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USMLE Step 2 (Fach) / Cardiology (Lektion)
- Amiodarone Lungs:- Pulmonary fibrosis - Chronic interstitial pneumonitis Thyroid:- May induce hypothyroidism and/or hyperthyroidism- May aggravate pre-existing thyroid conditions Liver:- AST/ALT > 2x normal If patients experience more than a two-fold elevation, drug therapy should be discontinued. LFTs should be monitored at baseline and every 6 months.- Hepatitis and cirrhosis Heart:- Bradycardia and AV block - Proarrhythmia Eyes:- Corneal micro-deposits - Optic neuritis GI tract:- Nausea, anorexia, and constipation Skin:- Photosensitivity- Blue discoloration CNS:- Various manifestations, esp. peripheral neuropathy (also ataxia, paresthesias, sleep disturbance, impaired memory, and tremor) GU tract:- Epididymitis and erectile dysfunction
- Cocaine-induced vasospasm ↓ Reuptake of norepinephrine → ↑ α- and β1‑stimulation → vasoconstriction and vasospasm → myocardial infarction, cerebrovascular accident, or ischemic colitisTreatment:- Same as STEMIs (percutaneous angioplasty or thrombolysis, aspirin, nitrates)- Calcium-channel blockers and α-blockers can reduce vasospasm.
- Thoracic aortic aneurysm Epidemiology: - Less common than abdominal aortic aneurysm (AAA)- Peak incidence: 60-65 years- Sex: ♂ > ♀ (∼ 3:1)- More common in white populations Risk factors:- Advanced age- Arterial hypertension- Trauma- Tertiary syphilis (due to obliterative endarteritis of the vasa vasorum)- Connective tissue diseases (e.g., Marfan syndrome, Ehlers-Danlos syndrome)- Bicuspid aortic valve - Positive family history- Smoking- Rare: vasculitis/infectious diseases with aortic involvement (e.g., Takayasu arteritis) Ascending thoracic aortic aneurysm: most often due to cystic medial necrosis Descending thoracic aortic aneurysm: typically a result of atherosclerosis Clinical features:- Feeling of pressure in the chest - Thoracic back pain- Features of mediastinal compression/obstruction→ Cough, wheeze, stridor (trachea)→ Difficulty swallowing (esophagus)→ Upper venous congestion (superior vena cava syndrome)→ Hoarseness (recurrent laryngeal nerve)→ Horner syndrome (sympathetic trunk), with the classic triad of ptosis, miosis, and hemifacial anhidrosis (with or without apparent enophthalmus) Diagnostics:- Chest x-ray: may be useful as an initial test in TAAs→ Bulging of the aorta: “aortic knob” (prominent shadow of the aortic arch)→ Widened mediastinum→ Tracheal deviation→ Calcification of the aortic wall- CT with contrast: best confirmatory test for TAAs Treatment:- Reduction of cardiovascular risk factors: Optimal blood pressure levels (< 120-80 mm Hg)- Cessation of smoking- Open or endovascular stent grafting repair: Indications:→ Diameter: ascending aneurysm ≥ 5.5 cm; descending aneurysm ≥ 6.5 cm → Aneurysm expanding rapidly: ≥ 1 cm per year→ Symptomatic
- Thromboangiitis obliterans (Buerger disease) Clinical features:- Age < 45- Ongoing or recent smoking history- Distal limb ischemia, gangrene, ulceration due to nonatherosclerotic occlusion, thrombosis Evaluation:- Ischemia on vascular studies (e.g., digital plethysmography)- Segmental occlusion of small & medium-sized vessels on angiography Treatment: Smoking cessation
- Mechanic prosthetic valve thrombosis (aortic & mitral valve) Prevention:- Aspirin 75-100 mg/day- Mitral valve: warfarin within target INR 2.5-3.5- Aortic valve: warfarin with target INR 2.0-3.0 Clinical features:- Inadequate anticoagulation- Mitral valve risk > aortic valve risk- Obstructive thrombus mimics valvular stenosis- Heart failure, cardiogenic shock- Systemic thromboembolic events (e.g., stroke) Diagnosis & treatment:- Echocardiogram visualizes thrombus- Anticoagulation (e.g., heparin)- Fibrinolytic therapy (typically avoided if possible)- Immediate surgery for severe heart failure or large thrombus
- Chemotherapy-induced cardiotoxicity Type I:- Associated with anthracyclines (e.g., doxorubicin, daunorubicin)- Myocyte necrosis & destruction (fibrosis)- Progression to overt clinical heart failure- Less likely to be reversible Type II:- Associated with trastuzumab- Myocardial stunning/hibernation without myocyte destruction (loss of myocardial contractility)- Asymptomatic left ventricular systolic dysfunction- More likely to be reversible
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