INTERNAL MEDICINE BOARDS - PART 3 pptx

CARDIOVASCULAR DISEASE Bradycardia Incidence ↑ with age. Etiologies are as follows: ■ Intrinsic causes: Idiopathic senile degeneration; ischemia (usually involv- ing the inferior wall); infectious processes (endocarditis, Chagas’ disease, Lyme disease); infiltrative diseases (sarcoidosis, amyloidosis, hemochro- matosis); autoimmune disease (SLE, RA, scleroderma); iatrogenic factors (heart transplant, surgery); inherited/congenital disease (myotonic muscu- lar dystrophy); conditioned heart (trained athletes). ■ Extrinsic causes: Autonomic (neurocardiac, carotid sinus hypersensitivity, situational), medications (β-blockers, calcium channel blockers, clonidine, digoxin, antiarrhythmics), metabolic (electrolyte abnormalities, hypothy- roidism, hypothermia), neurologic (↑ ICP, obstructive sleep apnea). SYMPTOMS Patients may be asymptomatic or may present with dizziness, weakness, fa- tigue, heart failure, or loss of consciousness (syncope). Symptoms can also be related to the underlying cause of the bradycardia. EXAM Look for evidence of ↓ pulse rate and evidence of the underlying cause of bradycardia. Look for cannon A waves in cases of complete AV dissociation (complete heart block). DIAGNOSIS ■ ECG: Look for the origin of the rhythm and whether dropped beats or AV dissociation is present (evidence of AV block; see Table 3.15). ■ Telemetry, event monitors, tilt-table testing, and electrophysiologic studies can also be helpful. TREATMENT ■ If the patient is unstable, follow ACLS protocols. ■ If possible, treat the underlying cause (e.g., endocarditis). ■ Medications: Atropine, glucagon (for β-blocker overdose), calcium (for If left untreated, Lyme disease can cause varying degrees of AV conduction block at any time in the course of the disease. TABLE 3.15. ECG Findings with AV Block TYPE OF BLOCK ECG FINDINGS First degree Prolonged PR interval (> 200 msec). Second degree Progressive prolongation of the PR interval until there is a dropped type I (Wenckebach) QRS. Progressive shortening of the RR interval and a constant PP interval are other signs. Second degree Regularly dropped QRS (e.g., every third QRS complex dropped). type II Constant PR interval (no prolongation). Usually associated with bundle branch blocks. Third degree Complete dissociation of P waves and QRS complexes (P-wave rate > QRS rate). 130 CARDIOVASCULAR DISEASE 131 calcium channel blocker overdose). Note: Calcium is contraindicated in digoxin toxicity. ■ Transcutaneous or transvenous pacing: Appropriate if medical therapy is ineffective. ■ Indication for permanent pacemakers: Documented symptomatic brady- cardia. If the patient is asymptomatic, pacemakers may be considered in patients with third-degree AV block with > 3 seconds of asystole or a heart rate < 40 bpm while the patient is awake. In second-degree type II AV block, pacemakers have a class II indication (there is conflicting evidence and opinion regarding the need for permanent pacing). Indications for Permanent Pacing Indications for permanent cardiac pacing, based on expert guidelines, are classified as follows: I (definite indications), II (indications with conflicting ev- idence or opinion), or III (not indicated or harmful). All indications assume that transient causes such as drugs, electrolytes, and ischemia have been corrected or excluded. CLASS I ■ Third-degree AV block and advanced second-degree AV block associated with the following: ■ Symptomatic bradycardia. ■ Arrhythmias or other conditions requiring medications that result in symptomatic bradycardia. ■ Documented asystole of > 3 seconds or escape rates < 40 bpm in awake, asymptomatic patients. ■ After AV junction ablation. ■ Post–cardiac surgery when AV block is not expected to resolve. ■ Neuromuscular diseases with AV block due to the unpredictable pro- gression of AV conduction disease in these patients. ■ Second-degree AV block (regardless of type) associated with symptomatic bradycardia. CLASS IIA ■ Asymptomatic third-degree AV block with awake escape rates of > 40 bpm. ■ Asymptomatic type II second-degree block with narrow QRS (with wide QRS, it becomes a class I indication). ■ Asymptomatic type I second-degree block with intra- or infra-His levels found on an electrophysiologic study done for another indication. ■ First- and second-degree AV block with symptoms suggestive of pacemaker syndrome. CLASS IIB ■ Marked first-degree AV block (PR > 300 msec) in patients with left ven- tricular dysfunction. ■ Neuromuscular diseases with any level of AV block due to the unpre- dictable progression of block in these patients. CARDIOVASCULAR DISEASE 132 C LASS III ■ Asymptomatic first-degree AV block. ■ Asymptomatic type I second-degree AV block not known to be due to a problem within or below the bundle of His. ■ AV block that is expected to resolve and/or is not likely to recur. Sudden Cardiac Death Approximately 450,000 sudden cardiac deaths occur annually in the United States. Etiologies include CAD, MI, pulmonary embolism, aortic dissection, cardiac tamponade, and other acute cardiopulmonary insults. Seventy-five percent of patients do not survive cardiac arrest. CAUSES IN YOUNG ATHLETES ■ In young athletes, the causes of sudden cardiac death differ from those in the overall population. Causes in this population include the following (in order of decreasing incidence): ■ Hypertrophic cardiomyopathy. ■ Commotio cordis (a sudden blow to the precordium causing ventricu- lar arrhythmia). ■ Coronary artery anomalies. ■ Myocarditis. ■ Ruptured aortic aneurysm (e.g., due to Marfan’s syndrome or Ehlers- Danlos syndrome). ■ Arrhythmogenic right ventricular dysplasia, in which the right ventricle is replaced by fat and fibrosis, causing ↑ frequency of ventricular ar- rhythmias. ■ Aortic stenosis. ■ Myocardial bridge causing coronary ischemia during ventricular con- traction. ■ Atherosclerotic CAD. ■ Coronary artery vasospasm. ■ Brugada syndrome, which is caused by a sodium channel defect that predisposes to VF. The baseline ECG shows incomplete RBBB and ST-segment elevation in the precordial leads. ■ Long QT syndrome. ■ Noncardiac precipitants of sudden cardiac death in young athletes in- clude asthma, illicit drug use (e.g., cocaine, ephedra, amphetamines), and heat stroke. SCREENING IN YOUNG ATHLETES ■ It is difficult to assess patients for risk factors of sudden cardiac death be- cause these conditions are rare and because millions of young athletes need to be screened. ■ Although screening usually involves history taking and physical examina- tion, these measures alone lack the sensitivity to detect even the most com- mon causes of sudden cardiac death in athletes (e.g., hypertrophic car- diomyopathy). ■ In patients with a suggestive history or physical examination, further workup with ECG and echocardiography is warranted. CARDIOVASCULAR DISEASE 133 Implantable Cardioverter-Defibrillators (ICDs) R ISK FACTORS FOR VENTRICULAR ARRHYTHMIAS Include dilated cardiomyopathy (with a reduced EF), hypertension, hyperlipi- demia, tobacco, diabetes, a family history of sudden cardiac death, myocardial ischemia and reperfusion, and toxins (e.g., cocaine). 2° PREVENTION ■ Goal: To prevent recurrent sudden cardiac death in patients with a history of VT or VF. ■ Drugs: Antiarrhythmic drugs have been disappointing in the 2° prevention of sudden cardiac death, especially in the large group of patients who are post-MI. Standard therapies for CAD alone (especially β-blockers) play a significant role in decreasing sudden cardiac death in these patients. ■ Devices: ICDs are superior to amiodarone in patients with CAD who have survived cardiac arrest and have a low EF. ■ There is no survival advantage of ICDs over amiodarone in patients who have an EF > 35%. 1° PREVENTION ■ Goal: To prevent sudden cardiac death in patients who have no history of VT and/or VF. ■ Studies have shown that in patients with a history of MI who have an EF < 30%, ICD therapy improves mortality and is superior to antiarrhythmic therapy. INDICATIONS FOR ICD USE ■ Etiology of heart failure: Recent studies indicate that ICD therapy ap- pears effective for both ischemic and nonischemic cardiomyopathy. ■ Severity of heart failure: Consider ICDs in patients with an EF < 30%. ■ Noninvasive testing: ■ T-wave alternans: Microfluctuations in the morphology of T waves on ECG may indicate an ↑ risk of sudden cardiac death (requires special- ized testing). ■ Heart rate variability: ↓ heart rate variability corresponds to worsening heart failure and may be associated with an ↑ risk of sudden cardiac death. VALVULAR HEART DISEASE Aortic Stenosis The most common causes are senile calcific aortic stenosis and congenital bi- cuspid aortic valve. Rheumatic aortic stenosis is usually not hemodynamically significant and almost always occurs in the presence of mitral valve disease. SYMPTOMS Presents with a long asymptomatic period followed by the development of the classic triad of angina, syncope, and heart failure. The normal valve area is 3 cm 2 , and symptoms usually do not develop until the area is < 1 cm 2 . Aortic valve replacement should be performed as soon as symptoms develop in aortic stenosis to prevent cardiac death. CARDIOVASCULAR DISEASE 134 E XAM ■ A crescendo-decrescendo systolic murmur is heard at the base of the heart with radiation to the carotid arteries. Late-peaking murmurs signify more severe stenosis. ■ Diminished carotid upstrokes (parvus et tardus) and a sustained PMI due to LVH may be present. ■ A systolic ejection click can occur in patients with a bicuspid aortic valve. A2 diminishes in intensity, and S2 may be single. DIFFERENTIAL ■ Sub- or supravalvular stenosis: Due to left ventricular outflow tract mem- brane or fibromuscular ring (rare). ■ Hypertrophic obstructive cardiomyopathy: Murmur accentuated with Valsalva or standing and ↓ by hand grip. DIAGNOSIS ■ Echocardiography: A modified Bernoulli equation is used to derive the pressure gradient across the aortic valve. The aortic valve area is derived by the continuity equation. The severity of aortic stenosis per the 2006 AHA/ACC guidelines can be classified as follows: ■ Mild disease: A valve area > 1.5 cm 2 , mean gradient < 25 mmHg. ■ Moderate disease: A valve area 1–1.5 cm 2 , mean gradient 25–40 mmHg. ■ Severe disease: A valve area < 1 cm 2 , mean gradient > 40 mmHg. ■ Follow-up echocardiography is recommended every year for severe aor- tic stenosis; every 1–2 years for moderate aortic stenosis; and every 3–5 years for mild aortic stenosis. ■ Cardiac catheterization: Required to exclude significant coronary stenoses in symptomatic patients who are scheduled for surgery and are at risk for CAD. Also needed to confirm the severity of aortic stenosis when there is a discrepancy between clinical and noninvasive data. ■ Dobutamine stress testing: Used in cases of low-gradient aortic stenosis (severe aortic stenosis by valve area, but mean gradient < 40 mmHg) to dis- tinguish true stenosis from pseudostenosis caused by ↓ systolic function. If true aortic stenosis is present, the gradient will ↑ and the valve area will re- main unchanged. If pseudostenosis is present, the valve area will ↑. TREATMENT ■ Aortic valve replacement: The only therapy for symptomatic aortic steno- sis. Older patients do quite well after aortic valve replacement and should not be disqualified by age alone. Patients who are unlikely to outlive a bio- prothesis can be spared the lifelong anticoagulation that is required for mechanical valves. ■ Antibiotic prophylaxis against subacute bacterial endocarditis: Indicated for all patients. ■ Aortic valvuloplasty: May be effective in young adults with congenital aortic stenosis. Less effective in patients with degenerative aortic steno- sis, and should be considered palliative therapy or a bridge to surgery. COMPLICATIONS ■ Sudden death occurs but is uncommon (< 1% per year) in patients with severe asymptomatic aortic stenosis. Aortic stenosis has been associated with an ↑ risk of GI bleeding, which is now thought to be due to acquired von Willebrand’s disease from disruption of von Willebrand factor multimers as they pass through the stenotic aortic valve. CARDIOVASCULAR DISEASE 135 ■ If left untreated, the average time to death is as follows: ■ After onset of syncope: 2.5–3 years. ■ After onset of angina: Three years. ■ After onset of dyspnea: Two years. ■ After onset of CHF: 1.5 years. Aortic Regurgitation Can be caused by destruction or malfunction of the valve leaflets (infective endocarditis, bicuspid aortic valve, rheumatic valve disease) or dilatation of the aortic root such that the leaflets no longer coapt (Marfan’s syndrome, aor- tic dissection). SYMPTOMS ■ Acute aortic regurgitation: Presents with rapid onset of cardiogenic shock. ■ Chronic aortic regurgitation: A long asymptomatic period followed by progressive dyspnea on exertion and other signs of heart failure. EXAM ■ Exam reveals a soft S1 (usually due to a long PR interval) and a soft or ab- sent A2 with a decrescendo blowing diastolic murmur at the base. ■ A wide pulse pressure with water-hammer peripheral pulses is also seen. ■ Other peripheral signs include a bruit over the femoral artery (Duroziez’s sign); nail-bed pulsations (Quincke’s pulse); and a popliteal-brachial BP difference of > 20 mmHg (Hill’s sign). ■ In acute aortic regurgitation, these signs are usually not present, and the only clues may be ↓ intensity of S1 and a short, blowing diastolic murmur. ■ In severe aortic regurgitation, the anterior mitral valve leaflet can vibrate in the aortic regurgitation jet, creating an apical diastolic rumble that mimics mitral stenosis (Flint murmur). DIFFERENTIAL Other causes of diastolic murmurs include mitral stenosis, tricuspid stenosis, pulmonic insufficiency, and atrial myxoma. DIAGNOSIS ■ Echocardiography: Essential for determining left ventricular size and function as well as the structure of the aortic valve. TEE is often necessary to rule out endocarditis in acute aortic regurgitation. ■ Cardiac catheterization: Aortography can be used to estimate the degree of regurgitation if noninvasive studies are inconclusive. Coronary angiog- raphy is indicated to exclude CAD in patients at risk prior to surgery. TREATMENT ■ In asymptomatic patients with normal left ventricular function, afterload reduction may be considered, but evidence for benefit is lacking. ACEIs or other vasodilators may ↓ left ventricular volume overload and progres- sion to heart failure. ■ Aortic valve replacement: Should be considered in symptomatic patients or in those without symptoms who develop worsening left ventricular di- latation and systolic failure. Indications for valve replacement in aortic regurgitation include the development of symptoms or left ventricular systolic failure even in the absence of symptoms. CARDIOVASCULAR DISEASE 136 ■ Acute aortic regurgitation: Surgery is the definitive therapy, since mortal- ity is high in this setting. IV vasodilators may be used as a bridge to surgery. ■ Endocarditis prophylaxis: Consider in all patients. COMPLICATIONS Irreversible left ventricular systolic dysfunction if valve replacement is de- layed. Mitral Stenosis Almost exclusively due to rheumatic heart disease, with rare cases due to congenital lesions and calcification of the mitral annulus. The normal mitral valve area is 4–6 cm 2 . Severe mitral stenosis occurs when the valve area is < 1 cm 2 . SYMPTOMS Characterized by a long asymptomatic period followed by gradual onset of dyspnea on exertion and findings of right heart failure and pulmonary hyper- tension. Hemoptysis and thromboembolic stroke are late findings. EXAM ■ Exam reveals a loud S1 and an opening snap of stenotic leaflets after S2 followed by an apical diastolic rumble. ■ Signs of pulmonary hypertension (a loud P2) and right heart failure (ele- vated JVP and hepatic congestion) are present in advanced disease. DIFFERENTIAL ■ Left atrial myxoma: Causes obstruction of mitral inflow. ■ Cor triatriatum: Left atrial septations cause postcapillary pulmonary hy- pertension. ■ Aortic insufficiency: Can mimic the murmur of mitral stenosis (Flint murmur) due to restriction of mitral valve leaflet motion by regurgitant blood from the aortic valve, but no opening snap is present. DIAGNOSIS ■ Echocardiography: Used to estimate valve area and to measure the trans- mitral pressure gradient. Mitral valve morphology on echocardiography determines a patient’s suitability for percutaneous valvuloplasty. ■ TEE: Indicated to exclude left atrial thrombus in patients scheduled for balloon valvotomy. ■ Cardiac catheterization: Can be used to directly measure the valve gradi- ent through simultaneous recording of PCWP and left ventricular diastolic pressure. Rarely needed for diagnosis; performed prior to percutaneous balloon valvotomy. TREATMENT ■ Percutaneous mitral balloon valvotomy: Unlike aortic valvuloplasty, bal- loon dilatation of the mitral valve has proven to be a successful strategy in patients without concomitant mitral regurgitation. Consider this interven- tion in symptomatic patients with isolated mitral stenosis and an effective valve area < 1.0 cm 2 . This is the appropriate intervention in pregnant CARDIOVASCULAR DISEASE 137 women for whom medical therapy has failed. Severe annular calcification, severe mitral regurgitation, and atrial thrombus are all contraindications to balloon valvuloplasty. ■ Mitral valve replacement: For patients who are not candidates for valvo- tomy or if the effective valve area is < 0.6 cm 2 . ■ Endocarditis prophylaxis is indicated for all patients. COMPLICATIONS ■ Left atrial enlargement and AF with resultant stasis is common and can re- sult in left atrial thrombus formation and embolic stroke. ■ Pulmonary hypertension and 2° tricuspid regurgitation. Mitral Regurgitation Common causes of mitral regurgitation include mitral valve prolapse, myxo- matous (degenerative) mitral valve disease, dilated cardiomyopathy (which causes functional mitral regurgitation due to dilatation of the mitral valve an- nulus), rheumatic heart disease (acute mitral valvulitis produces the Carey Coombs murmur of acute rheumatic fever), acute ischemia (due to rupture of a papillary muscle), mitral valve endocarditis, and trauma to the mitral valve. SYMPTOMS ■ Acute mitral regurgitation: Abrupt onset of dyspnea due to pulmonary edema. ■ Chronic mitral regurgitation: Can be asymptomatic. In severe cases, can present with dyspnea and symptoms of heart failure. EXAM ■ Presents with a soft S1 and a holosystolic, blowing murmur heard best at the apex with radiation to the axilla. S3 can be due to mitral regurgitation alone (in the absence of systolic heart failure), and its presence suggests se- vere mitral regurgitation. ■ Acute mitral regurgitation can be associated with hypotension and pul- monary edema; murmur may be early systolic. ■ The intensity of the murmur does not generally correlate with mitral re- gurgitation severity as documented by echocardiogram. DIFFERENTIAL ■ Aortic stenosis: Can mimic the murmur of mitral regurgitation (Gallavardin phenomenon). ■ Tricuspid regurgitation: Characterized by a holosystolic murmur best heard at the left sternal border; ↑ in intensity with inspiration. DIAGNOSIS ■ Early detection of mitral regurgitation is essential because treatment should be initiated before symptoms occur. ■ Exercise stress testing: Document exercise limitation before symptoms oc- cur at rest. ■ Echocardiography: Transthoracic echocardiography (TTE) is important for diagnosis as well as for grading the severity of mitral regurgitation. TEE Patients with rheumatic heart disease typically have involvement of the mitral valve. Isolated involvement of the aortic or tricuspid valve with sparing of the mitral valve is exceedingly rare in patients with rheumatic heart disease. CARDIOVASCULAR DISEASE is useful in patients who may need surgical repair or mitral valve replace- ment. ■ Echocardiography should be performed every 2–5 years in mild to moderate mitral regurgitation with a normal end-systolic diameter and an EF > 65%. ■ Echocardiography should be performed every 6–12 months in patients with severe mitral regurgitation, an end-systolic diameter > 4.0 cm, or an EF < 65%. ■ Catheterization: To exclude CAD prior to surgery. TREATMENT ■ See Figure 3.14 for an overview of the treatment of advanced mitral regur- gitation. ■ Medications: ACEIs are useful only in patients with left ventricular dys- function or hypertension. Medical therapy is generally the only option in patients with an EF < 30%. ■ Surgical intervention: ■ Indications for surgery include symptoms related to mitral regurgita- tion, left ventricular dysfunction, AF, or pulmonary hypertension. ■ Optimal timing of surgery is early in the course of the disease, when patients progress from a chronic, compensated state to symptomatic mitral regurgitation. ■ Surgical outcomes are best in patients who have an EF > 60% and a left ventricular end-systolic diameter < 4.5 cm. In patients with mitral regurgitation, the intensity of the murmur on physical exam does not correlate with disease severity. In patients with acute myocardial ischemia, even a low-intensity murmur of mitral regurgitation should alert the physician to the possibility of papillary rupture. FIGURE 3.14. Management of advanced mitral regurgitation. (Reproduced, with permission, from Braunwald E et al. Harrison’s Manual of Medicine, 15th ed. New York: McGraw-Hill, 2001.) Mitral regurgitation (MR) • Afterload reduction— e.g., IV nitroprusside • Diuretics if needed for LV failure ? acute severe MR yes • Control ventricular rate (e.g., β- blockers, digoxin) • Anticoagulation (heparin, warfarin) If AF poorly tolerated: • Chemical/electrical cardioversion (ideally ≥ 3 weeks of anticoagulation) ? atrial fibrillation no yes no yes no ? symptoms yes Surgical reconstruction or replacement ? surgical candidate no • Oral afterload reduction (ACEI or hydralazine) • Diuretics and/or digoxin for CHF symptoms yes no ? LV Progressive enlargement or ESD > 45 mm/m 2 Chronic management of asymptomatic patient: • Endocarditis prophylaxis • Serial assessment of LV function by echo 138 [...]... SYNDROME 2 23 HYPERALDOSTERONISM 224 PHEOCHROMOCYTOMA 226 ADRENAL INCIDENTALOMAS 227 Disorders of Lipid and Carbohydrate Metabolism 228 DIABETES MELLITUS 228 GESTATIONAL DIABETES 234 METABOLIC SYNDROME 234 HYPOGLYCEMIA 235 FAMILIAL LIPID ABNORMALITIES 236 Mineral Metabolism and Metabolic Bone Disease 236 CALCIUM METABOLISM 236 HYPERCALCEMIA 236 1° HYPERPARATHYROIDISM 240 HYPOCALCEMIA 242 2 03 Copyright... common noncyanotic heart defects will be presented here Table 3. 16 out- 140 TA B L E 3 16 Tolerance of Pregnancy by Patients with Congenital Cardiac Malformations WELL TOLERATED INTERMEDIATE EFFECT POORLY TOLERATED NYHA class I NYHA class II–III NHYA class IV Left-to-right shunts without pulmonary Repaired transposition of the great Right-to-left shunt; unrepaired cyanotic hypertension Aortic or mitral... Adapted, with permission, from Kerdel FA, Jimenez-Acosta F Dermatology: Just the Facts New York: McGraw-Hill, 20 03: 36 FIGURE 5.25 Toxic epidermal necrolysis Bulla formation with rapid desquamation (Reproduced, with permission, from Wolff K et al Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 5th ed New York: McGraw-Hill, 2005: 147.) 1 93 Clinical Features of Severe Cutaneous Reactions... bone, brain) Five-year survival rates with lymph node involvement and distant metastasis are 30 % and 10%, respectively TA B L E 5 14 Scheme for the Diagnostic Workup and Follow-up of Melanoma FOLLOW-UP BRESLOW DEPTH (mm) PHYSICAL EXAM CXR AND LABSa Stage I 6 months × 2 years; 12 months thereafter Initial Stage IIa 4 months × 3 years; 12 months thereafter Yearly Stage IIb 4 months × 3 years; 6 months... hypertension) Pulmonic stenosis (mild to moderate) Aortic or mitral stenosis (severe) Well-repaired tetralogy of Fallot Pulmonic stenosis (severe) Marfan’s or aortic coarctation Reproduced, with permission, from Kasper DL et al Harrison’s Principles of Internal Medicine, 16th ed New York: McGraw-Hill, 2005: 138 3 lines the extent to which patients with congenital cardiac malformations can tolerate pregnancy... for potentially life-threatening systemic disease involving the lungs, liver, and CNS 172 DE RMATOLOGY FIGURE 5.14 Dermatomyositis Heliotrope (reddish-purple) erythema of the upper eyelids can be seen along with edema of the lower lids (Reproduced, with permission, from Wolff K et al Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 5th ed New York: McGraw-Hill, 2005: 37 3.) KAPOSI’S SARCOMA... of any size Diuretics and vasodilators to ↓ left-to-right shunt and symptoms of right heart failure Surgical correction is appropriate for patients with significant shunt (Qp/Qs > 1.7:1) Once pulmonary hypertension occurs (systolic pulmonary artery pressure > 85 mmHg), mortality is ∼50% COMPLICATIONS ■ ■ ■ Eisenmenger’s syndrome: ■ Long-standing left-to-right shunting causes pulmonary vascular hyperplasia,... Dermatology Tara D Miller, MD Siegrid S Yu, MD Common Skin Disorders 1 63 ACNE 1 63 ROSACEA 1 63 SEBORRHEIC DERMATITIS 164 PSORIASIS 165 PITYRIASIS ROSEA 166 Cutaneous Infections 167 IMPETIGO 167 ERYSIPELAS 168 ANTHRAX 168 DERMATOPHYTOSIS (TINEA) 169 PITYRIASIS (TINEA) VERSICOLOR 170 CANDIDIASIS 171 HERPES SIMPLEX 171 HERPES ZOSTER 1 73 SMALLPOX 174 SCABIES 175 Dermatologic Manifestations of Systemic Diseases... collateral circulation involving the internal mammary, intercostal, and axillary arteries A bicuspid aortic valve is present in > 50% of patients with coarctation of the aorta More common in males than in females SYMPTOMS CARDIOVASC U LAR DISEASE Presents with headache, dyspnea, fatigue, and leg claudication EXAM Exam reveals diminished femoral pulses with a radial-to-femoral-pulse delay and a continuous... thereafter Regional (stage III) or distant (stage IV) disease 3 4 months × 5 years; 12 months thereafter Every other visit × 5 years; yearly thereafter; initial CT scans of head/chest/abdomen/pelvis or PET if available a LFTs and LDH Adapted, with permission, from Kerdel FA, Jimenez-Acosta F Dermatology: Just the Facts New York: McGraw-Hill, 20 03: 271 197 DE RMATOLOGY NOTES 202 CHAPTER 6 Endocrinology . permission, from Kasper DL et al. Harrison’s Principles of Internal Medicine, 16th ed. New York: McGraw-Hill, 2005: 138 3. Correction of ASD carries a long-term survival rate better than that of medical. ∼50% COMPLICATIONS ■ Eisenmenger’s syndrome: ■ Long-standing left-to-right shunting causes pulmonary vascular hyper- plasia, resulting in pulmonary arterial hypertension and shunt reversal (right-to-left shunt). ■ Symptoms. indication. ■ First- and second-degree AV block with symptoms suggestive of pacemaker syndrome. CLASS IIB ■ Marked first-degree AV block (PR > 30 0 msec) in patients with left ven- tricular dysfunction. ■ Neuromuscular