Internal Medicine EOR practice questions

Why Decrease levothyroxine dose is correct

• A suppressed TSH on levothyroxine increases the risk of atrial fibrillation and bone loss in postmenopausal women
• Target TSH for most patients on levothyroxine is 0.5–2.5 mIU/L; this patient's TSH of 0.2 mIU/L is below target, so reducing the dose is appropriate

Why the others are wrong

• A) Add liothyronine — combination T3/T4 therapy is not routinely recommended
• D) Increase levothyroxine dose — increasing the dose would further suppress TSH and worsen the risk of atrial fibrillation and bone loss

Why Discontinue alendronate and evaluate for esophageal injury is correct

• Oral bisphosphonates can cause esophageal irritation, esophagitis, and ulceration
• New dysphagia or chest pain after starting a bisphosphonate warrants discontinuation and evaluation, typically with upper endoscopy

Why the others are wrong

• A) Add a proton pump inhibitor and continue alendronate — PPI co-therapy does not address an already-symptomatic patient with possible esophageal injury
• B) Continue alendronate with strict upright dosing instructions — stricter upright/empty-stomach instructions do not address an already-symptomatic patient with possible esophageal injury
• D) Reassure and continue alendronate with food — alendronate must be taken on an empty stomach, and continuing it in the face of dysphagia and chest pain risks further esophageal injury

Additional high-yield points

• Alternatives after discontinuation include IV zoledronic acid or denosumab

Why Initiate high-intensity statin therapy and refer for genetic testing is correct

• This patient has heterozygous familial hypercholesterolemia (HeFH), suggested by markedly elevated LDL-C above 190 mg/dL, tendon xanthomas, corneal arcus before age 45, and a strong family history of premature coronary disease and sudden cardiac death
• HeFH is most often caused by loss-of-function mutations in the LDL receptor (also APOB or gain-of-function PCSK9), reducing hepatic LDL clearance
• Untreated HeFH carries up to a 20-fold increased risk of premature coronary disease
• High-intensity statin therapy (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) should be started immediately
• Ezetimibe and PCSK9 inhibitors are added to reach an LDL-C reduction of at least 50%
• Genetic testing and cascade screening of first-degree relatives are recommended

Why the others are wrong

• D) Begin a 6-month trial of dietary modification before pharmacotherapy — a prolonged diet-only trial inappropriately delays therapy in this very high-risk patient; lifestyle changes are adjunctive, not primary
• A) Initiate niacin monotherapy targeting HDL elevation — niacin has limited cardiovascular benefit and significant side effects, and does not address the LDL receptor defect
• B) Order coronary angiography before any lipid-lowering therapy — coronary angiography is not indicated in an asymptomatic patient without ischemic symptoms or abnormal noninvasive testing, and lipid therapy should never be delayed pending it

Why Etonogestrel subdermal implant is correct

• Migraines with aura and smoking are World Health Organization (WHO) category 4 (absolute contraindications) to combined estrogen-progestin methods due to increased stroke risk
• This eliminates combined oral contraceptives and the transdermal patch
• Among progestin-only options, the etonogestrel implant (Nexplanon) is the most effective reversible contraceptive (>99%), requires no daily compliance, and lasts 3 years

Why the others are wrong

• A) Combined oral contraceptive pills — WHO category 4 contraindication due to migraines with aura and smoking; increased stroke risk
• D) Transdermal estrogen-progestin patch — WHO category 4 contraindication for the same reasons as combined oral contraceptives
• B) Depot medroxyprogesterone acetate injection — progestin-only and safe in this patient, but is not long-acting reversible in the same sense (requires every-3-month injection, slower return to fertility) and carries bone mineral density concerns

Why Post-concussion syndrome is correct

• Post-concussion syndrome is defined by persistence of concussion-related symptoms (headache, dizziness, cognitive complaints, mood change, sleep disturbance) beyond the typical 7–10 day recovery window
• Diagnosis is clinical and supported by a documented preceding concussion, multidomain symptoms, and a normal neurologic exam with normal initial imaging

Why the others are wrong

• A) Chronic subdural hematoma — typically affects older adults or those on anticoagulants and shows a crescent-shaped extra-axial collection on imaging
• B) Vestibular migraine — causes episodic vertigo but does not account for the cognitive, mood, and sleep cluster
• C) Major depressive disorder — requires at least 2 weeks of depressed mood or anhedonia plus neurovegetative symptoms, and would not explain the prominent headache and dizziness

Why indefinite anticoagulation with a direct oral anticoagulant (DOAC) is correct

• Recurrent unprovoked venous thromboembolism (VTE) — two or more episodes without a provoking factor — is an indication for indefinite anticoagulation regardless of thrombophilia status
• The risk of recurrence after a second unprovoked VTE exceeds 40% at 5 years
• DOACs (rivaroxaban, apixaban) are preferred

Additional high-yield points

• Factor V Leiden heterozygosity alone does not mandate indefinite anticoagulation after a first unprovoked VTE, but after a second event the decision is clear