2

Question 1

What are the symptoms of myocarditis?

Answer 1

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

Question 2

What are the musculoskeletal causes of chest pain?

Answer 2

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

Question 3

What are the gastrointestinal causes of chest pain?

Answer 3

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

Question 4

What are the symptoms of pneumothorax?

Answer 4

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

Question 5

What are the symptoms of pleuritis?

Answer 5

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

Question 6

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

Answer 6

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

Question 7

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

Answer 7

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

Question 8

What is the risk of myocardial infarction in smokers?

Answer 8

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

Question 9

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

Answer 9

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

Question 10

What percentage of patients with diabetes die of cardiovascular disease?

Answer 10

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

Question 11

What are the clinical signs of stable angina?

Answer 11

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

Question 12

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

Answer 12

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

Question 13

How is ischemic heart disease diagnosed?

Answer 13

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

Question 14

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

Answer 14

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

Question 15

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

Answer 15

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

Question 16

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

Answer 16

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

Question 17

What is a nuclear stress test?

Answer 17

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

Question 18

What are the dobutamine and adenosine stress tests?

Answer 18

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

Question 19

What is a stress echocardiogram?

Answer 19

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

Question 20

What are the indications for cardiac catheterization?

Answer 20

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

Question 21

What is the treatment of ischemic heart disease?

Answer 21

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

Question 22

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

Answer 22

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

Question 23

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

Answer 23

200, HDL

Question 24

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

Answer 24

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

Question 25

What are the types of acute coronary syndromes?

Answer 25

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

Question 26

What is a non ST–segment elevation myocardial infarction?

Answer 26

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

Question 27

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

Answer 27

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

Question 28

What is unstable angina?

Answer 28

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

Question 29

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

Answer 29

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

Question 30

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

Answer 30

Repetitive or prolonged chest pain (>10 min), elevated markers, persistent ST depression >0.5 mm or new T–wave inversion, SBP

Question 31

What is the general management of NSTEMI?

Answer 31

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

Question 32

What are the drugs that are used in NSTEMI?

Answer 32

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

Question 33

What antiplatelet therapy should be given to patients with NSTEMI?

Answer 33

Aspirin and clopidogrel. Clopidogrel should be avoided if likely to require bypass surgery (severe ST–segment depression, SBP

Question 34

What are the indications for anticoagulants in NSTEMI?

Answer 34

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

Question 35

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

Answer 35

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

Question 36

What is the indication for tirofiban or eptifibatide in NSTEMI?

Answer 36

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

Question 37

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

Answer 37

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

Question 38

Which patients with NSTEMI should receive invasive management?

Answer 38

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

Question 39

What are the clinical signs of ST elevation myocardial infarction?

Answer 39

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

Question 40

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

Answer 40

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

Question 41

What are the physical signs of ST elevation myocardial infarction?

Answer 41

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

Question 42

What are the ECG criteria for STEMI?

Answer 42

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

Question 43

What is the initial nonspecific management of acute coronary syndrome?

Answer 43

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

Question 44

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

Answer 44

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

Question 45

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

Answer 45

II, III, aVF

Question 46

Which coronary artery is occluded in an inferior myocardial infarction?

Answer 46

Right coronary.

Question 47

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

Answer 47

V1–V3

Question 48

Which coronary artery is occluded in an anteroseptal myocardial infarction?

Answer 48

Left anterior descending

Question 49

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

Answer 49

V2–V4

Question 50

Which coronary artery is occluded in an anterior myocardial infarction?

Answer 50

Left anterior descending artery.

Question 51

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

Answer 51

I, aVL, V4, V5, and V6

Question 52

Which coronary artery is occluded in an anterior myocardial infarction?

Answer 52

Left anterior descending or circumflex artery.

Question 53

Which ECG leads have ST elevation in a posterior MI?

Answer 53

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

Question 54

Which coronary artery is occluded in a posterior myocardial infarction?

Answer 54

Posterior descending

Question 55

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

Answer 55

Immediately. Disappear in 6–24 hours.

Question 56

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

Answer 56

Immediately

Question 57

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

Answer 57

1–6 weeks

Question 58

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

Answer 58

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

Question 59

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

Answer 59

Years to never

Question 60

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

Answer 60

6–24 hours

Question 61

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

Answer 61

Disappear months to years later.

Question 62

What is the best emergent reperfusion therapy?

Answer 62

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

Question 63

What are the indications for thrombolytics?

Answer 63

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

Question 64

What are the contraindications to thrombolytic therapy?

Answer 64

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

Question 65

What are the relative contraindications to thrombolytic therapy?

Answer 65

Recent major surgery (

Question 66

What are the indications for antiplatelet agents in STEMI?

Answer 66

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

Question 67

What are the indications for antithrombin in STEMI?

Answer 67

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

Question 68

What are the indications for enoxaparin with fibrinolysis?

Answer 68

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

Question 69

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

Answer 69

Use abciximab with primary PCI in patients with STEMI.

Question 70

What are the recommended discharge medications after ACS?

Answer 70

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

Question 71

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

Answer 71

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

Question 72

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

Answer 72

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

Question 73

What are the indications for ACE inhibitors after ACS?

Answer 73

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

Question 74

What are the indications for statin therapy after ACS?

Answer 74

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

Question 75

What are the indications for nitrates after ACS?

Answer 75

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

Question 76

What are the indications for warfarin after ACS?

Answer 76

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

Question 77

What are the recommendations for exercise ECG testing after ACS?

Answer 77

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

Question 78

What are the complications of ACS?

Answer 78

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

Question 79

What is right ventricular infarction?

Answer 79

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

Question 80

What is Prinzmetal angina?

Answer 80

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

Question 81

What is the treatment of Prinzmetal angina?

Answer 81

Calcium channel blockers or nitrates.

Question 82

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

Answer 82

Congestive heart failure

Question 83

What is systolic heart failure?

Answer 83

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

Question 84

What is diastolic heart failure?

Answer 84

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

Question 85

What are the causes of decompensated heart failure?

Answer 85

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

Question 86

What are the causes of congestive heart failure?

Answer 86

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

Question 87

What are the symptoms of left ventricular heart failure?

Answer 87

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

Question 88

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

Answer 88

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

Question 89

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

Answer 89

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

Question 90

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

Answer 90

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

Question 91

What are the ECG findings in congestive heart failure?

Answer 91

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

Question 92

What is B–type natriuretic peptide?

Answer 92

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

Question 93

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

Answer 93

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

Question 94

What are the side effects of captopril?

Answer 94

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

Question 95

What are the side effects of enalapril?

Answer 95

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

Question 96

What are the side effects of lisinopril?

Answer 96

Hypotension, proteinuria, renal insufficiency, rash, cough.

Question 97

What are the side effects of nitroprusside?

Answer 97

Thiocyanate toxicity, methemoglobinemia.

Question 98

What are the side effects of nitroglycerin?

Answer 98

Headache, postural hypotension, methemoglobinemia.

Question 99

What are the side effects of isosorbide dinitrate?

Answer 99

Headache, postural hypotension

Question 100

What are the side effects of hydralazine?

Answer 100

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

Question 101

What is the treatment of congestive symptoms in heart failure?

Answer 101

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

Question 102

What is the mechanism of action of thiazides?

Answer 102

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

Question 103

What are the side effects of thiazides?

Answer 103

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

Question 104

What are the side effects of indapamide?

Answer 104

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

Question 105

What are the side effects of phthalimidine derivatives?

Answer 105

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

Question 106

What is the mechanism of action of loop diuretics?

Answer 106

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

Question 107

What are the side effects of loop diuretics?

Answer 107

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

Question 108

What are the side effects of potassium–sparing diuretics?

Answer 108

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

Question 109

What is the initial therapy for congestive heart failure?

Answer 109

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

Question 110

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

Answer 110

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

Question 111

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

Answer 111

Addition of spironolactone significantly reduces death and hospitalizations.

Question 112

What is the treatment of severe refractory heart failure?

Answer 112

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

Question 113

What is the mechanism of digitalis?

Answer 113

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

Question 114

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

Answer 114

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

Question 115

What conditions predispose to digitalis toxicity?

Answer 115

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

Question 116

What drug interaction occurs with digoxin and quinidine?

Answer 116

Decreases renal clearance of digoxin.

Question 117

What drug interaction occurs with digoxin and verapamil/diltiazem?

Answer 117

Decreases renal clearance of digoxin.

Question 118

What drug interaction occurs with digoxin and cholestyramine/colestipol?

Answer 118

Binds digoxin in gastrointestinal tract; interferes with enterohepatic circulation.

Question 119

What drug interaction occurs with digoxin and spironolactone?

Answer 119

Inhibits tubular secretion of digoxin.

Question 120

What drug interaction occurs with digoxin and thiazides/furosemide?

Answer 120

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

Question 121

What are the side effects of digoxin?

Answer 121

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

Question 122

What is the treatment for digoxin toxicity?

Answer 122

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

Question 123

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

Answer 123

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

Question 124

What is the treatment of diastolic heart failure?

Answer 124

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

Question 125

What are the signs of pulmonary edema?

Answer 125

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

Question 126

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

Answer 126

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

Question 127

What is the treatment of pulmonary edema?

Answer 127

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

Question 128

What is mitral stenosis?

Answer 128

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

Question 129

What is the most common lesion caused by rheumatic fever?

Answer 129

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

Question 130

What are the early clinical signs of mitral stenosis?

Answer 130

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

Question 131

What are the late clinical signs of severe mitral stenosis?

Answer 131

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

Question 132

What are the physical signs of mitral stenosis?

Answer 132

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

Question 133

What are the ECG findings in mitral stenosis?

Answer 133

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

Question 134

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

Answer 134

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

Question 135

What is the treatment of mitral stenosis?

Answer 135

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

Question 136

What are the hemodynamic findings in mitral regurgitation?

Answer 136

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

Question 137

What are the acute causes of mitral regurgitation?

Answer 137

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

Question 138

What are the chronic causes of mitral regurgitation?

Answer 138

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

Question 139

What are the physical signs of mitral regurgitation?

Answer 139

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

Question 140

What are the ECG signs of mitral regurgitation?

Answer 140

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

Question 141

What is the treatment of mitral regurgitation?

Answer 141

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

Question 142

What is mitral valve prolapse?

Answer 142

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

Question 143

What is the presentation of mitral valve prolapse?

Answer 143

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

Question 144

What are the complications of mitral valve prolapse?

Answer 144

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

Question 145

What is the treatment of mitral valve prolapse?

Answer 145

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

Question 146

What is aortic stenosis?

Answer 146

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

Question 147

What is the pathophysiology of aortic stenosis?

Answer 147

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

Question 148

What are the clinical signs of aortic stenosis?

Answer 148

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

Question 149

What are the ECG signs of aortic stenosis?

Answer 149

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

Question 150

What is the treatment of aortic stenosis?

Answer 150

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

Question 151

What is aortic valve sclerosis of the elderly?

Answer 151

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

Question 152

What are the clinical signs of hypertrophic obstructive cardiomyopathy?

Answer 152

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

Question 153

What are the clinical sings of mitral regurgitation?

Answer 153

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

Question 154

What are the clinical signs of pulmonic stenosis?

Answer 154

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

Question 155

What are the causes of aortic regurgitation?

Answer 155

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

Question 156

What is the pathophysiology of aortic regurgitation?

Answer 156

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

Question 157

What are the clinical signs of aortic regurgitation?

Answer 157

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

Question 158

How is aortic regurgitation diagnosed?

Answer 158

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

Question 159

What is the treatment of aortic regurgitation?

Answer 159

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

Question 160

What is hypertrophic obstructive cardiomyopathy?

Answer 160

Marked hypertrophy of left ventricle; usually disproportionate hypertrophy of septum

Question 161

What is restrictive cardiomyopathy?

Answer 161

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

Question 162

What is obliterative cardiomyopathy?

Answer 162

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

Question 163

What is dilated cardiomyopathy?

Answer 163

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

Question 164

What are the causes of dilated cardiomyopathy?

Answer 164

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

Question 165

What are the clinical signs of dilated cardiomyopathy?

Answer 165

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

Question 166

What are the x–ray signs of dilated cardiomyopathy?

Answer 166

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

Question 167

What is the cause of hypertrophic obstructive cardiomyopathy?

Answer 167

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

Question 168

What is the pathophysiology of hypertrophic obstructive cardiomyopathy?

Answer 168

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

Question 169

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

Answer 169

Increase obstruction because of increased contractility.

Question 170

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

Answer 170

Increase obstruction because of increased contractility.

Question 171

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

Answer 171

Increase obstruction because of increased contractility.

Question 172

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

Answer 172

Increase obstruction because of decreased preload.

Question 173

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

Answer 173

Increase obstruction because of decreased preload.

Question 174

What is the effect of standing on hypertrophic obstructive cardiomyopathy?

Answer 174

Increase obstruction because of decreased preload.

Question 175

What is the effect of nitroglycerin on hypertrophic obstructive cardiomyopathy?

Answer 175

Increase obstruction because of decreased preload.

Question 176

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

Answer 176

Increase obstruction because of decreased preload.

Question 177

What is the effect of tachycardia on hypertrophic obstructive cardiomyopathy?

Answer 177

Increase obstruction because of decreased preload and increased contractility.

Question 178

What is the effect of hypovolemia on hypertrophic obstructive cardiomyopathy?

Answer 178

Increase obstruction because of decreased afterload.

Question 179

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

Answer 179

Increase obstruction because of decreased afterload.

Question 180

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

Answer 180

Increase obstruction because of decreased afterload.

Question 181

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

Answer 181

Decreased obstruction because of decreased contractility.

Question 182

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

Answer 182

Decreased obstruction because of decreased contractility.

Question 183

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

Answer 183

Decreased obstruction because of decreased contractility.

Question 184

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

Answer 184

Decreased obstruction because of increased preload.

Question 185

What is the effect of squatting on hypertrophic obstructive cardiomyopathy?

Answer 185

Decreased obstruction because of increased preload.

Question 186

What is the effect of bradycardia on hypertrophic obstructive cardiomyopathy?

Answer 186

Decreased obstruction because of increased preload.

Question 187

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

Answer 187

Decreased obstruction because of increased preload.

Question 188

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

Answer 188

Decreased obstruction because of increased afterload.

Question 189

What is the effect of squatting on hypertrophic obstructive cardiomyopathy?

Answer 189

Decreased obstruction because of increased afterload.

Question 190

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

Answer 190

Decreased obstruction because of increased afterload.

Question 191

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

Answer 191

Decreased obstruction because of increased afterload.

Question 192

What are the symptoms of hypertrophic obstructive cardiomyopathy?

Answer 192

Dyspnea, angina, presyncope, syncope, and palpitations.

Question 193

What are the physical signs of hypertrophic obstructive cardiomyopathy?

Answer 193

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

Question 194

What are the ECG signs of hypertrophic obstructive cardiomyopathy?

Answer 194

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

Question 195

What is the treatment of hypertrophic obstructive cardiomyopathy?

Answer 195

Beta–blockers, calcium channel blockers, surgery.

Question 196

What is restrictive cardiomyopathy?

Answer 196

Least common cause of cardiomyopathy; rigid noncompliant ventricular walls.

Question 197

What are the causes of restrictive cardiomyopathy?

Answer 197

Sarcoidosis; amyloidosis, hemochromatosis, neoplasia, scleroderma, radiation

Question 198

What is the pathophysiology of restrictive cardiomyopathy?

Answer 198

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

Question 199

What are the signs of restrictive cardiomyopathy?

Answer 199

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

Question 200

What are the x–ray signs of restrictive cardiomyopathy?

Answer 200

Mild cardiomegaly, pulmonary congestion. Echocardiogram is diagnostic.

Question 201

What is the treatment of restrictive cardiomyopathy?

Answer 201

Heart transplantation; death from congestive heart failure or arrhythmias.

Question 202

What are the causes of acute pericarditis and myopericarditis?

Answer 202

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

Question 203

What are the clinical symptoms of acute pericarditis?

Answer 203

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

Question 204

What are the physical signs of acute pericarditis?

Answer 204

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

Question 205

What are the ECG signs of acute pericarditis?

Answer 205

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

Question 206

What is the treatment of acute pericarditis?

Answer 206

NSAIDs, aspirin, corticosteroids.

Question 207

What are the types of pericardial effusions?

Answer 207

Transudates, serosanguineous, blood.

Question 208

What are the causes of transudative pericardial effusions?

Answer 208

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

Question 209

What are the causes of serosanguineous pericardial effusions?

Answer 209

Serosanguineous pericardial fluid is sign in tuberculosis and neoplastic diseases.

Question 210

What are the causes of bloody pericardial effusions?

Answer 210

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

Question 211

How is pericardial effusion diagnosed?

Answer 211

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

Question 212

What is the treatment of pericardial effusion?

Answer 212

Pericardial fluid aspiration.

Question 213

What is cardiac tamponade?

Answer 213

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

Question 214

What are the causes of cardiac tamponade?

Answer 214

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

Question 215

What are the clinical manifestations of pericardial tamponade?

Answer 215

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

Question 216

What is the triad of pericardial tamponade?

Answer 216

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

Question 217

What is the treatment of cardiac tamponade?

Answer 217

Pericardiocentesis; subxiphoid surgical drainage.

Question 218

What is constrictive pericarditis?

Answer 218

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

Question 219

What are the causes of constrictive pericarditis?

Answer 219

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

Question 220

What are the clinical manifestations of constrictive pericarditis?

Answer 220

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

Question 221

How is constrictive pericarditis diagnosed?

Answer 221

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

Question 222

What is the treatment of constrictive pericarditis?

Answer 222

Sodium restriction, diuretics, pericardiectomy.

Question 223

What is sinus bradycardia?

Answer 223

Ventricular complexes are normal width, evenly spaced, rate is

Question 224

What are the causes of sinus bradycardia?

Answer 224

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

Question 225

What is the treatment of sinus bradycardia?

Answer 225

Atropine if symptoms. Pacemaker.

Question 226

What are the types of atrioventricular block?

Answer 226

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

Question 227

What is first–degree atrioventricular block?

Answer 227

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

Question 228

What are the causes of first–degree heart block?

Answer 228

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

Question 229

What are the types of second–degree atrioventricular block?

Answer 229

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

Question 230

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

Answer 230

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

Question 231

What is type II (Mobitz II) atrioventricular block?

Answer 231

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

Question 232

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

Answer 232

Usually AV nodal (supra–Hisian)

Question 233

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

Answer 233

Infranodal (infra– or infra–Hisian).

Question 234

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

Answer 234

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

Question 235

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

Answer 235

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

Question 236

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

Answer 236

PR interval lengthens progressively until ventricular beat dropped. PR shortens after dropped beat. RR narrows progressively up to the dropped beat. RR after blocked beat is

Question 237

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

Answer 237

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

Question 238

What is third–degree atrioventricular block?

Answer 238

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

Question 239

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

Answer 239

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

Question 240

What are Adams–Stoke attacks?

Answer 240

Sudden asystole or transient ventricular tachycardia or ventricular fibrillation.

Question 241

What is the treatment of third degree AV block?

Answer 241

Pacing.

Question 242

What is sinus tachycardia?

Answer 242

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

Question 243

What is paroxysmal supraventricular tachycardia?

Answer 243

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

Question 244

What are the ECG signs of paroxysmal supraventricular tachycardia?

Answer 244

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

Question 245

What is the treatment of paroxysmal supraventricular tachycardia?

Answer 245

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

Question 246

What are the ECG signs of multifocal atrial tachycardia?

Answer 246

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

Question 247

What are the causes of atrial flutter?

Answer 247

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

Question 248

What are the ECG signs of atrial flutter?

Answer 248

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

Question 249

What is the initial treatment of atrial flutter?

Answer 249

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

Question 250

What is the most common sustained cardiac rhythm disturbance?

Answer 250

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

Question 251

What are the ECG signs of atrial fibrillation?

Answer 251

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

Question 252

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

Answer 252

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

Question 253

What is the rate of ischemic stroke in atrial fibrillation?

Answer 253

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

Question 254

What are the signs of atrial fibrillation?

Answer 254

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

Question 255

What is lone atrial fibrillation?

Answer 255

Atrial fibrillation with no evidence of structural heart disease.

Question 256

What are the causes of atrial fibrillation?

Answer 256

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

Question 257

What tests are use in the evaluation of atrial fibrillation?

Answer 257

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

Question 258

What drugs are effective for pharmacologic cardioversion of atrial fibrillation?

Answer 258

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

Question 259

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

Answer 259

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

Question 260

What is the first step in managing atrial fibrillation?

Answer 260

Control rate to

Question 261

What is the recommended treatment strategy for atrial fibrillation?

Answer 261

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

Question 262

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

Answer 262

Electrical cardioversion.

Question 263

What is Wolff–Parkinson–White syndrome?

Answer 263

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

Question 264

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

Answer 264

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

Question 265

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

Answer 265

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

Question 266

What is ventricular tachycardia?

Answer 266

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

Question 267

What are the causes of ventricular tachycardia?

Answer 267

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

Question 268

What are the clinical manifestations of ventricular tachycardia?

Answer 268

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

Question 269

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

Answer 269

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

Question 270

What are the causes of torsade de pointes ventricular tachycardia?

Answer 270

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

Question 271

What is the treatment of torsade de pointes ventricular tachycardia?

Answer 271

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

Question 272

What are the indications for amiodarone?

Answer 272

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

Question 273

What are the side effects of amiodarone?

Answer 273

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

Question 274

What are the indications for disopyramide?

Answer 274

Ventricular ectopic activity and atrial ectopic activity.

Question 275

What are the adverse effects of disopyramide?

Answer 275

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

Question 276

What are the indications for lidocaine?

Answer 276

Ventricular ectopic activity

Question 277

What are the adverse effects of lidocaine?

Answer 277

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

Question 278

What are the cardiac indications for phenytoin?

Answer 278

Ventricular ectopic activity.

Question 279

What are the adverse effects of phenytoin?

Answer 279

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

Question 280

What are the indications for procainamide?

Answer 280

Ventricular ectopic activity, atrial ectopic activity

Question 281

What are the adverse effects of procainamide?

Answer 281

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

Question 282

What are the indications for quinidine?

Answer 282

Ventricular ectopic activity, atrial ectopic activity

Question 283

What are the adverse effects of quinidine?

Answer 283

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

Question 284

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

Answer 284

Atrial ectopic activity, ventricular ectopic activity.

Question 285

What are the adverse effects of beta–blockers?

Answer 285

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

Question 286

What are the antiarrhythmic indications for verapamil?

Answer 286

Atrial ectopic activity.

Question 287

What are the adverse effects of verapamil?

Answer 287

Congestive heart failure, asystole, constipation

Question 288

What are the indications for adenosine?

Answer 288

Ventricular tachycardia

Question 289

What are the adverse effects of adenosine?

Answer 289

Transient dyspnea, noncardiac chest pain, rarely hypotension.

Question 290

What are the indications for mexiletine?

Answer 290

Ventricular ectopic activity

Question 291

What is mexiletine?

Answer 291

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

Question 292

What are the indications for tocainide?

Answer 292

Ventricular ectopic activity

Question 293

What is tocainide?

Answer 293

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

Question 294

What are the indications for amiodarone?

Answer 294

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

Question 295

What are the adverse effects of amiodarone?

Answer 295

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

Question 296

What are the indications for encainide?

Answer 296

Ventricular tachycardia, Wolff–Parkinson–White syndrome.

Question 297

What are the adverse effects of encainide?

Answer 297

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

Question 298

What are the indications for flecainide?

Answer 298

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

Question 299

What are the adverse effects of flecainide?

Answer 299

Negative inotropism, QRS, PR prolongation

Question 300

What are the indications for propafenone?

Answer 300

Ventricular tachycardia, atrial fibrillation

Question 301

What the adverse effect of propafenone?

Answer 301

Negative inotropism

Question 302

What are the physiologic effects of low doses of nitrates?

Answer 302

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

Question 303

What are the physiologic effects of medium doses of nitrates?

Answer 303

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

Question 304

What are the physiologic effects of high doses of nitrates?

Answer 304

In high doses, nitrates increase coronary artery dilatation and increase oxygen supply.

Question 305

What are the side effects of nitrates?

Answer 305

Vasodilation can lead to orthostatic hypotension, reflex tachycardia, throbbing headache, and blushing.

Question 306

What is the contraindication to nitrates?

Answer 306

Contraindicated if systolic blood pressure is

Question 307

What is the dosing pattern for nitrates?

Answer 307

Requires a window–free period of more than 8 hours with nitrate therapy to reduce tachyphylaxis.

Question 308

What are the beneficial effects of beta–blockers?

Answer 308

Beta–blockers have been shown to improve survival after an acute myocardial infarction and in CHF.

Question 309

What are the adverse effects of beta–blockers?

Answer 309

Fatigue, mental depression, insomnia, adverse effects on lipid panel; hallucinations, Raynaud phenomenon, bronchoconstriction, mask signs and symptoms of insulin–induced hypoglycemia, sexual dysfunction.

Question 310

What are the adverse effects of nonselective beta–blockers?

Answer 310

Nonselective beta–blockers may mask hypoglycemic symptoms in insulin–dependent diabetics.

Question 311

What is the contraindication to beta–blockers?

Answer 311

Contraindicated in severe asthma.

Question 312

What are the physiologic effects of calcium–channel blockers?

Answer 312

Produces decreases in preload and afterload. May be harmful in postinfarction period, especially if left ventricular failure.

Question 313

What are the adverse effects of calcium channel blockers?

Answer 313

Congestive heart failure, reflex tachycardia, hypotension, lightheadedness; flushing, headache, weakness, nausea, constipation, nasal congestion, wheezing, peripheral edema.

Question 314

What is anemia?,

Answer 314

A hematocrit less than 41% in men or less than 36% in women, or a hemoglobin less than 13.5 gm/dL in men or less than 12 gm/dL in women.

Question 315

What is microcytic anemia?,

Answer 315

Microcytic anemia is a low mean corpuscular volume (MCV) less than 80; caused by iron deficiency, thalassemia, sideroblastosis, and lead poisoning. Anemia of chronic disease can be either microcytic or normocytic.

Question 316

What is macrocytic anemia?,

Answer 316

Elevated MCV >100 caused by vitamin B12 or folic acid deficiency, alcohol, liver disease, methotrexate, zidovudine, phenytoin. Normal MCV in early micro/macrocytic anemia and hemolysis.

Question 317

What is the presentation of anemia?,

Answer 317

Fatigue, tiredness, poor exercise tolerance. Dyspnea on exertion and light–headedness, confusion. Anemia may cause death from myocardial ischemia. Older patient will develop dyspnea or angina at a Hct

Question 318

What is the first step in diagnosing anemia?,

Answer 318

First step is to determine the MCV. Iron studies, reticulocyte count, peripheral smear, red cell distribution of width (RDW), Coombs test, B12, folate levels, and occasionally a bone marrow biopsy.

Question 319

What is the treatment for anemia?,

Answer 319

Packed red blood cells are used to maintain a hematocrit >25–30%. A healthy young patient can have transfusion withheld until the Hct is in the low 20%s. Older patient needs Hct >30%.

Question 320

How does one unit of packed red blood cells affect the hematocrit?,

Answer 320

The hematocrit should rise three points for every unit of packed red blood cells given.

Question 321

What is iron deficiency anemia?,

Answer 321

Diminished RBC production and an MCV

Question 322

What is the presentation of iron deficiency anemia?,

Answer 322

Hct 30% causes fatigue, poor exercise tolerance. Hct 25% cause tachycardia, palpitations, dyspnea, pallor. Older and CAD dyspneic at 30%. Lightheadedness, confusion, syncope, chest pain, death.

Question 323

What are the physical signs of iron deficiency?,

Answer 323

Brittle nails, spoon shaped nails, glossitis, and pica.

Question 324

How is iron deficiency anemia diagnosed?,

Answer 324

Low serum ferritin

Question 325

What is anemia of chronic disease?,

Answer 325

A defect in the ability to use iron; either microcytic or normocytic; caused by any chronic inflammatory, infectious, or neoplastic condition.

Question 326

How is anemia of chronic disease diagnosed?,

Answer 326

Serum ferritin level is normal or elevated. The serum iron level and total iron binding capacity (TIBC) are low. The reticulocyte count is low.

Question 327

What is the treatment for anemia of chronic disease?,

Answer 327

Correct underlying disease. Iron and erythropoietin are not effective, except in renal disease and anemia caused by chemotherapy or radiation therapy for malignancies.

Question 328

What is sideroblastic anemia?,

Answer 328

A microcytic anemia caused by a disorder in the synthesis of hemoglobin. Hereditary and acquired forms from chloramphenicol, isoniazid, or alcohol. Lead poisoning.

Question 329

How is sideroblastic anemia diagnosed?,

Answer 329

Ferritin is elevated. Transferrin saturation very high, and TIBC very low. Serum iron level is high. Prussian Blue stain of red blood cells in the marrow reveals ringed sideroblasts.

Question 330

What is thalassemia?,

Answer 330

Hereditary underproduction of either the alpha or beta globin chains of the hemoglobin molecule, resulting in a hypochromic, microcytic anemia.

Question 331

What populations more commonly have thalassemia?,

Answer 331

Alpha thalassemia is more common in Asian populations. Beta thalassemia is more common in Mediterranean populations.

Question 332

What is the presentation of thalassemia?,

Answer 332

Individuals with two genes deleted have a mild anemia with hematocrits ranging from 30–40% with a low MCV. In beta thalassemia there is a mild anemia with microcytosis (low MCV).

Question 333

How is thalassemia diagnosed?,

Answer 333

Thalassemia trait: mild anemia with microcytosis. Beta thalassemia major has severe symptoms, large spleen, bone abnormalities.

Question 334

How is thalassemia diagnosed?,

Answer 334

Microcytic anemia with normal iron studies, and hemoglobin electrophoresis. Beta thalassemia shows an increased level of hemoglobin F and hemoglobin A2.

Question 335

What is the treatment for thalassemia?,

Answer 335

Thalassemia traits do not require treatment. Beta thalassemia major patients require blood transfusions once or twice a month.

Question 336

A 73–year–old alcoholic man memory loss and tingling in his feet. Hematocrit of 32% with an MCV of 110. What is the diagnosis?,

Answer 336

Folic acid deficiency.

Question 337

What are the causes of vitamin B12 deficiency?,

Answer 337

Most common cause: pernicious anemia (hereditary, autoimmune, decreased intrinsic factor). Gastrectomy, atrophic gastritis, sprue, enteritis, blind loop. Pancreatic insufficiency, tapeworm. Decreased intake.

Question 338

What is the presentation of vitamin B12 deficiency?,

Answer 338

Peripheral neuropathy, decreased position and vibratory sense; psychiatric, autonomic, motor, cranial nerve, bowel, bladder, and sexual dysfunction. Glossitis, diarrhea, and abdominal pain.

Question 339

How is vitamin B12 deficiency diagnosed?,

Answer 339

Anemia with macrocytosis (increased MCV). Hypersegmented neutrophils. Indistinguishable from folate deficiency. Reticulocyte count is reduced. Pancytopenia. Most specific test is low B12 level.

Question 340

How is pernicious anemia diagnosed?,

Answer 340

Antibodies to intrinsic factor and parietal cells confirm the etiology as pernicious anemia. The Schilling test is not necessary if there is a low B12 level combined with the presence of antibodies to intrinsic factor.

Question 341

What is the treatment for vitamin B12 deficiency?,

Answer 341

Replace the vitamin B12 by the intramuscular route.

Question 342

What is folic acid deficiency?,

Answer 342

Deficiency in folic acid levels leading to anemia because of decreased dietary intake. Alcoholics have decreased folate intake.

Question 343

How is folic acid deficiency diagnosed?,

Answer 343

The hematologic presentation of folic acid deficiency is identical to B12 deficiency. Low red–blood–cell folic–acid level. Treatment is oral replacement of folic acid.

Question 344

What are some chronic causes of hemolytic anemia?,

Answer 344

Sickle cell disease, paroxysmal nocturnal hemoglobinuria, and hereditary spherocytosis

Question 345

What are some acute causes of hemolytic anemia?,

Answer 345

Drug–induced hemolysis, auto–immune hemolysis, or glucose 6–phosphate dehydrogenase deficiency.

Question 346

What is the presentation of hemolytic anemia?,

Answer 346

Fatigue and weakness. Dyspnea and confusion. Jaundice and dark urine. Fever, chills, chest pain, tachycardia, and backache may occur.

Question 347

How is hemolytic anemia diagnosed?,

Answer 347

Hemolytic anemias have a normal MCV. The reticulocyte count is elevated. LDH and indirect bilirubin are elevated. Peripheral smear shows fragmented cells. Hemoglobinuria.

Question 348

What is the treatment of hemolytic anemia?,

Answer 348

Transfusion when the hematocrit becomes low. Hydration prevents toxicity to the kidney tubule from free hemoglobin.

Question 349

What is sickle cell disease?,

Answer 349

A hereditary chronic hemolysis ranging from asymptomatic to severe crisis; irreversibly sickled cells and recurrent painful crises. Autosomal recessive.

Question 350

What is the pathophysiology of sickle cell disease?,

Answer 350

Hemoglobin S is due to a substitution of a valine for glutamic acid as the sixth amino acid of the beta globin chain.

Question 351

What is the prevalence of sickle cell disease?,

Answer 351

The heterozygous trait is present in 8% of the African–American population, and the homozygous form (disease) is present in 1 in 400 African Americans.

Question 352

What conditions may precipitate a painful crisis?,

Answer 352

Painful crisis can be precipitated by hypoxia, dehydration, acidosis, infection, and fever. Sudden drops in hematocrit may also be caused by Parvovirus B19 infection or folate deficiency.

Question 353

What is the presentation of sickle cell disease?,

Answer 353

Renal concentrating defects, ulcerations of legs, bilirubin gallstones, aseptic necrosis of femoral head, osteomyelitis, retinopathy, recurrent infections from Pneumococcus, Haemophilus, growth retardation, splenomegaly, autosplenectomy.

Question 354

What is an acute painful crisis of sickle cell disease?,

Answer 354

Back, rib, chest, leg pain. Acute chest syndrome is chest pain, fever, leukocytosis, hypoxia, and infiltrates. Stroke and TIA. Priapism, blindness, MI, cardiomyopathy. Spontaneous abortion, low birth weight.

Question 355

How is sickle cell disease diagnosed?,

Answer 355

Anemia with a normal MCV. Reticulocyte count 10–20%. LDH, bilirubin elevated. Hb electrophoresis most specific. Peripheral smear shows sickled cells. UA blood. WBC elevated.

Question 356

What is the treatment of acute sickle cell pain crisis?,

Answer 356

Fluids, analgesics, and oxygen. Antibiotics with infection, fever; leukocytosis. Ceftriaxone and cefotaxime are preferred because cover Pneumococcus and Haemophilus influenza.

Question 357

What is the treatment of sickle cell acute chest syndrome, CNS manifestations, priapism, and acute cardiac ischemia?,

Answer 357

PRBC if Hct low. Folic acid and vaccinations against Pneumococcus and influenza. Hydroxyurea to decrease frequency of pain crises. Bone marrow transplantation can be curative.

Question 358

What are autoimmune, cold agglutinin, and drug–induced hemolytic anemias?,

Answer 358

Various forms of acquired hemolytic anemias resulting from production of IgG, IgM, or activation of complement C3 against the red cell membrane. Often sudden and idiopathic.

Question 359

What are the causes of autoimmune hemolytic anemias?,

Answer 359

Antibodies in leukemia, viral infections, lymphoma, collagen vascular diseases or penicillins, cephalosporins, sulfa drugs, quinidine, alpha methyldopa, procainamide, rifampin, and thiazides.

Question 360

What percentage of autoimmune hemolytic anemias are idiopathic?,

Answer 360

50% do not have an underlying disorder.

Question 361

What is cold agglutinin disease?,

Answer 361

IgM against the red cell in association with lymphoma, Waldenstrom macroglobulinemia, Mycoplasma or mononucleosis.

Question 362

Which inflammatory bowel disease is associated with autoimmune hemolytic anemia?,

Answer 362

Ulcerative colitis.

Question 363

What is the presentation of autoimmune hemolysis?,

Answer 363

Sudden fever, syncope, congestive failure, hemoglobinuria. Splenomegaly; cold agglutinin disease results in cyanosis of the ears, nose, fingers, and toes. Weakness, pallor, jaundice, and dark urine.

Question 364

How is autoimmune hemolysis diagnosed?,

Answer 364

Normocytic anemia, reticulocytosis, increased LDH, increased indirect bilirubin. Coombs test is specific for autoimmune, cold agglutinin, drug–induced hemolysis. Spherocytes on smear.

Question 365

What is the treatment for autoimmune hemolysis?,

Answer 365

Steroids. Splenectomy for those unresponsive to steroids. Cold agglutinin disease is managed by avoiding cold.

Question 366

What is hereditary spherocytosis?,

Answer 366

Hemolysis with spherocytes, jaundice, splenomegaly. Autosomal dominant; loss of spectrin in RBC membrane results in spheres, which are not able to pass spleen. Anemia; splenomegaly jaundice; bilirubin stones.

Question 367

How is hereditary spherocytosis diagnosed?,

Answer 367

Decreased MCV anemia, elevated LDH, indirect bilirubin, reticulocytes. Hemolysis; negative Coombs. RBC sensitivity to lysis in osmotic fragility test. The mean corpuscular hemoglobin concentration is elevated.

Question 368

What is the treatment for hereditary spherocytosis?,

Answer 368

Folate replacement. Splenectomy.

Question 369

What is paroxysmal nocturnal hemoglobinuria?,

Answer 369

A red cell membrane defect leading to intermittent dark urine and venous thrombosis and a chronic hemolysis. A red cell membrane defect allows binding of complement to the red cell.

Question 370

What is the presentation of paroxysmal nocturnal hemoglobinuria?,

Answer 370

Dark urine from intravascular hemolysis. Thrombosis of the hepatic vein (Budd–Chiari syndrome). Hemoglobinuria in the first morning urine.

Question 371

How is paroxysmal nocturnal hemoglobinuria diagnosed?,

Answer 371

Increased LDH, bilirubin, and reticulocyte count, hemoglobinuria. Sugar–water test and the acidified–hemolysis (Ham) test. Decay accelerating factor is diminished in PNH.

Question 372

What is the treatment for paroxysmal nocturnal hemoglobinuria?,

Answer 372

Iron replacement. Corticosteroids.

Question 373

What is glucose–6–phosphate dehydrogenase deficiency?,

Answer 373

Hereditary deficiency of an enzyme for neutralizing oxidant stress to the red cell, resulting in acute hemolysis. Oxidant stress from infections, sulfa drugs, primaquine, dapsone, quinidine, and nitrofurantoin.

Question 374

What is the treatment of toxic shock syndrome?,

Answer 374

Beta–lactamase stable penicillin (nafcillin or oxacillin). Restoration of hypovolemic shock, remove infected tissue, prosthesis, tampons, diaphragm.

Question 375

What is acute renal failure?

Answer 375

Rapid rise in blood urea nitrogen or creatinine over a period of several hours to days. Decrease in glomerular filtration rate.

Question 376

What is renal insufficiency?

Answer 376

Renal insufficiency is renal failure, but not to the point of needing dialysis. The term azotemia can be used interchangeably with the term renal insufficiency.

Question 377

What is uremia?

Answer 377

Very severe renal failure requiring dialysis. Severe acidosis, mental status changes, hyper, fluid overload, anemia, hypocalcemia, pericarditis. Bleeding. Uremia is same as end stage renal disease.?

Question 378

What is blood urea nitrogen?

Answer 378

BUN becomes abnormally elevated in all forms of renal failure. BUN rises after a protein meal or from gastrointestinal bleeding. BUN is derived from protein waste products.

Question 379

What is creatinine?

Answer 379

Creatinine is the closest approximation of glomerular filtration rate. Creatinine is a metabolic product of skeletal muscle. Creatinine can be falsely low just because of a decrease in muscle mass.

Question 380

What is prerenal azotemia?

Answer 380

Renal insufficiency caused by diminished perfusion, hypovolemia (dehydration, burns, diuretic, vomiting, diarrhea, hemorrhage), hypotension (septic, cardiogenic, anaphylactic), third spacing in peritonitis.

Question 381

What is the laboratory criteria for prerenal azotemia?

Answer 381

BUN:creatinine ratio of 20:1. There is also a low urine sodium and low fractional excretion of sodium (FeNa 1.010) and a high urine osmolality (>500).

Question 382

What are the signs of renal artery stenosis?

Answer 382

High BUN and creatinine with a high BUN:creatinine ratio. HTN, prerenal azotemia. ACE inhibitors will markedly diminish renal perfusion in renal artery stenosis because of the high aldosterone.

Question 383

What is hepatorenal syndrome?

Answer 383

Renal failure caused by hepatic failure secondary to intense vasoconstriction of afferent arteriole, resulting in decreased renal perfusion.

Question 384

What are the laboratory abnormalities in hepatorenal syndrome?

Answer 384

Prerenal azotemia with a high BUN:creatinine ratio >20:1. Urine Na

Question 385

What is the effect of ACE inhibitors on the kidney?

Answer 385

Renal failure can be caused by vasodilation of the efferent arteriole. In elderly, diabetic, hypertensive, or renal disease such as from myeloma, an ACEI can result in a decreased renal function. Rise in BUN and creatinine.

Question 386

What is the hepatopulmonary syndrome?

Answer 386

Pulmonary failure is caused by hepatic disease. The oxygen saturation drops when the patient sits up and there is an increase in the A–a gradient.

Question 387

What is postrenal azotemia?

Answer 387

Bilateral blockage in outflow of urine. Small stone or clot in bladder. Bladder CA, prostate hypertrophy or CA, retroperitoneal fibrosis, neurogenic bladder. Creatinine will only begin to rise when 80% of renal function lost.

Question 388

What are the laboratory abnormalities in postrenal azotemia?

Answer 388

BUN and creatinine will elevate in a ratio of 20:1 as with prerenal azotemia. Low fractional excretion of sodium and low urine sodium.

Question 389

What are the consequences of prolonged postrenal obstruction?

Answer 389

Permanent damage occurs, and the kidney tubule cells die, then the BUN:creatinine ratio will lower to 10:1, such as that seen in acute tubular necrosis. Recovery is possible until 10 days of obstruction.

Question 390

What are the clinical findings in postrenal azotemia?

Answer 390

Distended bladder, bilateral hydronephrosis on renal sonogram or CT, or large volumes of urine in bladder after passing Foley catheter. After voiding, there should be no more than 50 mL of residual.

Question 391

What is acute tubular necrosis?

Answer 391

85% of acute renal failure is caused by intrinsic renal disease, such as ATN caused by either hypoperfusion of kidney or toxic injury (aminoglycoside). ATN is most common cause of ARF in hospitalized.

Question 392

What are the urine microscopic findings in acute tubular necrosis?

Answer 392

Severe ischemia causes the tubular cells to necrose and slough off into the urine and become visible as granular, muddy brown, or pigmented casts. At the point of necrosis, the renal insufficiency can be permanent.

Question 393

How is acute tubular necrosis diagnosed?

Answer 393

BUN:creatinine ratio 10:1. High urine sodium (>40), high fractional excretion of sodium (>1%), and low urine osm (

Question 394

What is the treatment of acute tubular necrosis?

Answer 394

Underlying cause must be corrected. Hydration is given to exclude possibility of prerenal component. Furosemide does not reverse ATN. Dopamine at low doses does not increase renal perfusion. Dialysis.

Question 395

What is allergic interstitial nephritis?

Answer 395

Allergic interstitial nephritis causes 10–15% of intrinsic renal; failure fever and rash, eosinophils in the urine. AIN is usually caused by an adverse effect of medications. Infections can also cause AIN.

Question 396

What medications can cause allergic interstitial nephritis?

Answer 396

Penicillin, cephalosporins, sulfas, allopurinol, rifampin, quinolones. Calcium blockers. Sulfa drugs include thiazides, furosemide, acetazolamide.

Question 397

What infections can cause allergic interstitial nephritis?

Answer 397

AIN is also caused by infections by viruses, bacteria, and fungi. Leptospirosis, legionella, CMV, rickettsia, and streptococci.

Question 398

What autoimmune disorders can cause allergic interstitial nephritis?

Answer 398

Systemic lupus erythematosus (SLE), Sjögren syndrome, sarcoidosis, and cryoglobulins.

Question 399

What laboratory abnormalities are associated with allergic interstitial nephritis?

Answer 399

Eosinophilia, eosinophiluria, hematuria, proteinuria, increased IgE. Best initial test is a urinalysis for white cells. Urine eosinophils on Wright stain. Kidney biopsy not necessary.

Question 400

What is the treatment of allergic intestinal nephritis?

Answer 400

AIN resolves spontaneously after stopping the offending agent. Short course of steroids may be administered.

Question 401

A 25–year–old man was exercising vigorously became very weak with painful muscles and dark urine. What is the most important test to do first?

Answer 401

Electrocardiogram

Question 402

What are the causes of rhabdomyolysis?

Answer 402

Rhabdomyolysis is caused by sudden, severe crush injury, seizures, severe exertion, hypokalemia, hypophosphatemia, and medications such as statins.

Question 403

What are the laboratory signs of rhabdomyolysis?

Answer 403

The most important test after a severe crush injury or seizure and rhabdomyolysis is an ECG or potassium level. UA is positive for blood but with no red cells because myoglobin reacts with the dipstick.

Question 404

What action should be taken if peaked T–waves are present on an ECG?

Answer 404

Acidosis and hyperkalemia can cause arrhythmia. If there are peaked T–waves, an amp of calcium gluconate should be given.

Question 405

How is rhabdomyolysis confirmed in the laboratory?

Answer 405

CPK skeletal muscle necrosis. Metabolic acidosis with a decreased serum bicarbonate, hyperphosphatemia, hypocalcemia. Severe hyperuricemia. Rapidly rising creatinine.

Question 406

What is the treatment for rhabdomyolysis?

Answer 406

If there are ECG abnormalities from the hyperkalemia, therapy is calcium chloride or gluconate. Hydration, mannitol. Alkalinize urine with bicarbonate to prevent precipitation of pigment in tubule.

Question 407

What is the most common cause of hyperoxaluria resulting in acute renal failure?

Answer 407

Ethylene glycol overdose from antifreeze. An intoxicated person with a metabolic acidosis with an elevated anion gap and renal insufficiency. Oxalate crystals on UA. Oxalate crystals are shaped like envelopes.

Question 408

What is the treatment of acute ethylene glycol overdose?

Answer 408

Fomepizole infusion to prevent the formation of the toxic metabolite of ethylene glycol (oxalic acid). Dialysis to then remove the ethylene glycol. Sodium bicarbonate to correct acidosis.

Question 409

What renal complication occurs in patients being given chemotherapy?

Answer 409

Acute renal failure from uric acid toxicity occurs in the setting of tumor lysis syndrome. Vigorous hydration and allopurinol should be given before chemotherapy.

Question 410

What is the effect of hypercalcemia on the kidneys?

Answer 410

Calcium precipitates in tubule, forming stones. Hypercalcemia can lead to distal RTA and nephrogenic diabetes insipidus. Most common cause of hypercalcemia is primary hyperparathyroidism.

Question 411

Which drugs are toxic to the kidneys?

Answer 411

NSAIDs, aminoglycosides, cephalosporins, contrast agents, amphotericin, cisplatin, radiation effect, lead, mercury, or gold, and cyclosporine.

Question 412

What method of administration of aminoglycosides reduces the risk of toxicity?

Answer 412

Ability of antibiotics to kill is associated with peak level, but toxicity is associated with the trough level. Once–a–day dosing allows high bactericidal levels and very low trough levels, which reduce toxicity.

Question 413

What is the affect of amphotericin B on the kidneys?

Answer 413

Renal insufficiency and distal renal tubular acidosis. After several weeks of amphotericin, the patient will develop high creatinine and decreased magnesium.

Question 414

How does atheroembolic disease affect the kidneys?

Answer 414

Vascular procedures (angioplasty) cause renal failure several days later. Atheroemboli are associated with eosinophilia, low complement, bluish discoloration of fingers, toes, livedo reticularis.

Question 415

What are the common nephrotoxic medications?

Answer 415

Radiocontrast for CT can result in renal failure 12 hours after. Pentamidine is associated with renal failure and pancreatitis. Vancomycin, aminoglycosides, cyclosporine, and lithium.

Question 416

Which antiretroviral is associated with renal failure?

Answer 416

Indinavir results in renal failure from the drug precipitating in the kidney tubules. Indinavir stones require contrast to be visualized on a spiral CT scan.

Question 417

Which persons are at risk for analgesic nephropathy?

Answer 417

NSAIDs are a frequent cause of renal failure. A rise in creatine occurs in persons with significant impairment such as the elderly or those with hypertension or diabetes.

Question 418

What are the causes of acute papillary necrosis?

Answer 418

Acute papillary necrosis occurs in sickle cell disease, diabetes, urinary obstruction, chronic pyelonephritis, and NSAIDs.

Question 419

What is the presentation of acute papillary necrosis?

Answer 419

Sudden flank pain, hematuria, pyuria, fever. Similar to pyelonephritis. Necrotic material in urine. Papillary necrosis will have a negative culture. The best test for papillary necrosis is CT.

Question 420

What is glomerulonephritis?

Answer 420

Glomerulonephritis is inflammation of the glomerulus caused by autoimmunity, antibodies, or vasculitis.

Question 421

What is the presentation of glomerulonephritis?

Answer 421

Edema, hematuria, red cell casts, and hypertension. The urine red cells are dysmorphic.

Question 422

What are the physical signs of glomerulonephritis?

Answer 422

Edema of GN initially appears in areas of low tissue tension, such as periorbital or scrotum. Edema can be diffuse. Salt and water retention leads to edema and hypertension.

Question 423

What amount of proteinuria is associated with glomerulonephritis?

Answer 423

Modest amounts of protein appear in the urine with the daily total being 3.5 grams per 24 hours the patient has nephrotic syndrome.

Question 424

What are the laboratory signs of glomerulonephritis?

Answer 424

Low urine Na with a fractional excretion of Na

Question 425

What is Wegener granulomatosis?

Answer 425

Vasculitis of kidney, lung, upper respiratory, sinuses, middle ear. Chronic upper/lower respiratory illness, not responding to antibiotics, with renal disease suggests WG. Involves skin, joints, eyes, GI; neuropathy.

Question 426

What are the laboratory abnormalities associated with Wegener granulomatosis?

Answer 426

Elevated ESR, anemia, leukocytosis. Rheumatoid factor in 50%. The best initial test that is specific for WG is the cytoplasmic antineutrophil cytoplasmic antibody. Complement levels are normal.