United States Medical Licensing Examination (USMLE) Internal Medicine and Clinical Knowledge (Step 2 CK) Flashcards

24 sample cards from the Internal Medicine and Clinical Knowledge (Step 2 CK) deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What is the danger of overly rapid correction of hyponatremia, and the safe correction rate?

   Overly rapid correction risks osmotic demyelination syndrome (central pontine myelinolysis). Limit correction to <=8 mEq/L per 24 hours (more conservative, ~6, in high-risk patients). For severe symptomatic hyponatremia, give 3% hypertonic saline boluses to raise Na ~4-6 mEq acutely.

2. How do you interpret a primary metabolic acidosis using the anion gap and Winter's formula?

   Anion gap = Na - (Cl + HCO3); normal ~12. High anion gap acidosis (MUDPILES). Winter's formula predicts respiratory compensation: expected PaCO2 = 1.5 x HCO3 + 8 (+/-2). Measured PaCO2 above expected = concurrent respiratory acidosis; below = concurrent respiratory alkalosis.

3. How are the categories of acute kidney injury (prerenal, intrinsic, postrenal) distinguished by FENa and urine findings?

   Prerenal: FENa <1%, BUN:Cr >20, bland sediment, concentrated urine (Uosm >500). Intrinsic (ATN): FENa >2%, muddy brown granular casts, isosthenuria. Postrenal: obstruction on imaging (hydronephrosis). FEurea <35% is useful for prerenal if on diuretics.

4. What are the emergent (AEIOU) indications for dialysis in acute kidney injury?

   Acidosis (refractory metabolic), Electrolytes (refractory hyperkalemia), Intoxications (dialyzable toxins-methanol, ethylene glycol, salicylates, lithium), Overload (refractory volume overload/pulmonary edema), Uremia (encephalopathy, pericarditis, bleeding).

5. How is chronic kidney disease staged by GFR, and what are the cornerstones of management?

   G1 >=90, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 <15 (with albuminuria categories A1-A3). Management: ACE inhibitor/ARB for proteinuria, SGLT2 inhibitor, BP and glycemic control, manage anemia (EPO/iron), mineral-bone disease (phosphate binders, vitamin D), and avoid nephrotoxins.

6. What is the difference between empiric and definitive (de-escalation) antimicrobial therapy in stewardship?

   Empiric therapy: broad-spectrum coverage started before culture results based on likely pathogens/site. Definitive therapy: narrow the spectrum once culture and susceptibility data return (de-escalation), choosing the narrowest effective agent for the shortest effective duration to limit resistance and toxicity.

7. At what CD4 count do major opportunistic infections occur in HIV, and what prophylaxis is given?

   CD4 <200: Pneumocystis jirovecii pneumonia-prophylax with TMP-SMX. CD4 <100: Toxoplasma (also TMP-SMX). CD4 <50: Mycobacterium avium complex (historically azithromycin, now often deferred with ART) and CMV retinitis. Start antiretroviral therapy in all HIV patients.

8. What is the empiric treatment and key diagnostic of Pneumocystis jirovecii pneumonia (PCP)?

   Presents with subacute dyspnea, dry cough, hypoxia, and elevated LDH; diffuse bilateral interstitial infiltrates. Treat with TMP-SMX; add adjunctive corticosteroids if PaO2 <70 mmHg or A-a gradient >=35 mmHg. Diagnosis via induced sputum/BAL with silver stain or PCR.

9. How are hospital-acquired (HAP) and ventilator-associated pneumonia (VAP) defined and treated?

   HAP: pneumonia >=48h after admission; VAP: >=48h after intubation. Empiric therapy must cover MRSA (vancomycin/linezolid) and Pseudomonas (e.g., piperacillin-tazobactam, cefepime), with double anti-pseudomonal coverage if high resistance risk or septic shock.

10. What is the diagnostic approach and treatment for Clostridioides difficile infection?

    Diagnose with stool PCR/toxin testing in patients with >=3 unformed stools/24h. First-line treatment: oral vancomycin or fidaxomicin (oral metronidazole only if non-severe and alternatives unavailable). Stop the inciting antibiotic; fulminant cases need oral vancomycin + IV metronidazole +/- surgery.

11. What is tumor lysis syndrome, its lab findings, and management?

    Massive tumor cell breakdown (often after chemo of high-grade lymphoma/leukemia) causing hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia, risking AKI and arrhythmia. Management: aggressive IV hydration, rasburicase (or allopurinol for prophylaxis), and treat electrolyte abnormalities.

12. What is the presentation and emergent management of malignant spinal cord compression?

    Back pain (often worse when lying down), progressive weakness, sensory level, and bowel/bladder dysfunction in a cancer patient. Give immediate IV dexamethasone and obtain urgent whole-spine MRI, followed by radiation oncology/neurosurgery for definitive decompression.

13. How is anemia classified by MCV, with key examples in each category?

    Microcytic (MCV <80): iron deficiency, thalassemia, anemia of chronic disease (late), sideroblastic. Normocytic (80-100): acute blood loss, hemolysis, anemia of chronic disease, CKD. Macrocytic (MCV >100): B12/folate deficiency (megaloblastic), alcohol, liver disease, hypothyroidism, drugs.

14. How do iron studies differentiate iron deficiency anemia from anemia of chronic disease?

    Iron deficiency: low ferritin, low serum iron, HIGH TIBC, low transferrin saturation. Anemia of chronic disease: normal/high ferritin, low serum iron, LOW/normal TIBC, often normal/low transferrin saturation due to iron sequestration.

15. What lab pattern identifies disseminated intravascular coagulation (DIC)?

    Prolonged PT and aPTT, low fibrinogen, elevated D-dimer/fibrin degradation products, and thrombocytopenia, with schistocytes on smear. Treat the underlying cause; support with platelets, FFP, and cryoprecipitate (for low fibrinogen) as needed for bleeding.

16. What are the diagnostic features and first-line treatment of systemic lupus erythematosus (SLE)?

    Multisystem autoimmune disease with malar rash, arthritis, serositis, nephritis, cytopenias; positive ANA (sensitive) and anti-dsDNA/anti-Smith (specific). Monitor disease with complement (C3/C4) and dsDNA. Treatment: hydroxychloroquine for all, with corticosteroids/immunosuppressants for organ involvement (e.g., lupus nephritis).

17. How is giant cell (temporal) arteritis diagnosed and managed urgently?

    Older patient with new headache, jaw claudication, scalp tenderness, visual changes, and markedly elevated ESR/CRP, often with polymyalgia rheumatica. Start high-dose corticosteroids IMMEDIATELY (do not wait for biopsy) to prevent irreversible blindness; confirm with temporal artery biopsy.

18. What synovial fluid features distinguish inflammatory, septic, and crystal arthritis?

    Non-inflammatory: WBC <2,000. Inflammatory: WBC 2,000-50,000. Septic: WBC >50,000 (often >75,000), high PMNs, positive Gram stain/culture. Gout: negatively birefringent needle-shaped (monosodium urate) crystals; pseudogout: positively birefringent rhomboid (calcium pyrophosphate) crystals.

19. How is rheumatoid arthritis distinguished from osteoarthritis clinically and serologically?

    RA: symmetric inflammatory polyarthritis of MCP/PIP/wrists with morning stiffness >1h, positive RF and anti-CCP, elevated ESR/CRP, erosions on X-ray; spares DIPs. OA: asymmetric, weight-bearing/DIP joints, brief stiffness, no systemic inflammation, osteophytes and joint-space narrowing on X-ray.

20. What is the time-sensitive treatment of acute ischemic stroke, including the tPA and thrombectomy windows?

    IV thrombolysis (alteplase/tenecteplase) within 4.5 hours of symptom onset after excluding hemorrhage with non-contrast CT. Mechanical thrombectomy for large-vessel occlusion up to 24 hours in selected patients with favorable perfusion imaging. Maintain permissive hypertension unless giving tPA (then BP <185/110).

21. How do you differentiate a TIA from a stroke, and what is secondary prevention?

    TIA: transient neurologic deficit from ischemia WITHOUT acute infarction on imaging (deficits typically resolve within an hour). Stroke: deficit with infarction. Secondary prevention: antiplatelet therapy (aspirin, or short-term dual antiplatelet for high-risk TIA/minor stroke), high-intensity statin, BP control, and carotid endarterectomy if stenosis 70-99% symptomatic.

22. What defines status epilepticus and what is the stepwise treatment?

    Continuous seizure >=5 minutes or recurrent seizures without recovery between them. Step 1: IV benzodiazepine (lorazepam). Step 2: IV antiseizure agent (levetiracetam, fosphenytoin, or valproate). Step 3 (refractory): anesthetic infusion (midazolam, propofol) with intubation; check glucose and treat reversible causes.

23. What headache features are 'red flags' requiring urgent imaging?

    Thunderclap (worst-ever, sudden) headache, focal neurologic deficit, papilledema, headache with fever/neck stiffness, onset after age 50, immunosuppression/cancer, headache worse with Valsalva/positional, or progressive worsening. A thunderclap headache mandates CT and possibly LP to rule out subarachnoid hemorrhage.

24. How is Parkinson disease characterized and treated, and what distinguishes essential tremor?

    Parkinson: bradykinesia plus resting (pill-rolling) tremor, cogwheel rigidity, and postural instability; treat with levodopa-carbidopa (or dopamine agonists). Essential tremor: bilateral ACTION/postural tremor improved by alcohol, often familial, treated with propranolol or primidone-no rest tremor or rigidity.

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Internal Medicine and Clinical Knowledge (Step 2 CK) flashcards FAQ