AIIMS PG (DM/MCh) Entrance General Medicine and Medical Super-Specialties Flashcards

24 sample cards from the General Medicine and Medical Super-Specialties deck

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

1. What characterizes IgA nephropathy clinically and histologically?

   Most common primary glomerulonephritis worldwide; presents with synpharyngitic gross hematuria (1-2 days after URI). Mesangial IgA deposition on immunofluorescence. Differs from post-strep GN, which occurs 1-3 weeks after infection with low complement.

2. Compare the timing and complement levels of post-streptococcal GN vs IgA nephropathy.

   PSGN: 1-3 weeks after pharyngitis/skin infection, LOW C3, subepithelial humps on EM. IgA: 1-2 days after URI (synpharyngitic), NORMAL complement, mesangial deposits.

3. Differentiate hemodialysis from peritoneal dialysis in mechanism of solute clearance.

   Hemodialysis clears solutes by diffusion across a semipermeable membrane (with convection via ultrafiltration) using extracorporeal blood. Peritoneal dialysis uses the peritoneum as the membrane, with diffusion and osmotic ultrafiltration driven by dextrose in dialysate.

4. Which kidney transplant rejection types correspond to T-cell vs antibody-mediated mechanisms, and the timing of hyperacute rejection?

   T-cell-mediated (cellular) rejection: tubulitis/interstitial infiltrate, days to weeks. Antibody-mediated: peritubular capillaritis, C4d positive, donor-specific antibodies. Hyperacute occurs within minutes-hours due to preformed antibodies (preventable by crossmatch).

5. Give the formulas for the anion gap and the expected respiratory (Winter's) compensation in metabolic acidosis.

   Anion gap = Na - (Cl + HCO3), normal 8-12. Winter's formula: expected PCO2 = 1.5 x [HCO3] + 8 (plus or minus 2). If measured PCO2 is higher, there is a concurrent respiratory acidosis; if lower, concurrent respiratory alkalosis.

6. List the causes of a high anion gap metabolic acidosis (mnemonic GOLD MARK).

   Glycols (ethylene, propylene), Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, Ketoacidosis. (Classic MUDPILES is an alternative.)

7. How is the corrected sodium calculated in hyperglycemia, and the correction for sodium in hyponatremia?

   Corrected Na = measured Na + 1.6 (or 2.4) mEq/L for every 100 mg/dL glucose above 100. Acute hyponatremia correction should not exceed ~8 mEq/L per 24 hours to avoid osmotic demyelination syndrome.

8. What ECG changes occur with progressive hyperkalemia, and the first drug to give?

   Peaked T waves, then PR prolongation/flattened P, widened QRS, sine wave, and asystole/VF. First give IV calcium gluconate to stabilize the myocardium (does not lower K); then shift K with insulin/glucose, beta-agonists, bicarbonate.

9. Differentiate ischemic stroke subtypes by the TOAST classification.

   Large-artery atherosclerosis, cardioembolism, small-vessel occlusion (lacunar), stroke of other determined etiology, and stroke of undetermined etiology (cryptogenic).

10. What are the time windows for IV thrombolysis (alteplase/tenecteplase) and mechanical thrombectomy in acute ischemic stroke?

    IV thrombolysis up to 4.5 hours from onset. Mechanical thrombectomy for large-vessel occlusion up to 24 hours in selected patients with favorable perfusion imaging (DAWN/DEFUSE-3 criteria).

11. What blood pressure threshold permits IV thrombolysis, and the target in spontaneous intracerebral hemorrhage?

    BP must be below 185/110 mmHg before and 180/105 after thrombolysis. In acute ICH, lowering SBP to ~140 mmHg (INTERACT/ATACH targets) is reasonable. In untreated ischemic stroke, permissive hypertension up to 220/120 is allowed.

12. Define status epilepticus and the first- and second-line drug treatments.

    Continuous seizure 5+ minutes, or recurrent seizures without recovery of consciousness. First-line: IV benzodiazepine (lorazepam/diazepam) or IM midazolam. Second-line: IV levetiracetam, fosphenytoin/phenytoin, or valproate.

13. Differentiate focal vs generalized seizures and give the drug of choice for absence seizures.

    Focal seizures begin in one hemisphere (with/without awareness); generalized involve both hemispheres at onset (e.g., absence, tonic-clonic, myoclonic). Drug of choice for absence seizures is ethosuximide (or valproate).

14. What is the pathophysiology of Parkinson disease and its cardinal motor features?

    Loss of dopaminergic neurons in the substantia nigra pars compacta with Lewy bodies (alpha-synuclein). Cardinal features: bradykinesia, resting tremor (4-6 Hz, pill-rolling), rigidity (cogwheel), and postural instability.

15. Differentiate essential tremor from Parkinsonian tremor and Huntington disease genetics.

    Essential tremor: action/postural tremor, improves with alcohol, treated with propranolol/primidone. Parkinsonian: resting tremor. Huntington: autosomal dominant CAG trinucleotide repeat expansion in HTT gene with chorea, caudate atrophy, anticipation.

16. Contrast Guillain-Barre syndrome with myasthenia gravis in pathophysiology and key tests.

    GBS: acute ascending areflexic paralysis, post-infectious (Campylobacter), albuminocytologic dissociation in CSF, autoimmune demyelination. Myasthenia gravis: anti-AChR (or MuSK) antibodies, fatigable weakness, decremental response on repetitive nerve stimulation, thymoma association.

17. What distinguishes the antibodies and weakness pattern of Lambert-Eaton from myasthenia gravis?

    Lambert-Eaton: anti-voltage-gated calcium channel antibodies, paraneoplastic (small cell lung cancer), weakness IMPROVES with repeated use (incremental response), proximal weakness with hyporeflexia. Myasthenia: anti-AChR, weakness WORSENS with use.

18. List the McDonald-relevant features and first-line acute treatment of multiple sclerosis.

    MS requires dissemination in space and time (CNS demyelination); MRI shows periventricular/juxtacortical/infratentorial/spinal lesions, CSF oligoclonal bands. Acute relapses treated with high-dose IV methylprednisolone; relapsing disease with disease-modifying therapies.

19. Differentiate the major primary headaches: migraine, tension-type, and cluster.

    Migraine: unilateral, pulsating, 4-72 hr, photophobia/phonophobia/nausea, +/- aura. Tension: bilateral, pressing, non-pulsatile, no nausea. Cluster: severe unilateral orbital pain, 15-180 min, with ipsilateral autonomic features (lacrimation, ptosis), male predominance.

20. What protein pathologies underlie Alzheimer disease, and the characteristic CSF/imaging findings?

    Extracellular beta-amyloid plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau. CSF shows low Abeta42 and high tau/p-tau; MRI shows hippocampal/medial temporal atrophy. Anti-amyloid monoclonal antibodies (lecanemab) are disease-modifying options.

21. State the diagnostic thresholds for diabetes mellitus.

    Fasting plasma glucose 126+ mg/dL, 2-hour OGTT 200+ mg/dL, HbA1c 6.5%+, or random glucose 200+ with symptoms. Prediabetes: FPG 100-125, A1c 5.7-6.4%, OGTT 140-199.

22. Differentiate DKA from hyperosmolar hyperglycemic state.

    DKA: glucose usually 250-600, marked ketonemia/ketonuria, high anion gap metabolic acidosis (pH <7.3, HCO3 <18), in type 1. HHS: glucose often >600, serum osmolality >320, minimal ketosis, pH >7.3, profound dehydration, in type 2; higher mortality.

23. How are primary, secondary, and tertiary hyperthyroidism distinguished by TSH/T4, and what is the most common cause of hyperthyroidism?

    Primary (Graves): low TSH, high free T4 (TSH-receptor antibodies, diffuse uptake). Secondary (TSH-secreting adenoma): high TSH, high T4. Subclinical: low TSH, normal T4. Graves disease is the most common cause of hyperthyroidism.

24. Differentiate Cushing syndrome screening tests and the dexamethasone suppression interpretation.

    Screen with late-night salivary cortisol, 24-hr urinary free cortisol, or 1 mg overnight dexamethasone suppression test (cortisol fails to suppress). ACTH-dependent (pituitary/ectopic) vs ACTH-independent (adrenal). High-dose dexamethasone suppresses pituitary (Cushing disease) but not ectopic ACTH.

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