2 Flashcards
(426 cards)
1
Q
What are the symptoms of myocarditis?
A
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.
2
Q
What are the musculoskeletal causes of chest pain?
A
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.
3
Q
What are the gastrointestinal causes of chest pain?
A
Esophageal reflux is worse with recumbency or meals; regurgitation; relieved by antacids, nitroglycerin. Ulcers, cholecystitis. Pancreatitis causes abdominal tenderness, with radiation to back, hyperamylasemia.
4
Q
What are the symptoms of pneumothorax?
A
Onset abrupt with sharp pleuritic chest pain and dyspnea; breath sounds are absent, chest x–ray confirms.
5
Q
What are the symptoms of pleuritis?
A
Pain is sharp and increases on inspiration; pleural friction rub; underlying pulmonary infection.
6
Q
What are the major modifiable risk factors for ischemic heart disease?
A
Hypercholesterolemia, smoking hypertension, physical inactivity, obesity, diabetes.
7
Q
What subgroup of hypercholesterolemia is the most important risk factor for ischemic heart disease?
A
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.
8
Q
What is the risk of myocardial infarction in smokers?
A
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.
9
Q
What degree of hypertension is a risk factor for cardiovascular events?
A
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.
10
Q
What percentage of patients with diabetes die of cardiovascular disease?
A
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.
11
Q
What are the clinical signs of stable angina?
A
Substernal pressure lasting 5–15 min; not affected by respiration/position. Stable angina occurs when myocardium becomes ischemic during exercise, hypotension, anemia.
12
Q
What is the most common ECG sign in patients with angina?
A
Most commonly ST segment depression is seen. ST segment elevation typically occurs in variant angina (Prinzmetal angina) where coronary artery spasm is responsible.
13
Q
How is ischemic heart disease diagnosed?
A
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.
14
Q
What is the criteria for a positive exercise stress test for myocardial ischemia?
A
>2 mm ST–segment depressions or hypotension (a drop of more than 10 mm Hg in systolic pressure) occur either alone or in combination.
15
Q
What type of noninvasive test for ischemic heart disease is indicated for patients who are unable to exercise?
A
Patients who are unable to exercise or walk should be considered for chemical stress testing, such as dipyridamole (Persantine) or dobutamine stress tests.
16
Q
What type of noninvasive test for ischemic heart disease is indicated for patients with bundle branch block?
A
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.
17
Q
What is a nuclear stress test?
A
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.
18
Q
What are the dobutamine and adenosine stress tests?
A
This test is used in people who are unable to exercise. A drug is given to induce tachycardia.
19
Q
What is a stress echocardiogram?
A
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.
20
Q
What are the indications for cardiac catheterization?
A
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.
21
Q
What is the treatment of ischemic heart disease?
A
Nitroglycerin SL alleviates pain. Long–acting nitrates, beta blockers. Aspirin and statins. All patients with stable angina need cardiac angiography or stress testing.
22
Q
What are the target goals for treatment of hyperlipidemic patients with coronary artery disease?
A
LDL less than 100 mg/dL. HDL 40 mg/dL or greater. Triglycerides less than 150 mg/dL.
23
Q
What is the optimal LDL–cholesterol goal for patients at very high risk of coronary artery disease?
A
200, HDL
24
Q
What are the indications for coronary bypass graft in ischemic heart disease?
A
Left main coronary disease or three vessel disease and left ventricular (LV) dysfunction. More efficacious in diabetes. More beneficial in low ejection fraction.
25
What are the types of acute coronary syndromes?
Acute coronary syndromes (ACS) include a range of thrombotic coronary diseases, including unstable angina (UA), non–ST elevation myocardial infarction, and STEMI.
26
What is a non ST–segment elevation myocardial infarction?
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.
27
What are the indications for thrombotic therapy in patients with acute coronary syndrome?
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.
28
What is unstable angina?
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.
29
What are the ECG findings in non–segment elevation MI?
Dynamic ST–segment depression (\>5 mm), or new T–wave inversion ( 2 mm), but the ECG may be normal or show minor changes.
30
What are the high–risk features for patients with UA/NSTEMI?
Repetitive or prolonged chest pain (\>10 min), elevated markers, persistent ST depression \>0.5 mm or new T–wave inversion, SBP
31
What is the general management of NSTEMI?
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.
32
What are the drugs that are used in NSTEMI?
Aspirin, clopidogrel, heparin, tirofiban, metoprolol, nitroglycerine.
33
What antiplatelet therapy should be given to patients with NSTEMI?
Aspirin and clopidogrel. Clopidogrel should be avoided if likely to require bypass surgery (severe ST–segment depression, SBP
34
What are the indications for anticoagulants in NSTEMI?
Unfractionated heparin or subcutaneous enoxaparin should be given until angiography or for 48–72 hours. Enoxaparin dose must be reduced in patients with impaired renal function.
35
What is the mechanism of the glycoprotein (GP) Hb/IIIa inhibitors?
Inhibit platelet function by blocking a receptor involved in platelet aggregation, providing a more comprehensive platelet blockade than the combination of aspirin and heparin.
36
What is the indication for tirofiban or eptifibatide in NSTEMI?
High–risk patients in whom an invasive strategy is planned. Tirofiban is particularly beneficial and recommended in patients with diabetes. Complications are bleeding and thrombocytopenia.
37
What are the indications for a beta–blocker in patients with NSTEMI?
A beta–blocker should be given unless contraindicated. Intravenous nitroglycerin is given for refractory pain.
38
Which patients with NSTEMI should receive invasive management?
Early angiography (48 h) and revascularization is recommended in NSTEMI with high–risk features. Refractory ischemia, and high–risk features on early exercise testing need early invasive.
39
What are the clinical signs of ST elevation myocardial infarction?
Substernal, diffuse, pressure pain. Radiation neck, jaw, shoulders, arms. Lightheadedness, nausea, vomiting, diaphoresis, dyspnea. Pain lasts longer than 20 min, does not respond completely to nitroglycerin.
40
What are the signs of STEMI in elderly and diabetic patients?
Elderly and diabetic patients are prone to atypical symptoms, such as nausea or dyspnea. 20% of MI are silent
41
What are the physical signs of ST elevation myocardial infarction?
Bradycardia in inferior MI. Tachycardia with large MI. BP elevated. Left ventricular failure, valve dysfunction. S4 of stiffened ventricle. Mitral regurgitation if papillary muscle malfunction. S2 paradoxical split as LV contraction time increases due to
42
What are the ECG criteria for STEMI?
Persistent ST–segment elevation of \>1 mm in two contiguous limb leads. ST–segment elevation of \>2 mm in two contiguous chest leads. New LBBB. Initially, markers are not elevated in STEMI (eventually positive).
43
What is the initial nonspecific management of acute coronary syndrome?
Initial nonspecific management for all patients with possible MI (chest pain) is oxygen therapy, aspirin (unless contraindicated), nitroglycerin and morphine.
44
What is the management of STEMI in patients who present within 12 hours of the onset of ischemic symptoms?
Completely occluded coronary artery with thrombus at the site of a ruptured plaque. Reperfusion strategy with fibrinolytic therapy or percutaneous coronary intervention.
45
Which ECG leads have ST elevation in an inferior myocardial infarction?
II, III, aVF
46
Which coronary artery is occluded in an inferior myocardial infarction?
Right coronary.
47
Which ECG leads have ST elevation in an anteroseptal myocardial infarction?
V1–V3
48
Which coronary artery is occluded in an anteroseptal myocardial infarction?
Left anterior descending
49
Which ECG leads have ST elevation in an anterior myocardial infarction?
V2–V4
50
Which coronary artery is occluded in an anterior myocardial infarction?
Left anterior descending artery.
51
Which ECG leads have ST elevation in a lateral myocardial infarction?
I, aVL, V4, V5, and V6
52
Which coronary artery is occluded in an anterior myocardial infarction?
Left anterior descending or circumflex artery.
53
Which ECG leads have ST elevation in a posterior MI?
V1–V2: Tall broad initial R wave, ST depression, tall upright T wave; usually occurs in association with inferior or lateral MI.
54
Which coronary artery is occluded in a posterior myocardial infarction?
Posterior descending
55
What is the time of onset of hyperacute T waves (tall, peaked T waves) after a myocardial infarction?
Immediately. Disappear in 6–24 hours.
56
What is the time of onset of ST–segment elevations after a myocardial infarction?
Immediately
57
At what time do ST–segment elevations disappear after a myocardial infarction?
1–6 weeks
58
What is the time of onset of Q waves longer than 0.04 seconds after a myocardial infarction?
One to several days. 0.04 seconds is one small ECG box.
59
At what time do Q waves longer than 0.04 seconds disappear after a myocardial infarction?
Years to never
60
What is the time of onset of T wave inversions after a myocardial infarction?
6–24 hours
61
At what time do T wave inversions disappear after a myocardial infarction?
Disappear months to years later.
62
What is the best emergent reperfusion therapy?
PCI is the best available treatment because of improved short–term and long–term reduction of deaths and MI in patients with STEMI presenting within 12 hours when compared with thrombolytic therapy.
63
What are the indications for thrombolytics?
tPA is the most common agent used in the US. Thrombolytic agent is an alternative to primary PCI in suitable candidates with: ST–elevation MI (\>1 mm ST elevation in two contiguous leads). New LBBB
64
What are the contraindications to thrombolytic therapy?
Active bleeding or bleeding diathesis, head or facial trauma within 3 months, suspected aortic dissection, prior intracranial hemorrhage, ischemic stroke within 3 months.
65
What are the relative contraindications to thrombolytic therapy?
Recent major surgery (
66
What are the indications for antiplatelet agents in STEMI?
Aspirin (300 mg) should be given to all STEMI; 75 mg/d long term. Clopidogrel (300–600 mg loading) in addition to aspirin if undergoing PCI. If fibrinolytic therapy, clopidogrel given in addition to ASA. If CABG planned, clopidogrel withheld.
67
What are the indications for antithrombin in STEMI?
With PCI: Antithrombin therapy should be used in conjunction with PCI. Enoxaparin in acute STEMI in conjunction with PCI is effective.
68
What are the indications for enoxaparin with fibrinolysis?
Enoxaparin may be used in conjunction with fibrin–specific fibrinolytic agents in patients under the age of 75 years if there is no significant renal dysfunction.
69
What are the indications for glycoprotein IIb/IIIa inhibitors in STEMI?
Use abciximab with primary PCI in patients with STEMI.
70
What are the recommended discharge medications after ACS?
Aspirin, clopidogrel, beta–blocker, statin, nitrates.
71
What discharge antiplatelet therapy should be given to patients after ACS?
Aspirin: All patients should take 75–325 mg daily unless contraindicated. Clopidogrel should be prescribed for up to 9–12 months after ACS, particularly after stent placement.
72
What are the indications for a beta–blocker after ACS?
Beta–blocker should be prescribed for all patients after an ACS unless contraindicated, and continued indefinitely. Metoprolol and carvedilol should be used in patients after ACS who have heart failure.
73
What are the indications for ACE inhibitors after ACS?
ACE inhibitors should be given in patients with ACS in congestive heart failure, left ventricular dysfunction (ejection fraction 40%).
74
What are the indications for statin therapy after ACS?
Statin therapy should be initiated in the hospital in all patients with ACS.
75
What are the indications for nitrates after ACS?
All patients should be prescribed short–acting nitrates. Long–acting nitrates (isosorbide) are given if there is continuous and frequent chest pain.
76
What are the indications for warfarin after ACS?
Warfarin is recommended after ACS only for those at high risk of systemic thromboembolism because of atrial fibrillation, mural thrombus, or congestive heart failure.
77
What are the recommendations for exercise ECG testing after ACS?
Submaximal testing 4–7 days after infarction. A maximal test can be performed at 3–6 weeks postinfarction. Myocardial perfusion imaging can be performed before hospital discharge to assess residual ischemia.
78
What are the complications of ACS?
Pump dysfunction, ischemia, pericarditis (Dressler syndrome), thromboembolism, sudden cardiac death due to arrhythmia (most commonly ventricular fibrillation). Ventricular tachycardia.
79
What is right ventricular infarction?
Accompanies 30% of inferior MIs. It is diagnosed with right side leads and treated with fluids.
80
What is Prinzmetal angina?
Uncommon condition: episodes of angina are triggered when a coronary artery goes into spasm with ST–segment elevation. May cause acute MI, ventricular arrhythmias, sudden death.
81
What is the treatment of Prinzmetal angina?
Calcium channel blockers or nitrates.
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?
Congestive heart failure
83
What is systolic heart failure?
Systolic dysfunction is caused by a loss of contractile strength of the myocardium with ventricular dilatation. Ischemic cardiomyopathy and dilated cardiomyopathy.
84
What is diastolic heart failure?
Filling of one or both ventricles is impaired while the emptying capacity is normal (the ejection fraction is normal). Infiltrative cardiomyopathies (amyloidosis).
85
What are the causes of decompensated heart failure?
Exacerbation of HF can be caused by nonadherence to medication, increase in dietary salt, acute ischemia, tachycardia or pulmonary infection, arrhythmias, hypertension, thyrotoxicosis, and anemia.
86
What are the causes of congestive heart failure?
Ischemic heart disease causes 70%. Other:: hypertensive heart disease, cardiomyopathies (idiopathic, alcohol), valvular, congenital. With exacerbation of HF, always check troponin to exclude myocardial infarction.
87
What are the symptoms of left ventricular heart failure?
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, and weakness.
88
What is the New York Heart Association Functional Classification of heart failure?
Class I: no limitation. Class II: slight, mild limitation of activity. Class III: marked limitation. Class IV: confined to bed or chair.
89
What is the best test to confirm the diagnosis of heart failure?
Echocardiography is the test–of–choice for diagnosis and to classify the type (systolic vs. diastolic). Echocardiography measures ejection fraction.
90
What are the chest x–ray findings in congestive heart failure?
The chest x–ray may show cardiomegaly, vascular redistribution, Kerley B–lines, and interstitial edema.
91
What are the ECG findings in congestive heart failure?
Electrocardiogram identifies ventricular hypertrophy, ischemic heart disease, arrhythmias or conduction delays which may cause HF.
92
What is B–type natriuretic peptide?
BNP is a polypeptide secreted by the heart in response to excessive stretching of the myocytes. The BNP is elevated (97% sensitivity) in decompensated HF.
93
What are the beneficial effects of ACE inhibitors in congestive heart failure?
ACE reduce preload and afterload through vasodilation, reducing right atrial, pulmonary arterial, pulmonary capillary wedge pressures. Angiotensin receptor blockers if unable to tolerate ACEI (cough).
94
What are the side effects of captopril?
Rash, nonproductive cough, proteinuria, renal failure, taste disturbance, agranulocytosis, hypotension
95
What are the side effects of enalapril?
Hypotension, angioedema, renal failure, laryngeal edema, cough.
96
What are the side effects of lisinopril?
Hypotension, proteinuria, renal insufficiency, rash, cough.
97
What are the side effects of nitroprusside?
Thiocyanate toxicity, methemoglobinemia.
98
What are the side effects of nitroglycerin?
Headache, postural hypotension, methemoglobinemia.
99
What are the side effects of isosorbide dinitrate?
Headache, postural hypotension
100
What are the side effects of hydralazine?
Headache, positive ANA, SLE–like syndrome (10–20%) drug fever, rash.
101
What is the treatment of congestive symptoms in heart failure?
Loop diuretics. Furosemide is most commonly used. Spironolactone and eplerenone (aldosterone antagonists) are used as add–on therapy to ACE inhibitors in severe heart failure.
102
What is the mechanism of action of thiazides?
Inhibits NaCl cotransport; used mostly for treatment of hypertension; hydrochlorothiazide, chlorothiazide
103
What are the side effects of thiazides?
HypoNa, hypoK, hyperlipidemia, hyperCa, metabolic alkalosis, hyperuricemia, reduced GFR, allergy, thrombocytopenia, agranulocytosis, leukopenia, anemia, pancreatitis, sexual dys, glucose intolerance.
104
What are the side effects of indapamide?
Hypokalemia and lipid abnormalities are less common than with other thiazides. Hyponatremia, hypercalcemia, metabolic alkalosis, hyperuricemia, reduced glomerular filtration rate, allergy.
105
What are the side effects of phthalimidine derivatives?
Similar to thiazides, but hypokalemia may be profound. Chlorthalidone, metolazone.
106
What is the mechanism of action of loop diuretics?
Inhibitors of Na/K/Cl cotransport; most commonly used diuretics in heart failure; furosemide, ethacrynic acid, bumetanide.
107
What are the side effects of loop diuretics?
Hyponatremia, hypokalemia, hypocalcemia, metabolic alkalosis, hyperuricemia, interstitial nephritis, ototoxicity, thrombocytopenia, agranulocytosis, leukopenia, anemia.
108
What are the side effects of potassium–sparing diuretics?
Hyperkalemia, mental confusion, nausea, and gynecomastia (spironolactone only).
109
What is the initial therapy for congestive heart failure?
ACE inhibitor and furosemide is considered first line for all HF. Once stable, add on carvedilol or metoprolol. Chronic adrenergic activation is associated with HF.
110
What treatment is recommended for black patients with severe heart failure who have already been treated with the standard therapy?
Reduction in death and a decrease in hospitalization occurs with the combination of hydralazine and isosorbide.
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)?
Addition of spironolactone significantly reduces death and hospitalizations.
112
What is the treatment of severe refractory heart failure?
Inotropic agents for severe heart failure improves symptoms, quality of life and reduces hospitalizations, but does not improve survival.
113
What is the mechanism of digitalis?
Inhibits Na+/K+ – ATPase pump which results in increased intracellular Na+ and decreased intracellular Ca. Increase in intracellular Ca results in improved cardiac contractility.
114
What is the effect of potassium levels on the effect of digitalis?
Hyperkalemia will decrease digitalis activity, whereas hypokalemia results in toxicity.
115
What conditions predispose to digitalis toxicity?
Renal insufficiency, hypokalemia, hypercalcemia, hypomagnesemia, advanced age, sinoatrial and atrioventricular block; hypothyroidism, hypoxic states, pulmonary disease; multiple drug therapy.
116
What drug interaction occurs with digoxin and quinidine?
Decreases renal clearance of digoxin.
117
What drug interaction occurs with digoxin and verapamil/diltiazem?
Decreases renal clearance of digoxin.
118
What drug interaction occurs with digoxin and cholestyramine/colestipol?
Binds digoxin in gastrointestinal tract; interferes with enterohepatic circulation.
119
What drug interaction occurs with digoxin and spironolactone?
Inhibits tubular secretion of digoxin.
120
What drug interaction occurs with digoxin and thiazides/furosemide?
Diuretic–induced hypokalemia and/or bumetanide. Hypomagnesemia potentiates digitalis action.
121
What are the side effects of digoxin?
Nausea, vomiting, gynecomastia, blurred vision; yellow halo around objects; paroxysmal atrial tachycardia with block, PVCs, and bradycardia.
122
What is the treatment for digoxin toxicity?
Stop the drug. K+ administration if needed. Lidocaine and phenytoin. Digibind only for acute overdose.
123
What is the treatment of severe heart failure that does not respond to standard therapy?
Sympathomimetic amines (dopamine, dobutamine) and phosphodiesterase inhibitors (amrinone, milrinone) IV infusion. Other options: pacing, implantable defibrillator, heart transplantation.
124
What is the treatment of diastolic heart failure?
Diastolic HF may worsen when diuretics and vasodilators. Reducing the heart rate with beta blockers and calcium channel blockers (verapamil, diltiazem) to allow adequate diastolic filling.
125
What are the signs of pulmonary edema?
Increased respiratory rate, nocturnal dyspnea, cough with expectoration of pink frothy sputum, cyanosis, crackles, rhonchi, wheezing.
126
What are the chest x–ray findings in pulmonary edema?
Prominent pulmonary vasculature, enlarged cardiac silhouette, Kerley B lines, effusions.
127
What is the treatment of pulmonary edema?
Morphine sulfate. Furosemide reduces preload. Nitroglycerin reduces preload. Digoxin if atrial fibrillation. Intravenous ACE inhibitors.
128
What is mitral stenosis?
Thickened valve leaflets impede left ventricular filling; increased left atrial pressure causes pulmonary congestion; cardiac output reduced, secondary pulmonary vasoconstriction and RV failure occurs
129
What is the most common lesion caused by rheumatic fever?
Mitral stenosis is the most common lesion caused by rheumatic fever. Rarely congenital.
130
What are the early clinical signs of mitral stenosis?
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, wasting, hemoptysis (rupture of pulmonary vessels); systemic embolism from stasis of blood in an enlarged left atrium
131
What are the late clinical signs of severe mitral stenosis?
Hoarseness due to impingement of an enlarged left atrium on recurrent laryngeal nerve; right–sided heart failure; hepatomegaly, ascites; peripheral edema.
132
What are the physical signs of mitral stenosis?
Atrial fibrillation (irregular rhythm); pulmonary rales; decreased pulse pressure; loud S1, opening snap following S2, diastolic rumble, sternal lift (right ventricular enlargement).
133
What are the ECG findings in mitral stenosis?
Right ventricular hypertrophy; left and right atrial enlargement; atrial fibrillation may occur.
134
What are the chest x–ray findings in mitral stenosis?
Large left atrium (double–density right heart border, straightening of the left heart border). Signs of pulmonary hypertension, including Kerley B lines and increased vascular markings. Large pulmonary artery.
135
What is the treatment of mitral stenosis?
Diuretics and salt–restricted diet; digitalis, anticoagulants if atrial fibrillation; when symptomatic: mitral commissurotomy or valve replacement.
136
What are the hemodynamic findings in mitral regurgitation?
LV stroke volume is pumped backward into LA, resulting in decreased CO. Volume overload, increased preload. LV failure causes dyspnea, orthopnea, paroxysmal nocturnal dyspnea. Pulmonary HTN.
137
What are the acute causes of mitral regurgitation?
Rupture chordae tendineae; papillary muscle rupture; endocarditis, trauma.
138
What are the chronic causes of mitral regurgitation?
Rheumatic heart disease, papillary muscle dysfunction, mitral prolapse/calcification, endocarditis; HCM; endocardial cushion defect, corrected transposition; endocardial fibroelastosis; LV dilatation.
139
What are the physical signs of mitral regurgitation?
Hyperdynamic and downward left ventricular impulse. Holosystolic apical murmur radiating to the axilla with a thrill (palpable turbulence). S3 with a soft S1 and widely split S2. Distended neck veins.
140
What are the ECG signs of mitral regurgitation?
Left ventricular hypertrophy and left atrial enlargement. Chest x–ray: cardiac enlargement vascular congestion.
141
What is the treatment of mitral regurgitation?
Digitalis, diuretics, arteriolar vasodilators (ACE inhibitors), warfarin; mitral valve replacement when symptoms.
142
What is mitral valve prolapse?
Most common congenital valvular abnormality; also in young women with connective tissue disease (e.g., Marfan or idiopathic).
143
What is the presentation of mitral valve prolapse?
Asymptomatic. Lightheadedness, palpitations, syncope, chest pain. Arrhythmias. Mid–to–late systolic click, late systolic murmur at apex which worsens with Valsalva; improves with squatting.
144
What are the complications of mitral valve prolapse?
Serious arrhythmias, sudden death, congestive heart failure, bacterial endocarditis, calcifications, transient cerebral ischemic attacks, mitral regurgitation.
145
What is the treatment of mitral valve prolapse?
Endocarditis prophylaxis only in severe cases. Beta–blocker for chest pain. Mitral valve replacement is rarely necessary.
146
What is aortic stenosis?
Calcification and degeneration; more common in elderly. Calcification and fibrosis of a congenitally bicuspid aortic valve. Rheumatic valvular disease.
147
What is the pathophysiology of aortic stenosis?
Elevation LV systolic pressure and LV hypertrophy. Noncompliant left ventricle causes a prominent S4 gallop. LV diastolic pressure increases; pulmonary congestion.
148
What are the clinical signs of aortic stenosis?
Angina, syncope, dyspnea. Pulsus tardus et parvus (carotid pulse weak, late), carotid thrill. Systolic ejection murmur aortic area; harsh, S4 gallop; A2 decreased, S2 single or paradoxically split; aortic ejection click.
149
What are the ECG signs of aortic stenosis?
Left ventricular hypertrophy. Chest x–ray: calcification, cardiomegaly, pulmonary congestion.
150
What is the treatment of aortic stenosis?
Endocarditis prophylaxis is not recommended. Valve replacement when the valve area is reduced below 0.8 cm or symptoms. Balloon valvuloplasty if too ill to tolerate surgery.
151
What is aortic valve sclerosis of the elderly?
Systolic murmur may mimic aortic stenosis. Systolic murmur ends early and does not peak late. Carotids do not have delayed upstrokes. No left ventricular hypertrophy by ECG. There is no stenosis on echo.
152
What are the clinical signs of hypertrophic obstructive cardiomyopathy?
Brisk bifid carotid. Systolic crescendo–decrescendo–murmur at left sternal border, which does not radiate to neck. Murmur increases with Valsalva (all other murmurs decrease). Pseudoinfarct (large septal Q).
153
What are the clinical sings of mitral regurgitation?
Murmur is holosystolic and radiates to axilla and not carotids. Carotid upstroke is normal; dilated left ventricle.
154
What are the clinical signs of pulmonic stenosis?
Murmur does not radiate into neck; loudest along the left sternal border; increases with inspiration.
155
What are the causes of aortic regurgitation?
Hypertension is the most common cause; infectious endocarditis, syphilis, ankylosing spondylitis; Marfan syndrome, rheumatic fever, aortic dissection, aortic trauma.
156
What is the pathophysiology of aortic regurgitation?
Aortic regurgitation results in a volume overload of the left ventricle.
157
What are the clinical signs of aortic regurgitation?
Dyspnea is most common. Diastolic decrescendo murmur. Systolic flow murmur. S3 in left ventricular failure, Austin–Flint murmur: low pitched, late diastolic apex murmur
158
How is aortic regurgitation diagnosed?
ECG: LV hypertrophy; chest x–ray: LV and aortic dilation; echocardiogram
159
What is the treatment of aortic regurgitation?
Endocarditis prophylaxis is not recommended. Salt restriction, diuretics, ACE inhibitors. Aortic valve replacement when symptoms worsen.
160
What is hypertrophic obstructive cardiomyopathy?
Marked hypertrophy of left ventricle; usually disproportionate hypertrophy of septum
161
What is restrictive cardiomyopathy?
Reduced ventricular compliance; usually caused by infiltration of myocardium (by amyloid, hemosiderin, or glycogen deposits).
162
What is obliterative cardiomyopathy?
Thickened endocardium or mural thrombi, or both, act as space–occupying lesions and reduce left ventricular filling.
163
What is dilated cardiomyopathy?
Characterized by diminished myocardial contractility, usually involving both ventricles; most common cause for heart transplants.
164
What are the causes of dilated cardiomyopathy?
Idiopathic, alcoholic, peripartum; viruses, parasites, mycobacteria, Rickettsiae; toxins (cobalt, lead, arsenic); doxorubicin cyclophosphamide, vincristine. Hypophosphatemia, hypoK, hypoCa, uremia.
165
What are the clinical signs of dilated cardiomyopathy?
Symptoms of left and right ventricular failure: dyspnea, orthopnea; peripheral edema.
166
What are the x–ray signs of dilated cardiomyopathy?
Cardiomegaly with pulmonary congestion. ECG: sinus tachycardia, arrhythmias, conduction disturbances.
167
What is the cause of hypertrophic obstructive cardiomyopathy?
Hypertrophic cardiomyopathy can develop sporadically; it is hereditary in 60%; autosomal dominant.
168
What is the pathophysiology of hypertrophic obstructive cardiomyopathy?
Thickening of interventricular septum. LV compliance reduced. Heart is hypercontractile. EJECTION FRACTION 80% (normal is 60%). Obstruction worsened by increased contractility.
169
What is the effect of digitalis glycosides on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of increased contractility.
170
What is the effect of beta–adrenergic stimulation (eg, isoproterenol, epinephrine) on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of increased contractility.
171
What is the effect of premature beats on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of increased contractility.
172
What is the effect of Valsalva maneuver on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of decreased preload.
173
What is the effect of decrease in intravascular volume (eg, hemorrhage, diuresis, gastrointestinal losses) on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of decreased preload.
174
What is the effect of standing on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of decreased preload.
175
What is the effect of nitroglycerin on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of decreased preload.
176
What is the effect of vasodilator drugs on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of decreased preload.
177
What is the effect of tachycardia on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of decreased preload and increased contractility.
178
What is the effect of hypovolemia on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of decreased afterload.
179
What is the effect of nitroglycerin and related drugs on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of decreased afterload.
180
What is the effect of vasodilator drugs on hypertrophic obstructive cardiomyopathy?
Increase obstruction because of decreased afterload.
181
What is the effect of beta–adrenergic blockade (eg, propranolol) on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of decreased contractility.
182
What is the effect of heavy sedation and general anesthesia on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of decreased contractility.
183
What is the effect of calcium channel blockers, disopyramide, and other drugs that depress myocardial function on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of decreased contractility.
184
What is the effect of intravascular volume expansion on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of increased preload.
185
What is the effect of squatting on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of increased preload.
186
What is the effect of bradycardia on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of increased preload.
187
What is the effect of beta–adrenergic blockade on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of increased preload.
188
What is the effect of intravascular volume expansion on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of increased afterload.
189
What is the effect of squatting on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of increased afterload.
190
What is the effect of alpha–adrenergic stimulation (e.g., phenylephrine, mephentermine) on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of increased afterload.
191
What is the effect of handgrip exercise on hypertrophic obstructive cardiomyopathy?
Decreased obstruction because of increased afterload.
192
What are the symptoms of hypertrophic obstructive cardiomyopathy?
Dyspnea, angina, presyncope, syncope, and palpitations.
193
What are the physical signs of hypertrophic obstructive cardiomyopathy?
Large jugular A wave, bifid carotid pulse, palpable S4 gallop, systolic murmur and thrill, mitral regurgitation murmur; sudden death.
194
What are the ECG signs of hypertrophic obstructive cardiomyopathy?
Left ventricular hypertrophy, pseudo Q waves (V1–V3), ventricular arrhythmias.
195
What is the treatment of hypertrophic obstructive cardiomyopathy?
Beta–blockers, calcium channel blockers, surgery.
196
What is restrictive cardiomyopathy?
Least common cause of cardiomyopathy; rigid noncompliant ventricular walls.
197
What are the causes of restrictive cardiomyopathy?
Sarcoidosis; amyloidosis, hemochromatosis, neoplasia, scleroderma, radiation
198
What is the pathophysiology of restrictive cardiomyopathy?
Myocardium is rigid and noncompliant, impeding ventricular filling and raising cardiac filling pressures. Systolic performance reduced.
199
What are the signs of restrictive cardiomyopathy?
Dyspnea, exercise intolerance, weakness. Elevated jugular venous pressure, edema, hepatomegaly, ascites, S4 and S3 gallop, Kussmaul sign.
200
What are the x–ray signs of restrictive cardiomyopathy?
Mild cardiomegaly, pulmonary congestion. Echocardiogram is diagnostic.
201
What is the treatment of restrictive cardiomyopathy?
Heart transplantation; death from congestive heart failure or arrhythmias.
202
What are the causes of acute pericarditis and myopericarditis?
Idiopathic, infections (viral), vasculitis (connective tissue disease), disorders of metabolism, neoplasms, trauma, drug reactions.
203
What are the clinical symptoms of acute pericarditis?
Chest pain at left of sternum, worsened by lying down, coughing, and deep inspiration, relieved by sitting up and leaning forward.
204
What are the physical signs of acute pericarditis?
Scratchy, high–pitched rub that has 1–3 components. The rub is best heard with the diaphragm of the stethoscope as the patient sits forward at forced–end expiration.
205
What are the ECG signs of acute pericarditis?
Diffuse ST–segment elevation with upright T waves. The diffuseness of the ST–segment elevation, and absence of Q waves distinguish pericarditis from acute MI.
206
What is the treatment of acute pericarditis?
NSAIDs, aspirin, corticosteroids.
207
What are the types of pericardial effusions?
Transudates, serosanguineous, blood.
208
What are the causes of transudative pericardial effusions?
Transudates occur with congestive heart failure, overhydration, or hypoproteinemia. Exudates occur in the presence of pericardial injury.
209
What are the causes of serosanguineous pericardial effusions?
Serosanguineous pericardial fluid is sign in tuberculosis and neoplastic diseases.
210
What are the causes of bloody pericardial effusions?
Blood in the pericardial space may occur in aortic aneurysm or aortic dissection, trauma, rupture of the heart in acute MI, and bleeding caused by coagulation defects.
211
How is pericardial effusion diagnosed?
Echocardiography. Chest x–ray may show a water–bottle cardiac silhouette.
212
What is the treatment of pericardial effusion?
Pericardial fluid aspiration.
213
What is cardiac tamponade?
A life–threatening condition in which a pericardial effusion compresses the heart.
214
What are the causes of cardiac tamponade?
Neoplasia, idiopathic (viral) pericarditis, tuberculosis, suppurative, intrapericardial hemorrhage, central line extravasation, surgery, postpericardiotomy syndrome, uremia, radiation therapy, vasculitis.
215
What are the clinical manifestations of pericardial tamponade?
Dyspnea, fatigue, orthopnea. Pulsus paradoxus (decrease in systolic blood more than 10 with inspiration or disappearance pulse with inspiration).
216
What is the triad of pericardial tamponade?
Triad of neck vein distension with clear lung, hypotension, and muffled heart sounds.
217
What is the treatment of cardiac tamponade?
Pericardiocentesis; subxiphoid surgical drainage.
218
What is constrictive pericarditis?
Diffuse thickening of the pericardium caused by inflammation; reduced distensibility of the cardiac chambers. Cardiac output is limited and filling pressures are increased; abnormal diastolic filling.
219
What are the causes of constrictive pericarditis?
Idiopathic; following open–heart surgery; thoracic radiation; postviral infection.
220
What are the clinical manifestations of constrictive pericarditis?
Dyspnea on exertion, orthopnea; ascites, edema, jaundice, hepatic tenderness, and hepatomegaly (right–side failure). Jugular venous distension that increases with inspiration (Kussmaul sign).
221
How is constrictive pericarditis diagnosed?
CT: thickened pericardium; pericardial calcifications in tuberculous constriction. Left ventricular ejection fraction is decreased in restrictive cardiomyopathy, but not in constrictive pericarditis.
222
What is the treatment of constrictive pericarditis?
Sodium restriction, diuretics, pericardiectomy.
223
What is sinus bradycardia?
Ventricular complexes are normal width, evenly spaced, rate is
224
What are the causes of sinus bradycardia?
Acute MI, carotid sinus pressure, vomiting, Valsalva maneuver, phenothiazines, digitalis glycosides, beta–adrenergic blocking agents, calcium blockers, marathoners and swimming, hypothyroidism, normal variant.
225
What is the treatment of sinus bradycardia?
Atropine if symptoms. Pacemaker.
226
What are the types of atrioventricular block?
The three classic clinical types are first–, second–, and third–degree (or complete) atrioventricular block.
227
What is first–degree atrioventricular block?
PR interval greater than 0.20 s at a heart rate of 70 beats/min.
228
What are the causes of first–degree heart block?
Digitalis; exaggerated vagal tone after tracheal suctioning; ischemia, inflammation (myocarditis, acute rheumatic fever), cardiomyopathies.
229
What are the types of second–degree atrioventricular block?
Type I (Mobitz I, Wenckebach) and type II (Mobitz II).
230
What is type I atrioventricular block (Mobitz I, Wenckebach)?
There is progressive prolongation of the PR interval until a P wave is blocked and a ventricular beat is dropped. The PR interval of the next conducted beat is shorter than the preceding PR interval.
231
What is type II (Mobitz II) atrioventricular block?
An intermittent blocked beat occurs suddenly and is not preceded by a change in the duration of the PR interval.
232
What is the site of the block in type I second–degree atrioventricular block?
Usually AV nodal (supra–Hisian)
233
What is the site of the block in type II second degree atrioventricular block?
Infranodal (infra– or infra–Hisian).
234
What are the causes of type I second degree atrioventricular block?
Degenerative changes in AV node; diaphragmatic myocardial infarct; digitalis toxicity; myocarditis; rheumatic fever; increased vagal tone.
235
What are the causes of type II second degree AV block?
Extensive anterior myocardial infarct; degenerative changes in His–Purkinje system; calcification of mitral or aortic valve annulus.
236
What are the ECG findings in type I second degree AV block?
PR interval lengthens progressively until ventricular beat dropped. PR shortens after dropped beat. RR narrows progressively up to the dropped beat. RR after blocked beat is
237
What are the ECG findings in type II second degree AV block?
PR interval is normal duration and constant length; blocked beats occur suddenly without progressive lengthening of PR. RR interval of conducted beats is constant or a multiple of a basic RR interval.
238
What is third–degree atrioventricular block?
In 3rd degree block, all atrial beats are blocked, and ventricles are driven by an escape focus.
239
What are the most common causes of 3rd degree atrioventricular block?
Most common is fibrous degeneration of conduction system from aging; inferior/ posterior infarction; infection, inflammation, digitalis, ankylosing spondylitis, Adams–Stokes, heart failure.
240
What are Adams–Stoke attacks?
Sudden asystole or transient ventricular tachycardia or ventricular fibrillation.
241
What is the treatment of third degree AV block?
Pacing.
242
What is sinus tachycardia?
Rhythm with a rate \>100. Ventricular complexes are normal width, evenly spaced, normal P precedes a QRS. Caused by fever, hypotension, volume depletion, anxiety, pain. Thyrotoxicosis, anemia, beta–agonists.
243
What is paroxysmal supraventricular tachycardia?
Group of ectopic tachyarrhythmias that are characterized by sudden onset and abrupt termination. Includes paroxysmal atrial tachycardia. 80% are caused by re–entry, mainly in the AV node.
244
What are the ECG signs of paroxysmal supraventricular tachycardia?
Paroxysmal supraventricular tachycardia has an absolutely regular rhythm at a rate between 130 and 220 beats/min. P–wave is abnormal.
245
What is the treatment of paroxysmal supraventricular tachycardia?
Right side carotid sinus massage to increase vagal tone; adenosine is effective in more than 90%. IV propranolol, esmolol, digitalis; synchronized external cardioversion if patient is unstable.
246
What are the ECG signs of multifocal atrial tachycardia?
Irregular supraventricular rhythm rate 100–200. At least 3 different P wave morphologies; PR interval varies. Each QRS complex is preceded by a P wave. Occurs in elderly patients or chronic lung disease.
247
What are the causes of atrial flutter?
Chronic obstructive lung disease, pulmonary embolism, thyrotoxicosis, mitral valve disease, alcohol.
248
What are the ECG signs of atrial flutter?
Atrial flutter has an absolutely regular rhythm with a ventricular rate of 125–150 beats/min and an atrial rate of 250–300 beats/min (ie, 2:1 block).
249
What is the initial treatment of atrial flutter?
Cardioversion if hemodynamically unstable (e.g., hypotension); digitalis, verapamil, diltiazem, beta–blockers.
250
What is the most common sustained cardiac rhythm disturbance?
Atrial fibrillation, which is often associated with heart disease but occurs commonly in patients with no disease. AF may cause thromboembolic events and hemodynamic impairment.
251
What are the ECG signs of atrial fibrillation?
No p waves. Fibrillatory waves with an irregular, rapid ventricular response (irregularly, irregular).
252
What is the sign of Wolf–Parkinson White syndrome with atrial fibrillation?
Extremely rapid rates (over 200 bpm) suggest the presence of an accessory pathway (W–P–W syndrome), which may manifest as AF. There is a delta wave.
253
What is the rate of ischemic stroke in atrial fibrillation?
The rate of ischemic stroke among patients with nonrheumatic atrial fibrillation averages 5% per year.
254
What are the signs of atrial fibrillation?
Elderly patients with shortness of breath, dizziness, or palpitations. Acute fatigue or exacerbation of congestive heart failure. Irregularly irregular pulse.
255
What is lone atrial fibrillation?
Atrial fibrillation with no evidence of structural heart disease.
256
What are the causes of atrial fibrillation?
Rheumatic mitral disease, CAD, CHF, HTN (atrial dilation). Hyperthyroidism, hypoxemia, alcohol. In younger patients, 30–45% of paroxysmal cases and 20–25% of persistent cases of AF occur as lone AF.
257
What tests are use in the evaluation of atrial fibrillation?
ECG: AF, left ventricular hypertrophy, pre–excitation, prior myocardial infarction. Echocardiogram: identifies LVH, valvular disease, atrial size, and left atrial thrombus. Thyroid function tests.
258
What drugs are effective for pharmacologic cardioversion of atrial fibrillation?
Amiodarone, dofetilide, flecainide, ibutilide, propafenone, and quinidine.
259
Which drugs are used to maintain sinus rhythm in patients with atrial fibrillation?
Drugs used to maintain sinus rhythm in patients with atrial fibrillation include amiodarone, disopyramide, dofetilide, flecainide, propafenone, and sotalol.
260
What is the first step in managing atrial fibrillation?
Control rate to
261
What is the recommended treatment strategy for atrial fibrillation?
Rate control with chronic anticoagulation for the majority of patients with chronic AR. Rhythm control has not been shown to be superior to rate control in reducing morbidity and mortality.
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?
Electrical cardioversion.
263
What is Wolff–Parkinson–White syndrome?
Ventricle is activated by atrial impulses early by accessory pathway (Kent bundle). Short PR interval followed by a wide QRS complex with a slurred initial deflection (delta), which represents early ventricular activation.
264
What is the treatment of Wolff–Parkinson–White syndrome?
If unstable, then synchronized cardioversion. If stable, then procainamide. Ablation.
265
What drugs should be avoided in Wolff–Parkinson–White syndrome?
Avoid digoxin, beta–blockers, calcium–blockers because inhibit conduction in the normal conduction pathway and cause ventricular or supraventricular tachycardia via in the aberrant conduction pathway.
266
What is ventricular tachycardia?
VT is three or more consecutive beats of ventricular origin at a rate greater than 120 beats/min. QRS complexes are wide and bizarre.
267
What are the causes of ventricular tachycardia?
Ischemic heart disease after an acute MI; cardiomyopathies, hypokalemia, hypercalcemia, hypomagnesemia, hypoxia, digitalis toxicity and thioridazine drugs.
268
What are the clinical manifestations of ventricular tachycardia?
Hypotension, congestive heart failure, syncope, or cardiac arrest.
269
What are the ECG signs of torsade de pointes ventricular tachycardia?
Undulating rotations of QRS complexes around baseline. Initiated by a PVC in setting of abnormal ventricular repolarization, characterized by prolongation of QT interval. Episodes of dizziness or syncope.
270
What are the causes of torsade de pointes ventricular tachycardia?
Antiarrhythmics that prolong ventricular repolarization (prolong QT); quinidine, procainamide, disopyramide, phenothiazines, thioridazine, tricyclics, lithium, hypoK hypoMg, intracerebral hemorrhage.
271
What is the treatment of torsade de pointes ventricular tachycardia?
Treat underlying electrolyte disorders. Magnesium and potassium are first–line therapies. Isoproterenol and short–acting beta–blockers. Overdrive pacing. If unstable, perform electrical cardioversion.
272
What are the indications for amiodarone?
Amiodarone is a very effective antiarrhythmic drug, used in ventricular tachycardia, AF, and atrial flutter. Amiodarone has a very long half–life (over 50 days).
273
What are the side effects of amiodarone?
Cough, fever; painful breathing can be fatal. 20% neurotoxicity with imbalance, tremor, numbness, weakness. Hypothyroidism/ hyperthyroidism; blue–gray skin; halos, blurred vision; corneal deposits.
274
What are the indications for disopyramide?
Ventricular ectopic activity and atrial ectopic activity.
275
What are the adverse effects of disopyramide?
Anticholinergic effects; hypotension, heart failure, heart block, tachyarrhythmia.
276
What are the indications for lidocaine?
Ventricular ectopic activity
277
What are the adverse effects of lidocaine?
Drowsiness, agitation, seizures; rarely congestive heart failure or heart block.
278
What are the cardiac indications for phenytoin?
Ventricular ectopic activity.
279
What are the adverse effects of phenytoin?
Ataxia, nystagmus, drowsiness; hypotension and heart block with rapid IV injection
280
What are the indications for procainamide?
Ventricular ectopic activity, atrial ectopic activity
281
What are the adverse effects of procainamide?
Lupus–like syndrome; nausea/vomiting; insomnia; rash; hypotension; aggravation of arrhythmia; blood, dyscrasias
282
What are the indications for quinidine?
Ventricular ectopic activity, atrial ectopic activity
283
What are the adverse effects of quinidine?
Aggravation of arrhythmias; thrombocytopenia; fever, rash; cinchonism; nausea; digoxin–quinidine interaction (elevation of digoxin levels).
284
What are the antiarrhythmic indications for beta–adrenergic blocking agents?
Atrial ectopic activity, ventricular ectopic activity.
285
What are the adverse effects of beta–blockers?
Heart block, hypotension, heart failure, asthma, hypoglycemia, lethargy, impotence.
286
What are the antiarrhythmic indications for verapamil?
Atrial ectopic activity.
287
What are the adverse effects of verapamil?
Congestive heart failure, asystole, constipation
288
What are the indications for adenosine?
Ventricular tachycardia
289
What are the adverse effects of adenosine?
Transient dyspnea, noncardiac chest pain, rarely hypotension.
290
What are the indications for mexiletine?
Ventricular ectopic activity
291
What is mexiletine?
Lidocaine–like drug. Local anesthetic; half–life, 8–14 h.
292
What are the indications for tocainide?
Ventricular ectopic activity
293
What is tocainide?
Lidocaine–like drug. Half–life 14–16 h in patients with high–grade ventricular ectopic activity.
294
What are the indications for amiodarone?
Atrial ectopic activity (especially WPW), ventricular ectopic activity.
295
What are the adverse effects of amiodarone?
Very long half–life (20–40 d). May increase digoxin level. May worsen existing cardiac conduction disturbances. May prolong Coumadin effect.
296
What are the indications for encainide?
Ventricular tachycardia, Wolff–Parkinson–White syndrome.
297
What are the adverse effects of encainide?
Negative inotropism; QRS and PR prolongation. Hepatic metabolism to active metabolites.
298
What are the indications for flecainide?
Ventricular tachycardia, supraventricular tachycardia, Wolff–Parkinson–White syndrome.
299
What are the adverse effects of flecainide?
Negative inotropism, QRS, PR prolongation
300
What are the indications for propafenone?
Ventricular tachycardia, atrial fibrillation
301
What the adverse effect of propafenone?
Negative inotropism
302
What are the physiologic effects of low doses of nitrates?
In low doses, nitrates increase venous dilation and reduce preload.
303
What are the physiologic effects of medium doses of nitrates?
In medium doses, nitrates increase arteriolar dilatation and decrease afterload and preload.
304
What are the physiologic effects of high doses of nitrates?
In high doses, nitrates increase coronary artery dilatation and increase oxygen supply.
305
What are the side effects of nitrates?
Vasodilation can lead to orthostatic hypotension, reflex tachycardia, throbbing headache, and blushing.
306
What is the contraindication to nitrates?
Contraindicated if systolic blood pressure is
307
What is the dosing pattern for nitrates?
Requires a window–free period of more than 8 hours with nitrate therapy to reduce tachyphylaxis.
308
What are the beneficial effects of beta–blockers?
Beta–blockers have been shown to improve survival after an acute myocardial infarction and in CHF.
309
What are the adverse effects of beta–blockers?
Fatigue, mental depression, insomnia, adverse effects on lipid panel; hallucinations, Raynaud phenomenon, bronchoconstriction, mask signs and symptoms of insulin–induced hypoglycemia, sexual dysfunction.
310
What are the adverse effects of nonselective beta–blockers?
Nonselective beta–blockers may mask hypoglycemic symptoms in insulin–dependent diabetics.
311
What is the contraindication to beta–blockers?
Contraindicated in severe asthma.
312
What are the physiologic effects of calcium–channel blockers?
Produces decreases in preload and afterload. May be harmful in postinfarction period, especially if left ventricular failure.
313
What are the adverse effects of calcium channel blockers?
Congestive heart failure, reflex tachycardia, hypotension, lightheadedness; flushing, headache, weakness, nausea, constipation, nasal congestion, wheezing, peripheral edema.
314
What is anemia?,
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.
315
What is microcytic anemia?,
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.
316
What is macrocytic anemia?,
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.
317
What is the presentation of anemia?,
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
318
What is the first step in diagnosing anemia?,
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.
319
What is the treatment for anemia?,
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%.
320
How does one unit of packed red blood cells affect the hematocrit?,
The hematocrit should rise three points for every unit of packed red blood cells given.
321
What is iron deficiency anemia?,
Diminished RBC production and an MCV
322
What is the presentation of iron deficiency anemia?,
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.
323
What are the physical signs of iron deficiency?,
Brittle nails, spoon shaped nails, glossitis, and pica.
324
How is iron deficiency anemia diagnosed?,
Low serum ferritin
325
What is anemia of chronic disease?,
A defect in the ability to use iron; either microcytic or normocytic; caused by any chronic inflammatory, infectious, or neoplastic condition.
326
How is anemia of chronic disease diagnosed?,
Serum ferritin level is normal or elevated. The serum iron level and total iron binding capacity (TIBC) are low. The reticulocyte count is low.
327
What is the treatment for anemia of chronic disease?,
Correct underlying disease. Iron and erythropoietin are not effective, except in renal disease and anemia caused by chemotherapy or radiation therapy for malignancies.
328
What is sideroblastic anemia?,
A microcytic anemia caused by a disorder in the synthesis of hemoglobin. Hereditary and acquired forms from chloramphenicol, isoniazid, or alcohol. Lead poisoning.
329
How is sideroblastic anemia diagnosed?,
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.
330
What is thalassemia?,
Hereditary underproduction of either the alpha or beta globin chains of the hemoglobin molecule, resulting in a hypochromic, microcytic anemia.
331
What populations more commonly have thalassemia?,
Alpha thalassemia is more common in Asian populations. Beta thalassemia is more common in Mediterranean populations.
332
What is the presentation of thalassemia?,
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).
333
How is thalassemia diagnosed?,
Thalassemia trait: mild anemia with microcytosis. Beta thalassemia major has severe symptoms, large spleen, bone abnormalities.
334
How is thalassemia diagnosed?,
Microcytic anemia with normal iron studies, and hemoglobin electrophoresis. Beta thalassemia shows an increased level of hemoglobin F and hemoglobin A2.
335
What is the treatment for thalassemia?,
Thalassemia traits do not require treatment. Beta thalassemia major patients require blood transfusions once or twice a month.
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?,
Folic acid deficiency.
337
What are the causes of vitamin B12 deficiency?,
Most common cause: pernicious anemia (hereditary, autoimmune, decreased intrinsic factor). Gastrectomy, atrophic gastritis, sprue, enteritis, blind loop. Pancreatic insufficiency, tapeworm. Decreased intake.
338
What is the presentation of vitamin B12 deficiency?,
Peripheral neuropathy, decreased position and vibratory sense; psychiatric, autonomic, motor, cranial nerve, bowel, bladder, and sexual dysfunction. Glossitis, diarrhea, and abdominal pain.
339
How is vitamin B12 deficiency diagnosed?,
Anemia with macrocytosis (increased MCV). Hypersegmented neutrophils. Indistinguishable from folate deficiency. Reticulocyte count is reduced. Pancytopenia. Most specific test is low B12 level.
340
How is pernicious anemia diagnosed?,
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.
341
What is the treatment for vitamin B12 deficiency?,
Replace the vitamin B12 by the intramuscular route.
342
What is folic acid deficiency?,
Deficiency in folic acid levels leading to anemia because of decreased dietary intake. Alcoholics have decreased folate intake.
343
How is folic acid deficiency diagnosed?,
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.
344
What are some chronic causes of hemolytic anemia?,
Sickle cell disease, paroxysmal nocturnal hemoglobinuria, and hereditary spherocytosis
345
What are some acute causes of hemolytic anemia?,
Drug–induced hemolysis, auto–immune hemolysis, or glucose 6–phosphate dehydrogenase deficiency.
346
What is the presentation of hemolytic anemia?,
Fatigue and weakness. Dyspnea and confusion. Jaundice and dark urine. Fever, chills, chest pain, tachycardia, and backache may occur.
347
How is hemolytic anemia diagnosed?,
Hemolytic anemias have a normal MCV. The reticulocyte count is elevated. LDH and indirect bilirubin are elevated. Peripheral smear shows fragmented cells. Hemoglobinuria.
348
What is the treatment of hemolytic anemia?,
Transfusion when the hematocrit becomes low. Hydration prevents toxicity to the kidney tubule from free hemoglobin.
349
What is sickle cell disease?,
A hereditary chronic hemolysis ranging from asymptomatic to severe crisis; irreversibly sickled cells and recurrent painful crises. Autosomal recessive.
350
What is the pathophysiology of sickle cell disease?,
Hemoglobin S is due to a substitution of a valine for glutamic acid as the sixth amino acid of the beta globin chain.
351
What is the prevalence of sickle cell disease?,
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.
352
What conditions may precipitate a painful crisis?,
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.
353
What is the presentation of sickle cell disease?,
Renal concentrating defects, ulcerations of legs, bilirubin gallstones, aseptic necrosis of femoral head, osteomyelitis, retinopathy, recurrent infections from Pneumococcus, Haemophilus, growth retardation, splenomegaly, autosplenectomy.
354
What is an acute painful crisis of sickle cell disease?,
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.
355
How is sickle cell disease diagnosed?,
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.
356
What is the treatment of acute sickle cell pain crisis?,
Fluids, analgesics, and oxygen. Antibiotics with infection, fever; leukocytosis. Ceftriaxone and cefotaxime are preferred because cover Pneumococcus and Haemophilus influenza.
357
What is the treatment of sickle cell acute chest syndrome, CNS manifestations, priapism, and acute cardiac ischemia?,
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.
358
What are autoimmune, cold agglutinin, and drug–induced hemolytic anemias?,
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.
359
What are the causes of autoimmune hemolytic anemias?,
Antibodies in leukemia, viral infections, lymphoma, collagen vascular diseases or penicillins, cephalosporins, sulfa drugs, quinidine, alpha methyldopa, procainamide, rifampin, and thiazides.
360
What percentage of autoimmune hemolytic anemias are idiopathic?,
50% do not have an underlying disorder.
361
What is cold agglutinin disease?,
IgM against the red cell in association with lymphoma, Waldenstrom macroglobulinemia, Mycoplasma or mononucleosis.
362
Which inflammatory bowel disease is associated with autoimmune hemolytic anemia?,
Ulcerative colitis.
363
What is the presentation of autoimmune hemolysis?,
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.
364
How is autoimmune hemolysis diagnosed?,
Normocytic anemia, reticulocytosis, increased LDH, increased indirect bilirubin. Coombs test is specific for autoimmune, cold agglutinin, drug–induced hemolysis. Spherocytes on smear.
365
What is the treatment for autoimmune hemolysis?,
Steroids. Splenectomy for those unresponsive to steroids. Cold agglutinin disease is managed by avoiding cold.
366
What is hereditary spherocytosis?,
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.
367
How is hereditary spherocytosis diagnosed?,
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.
368
What is the treatment for hereditary spherocytosis?,
Folate replacement. Splenectomy.
369
What is paroxysmal nocturnal hemoglobinuria?,
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.
370
What is the presentation of paroxysmal nocturnal hemoglobinuria?,
Dark urine from intravascular hemolysis. Thrombosis of the hepatic vein (Budd–Chiari syndrome). Hemoglobinuria in the first morning urine.
371
How is paroxysmal nocturnal hemoglobinuria diagnosed?,
Increased LDH, bilirubin, and reticulocyte count, hemoglobinuria. Sugar–water test and the acidified–hemolysis (Ham) test. Decay accelerating factor is diminished in PNH.
372
What is the treatment for paroxysmal nocturnal hemoglobinuria?,
Iron replacement. Corticosteroids.
373
What is glucose–6–phosphate dehydrogenase deficiency?,
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.
374
What is the treatment of toxic shock syndrome?,
Beta–lactamase stable penicillin (nafcillin or oxacillin). Restoration of hypovolemic shock, remove infected tissue, prosthesis, tampons, diaphragm.
375
What is acute renal failure?
Rapid rise in blood urea nitrogen or creatinine over a period of several hours to days. Decrease in glomerular filtration rate.
376
What is renal insufficiency?
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.
377
What is uremia?
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.?
378
What is blood urea nitrogen?
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.
379
What is creatinine?
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.
380
What is prerenal azotemia?
Renal insufficiency caused by diminished perfusion, hypovolemia (dehydration, burns, diuretic, vomiting, diarrhea, hemorrhage), hypotension (septic, cardiogenic, anaphylactic), third spacing in peritonitis.
381
What is the laboratory criteria for prerenal azotemia?
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).
382
What are the signs of renal artery stenosis?
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.
383
What is hepatorenal syndrome?
Renal failure caused by hepatic failure secondary to intense vasoconstriction of afferent arteriole, resulting in decreased renal perfusion.
384
What are the laboratory abnormalities in hepatorenal syndrome?
Prerenal azotemia with a high BUN:creatinine ratio \>20:1. Urine Na
385
What is the effect of ACE inhibitors on the kidney?
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.
386
What is the hepatopulmonary syndrome?
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.
387
What is postrenal azotemia?
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.
388
What are the laboratory abnormalities in postrenal azotemia?
BUN and creatinine will elevate in a ratio of 20:1 as with prerenal azotemia. Low fractional excretion of sodium and low urine sodium.
389
What are the consequences of prolonged postrenal obstruction?
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.
390
What are the clinical findings in postrenal azotemia?
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.
391
What is acute tubular necrosis?
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.
392
What are the urine microscopic findings in acute tubular necrosis?
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.
393
How is acute tubular necrosis diagnosed?
BUN:creatinine ratio 10:1. High urine sodium (\>40), high fractional excretion of sodium (\>1%), and low urine osm (
394
What is the treatment of acute tubular necrosis?
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.
395
What is allergic interstitial nephritis?
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.
396
What medications can cause allergic interstitial nephritis?
Penicillin, cephalosporins, sulfas, allopurinol, rifampin, quinolones. Calcium blockers. Sulfa drugs include thiazides, furosemide, acetazolamide.
397
What infections can cause allergic interstitial nephritis?
AIN is also caused by infections by viruses, bacteria, and fungi. Leptospirosis, legionella, CMV, rickettsia, and streptococci.
398
What autoimmune disorders can cause allergic interstitial nephritis?
Systemic lupus erythematosus (SLE), Sjögren syndrome, sarcoidosis, and cryoglobulins.
399
What laboratory abnormalities are associated with allergic interstitial nephritis?
Eosinophilia, eosinophiluria, hematuria, proteinuria, increased IgE. Best initial test is a urinalysis for white cells. Urine eosinophils on Wright stain. Kidney biopsy not necessary.
400
What is the treatment of allergic intestinal nephritis?
AIN resolves spontaneously after stopping the offending agent. Short course of steroids may be administered.
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?
Electrocardiogram
402
What are the causes of rhabdomyolysis?
Rhabdomyolysis is caused by sudden, severe crush injury, seizures, severe exertion, hypokalemia, hypophosphatemia, and medications such as statins.
403
What are the laboratory signs of rhabdomyolysis?
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.
404
What action should be taken if peaked T–waves are present on an ECG?
Acidosis and hyperkalemia can cause arrhythmia. If there are peaked T–waves, an amp of calcium gluconate should be given.
405
How is rhabdomyolysis confirmed in the laboratory?
CPK skeletal muscle necrosis. Metabolic acidosis with a decreased serum bicarbonate, hyperphosphatemia, hypocalcemia. Severe hyperuricemia. Rapidly rising creatinine.
406
What is the treatment for rhabdomyolysis?
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.
407
What is the most common cause of hyperoxaluria resulting in acute renal failure?
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.
408
What is the treatment of acute ethylene glycol overdose?
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.
409
What renal complication occurs in patients being given chemotherapy?
Acute renal failure from uric acid toxicity occurs in the setting of tumor lysis syndrome. Vigorous hydration and allopurinol should be given before chemotherapy.
410
What is the effect of hypercalcemia on the kidneys?
Calcium precipitates in tubule, forming stones. Hypercalcemia can lead to distal RTA and nephrogenic diabetes insipidus. Most common cause of hypercalcemia is primary hyperparathyroidism.
411
Which drugs are toxic to the kidneys?
NSAIDs, aminoglycosides, cephalosporins, contrast agents, amphotericin, cisplatin, radiation effect, lead, mercury, or gold, and cyclosporine.
412
What method of administration of aminoglycosides reduces the risk of toxicity?
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.
413
What is the affect of amphotericin B on the kidneys?
Renal insufficiency and distal renal tubular acidosis. After several weeks of amphotericin, the patient will develop high creatinine and decreased magnesium.
414
How does atheroembolic disease affect the kidneys?
Vascular procedures (angioplasty) cause renal failure several days later. Atheroemboli are associated with eosinophilia, low complement, bluish discoloration of fingers, toes, livedo reticularis.
415
What are the common nephrotoxic medications?
Radiocontrast for CT can result in renal failure 12 hours after. Pentamidine is associated with renal failure and pancreatitis. Vancomycin, aminoglycosides, cyclosporine, and lithium.
416
Which antiretroviral is associated with renal failure?
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.
417
Which persons are at risk for analgesic nephropathy?
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.
418
What are the causes of acute papillary necrosis?
Acute papillary necrosis occurs in sickle cell disease, diabetes, urinary obstruction, chronic pyelonephritis, and NSAIDs.
419
What is the presentation of acute papillary necrosis?
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.
420
What is glomerulonephritis?
Glomerulonephritis is inflammation of the glomerulus caused by autoimmunity, antibodies, or vasculitis.
421
What is the presentation of glomerulonephritis?
Edema, hematuria, red cell casts, and hypertension. The urine red cells are dysmorphic.
422
What are the physical signs of glomerulonephritis?
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.
423
What amount of proteinuria is associated with glomerulonephritis?
Modest amounts of protein appear in the urine with the daily total being 3.5 grams per 24 hours the patient has nephrotic syndrome.
424
What are the laboratory signs of glomerulonephritis?
Low urine Na with a fractional excretion of Na
425
What is Wegener granulomatosis?
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.
426
What are the laboratory abnormalities associated with Wegener granulomatosis?
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.
