and posterior cervical chain, and there diffuse scattered rhonchi on lung exam. She has an enlarged liver and the remainder of the exam is normal. X-rays show hilar adenopathy. Sarcoidosis · Chronic multisystem disease with noncaseating granulomas in affected organs · Pulmonary involvement in > 90% of patients o Stage 0 – normal o Stage I – hilar lymphadenopathy o Stage IIA – hilar lymphadenopathy and parenchymal infiltrates o Stage IIB – infiltrates without hilar lymphadenopathy o Stage III – advanced fibrosis and bullae Sarcoidosis Extrapulmonary features · Lymphadenopathy, hepatosplenomegaly · Skin o Lupus pernio (blue-purple lesion of face, fingers) o Erythema nodosum · Eye o Uveitis o Sjögren’s syndrome Sarcoidosis Extrapulmonary features · Nervous system – Bell’s palsy · Myocardium – conduction disturbances · Hypercalcemia o Nephrocalcinosis o Nephrolithiasis Sarcoidosis Diagnosis · Typical clinical or x-ray findings · Histologic demonstration of noncaseating granulomas · Negative bacterial, fungal, and tissue studies, ie, rule out infections Sarcoidosis Treatment · Steroids for severe lung involvement · Steroids for the following extrapulmonary findings: o Ocular disease o Hypercalcemia o Cardiac arrhythmia o Neurologic involvement o Arthritis o Disfiguring skin lesions A patient presents with a cough for the last 3- 6 months but not acute. Patient also complains of a sinus infection. Exam will show a normal upper respiratory tract exam. On routine physical, acute rhonchi and hematuria in the urine and on electrolytes renal insufficiency. Granulomatous Vasculitis Wegener’s granulomatosis · CXR – multiple nodular infiltrates · Labs – elevated C-ANCA (cytoplasmic anti-neutrophilic cytoplasm antibodies) · Treatment – prednisone and cyclophosphamide
USMLE Step 2 — Lesson 2: Pulmonary
A patient presents with a non-productive cough for the past 5 days. He has increased pain with deep inspiration, described as sharp pain. He has a history of congestive heart failure. On exam, there is diffuse crackling halfway up both lung fields and there is an S3 present. On lung exam, there is dullness to percussion and decreased fremitus at both bases. A patient with a history of IV drug abuse presents to the ED with a productive cough, very sharp chest pain on deep inspiration, and a temperature of 39 C (102.8 F). On exam, the patient has dense rhonchi in the right posterior lung field in association with dullness to percussion, decreased fremitus, and diminished breath sounds just under the area of dense rhonchi. CXR shows a dense right lower lobe infiltrate and a pleural effusion. Diseases Of The Pleura Pleural effusions: General features · Signs o Diminished breath sounds o Dullness to percussion o Decreased tactile fremitus o Friction rub Diseases Of The Pleura Pleural effusions: General features · Symptoms o Pleuritic chest pain o Dyspnea o Cough Diseases Of The Pleura Pleural effusions: General features · CXR findings o Blunting costophrenic angle > 300 cc fluid o Free-flowing fluid seen with lateral decubitus film o Ultrasound or CT if fluid loculated Diseases Of The Pleura Pleural effusions: General Features · Thoracentesis o Cell count and differential o Chemistries – LDH & protein, glucose, amylase, pH o Culture – bacteria, TB, fungi o Stains – gram, AFB, fungal o Cytology DISEASES OF THE PLEURA Pleural effusions: Exudate Types · More than 100,000 RBC – pulmonary embolism, TB, hemothorax o Glucose < 60 mg/dL – para pneumonic effusion, malignancy, TB, rheumatoid arthritis (< 30) o High amylase – pancreatitis, esophageal rupture o pH < 7.0 – para pneumonic effusions, empyema, TB, esophageal rupture Pleural effusions: Exudates Types (cont’d) · Immunologic markers – ANA in SLE, RF in RA · Cytology – yield depends on amount of fluid, skill of the cytologist; positive cytology 40-90% of patients with malignant effusions · Pleural biopsy – TB; culture, AFB, malignancy DISEASES OF THE PLEURA Pleural effusions: Exudates · Empyema o Pus in pleural space; since pus is a surgical disease, drain the pleura (ie, chest tube) o Also consider chest tube if pleural fluid shows: § pH < 7.0 § Glucose < 50 in setting of para pneumonic effusion § Organisms on gram stain DISEASES OF THE PLEURA Pleural effusions: Exudates · Malignant effusions o Most commonly seen in cancer of § Lung § Breast § Stomach § Lymphoma § Mesothelioma DISEASES OF THE PLEURA Pleural effusions: Exudates · Malignant effusions o May require pleurodesis – injection of a sclerosant to close the pleural space by fibrosis DISEASES OF THE PLEURA Pleural effusions: Transudates · Occur with either reduced serum oncotic pressure or increased hydrostatic pressure · Causes o CHF o Cirrhosis o Nephrosis o Myxedema
USMLE Step 2 — Lesson 3: Pulmonary
A 59-year-old obese woman presents with pleuritic type cough mild hemophilosis. Came on suddenly. She has no fever. Has normal lung exam remainder exam normal. Reports she just came back from Milan, Italy. She is a fashion consultant and was covering Spring fashion shows. PULMONARY EMBOLISM (PE) Features · Blood clot lodged within the pulmonary circulation · Most originate from deep venous thromboses (DVT) from legs or pelvis · 10% may be fatal!!! PULMONARY EMBOLISM (PE) Pathophysiologic consequences · Pulmonary vascular resistance rises · High pulmonary artery pressure · Increased right ventricular afterload PULMONARY EMBOLISM (PE) Risk factors · Immobilization (especially post-op) · Pelvic/leg surgery or trauma · Malignancy – Trousseau’s syndrome PULMONARY EMBOLISM (PE) Risk factors (cont’d) · Obesity · CHF (predisposes to vascular stasis) · Oral contraceptives/estrogen --> hypercoagulability · Hypercoagulable conditions PULMONARY THROMBOEMBOLISM (PE) Clinical features · Dyspnea · Pleuritic chest pain · Hemoptysis (pleural infarct) PULMONARY EMBOLISM (PE) Clinical features · Signs of RV overload (loud P2, RV heave) · Look for signs of DVT · 50% of patients have no suggestive physical findings PULMONARY EMBOLISM (PE) Diagnosis · History and physical · CXR o Normal -- most common o Regional oligemia o Pleural infarct o Pleural effusion PULMONARY EMBOLISM (PE) Diagnosis · ABG · Respiratory alkalosis · Hypocapnia · Varying hypoxemia · Increased arterial-alveolar oxygen difference PULMONARY EMBOLISM (PE) Diagnosis · Ventilation-perfusion (V/Q) scan – high probability, ie, segmental perfusion defect with normal ventilation · Pulmonary angiography – gold standard but invasive · Venogram or non-invasive testing for lower extremity DVT SOURCES OF PE: DEEP VEIN THROMBOSIS (DVT) Physical findings · Leg pain, tenderness, warmth, redness · Palpable cord · Homan’s sign · Physical exam unreliable for diagnosis; nonspecific and insensitive SOURCES OF PE: DEEP VEIN THROMBOSIS (DVT) Diagnosis · Venogram – gold standard but invasive · Duplex sonography – only 50% sensitive in calves · Impedance plethysmography (IPG) – insensitive for calf-vein thrombosis · 125I-fibrinogen – best for calf-vein thrombi, therefore useful in combination with IPG SOURCES OF PE: DEEP VEIN THROMBOSIS (DVT) Treatment · IV heparin followed by oral warfarin for 3-6 months · Longer duration therapy if recurrent emboli or ongoing risk · Inferior vena caval interruption if anticoagulation contraindicated PE: HYPERCOAGULABLE STATES Suspect in patients with · Strong family history · Recurrent thromboembolism without predisposing cause · Early age · Difficulty anticoagulating · Unusual sites of thrombosis PE: HYPERCOAGULABLE STATES Causes · Antithrombin III deficiency – most common inherited defect; life-long anticoagulation if thrombosis occurs · Protein C, protein S deficiency · Lupus “anticoagulant” PE: HYPERCOAGULABLE STATES Causes · Malignancy · DIC · Myeloproliferative syndromes, ie, polycythemia vera PE ANTICOAGULATION Heparin · Enhances antithrombin III activity to inhibit thrombin formation · Follow with PTT · SQ or IV - ok during pregnancy · Thrombocytopenia is important side effect · Antidote – protamine PE ANTICOAGULATION Warfarin, coumadin · Vitamin K antagonists · Inhibit synthesis of factor II, VII, IX, X (also protein C,S) · Skin necrosis (rare) · Beware of drug interactions · Contraindicated during pregnancy · Antidote – vitamin K or FFP PE ANTICOAGULATION Thrombolytic therapy – streptokinase, urokinase, tPA · Stimulates fibrinolysis · Risk of bleeding very high · Use only with life-threatening PE, ie, hypotension or refractory hypoxemia
USMLE Step 2 — Lesson 4: Respiratory
LUNG CANCER LUNG CANCER Paraneoplastic syndromes · SIADH – most commonly in small cell · Cushing’s syndrome – small cell o HTN, hypokalemia, hyperglycemia, proximal muscle weakness o High AM cortisol that does not suppress with dexamethasone · Hypercalcemia – from either bone metastasis or osteoclastic activity in absence of bone metastasis (squamous) LUNG CANCER Paraneoplastic syndromes · Eaton Lambert – with small cell o Myasthenia-like symptoms (but in contrast to myasthenia, muscles increase in strength with repetition) o Muscle weakness o Decreased tendon reflexes o Autonomic dysfunction LUNG CANCER Paraneoplastic syndromes · SIADH – most commonly in small cell · Cushing’s syndrome – small cell o HTN, hypokalemia, hyperglycemia, proximal muscle weakness o High AM cortisol that does not suppress with dexamethasone · Hypercalcemia – from either bone metastasis or osteoclastic activity in absence of bone metastasis (squamous) APPROACH TO THE PATIENT WITH SOLITARY PULMONARY NODULE Definition – single nodule in the lung parenchyma < 6.0 cm Benign vs. malignant · Favor benign o Younger age o No growth in 2 years (review old CXR) o Small size; 90% < 1 cm are benign APPROACH TO THE PATIENT WITH SOLITARY PULMONARY NODULE Favor benign (con'd) · Pattern of calcification: dense central, multiple punctate, laminated pattern all suggest benign · “Popcorn” pattern = hamartoma · Smooth margins APPROACH TO THE PATIENT WITH SOLITARY PULMONARY NODULE Benign vs. malignant · Favor malignant o Older age o Smoking history o Large size; 90% > 3 cm are malignant o Eccentric calcification o Irregular margins APPROACH TO THE PATIENT WITH SOLITARY PULMONARY NODULE Work-up · CT – accurately evaluates size, margin contours and calcification pattern; also assesses for nodes, other masses, mediastinum · Bronchoscopy and biopsy – especially if proximal or endobronchial APPROACH TO THE PATIENT WITH SOLITARY PULMONARY NODULE Work-up · Percutaneous needle biopsy – helpful if granulomas or hamartoma found; otherwise, cannot exclude a malignant diagnosis · Mini thoracotomy RESPIRATORY THERAPY TECHNIQUES Supplemental oxygen · Indicated for patients with pO2 < 55 mmHg on room air at rest · Beware of suppressing hypoxic drive in patients with chronic CO2 retention · High concentrations of supplemental oxygen --> oxygen toxicity and parenchymal damage RESPIRATORY THERAPY TECHNIQUES Mechanical ventilation: Indications · Apnea or inadequate alveolar ventilation · Severe hypoxemia despite O2 supplementation · Airway protection ADULT RESPIRATORY DISTRESS SYNDROME (ARDS) Features · Non cardiogenic pulmonary edema; due to damage to alveolar-capillary membrane --> stiff lungs · Severe hypoxemia; pO2 < 60 or FIO2 > 60 · CXR – bilateral pulmonary infiltrates ADULT RESPIRATORY DISTRESS SYNDROME (ARDS) Features · Normal or low pulmonary artery, capillary pressures · Mortality – 50%!! · Treat underlying illness ADULT RESPIRATORY DISTRESS SYNDROME (ARDS) Causes of ARDS · Sepsis syndrome · Overwhelming pneumonia · DIC · Major trauma · Multiple transfusions · Pancreatitis · Drowning ADULT RESPIRATORY DISTRESS SYNDROME (ARDS) Mechanical Ventilator – Know the Dials · Respiratory Rate = 12-20 · Volume = 10 cc/kg · FIO2 = as low as possible ADULT RESPIRATORY DISTRESS SYNDROME (ARDS) Causes of ARDS · Sepsis syndrome · Overwhelming pneumonia · DIC · Major trauma · Multiple transfusions · Pancreatitis · Drowning ADULT RESPIRATORY DISTRESS SYNDROME (ARDS) Treatment · Treat underlying cause · Correct hypoxemia but intrapulmonary shunting limits effectiveness of supplemental O2 · PEEP (positive-end expiratory pressure) o Increases lung volumes, allows lower FIO2 o Risks – diminished cardiac output, barotrauma
USMLE Step 2 — Lesson 5: Respiratory Disorders
RESPIRATORY DISORDERS ASTHMA Pathophysiology · Reversible increased resistance to airflow due to airway narrowing · Causes o Airway bronchospasm o Airway inflammation ASTHMA Triggering factors · Airway irritants, environmental pollutants (including occupational exposure) · Exercise, cold air, dry air · Upper and lower respiratory tract infection · Aspirin, NSAIDs (triad of aspirin sensitivity, sinusitis, and nasal polyposis) · Gastroesophageal reflux ASTHMA Treatment · Anti-inflammatory drugs o Inhaled steroids o Systemic steroids o Cromolyn – prevents mast cell degranulation; useful for prophylaxis, not for an acute attack o Zileuton o Zafirlukast ASTHMA Treatment · Bronchodilators o b2 agonists – inhaled and nebulized o Anticholinergics – atropine, ipratropium o Aminophylline preparations – narrow therapeutic/toxicity window ASTHMA Management of acute attack · b2 agonist + steroid inhalers + ipratropium · Systemic steroids · Aminophylline not helpful in control of severe acute attack CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Features · Emphysema – alveolar destruction · Chronic bronchitis – airway inflammatory damage · Both characterized by chronic airway obstruction, dyspnea, cough, sputum production · Cigarette smoking most common factor in both CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Diagnosis · Physical exam o Hyperinflation --> increased A-P diameter, low diaphragm o Diminished breath sounds o Cor pulmonale – jugular venous distention (JVD), hepatomegaly, peripheral edema CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Features · Polycythemia secondary to hypoxemia · Compensated respiratory acidosis · CXR o Hyperinflation o Flat diaphragms o Reduction in vascular markings o Bullae CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Treatment · Smoking cessation · Antibiotics if sputum purulent, with coverage for H. influenzae, S. pneumoniae, M. catarrhalis · Bronchodilators if there is evidence of reversibility –b2 agonists, ipratropium, aminophylline CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Treatment · Steroids – but demonstrate effectiveness with PFTs · Supplemental O2 with pO2 < 55 mmHg – improves survival
USMLE Step 2 — Lesson 6: Esophagus:
Esophagus A patient presents complaining of 6 months of difficulty swallowing; symptoms occur with liquids as well as solids. The patient has lost 10 lbs. Physical exam is normal. Plain AP chest film shows an air fluid level. CLASSIC MOTILITY DISORDERS: ACHALASIA · Pathophysiology: reduced or absent peristalsis in body and high pressure at LES; incomplete relaxation with swallow · Dysphagia to both solids and liquids (always suggests a motility problem) X-ray: upper GI series shows very dilated esophagus with tapering ("bird beak") · Diagnosis: confirmed manometrically · Treatment: pneumatic dilation or surgical myotomy A 42-year-old woman presents complaining with difficulty swallowing solids as well as liquids. She has had these symptoms over the last few months and has lost weight. She also complains that she has had pain in her hands particularly when it is cold. CLASSIC MOTILITY DISORDERS: SCLERODERMA ESOPHAGUS · Pathophysiology: reduced peristalsis and reduced LES resting pressure · Symptoms: dysphagia and terrible reflux symptoms · Late symptoms may be secondary to peptic stricture CLASSIC MOTILITY DISORDERS: NONCARDIAC CHEST PAIN · R/O cardiac chest pain · May be secondary to nonspecific motility problem (eg, diffuse esophageal spasm, "nutcracker" esophagus) · R/O cardiac chest pain · GERD most common cause of noncardiac chest pain · R/O cardiac chest pain CLASSIC MOTILITY DISORDERS: GASTROESOPHAGEAL REFLUX DISEASE (GERD) · Pathophysiology · Reduced LES pressure – most important · Reflux of caustic material · Reduced esophageal peristalsis · Diminished esophageal bicarb/saliva · Delayed gastric emptying CLASSIC MOTILITY DISORDERS: GASTROESOPHAGEAL REFLUX DISEASE (GERD) · LES is vagal mediated; anticholinergic drugs increase reflux · Symptoms o Esophageal (heartburn, dysphagia, odynophagia) o Extra-esophageal (hoarseness, wheezing, aspiration) CLASSIC MOTILITY DISORDERS: GERD Diagnosis · Suggested by history · X-rays: often normal, can demonstrate ulcers, strictures · Endoscopy: often normal, can demonstrate esophagitis, ulcers, Barrett's (see below), and strictures; allows biopsy · 24-hour pH monitor: definitive proof that acid reflux is causing symptoms CLASSIC MOTILITY DISORDERS: GERD Treatment: Lifestyle Modifications · Elevate HOB · Lose weight · Eliminate ETOH, HS snacks, certain drugs, fat, chocolate, peppermint BUT LIFE IS THEN NOT WORTH LIVING, so… CLASSIC MOTILITY DISORDERS: GERD Treatment: · Drug therapy: neutralizing (antacids, alginic acid, sucralfate); acid inhibition (H2 blockers, omeprazole); prokinetic agents (metoclopramide, cisapride) · Surgery: reduce hiatal hernia, perform fundoplication CLASSIC MOTILITY DISORDERS: GERD Complications · Peptic stricture: gradual progression of obstructive type dysphagia, ie, solids >> liquids · Barrett's esophagus: transformation of squamous to columnar mucosa; premalignant, requires surveillance biopsies searching for dysplasia; resulting cancer, adenocarcinoma RINGS, TIC, TEARS Schatzki ring · May cause intermittent dysphagia · Located at G-E junctionPlummer-Vinson syndrome · Upper esophageal web causing dysphagia · Associated with an iron deficiency anemia RINGS, TIC, TEARS Zenker's diverticulum · Classic symptom: post-prandial cough and gurgling · Diverticulum in proximal esophagus; food may be expelled by pressing on throat Mallory-Weiss tear · Superficial laceration at G-E junction · May cause upper GI bleeding · Classic symptom: retching followed by hematemesis
USMLE Step 2 — Lesson 7: Stomach
STOMACH PEPTIC ULCER Symptoms and complications · Pain · Bleeding · Obstruction · Perforation PEPTIC ULCER Therapy · Antacids · Sucralfate · H2 blockers · Omeprazole · Prostaglandin analogues Importance of H. pylori detection and eradication GASTRIC MOTILITY DISORDERS Gastroparesis · Early satiety · Bloating · Distension · Pain GASTRIC MOTILITY DISORDERS Diagnosis · Gastric emptying scan · Exclude mechanical causes such as ulcer, cancer (gastric or pancreatic) GASTRIC MOTILITY DISORDERS Medical therapy: prokinetic drugs · Metoclopramide · Cisapride · Erythromycin
USMLE Step 2 — Lesson 8: Small & Large Intestine
Diseases of the Smalland Large Intestine MALABSORPTION: General Considerations History · Diarrhea · Weight loss · Fat-soluble vitamin deficiency Physical exam · Edema · Tremors/tetany · B12 deficiency · Fat-soluble vitamin deficiency MALABSORPTION: General Considerations Labs · Anemia: low iron, B12, or folate · Low cholesterol, carotene · Low calcium, magnesium, albumin, folate, B12; high PT MALABSORPTION: Celiac Sprue · Chronic sensitivity to dietary gluten · Biopsy characteristic but nonspecific · Lesion is more severe proximally (low in “FIC”) · “Honeymoon” period but a lifelong disease · Association with dermatitis herpetiformis MALABSORPTION: Celiac Sprue · If patient doesn’t respond to gluten withdrawal o Noncompliance with diet (most common) o Wrong diagnosis o Superimposed lymphoma or ulcerative jejunoileitis MALABSORPTION: Tropical Sprue · Caribbean, India, northern coast of South America · Biopsy may be identical to celiac but process more distal (B12 deficiency!) · Responds to folate and/or broad spectrum antibiotics MALABSORPTION: Infectious Etiology Giardia: trophozoites in lumen and on mucosa · Upper GI symptoms may predominate · Stool tests unreliable; need duodenal aspirate · Consider after trip to national parks, skiing, Middle East, Russia, Mexico TRAVELER’S DIARRHEA · Usually due to enterotoxigenic E. coli · Bismuth prophylactic · Antibiotics prophylactic but controversial · Treatment consists of loperamide and antibiotic (trimethaprim/sulfamethoxazole or Cipro) INFLAMMATORY BOWEL DISEASE:Ulcerative Colitis (UC) General considerations · Ulcerated mucosa; hallmark symptom – bloody diarrhea · Involves colon in continuous, symmetric fashion – disease begins distally, spreads to involve variable portions of colon · Typically affects young people; if new onset colitis in elderly, suspect ischemic colitis INFLAMMATORY BOWEL DISEASE:Ulcerative colitis Extraintestinal manifestations related to bowel activity · Peripheral arthritis · Pyoderma gangrenosum · Episcleritis, conjunctivitis · Erythema nodosum INFLAMMATORY BOWEL DISEASE: Ulcerative colitis Extraintestinal manifestations not related to bowel activity · Ankylosing spondylitis and sacroileitis (HLA-B27) · Uveitis · Sclerosing cholangitis INFLAMMATORY BOWEL DISEASE: Ulcerative Colitis Cancer risk · Duration of disease (>10 years) · Extent of disease (proctosigmoiditis not at risk) · Surveillance with colonoscopy, biopsy; looking for dysplasia
USMLE Step 2 — Lesson 9: Inflammatory Bowel Disease
INFLAMMATORY BOWEL DISEASE:Crohn Disease INFLAMMATORY BOWEL DISEASE: Crohn Disease General considerations · Transmural inflammation most commonly in ileum and colon; granulomas may occur · Perianal disease with fistulas, abscess; may be severe · Discontinuous or skip lesions (compared continuous lesions in UC) INFLAMMATORY BOWEL DISEASE: Crohn Disease Clinical presentation · Inflammatory symptoms o Ileitis: may behave like appendicitis o Colitis: diarrhea with or without blood · Obstructive symptoms: may occur secondary to inflammation or fibrosis INFLAMMATORY BOWEL DISEASE: Crohn Disease NON-IBD COLITIDES: Clostridium difficile Clinical presentation · Fistulizing disease: occurs from transmural inflammation to adjacent organs (bladder, skin, vagina, psoas muscle); may result in intraabdominal abscesses · Increased cancer risk after long-standing inflammation · Related to treatment with antibiotics: cephalosporins, ampicillin, clindamycin · Nosocomial spread · Clinical presentation o Diarrhea o Fever o Abdominal tenderness o Leukocytosis NON-IBD COLITIDES: Clostridium difficile · Diagnosis o C. difficile toxin assay o Flexible sigmoidoscopy demonstrating pseudomembranes · Treatment: PO metronidazole or PO vancomycin · Relapses in 10-20% of cases NON-IBD COLITIDES Shigella o Classic presentation is dysentery: toxic patient, bloody diarrhea, many fecal WBCs Campylobacter · Most common cause of bacterial diarrhea · Symptoms vary from mild diarrhea to colitis, closely mimicking UC NON-IBD COLITIDES Yersinia enterocolitica · Typically ileitis or ileocolitis: may mimic UC or Crohn disease · Diagnosis with serology or stool culture NON-IBD COLITIDES Amebiasis – Entameoba histolytica · Seen in homosexual men and as traveler’s diarrhea · Can cause ileocolitis, mimicking UC or Crohn disease · Ameboma can cause mass effect · Diagnosis o Stool culture o Biopsy o Serology VACULAR DISEASES OF THE BOWEL: Angiodysplasia (or vascular ectasias) · Typical presentation: painless lower GI bleeding in elderly · Most commonly cecal but can occur in entire GI tract · Diagnose and treat endoscopically · May be associated with aortic stenosis · Think Osler-Weber-Rendu if nosebleeds or other telangiectasias · Gastric arteriovenous malformations common in chronic renal failure VACULAR DISEASES OF THE BOWEL: Mesenteric Ischemia Refers to ischemia of superior mesenteric artery · Usually nonocclusive: low-flow (CHF, hypotension) vs. occlusive (embolus in atrial fibrillation; thrombus) · Pain out of proportion to exam · Labs: high potassium, acidosis, leukocytosis · Fingerprinting on abdominal x-ray · Diagnosis – angiogram early! VACULAR DISEASES OF THE BOWEL: Ischemic Colitis · Due to IMA inferior mesenteric artery (IMA) ischemia · Usually due to low flow and with small vessel disease; angiogram not helpful · Can occur after abdominal aortic aneurysm repair and IMA damage VACULAR DISEASES OF THE BOWEL: Ischemic Colitis Clinical presentation · Painless bleeding · Typical colitis: bloody diarrhea, pain · Acute left-sided abdominal findings · Most commonly in “watershed” areas: splenic flexure and rectosigmoid
USMLE Step 2 — Lesson 10: Liver and Biliary Tract Disorders
LIVER AND BILIARY TRACT DISORDERS ACUTE HEPATITIS: Hepatitis A · Incubation 30 days · Fecal-oral transmission · Dx: HAV IgM · Course: cholestatic or hepatocellular · Rarely fulminant, never chronic · Exposure: immunize human immunoglobulin ACUTE HEPATITIS: Hepatitis B · DNA · Perinatal, parenteral, sexual transmission · Incubation 3 months · Diagnosis o HBsAg o HBcAb - IgM o HBeAg ACUTE HEPATITIS: Hepatitis B · Exposure: vaccine + HBIG · Clinical course: symptomatic vs asymptomatic · Serum sickness: arthritis, rash, glomerulonephritis · May become fulminant, chronic, risk for hepatoma ACUTE HEPATITIS: Hepatitis C Post-transfusion hepatitis · Sporadic (? sexual) frequent · Anti-HCV not useful in acute phase · 90% evolve to chronic hepatitis · 20% evolve to cirrhosis ACUTE HEPATITIS: Hepatitis D Obligate co-infection with hepatitis B · Either simultaneous or superinfection in chronic carrier · More severe course · More prevalent in IV drug abusers, hemophiliacs ACUTE HEPATITIS: Hepatitis E · Epidemic (India, Southeast Asia, Mexico) · Fecal-oral transmission · Usually self-limited, not chronic · Fulminant disease in pregnancy DRUG INDUCED LIVER DISEASE: Acetaminophen Dose related · Can be severe, fatal · Mediated by cytochrome P-450 system · Severe toxicity with low dose = ETOH · Treatment with acetylcysteine ALCOHOLIC LIVER DISEASE: Alcoholic Hepatitis Clinical: fever, tachycardia, jaundice, RUQ symptoms · Lab: SGOT > SGPT and < 300 · Treatment: ? steroids if jaundice and elevated PT or encephalopathy Autoimmune Hepatitis · Formerly known as “lupoid” hepatitis (but not associated with lupus) · Typically a disease of young women · May appear hirsute, Cushingoid · Associated with other autoimmune disorders (thyroid, Sjögren’s) · Treatment with immunosuppressives: steroids and azathioprine Primary Sclerosing Cholangitis (PSC) · Obstruction (fibrosis) of intra- and extrahepatic bile ducts · Association with IBD (UC>CD) · Symptoms of cholestasis, jaundice, pruritus Primary Biliary Cirrhosis (PBC) · Female:male = 9:1 · Onset early to mid adulthood · Cholestatic: either biochemical (alk phos, GGTP, bilirubin) or clinical (pruritus) · Clinical findings o Asymptomatic o Pruritus o Cholestatic Sx: xanthelasma, osteoporosis, fat-soluble vitamin deficiency
USMLE Step 2 — Lesson 11: Vascular Disorders of the Liver
PORTAL HYPERTENSION: Esophagogastric Varices · Portal pressure >12 mm Hg necessary o Somatostatin: safer and more effective than pitressin · Risk factors for bleeding: variceal size, endoscopic stigmata · Medical treatment o Propranolol: prophylaxis of first bleed and rebleeds PROTAL HYPERTENSION: Esophagogastric Varices Endoscopic sclerotherapy or banding o Ineffective in prevention of first bleed o Highly effective in control of active bleeding o Adverse effects common: esophageal ulcers, stricture, bacteremia, o spontaneous bacterial peritonitis (SBP) o Advantage of banding: reduced complications Laboratory test · Cell count and differential (250 PMN = SBP) · Culture in bedside blood culture bottles · Serum and ascitic albumin (gradient >1.1 g/dL = portal hypertension) PORTAL HYPERTENSION: Ascites PORTAL HYPERTENSION: Ascites Treatment · Diuresis and sodium restriction · Large volume paracentesis · Albumin infusion if no peripheral edema · Perivenous shunt; adverse effects – DIC, infection, thrombosis SPONTANEOUS BACTERIAL PERITONITIS (SBP) Glycolysis · Low threshold for diagnostic tap · Low protein ascites at high risk · Dx: > 250 PMN + bedside BD inoculation · E. coli and enteric gram-negative organisms · Polymicrobial infection: think “secondary” bacterial peritonitis SPONTANEOUS BACTERIAL PERITONITIS (SBP) Treatment · Cefotaxime, 5–10 days · Repeat paracentesis to monitor therapy · Avoid aminoglycosides HEPATORENAL SYNDROME Definition · Azotemia · Oliguria · Urine sodium <10mEq/L · Distinguish from prerenal azotemia HEPATORENAL SYNDROME Precipitant factors · Aminoglycosides · NSAIDs · Volume loss (diuretics, paracentesis, excess lactulose) PORTOSYSTEMIC ENCEPHALOPATHY Precipitating factors · Infection (think SBP) · Hypokalemia · Alkalosis · Azotemia (iatrogenic) · GI bleed · Sedatives PORTOSYSTEMIC ENCEPHALOPATHY Treatment · Correct exacerbating factors · Restriction of animal protein · Lactulose · Neomycin · ? Flumazenil
USMLE Step 2 — Lesson 12: Renal Disorders
RENAL DISORDERS DIAGNOSTIC TESTS Urinanalysis (U/A) · Hematuria with RBC casts --> glomerulonephritis · Heavy proteinuria (>3.5 g/dL) --> glomerulonephritis · Granular and epithelial cell casts --> acute tubular necrosis (ATN) · WBC, waxy cast --> tubulointerstitial disease DIAGNOSTIC TESTS Urinanalysis (U/A) · Hematuria alone ? vasculitis or postrenal disease · Normal U/A --> prerenal, ATN, tubulointerstitial · Pyuria alone --> infection OTHER DIAGNOSTIC TESTS · Intravenous pyelography (IVP): assesses function and structure of kidney, collecting system and bladder · Ultrasound (US): outlines size, obstructions, cysts, and masses · Computerized tomography (CT): more detailed information regarding masses or complex cysts OTHER DIAGNOSTIC TESTS · Renal arteriography: evaluation for renal artery stenosis and of renal masses · Nuclear scan: assess function without contrast · Renal biopsy: useful for evaluation of glomerular disease, vasculitis PRERENAL AZOTEMIA Causes · Volume depletion · Heart failure and poor forward flow · Bilateral renal artery stenosis Diagnosis: UNa < 10 mEq/L and/or FeNa = < 1% POSTRENAL AZOTEMIA: OBSTRUCTIVE UROPATHY Causes · Prostatic disease · Pelvic or retroperitoneal malignancy · Stones Diagnosis · Sonogram · IVP Treatment: Relieve obstruction TUBULINTERSTITIAL DISEASE Acute interstitial nephritis · Common causes o Adults: drugs (pen, ceph, sulfa, NSAIDs) o Kids: infections (diphtheria, streptococcus) · Presentation: hypersensitivity reaction o Fever o Rash o Peripheral and urine eosinophilia RENAL VASCULAR DISEASE Renal artery stenosis · Children: fibromuscular dysplasia · Adults: atherosclerosis · Presents with bruit · High renin, high aldo -->renovascular hypertension · Diagnosis: angiography, renal vein renins, captopril challenge, nuclear scan · Treatment: correct stenosis (PTCA, surgery) RENAL VASCULAR DISEASE Scleroderma · Acute presentation in setting of severe hypertension · Sclerosis of renal vessels -->high renin, high aldo · Treatment with ACE inhibitors CHRONIC RENAL FAILURE: UREMIA Clinical presentation · Neurologic: lethargy, confusion · Cardiovascular: hypertension, CHF, pericarditis · GI: anorexia, nausea, vomiting · Metabolic: pruritus (urea); bone pain (secondary hyperparathyroidism) · Anemia CHRONIC RENAL FAILURE: UREMIA Therapy · Dietary restrictions: protein, sodium, potassium, fluids · Renal replacement therapy o Hemodialysis o Peritoneal dialysis o Transplantation CHRONIC RENAL FAILURE: UREMIA Therapy · Replacement therapy indications o Clinical uremia o Severe azotemia, ie, GFR < 10cc/min o Volume overload o Hyperkalemia o Acidemia
USMLE Step 2 — Lesson 13: Musculoskeletal & Connective Tissue Disorders
MUSCULOSKELETAL & CONNECTIVE TISSUE DISORDERS OSTEOARTHRITIS Features · Degenerative joint disease, AKA “wear-and-tear” arthritis · Represents deterioration of articular cartilage and underlying bone · Symptoms: pain that worsens with activity, relieved with rest · Less morning stiffness than with RA OSTEOARTHRITIS Physical findings · Tenderness may be present in involved joints · Involved joints may feel slightly warm with a flare-up, though they are usually cool · Pain with motion in larger joints · Crepitus can be felt OSTEOARTHRITIS Physical findings · Joint enlargement and deformity occur · Heberden's nodes: enlargement of distal interphalangeal (DIP) joints · Bouchard's nodes: enlargement of proximal interphalangeal (PIP) joints OSTEOARTHRITIS Diagnosis · History and physical findings · Absence of inflammatory lab findings, eg, leukocytosis, fevers, high ESR · Non-inflammatory synovial fluid · X-ray degeneration of joint o Narrowed joint space o Osteophytes o Increased bone density of subchondral area OSTEOARTHRITIS Treatment · Nonpharmacologic o Lifestyle changes o Weight loss o Rest of affected joint o Ice/heat · Pharmacologic o NSAIDs GOUT General Features · Caused by serum uric acid elevation resulting in urate deposition in articular as well as extra-articular areas · Only 10% of hyperuricemic patients develop · Patients with gout have serum uric acid >7mg/dL · Patients may be overproducers or underexcreters of uric acid GOUT Acute gouty attack: Features · Most patients are middle-aged or elderly men · Typical attack: monoarticular lower extremity arthritis · 60% of patients develop podagra (painful swelling of first MTP joint) · May occur very suddenly; rapid progression of joint inflammation that may extend into the soft tissues · Attack usually subsides within several days GOUT Acute gouty attack: Diagnosis · Serum uric acid may be normal during acute attack · Diagnosis made by demonstrating urate crystals in synovial fluid · Crystals are needle shaped and negatively birefringent in polarized light · Synovial fluid WBC is generally elevated GOUT Acute gouty attack: Therapy · NSAIDs: very effective; used in high dose and quickly tapered · Colchicine: IV or oral; nausea, vomiting, and diarrhea often occur with oral dosing RHEUMATOID ARTHRITIS (RA) Features · Chronic inflammatory, polyarticular, symmetric arthritis · Extra-articular manifestations · Rheumatoid factor usually present · Seropositive patients usually have more severe disease with increased frequency of extra-articular features RHEUMATOID ARTHRITIS (RA) Clinical features · Symmetric and bilateral joint inflammation usually sparing DIP joints; most common joints involved: MCP, PIP, and wrist · Tendons and ligaments may be inflamed causing carpal tunnel syndrome, rotator cuff tendinitis, and ligament involvement at atlantoaxial joint between C1 and C2 vertebrae RHEUMATOID ARTHRITIS (RA) History · Chronic inflammatory polyarthritis · Prolonged morning stiffness is classic feature · Constitutional symptoms: weight loss, anorexia, malaise · Pain in involved joints typically worse in morning RHEUMATOID ARTHRITIS (RA) Physical examination · Sparing of DIP and involvement of MCP, PIP, and wrists with associated soft tissue swelling · Rheumatoid nodules over extensor surfaces, especially near olecranon RHEUMATOID ARTHRITIS (RA) Laboratory features · Anemia of chronic disease · Leukocytosis · Thrombocytosis · Increased sedimentation rate · Rheumatoid factor in approximately 60-80% of patients · Synovial fluid with WBC 5000-20,000 RHEUMATOID ARTHRITIS (RA) Nonpharmacologic treatment · Rest of acutely inflamed joints; exercise to strengthen muscles around involved joints · Physical and occupational therapy RHEUMATOID ARTHRITIS (RA) Drug therapy · NSAIDs: used to control inflammation and pain; frequent toxicity including GI upset and ulcers, renal dysfunction, and mental status changes in the elderly · Corticosteroids: used as potent anti-inflammatory drugs; given either systemically or as intra-articular injections · DMARDs (disease modifying anti-rheumatic drugs): used when patient is not improving on steroids or is improving but cannot get off steroids INFECTIOUS ARTHRITIS: Bacterial Arthritis Predisposing factors · Previous joint damage · Repeated septicemia · IV drug abuse · Prosthetic joints · Immunosuppression INFECTIOUS ARTHRITIS: Bacterial Arthritis Gonococcal Arthritis · Disseminated gonococcal infection often evolves into acute mono- or oligoarthritis with purulent joint effusions · Sexually active adult with acute monoarthritis without crystals: treat for gonococcal arthritis until proven otherwise · Cultures taken from all sites prone to gonococcal exposure INFECTIOUS ARTHRITIS: Bacterial Arthritis Diagnosis of Non-gonococcal Arthritis · Synovial fluid must be aspirated and sent for: o Gram stain o Culture and sensitivity o WBC and differential · WBC >50,000 with > 90% neutrophils: very suggestive of bacterial infection INFECTIOUS ARTHRITIS: Bacterial Arthritis Treatment · Treat for gonococcal arthritis in all adults unless certain of another diagnosis or there has been no sexual contact · Gonococcal arthritis: IM ceftriaxone, 1 g daily for 2 days, followed by cefuroxime · Staphylococcal infections: IV nafcillin
USMLE Step 2 — Lesson 14: Musculoskeletal & Connective Tissue Disorders
MUSCULOSKELETAL & CONNECTIVE TISSUE DISORDERS INFECTIOUS ARTHRITIS: Lyme Disease Multisystemic Illness · Skin · Joints · Neurologic system · Cardiac system SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Features · Chronic immune disorder with multisystemic involvement · Circulating immune complex and antibodies lead to tissue damage and dysfunction · Female to male ratio: 10:1; African-American women are affected 3 times as often as Caucasian women SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Dermatologic manifestations · Butterfly rash consists of erythema over the cheeks and nose (ie, malar rash) · Discoid (coin-shaped) lesions · Mucous membrane ulceration · Focal or generalized alopecia SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Nervous system manifestations · Central nervous system o Depression o Psychosis o Cognitive abnormalities o Seizures o Requires steroid therapy SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Pulmonary manifestations · 1/3 of patients have pleuritis · Restrictive changes may occur · Pulmonary hypertension secondary to pulmonary vasculitis SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Renal manifestations · Renal disease is very common · Patients with active renal disease generally have abnormalities on urinalysis with RBCs, WBCs, or casts · Elevated serum creatinine and BUN SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Renal manifestations · dsDNA antibodies and low levels of serum complement, generally associated with active renal disease · Glomerulonephritis can take form of mesangial disease (most common), focal proliferative, diffuse proliferative (most severe lesion), or membranous (significant nephrotic syndrome) SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Musculoskeletal manifestations · Arthralgias · Symmetric arthritis · Joint deformities may occur due to tendon or ligament laxity · Erosive joint disease is uncommon · Inflammatory myopathy may cause muscle weakness SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Hematologic manifestations · Anemia of chronic disease · Hemolytic anemia · Lymphopenia · ITP (immune thrombocytopenia) · Elevation in ESR SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Hematologic manifestations · Coagulation abnormalities o Phospholipid antibody (ie, lupus anticoagulant) o Interferes with coagulation profile testing; causes prolongation of PTT o Patients not prone to bleeding; higher incidence of thrombosis o Recurrent 2nd trimester abortions SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Serologic findings · False-positive VDRL · Testing for FTA-ABS usually normal in the absence of syphilitic infection SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Immunologic abnormalities · Autoantibodies are common o Antinuclear antibodies present in almost all patients o Antibodies to dsDNA present in 2/3 of patients with active disease o Histone antibodies present in patients with drug-induced lupus SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Immunologic abnormalities · Autoantibodies are common o Smith (Sm) antibodies specific for SLE o Anti-Ro and anti-La in patients with prominent skin and photosensitive findings SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Treatment · Should be tailored to individual patient's findings · Sunscreen for photosensitive patients · NSAIDs for serositis, joint complaints, fever · Antimalarial drugs (ie, chloroquine or hydroxychloroquine) to treat arthritis and skin findings SCLERODERMA Features · Connective tissue disease characterized by fibrosis of the skin and multiple organs · Multisystemic involvement o Heart o Lungs o Kidneys o GI tract SCLERODERMA Skin changes · Occurs in almost all patients with scleroderma · Most begin in the fingers and hands · Raynaud's phenomenon occurs in almost all patients; results in tri-phasic color change of white, blue, and red · Telangiectasias · Skin ulcers most commonly on fingers and are due to infarctions SCLERODERMA Kidney disease · Scleroderma renal crisis occurs in setting of uncontrolled hypertension; acute renal failure may occur. Malignant hypertension best treated with ACE inhibitors · Renal crisis often accompanied by a microangiopathic hemolytic anemia SCLERODERMA Kidney disease · Chronic renal failure may occur in patients with long-standing, poorly controlled hypertension SCLERODERMA CREST syndrome · CREST = calcinosis, Raynaud's phenomena, esophageal dysfunction, sclerodactyly, and telangiectasias · Milder form of disease · Associated with anticentromere antibody · Internal organ involvement usually less severe than with diffuse scleroderma LARGE VESSEL VASCULITIS Temporal arteritis · Pathologically identical to Takayasu's arteritis · Occurs in patients >50 · Half the patients have polymyalgia rheumatica LARGE VESSEL VASCULITIS Temporal arteritis · Symptoms due to ischemia of vessels in the carotid artery region; include headache, visual disturbances, and jaw claudication · Patients may have tenderness over the temporal artery distribution · Diagnosis is made with temporal artery biopsy · Treatment with steroids to prevent blindness
USMLE Step 2 — Lesson 15: Thyroid Disease
THYROID DISEASE HYPOTHYROIDISM Clinical features · Signs of metabolic slow-down, ie, lethargy, fatigue, slowness of speech · Cold intolerance · Constipation · Weight gain HYPOTHYROIDISM Clinical features · Voice and hair change · Nonpitting edema, ie, myxedema · Diminished deep tendon reflexes · Bradycardia HYPOTHYROIDISM Myxedema coma · Untreated severe hypothyroidism · May be triggered by acute precipitant, eg, infection · Patients may present with hypothermia, hypoglycemia, shock, and hypoventilation · Therapy: thyroid and adrenal hormone replacement HYPOTHYROIDISM Diagnosis of hypothyroidism · Low total T4 and T3 · Elevated TSH · Low radioactive iodine uptake HYPOTHYROIDISM: Chronic Thyroiditis (Hashimoto’s Thyroiditis) · Autoimmune disorder usually affecting women · Antithyroid antibodies present · Thyromegaly due to lymphocytic infiltration · Hypothyroidism gradually develops HYPOTHYROIDISM: Chronic Thyroiditis (Hashimoto’s Thyroiditis) Diagnosis · Antimicrosomal antibodies or antithyroglobulin antibodies · Suspected in patients with symmetric, usually nontender, nontoxic goiters · Patients may be euthyroid or hypothyroid · Treat with L-thyroxine to decrease size of gland and for the hypothyroidism HYPOTHYROIDISM Therapy · Thyroid hormone replacement, ie, synthetic L-thyroxine · Begin with low doses in older patients and in those with severe hypothyroidism HYPERTHYROIDISM Clinical features · "Overactive" metabolism · Sweating · Heat intolerance · Weight loss · Sinus tachycardia · Atrial fibrillation (apathetic hyperthyroidism in the elderly) HYPERTHYROIDISM Etiology · Graves' disease · Nodular toxic goiter · Subacute thyroiditis · Factitious · Pituitary tumors HYPERTHYROIDISM Clinical features · Diarrhea · Warm, moist skin · Restlessness and tremor · Ophthalmic findings: lid lag and the hyperthyroid “stare” · Thyroid exophthalmos: seen only in Graves’ disease; due to infiltration of the extraocular muscles HYPERTHYROIDISM Thyroid storm · Severe exacerbation of hyperthyroidism · Often precipitated by infection, surgery, or delivery · High fevers, tachycardia with associated high mortality HYPERTHYROIDISM XSLaboratory studies · Elevated total T4 and T3 · Elevated T3 resin uptake · Elevated radioactive iodine uptake · Low TSH HYPERTHYROIDISM Treatment · Antithyroid drugs · Methimazole and propylthiouracil (PTU) o Decrease the synthesis of thyroid hormone by inhibiting the oxidation of iodide o PTU also inhibits the conversion of T4 to T3 o Skin rash, joint pain, or agranulocytosis may occur HYPERTHYROIDISM Treatment · Methimazole and propylthiouracil (PTU) o Allows out-patient therapy o Less likelihood of subsequent hypothyroidism · Beta-blockers: do not affect thyroid function but will block adrenergic effects of hyperthyroidism HYPERTHYROIDISM Treatment · Subtotal thyroidectomy o Allows for cure of hyperthyroidism o Patient compliance with long-term medication is necessary o Less hypothyroidism than with radioactive iodine o Patient should be euthyroid before surgery HYPERTHYROIDISM Treatment · Radioactive iodine o Most patients require 1 or 2 doses of radioactive iodine to cause decrease in function and size o Allows outpatient treatment o Very high success rate HYPERTHYROIDISM Treatment · After 10 years, up to half of patients may become hypothyroid and require thyroid hormone replacement · No increase in leukemia risk, thyroid cancer, or other malignancies; slight risk of genetic defects in offspring HYPERTHYROIDISM Treatment of thyroid storm · IV sodium iodide inhibits the release of thyroid hormones · Antithyroid drugs block further hormone synthesis · Beta-blockers block peripheral effects of thyroid hormone
USMLE Step 2 — Lesson 16: Diabetes
DIABETES OVERVIEW Type 1 diabetes · Autoimmune disease · Complete or near-complete absence of insulin. Prone to diabetic ketoacidosis (DKA) · Generally in thin, young adults and children · Only ~10% of diabetics are true type 1 OVERVIEW Type 2 diabetes · Reduced insulin secretion or insulin resistance · Usually patients are overweight; obesity increases insulin resistance · Not prone to ketoacidosis CLINICAL FEATURES AND DIAGNOSIS Clinical features · Polyuria, polydipsia · Weight loss; insulin deficiency catabolic · Decreased resistance to infection · Visual changes; acutely worsen with hyperglycemia CLINICAL FEATURES AND DIAGNOSIS Diagnosis of diabetes · Fasting hyperglycemia · Postprandial glucose level · Glucose tolerance test · Urine glucose very unreliable CHRONIC COMPLICATIONS OF DIABETES Diabetic retinopathy · 1/3 - 1/2 of patients after 10 years · Non proliferative: exudates, hemorrhage, microaneurysm; treat with tight glucose control CHRONIC COMPLICATIONS OF DIABETES Diabetic retinopathy · Proliferative: only ~10% of patients o Neovascularization may cause vitreous hemorrhage scar formation o May cause acute blindness o Treated with laser CHRONIC COMPLICATIONS OF DIABETES Diabetic nephropathy · “Kimmelstiel-Wilson” lesion = intercapillary glomerulosclerosis · Papillary necrosis · Arteriosclerotic renal disease · Chronic interstitial nephritis · Earliest marker is microalbuminuria · May progress to nephrotic syndrome CHRONIC COMPLICATIONS OF DIABETES Diabetic nephropathy · Hypertension accelerates renal failure; treat hypertension aggressively · High protein diet may accelerate renal damage · Captopril may slow progression of renal disease CHRONIC COMPLICATIONS OF DIABETES Accelerated atherosclerosis · Coronary artery disease: large and small vessel · Silent cardiac ischemia common · Peripheral vascular disease most commonly in lower legs and feet · Small vessel disease may lead to foot infections ulcers gangrene progressive amputation CHRONIC COMPLICATIONS OF DIABETES Diabetic neuropathy · Peripheral neuropathy o Symmetric “stocking-glove” sensory loss o Numbness, tingling, burning o Charcot’s joints o Foot care, foot care, foot care! CHRONIC COMPLICATIONS OF DIABETES Diabetic neuropathy · Autonomic neuropathy o Postural hypotension o Gastroparesis difficult diabetic control o Impotence in men o Urinary retention UTI DIABETIC KETOACIDOSIS (DKA) Etiology · Search for precipitating factors · Insulin noncompliance · Trauma DIABETIC KETOACIDOSIS (DKA) Pathophysiology · Insulin deficiency hyperglycemia · Hyperglycemia osmotic diuresis · Insulin deficiency lipolysis free fatty acids ketone production · Ketone bodies buffered by bicarbonate high anion gap metabolic acidosis DIABETIC KETOACIDOSIS (DKA) Treatment · Insulin to achieve gradual reduction in serum glucose, serum ketones; rise in serum pH · Fluids o Start NaCl o When glucose <200-300 mg/dL, start D5W; continue insulin DIABETIC KETOACIDOSIS (DKA) Treatment · Replete potassium, phosphate, and bicarbonate if very acidotic · Find and treat underlying cause HYPEROSMOLAR NONKETOTIC COMA Features · Usually in type 2 diabetics · May be initial presentation · Severe hyperglycemia causes profound osmotic diuresis with severe dehydration · Severe dehydration very high osmolality mental status changes · Treatment: like DKA but usually requires more fluid and (maybe) less insulin TREATMENT OF DIABETES Diet · Estimate ideal body weight · Determine daily caloric requirement · Balance protein 20%, carbohydrates 50%, and fat 30% · Eat at regular intervals, ie, 3 meals and bedtime snack TREATMENT OF DIABETES Oral hypoglycemic agents · Increase insulin secretion · Used when diet alone is not enough · Generally most useful in recent onset type 2 patients with <20 m insulin requirement/day · Newer sulfonylureas (glipizide, glyburide); avoid hyponatremia seen with older drugs (chlorpropamide) TREATMENT OF DIABETES Insulin therapy · Type 1 diabetics · Type 2 diabetics not responsive to diet and oral agents · Know the different preparations! TREATMENT OF DIABETES Insulin therapy · Onset – Peak – Duration o Fast acting = regular: 1/2 hr, 4 hr, 8 hr o Intermediate = NPH: 1-2 hr, 4-12 hr, 24 hr § Lente § 70% NPH/30% regular o Long-acting = Ultralente: 4 hr, 10-30 hr, 36 hr HYPOGLYCEMIA Symptoms · Adrenergic symptoms: sweating, tachycardia, palpitations, tremulousness · CNS symptoms – occur later and may cause irreversible damage: lethargy, confusion, seizures, coma
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