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General medicine neetpg questions with explanation

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I have enough rich content to write 20 high-quality NEET PG case-based vignette questions with detailed explanations. Let me now compose them comprehensively.

20 NEET PG General Medicine - Case-Based Vignette Questions

CARDIOLOGY

Q1. A 45-year-old man with a history of rheumatic heart disease presents with 3 weeks of fever, fatigue, and a new murmur of mitral regurgitation. Blood cultures on two separate occasions grow alpha-hemolytic streptococcus. Echocardiography shows a mobile vegetation on the mitral valve.
Which of the following correctly categorizes this patient's diagnosis using the Duke criteria?
A) Possible infective endocarditis - one major + one minor criterion B) Definite infective endocarditis - two major criteria C) Definite infective endocarditis - one major + three minor criteria D) Rejected - alternative diagnosis more likely
Answer: B
Explanation: This patient meets two major Duke criteria:
  1. Blood culture major criterion - Two separate blood cultures positive for alpha-hemolytic streptococcus, a "typical organism" for IE
  2. Endocardial involvement - Echocardiographic mobile vegetation on the mitral valve
Duke Criteria (Modified):
  • Major: (1) Positive blood culture for typical organisms or persistent bacteremia; (2) Echocardiographic evidence of vegetation/abscess/new valvular regurgitation
  • Minor: Predisposing condition, fever ≥38°C, vascular phenomena (Janeway lesions, septic emboli), immunologic phenomena (Osler nodes, Roth spots, glomerulonephritis), positive blood culture not meeting major criteria
Definite IE requires: 2 major criteria OR 1 major + 3 minor OR 5 minor criteria. The mnemonic for immunologic phenomena: "GORE" - Glomerulonephritis, Osler nodes, Rheumatoid factor, Exposed Roth spots
  • Goldman-Cecil Medicine
Q2. A 55-year-old man is brought to the ER 8 hours after an acute inferior wall MI. He is treated conservatively. Two weeks later he returns with fever, pleuritic chest pain, and pericardial friction rub. Echo shows pericardial effusion. ESR is elevated.
What is the most likely diagnosis?
A) Reinfarction B) Dressler syndrome C) Acute pericarditis (primary viral) D) Pulmonary embolism
Answer: B
Explanation: Dressler syndrome (post-MI pericarditis / post-cardiac injury syndrome - PCIS) presents weeks after myocardial infarction (classically 2-10 weeks). It is an autoimmune reaction to myocardial antigens released after necrosis.
Key features:
  • Fever, pleuritic chest pain, pericardial friction rub
  • Elevated ESR/CRP
  • Pericardial (and sometimes pleural) effusion
  • Responds to NSAIDs/aspirin ± colchicine
Distinguishing from early infarct pericarditis (occurs within 24-72 hours after MI): Dressler's is delayed, has a more systemic inflammatory picture, and can recur.
Treatment: High-dose aspirin (or NSAIDs) + colchicine; avoid systemic steroids if possible (can impair myocardial healing).
  • Tintinalli's Emergency Medicine
Q3. A 60-year-old hypertensive woman develops sudden-onset severe tearing chest pain radiating to her back. BP is 190/110 mmHg in the right arm and 150/90 in the left arm. CXR shows a widened mediastinum.
The drug of FIRST choice to reduce aortic wall stress in this condition is:
A) Nitroglycerin B) Furosemide C) IV Labetalol (or esmolol) D) Hydralazine
Answer: C
Explanation: This is aortic dissection (Type A - ascending, given the BP differential and classic presentation). The priority is to reduce dP/dt (rate of pressure rise) and heart rate simultaneously to reduce shear force on the aortic wall.
Beta-blockers (IV esmolol, labetalol, metoprolol) are the agents of first choice because they reduce both BP and HR. If further BP control is needed, a vasodilator like nitroprusside can be added AFTER beta-blockade (never first - vasodilators alone cause reflex tachycardia, worsening aortic stress).
  • Type A dissection (involving ascending aorta) - requires emergency surgery
  • Type B dissection (descending only) - managed medically unless complications

NEPHROLOGY

Q4. A 6-year-old boy is brought with periorbital puffiness, frothy urine, and swelling of the legs for the past 2 weeks. Urinalysis shows 4+ proteinuria. Serum albumin is 1.8 g/dL. Serum cholesterol is 380 mg/dL. Blood pressure is normal. No hematuria.
The most likely underlying glomerular lesion is:
A) Membranous nephropathy B) Minimal change disease C) Focal segmental glomerulosclerosis D) IgA nephropathy
Answer: B
Explanation: This is classic Nephrotic Syndrome in a child - the triad of:
  • Massive proteinuria (>3.5 g/day in adults, proportionally less in children)
  • Hypoalbuminemia (albumin <3 g/dL)
  • Edema (periorbital puffiness characteristic in children) + Hyperlipidemia/lipiduria
Minimal Change Disease (MCD) is by far the most common cause of nephrotic syndrome in children (>80%). It is characterized by:
  • No changes on light microscopy
  • No immune deposits on immunofluorescence
  • Fusion/effacement of podocyte foot processes on electron microscopy (the key finding)
  • Highly selective proteinuria (mostly albumin)
  • Responds dramatically to steroids
In adults, the most common primary causes are membranous nephropathy (most common adult primary nephrotic) and FSGS. The most common systemic causes overall are diabetes mellitus, amyloidosis, and SLE.
  • Robbins, Cotran & Kumar Pathologic Basis of Disease
Q5. A 35-year-old man with recurrent nephrotic syndrome fails to respond to steroids. Biopsy shows segmental sclerosis involving some but not all glomeruli on light microscopy.
The most likely diagnosis is:
A) Minimal change disease B) Membranous nephropathy C) Focal segmental glomerulosclerosis (FSGS) D) Membranoproliferative GN
Answer: C
Explanation: FSGS (Focal Segmental Glomerulosclerosis):
  • "Focal" = only some glomeruli affected
  • "Segmental" = only part of each affected glomerulus shows sclerosis
  • Most common cause of nephrotic syndrome in adults in the USA and common in HIV patients (collapsing variant)
  • Associated with heroin abuse, obesity, sickle cell disease, reduced renal mass
  • Poor prognosis - ~50% progress to ESRD in 10 years
  • Resistant to steroids in many cases
Memory tip:
  • MCD: children, electron microscopy only finding (foot process effacement), steroid-responsive
  • FSGS: adults, focal segmental on LM, often steroid-resistant
  • Membranous: adults, "spike and dome" on EM, subepithelial deposits, associated with HBV/malignancy/drugs
Q6. A 22-year-old woman develops hematuria, RBC casts, and mild proteinuria 10 days after a throat infection with group A Streptococcus. Serum complement (C3) is low. ASO titer is elevated.
The most likely diagnosis is:
A) IgA nephropathy (Berger's disease) B) Post-streptococcal glomerulonephritis (PSGN) C) Membranoproliferative GN D) Lupus nephritis
Answer: B
Explanation: Post-Streptococcal GN (PSGN):
  • Presents 2-3 weeks after throat infection (or 4-6 weeks after skin infection)
  • Classic nephritic syndrome: hematuria, RBC casts, oliguria, hypertension, mild proteinuria
  • Low C3 (with normal C4 - alternate pathway activation)
  • High ASO titer (from throat infection; anti-DNase B more sensitive for skin)
  • Resolves spontaneously in most children; adults may progress
Key distinction from IgA nephropathy (Berger's disease):
  • IgA nephropathy presents with synpharyngitic hematuria - hematuria occurring within 24-48 hours of the throat infection (concurrent), not weeks later
  • IgA is the most common glomerulonephritis worldwide

ENDOCRINOLOGY

Q7. A 28-year-old woman presents with weight gain, cold intolerance, constipation, dry skin, periorbital puffiness, and bradycardia. TSH is markedly elevated at 85 mIU/L. Free T4 is very low.
The most common cause of this condition worldwide is:
A) Hashimoto's thyroiditis B) Iodine deficiency C) Post-thyroidectomy hypothyroidism D) Riedel's thyroiditis
Answer: B - worldwide; Answer: A - in iodine-sufficient countries (NEET PG context = A or B depending on framing)
Explanation:
  • Worldwide: Iodine deficiency is the most common cause of hypothyroidism
  • In India / iodine-sufficient areas: Hashimoto's thyroiditis (chronic autoimmune thyroiditis) is the most common cause
For NEET PG (India), the expected answer is typically Hashimoto's thyroiditis (autoimmune, anti-TPO antibodies, anti-thyroglobulin antibodies, lymphocytic infiltration with germinal center formation on histology).
Clinical features of hypothyroidism:
  • Slowing of all body functions: fatigue, cold intolerance, weight gain, constipation, bradycardia
  • Myxedema: non-pitting edema (due to glycosaminoglycan deposition)
  • Delayed relaxation of deep tendon reflexes (pathognomonic)
  • Pericardial effusion, low voltage ECG
  • In children: cretinism (irreversible if untreated)
Treatment: Levothyroxine (T4), adjusted by TSH levels.
  • Robbins & Kumar Basic Pathology
Q8. A 55-year-old obese man with poorly controlled diabetes presents with nausea, vomiting, and polyuria for 2 days. Blood glucose is 490 mg/dL, pH 7.1, bicarbonate 10 mEq/L, anion gap 24, urine ketones 3+. He is obtunded.
Which of the following is the FIRST priority in management?
A) IV insulin infusion B) IV fluid resuscitation with normal saline C) Sodium bicarbonate D) Potassium replacement
Answer: B
Explanation: This is Diabetic Ketoacidosis (DKA) - triad of:
  1. Hyperglycemia (usually >250 mg/dL)
  2. Metabolic acidosis (pH <7.3, bicarbonate <18)
  3. Ketonemia/ketonuria
Management priorities (in order):
  1. IV fluid resuscitation - 1-1.5 L 0.9% NaCl in the first hour (most important - corrects hypovolemia and hyperosmolarity)
  2. Insulin infusion - after fluid started and K+ confirmed ≥3.5 mEq/L (insulin drives K+ into cells - dangerous to start insulin if K+ is already low)
  3. Potassium replacement - start if K+ <5.2 mEq/L once urine output established
  4. Bicarbonate - only if pH <6.9 (controversial, not routine)
Why not insulin first? Insulin without adequate volume resuscitation causes vascular collapse; also insulin lowers K+ rapidly and can precipitate life-threatening hypokalemia.
Q9. A 30-year-old woman has episodic hypertension, headache, palpitations, and diaphoresis. 24-hour urine shows markedly elevated catecholamines and metanephrines. CT abdomen reveals a 4 cm right adrenal mass.
Before surgical resection, the MOST important step is:
A) Start beta-blocker immediately B) Start alpha-blocker (phenoxybenzamine) first, then add beta-blocker C) Administer IV corticosteroids D) Start ACE inhibitor
Answer: B
Explanation: This is Pheochromocytoma - catecholamine-secreting tumor of adrenal medulla (chromaffin cells). The classic "5 H's": Hypertension (episodic), Headache, Hyperhidrosis, Hypermetabolism, Hyperglycemia.
Preoperative preparation (critical for safety):
  1. Alpha-blockade FIRST (phenoxybenzamine - non-competitive, or doxazosin) for at least 10-14 days to normalize BP and allow volume expansion
  2. Then add beta-blocker (propranolol/atenolol) to control reflex tachycardia
Never give beta-blocker first - this leaves alpha-receptors unopposed, causing severe hypertension (paradoxical hypertensive crisis). This is a classic NEET PG trap question.
Tumor of rule of 10's: 10% malignant, 10% bilateral, 10% extra-adrenal, 10% familial, 10% in children.

RHEUMATOLOGY / IMMUNOLOGY

Q10. A 25-year-old woman presents with a malar rash, photosensitivity, oral ulcers, and arthralgia. Investigations show: ANA positive (1:640), anti-dsDNA positive, low complement (C3, C4), urine protein 3+, RBC casts.
According to the ACR/EULAR 2019 criteria, which of the following findings carries the highest weight/points?
A) Anti-dsDNA antibody B) Malar rash C) Oral ulcers D) Arthritis
Answer: A
Explanation: This patient has Systemic Lupus Erythematosus (SLE) with lupus nephritis (proteinuria + RBC casts).
The 2019 EULAR/ACR classification criteria use a weighted scoring system (entry criterion: ANA ≥1:80). Anti-dsDNA and anti-Sm antibodies carry high immunological weights (6 points each for anti-dsDNA).
Classic SLE features (older 1997 ACR - 11 criteria, need 4 of 11): Mnemonic "SOAP BRAIN MD":
  • Serositis
  • Oral ulcers
  • Arthritis
  • Photosensitivity
  • Blood disorders (hemolytic anemia, leukopenia, thrombocytopenia)
  • Renal (proteinuria >0.5 g/day or RBC casts)
  • ANA positive
  • Immunologic (anti-dsDNA, anti-Sm, antiphospholipid)
  • Neurologic (seizures, psychosis)
  • Malar rash
  • Discoid rash
Anti-dsDNA is also useful for monitoring disease activity - titres rise with flares.
  • Rheumatology, 2-Volume Set (Elsevier)
Q11. A 50-year-old man with longstanding rheumatoid arthritis presents with Raynaud phenomenon, puffy fingers, and skin tightening extending from the fingers to the forearm. He has difficulty swallowing and exertional dyspnea. ANA is positive with anti-Scl-70 (anti-topoisomerase I).
The most feared complication responsible for mortality in this condition is:
A) Pulmonary arterial hypertension (limited type) B) Scleroderma renal crisis C) Pulmonary fibrosis (diffuse type) D) Cardiac conduction defects
Answer: C (in diffuse systemic sclerosis with anti-Scl-70)
Explanation: This patient has Diffuse Cutaneous Systemic Sclerosis (dcSSc) - the more severe form:
  • Skin involvement proximal to elbows/knees and trunk
  • Associated with anti-Scl-70 (anti-topoisomerase I) antibodies
  • Leading cause of death: Interstitial lung disease/pulmonary fibrosis
Contrast with Limited cutaneous SSc (CREST syndrome):
  • Calcinosis, Raynaud, Esophageal dysmotility, Sclerodactyly, Telangiectasia
  • Associated with anti-centromere antibodies
  • Leading complication: Pulmonary arterial hypertension (PAH)
Scleroderma renal crisis (abrupt onset malignant hypertension + AKI) is associated with dcSSc and anti-RNA polymerase III antibodies; treated with ACE inhibitors.

NEUROLOGY

Q12. A 70-year-old man presents with progressive resting tremor in the right hand, rigidity, bradykinesia, and a stooped, shuffling gait. There is no cerebellar sign, no dementia, and no autonomic dysfunction. He responds excellently to levodopa.
The hallmark pathological finding in this condition is:
A) Neurofibrillary tangles B) Lewy bodies (alpha-synuclein aggregates) in substantia nigra C) Pick bodies D) Senile plaques with amyloid
Answer: B
Explanation: This is Parkinson's disease - classic features: TRAP mnemonic:
  • Tremor (resting, pill-rolling, 4-6 Hz)
  • Rigidity (cogwheel)
  • Akinesia/bradykinesia
  • Postural instability (late)
Pathology: Degeneration of dopaminergic neurons in the substantia nigra pars compacta with presence of Lewy bodies (eosinophilic intracytoplasmic inclusions containing alpha-synuclein and ubiquitin).
Pathological distinction:
  • Parkinson's: Lewy bodies in substantia nigra
  • Alzheimer's: neurofibrillary tangles (tau) + senile plaques (beta-amyloid)
  • Pick's disease (frontotemporal dementia): Pick bodies (tau)
Treatment: Levodopa + carbidopa (carbidopa is a peripheral dopa decarboxylase inhibitor that prevents peripheral conversion of levodopa, allowing more to reach the brain and reducing side effects).
Q13. A 65-year-old hypertensive man suddenly develops left-sided weakness, face drooping, and slurred speech. Symptoms began 1.5 hours ago. NIHSS score is 8. CT head shows no hemorrhage.
The time window for IV thrombolysis with alteplase is:
A) 6 hours from onset B) 4.5 hours from onset C) 3 hours from onset (only) D) 12 hours from onset
Answer: B
Explanation: This is an acute ischemic stroke - the "FAST" rule (Face drooping, Arm weakness, Speech difficulty, Time to call).
IV thrombolysis (alteplase, tPA):
  • Window: up to 4.5 hours from symptom onset (extended from the initial 3-hour window)
  • Dose: 0.9 mg/kg IV (max 90 mg), 10% as bolus, rest over 60 minutes
  • Contraindications: hemorrhage, BP >185/110 uncontrolled, recent surgery, prior stroke within 3 months, INR >1.7, platelet <100,000
Mechanical thrombectomy (endovascular):
  • For large vessel occlusion
  • Window: up to 24 hours in selected patients (DAWN/DEFUSE-3 trial criteria)
Key point for NEET PG: The 4.5-hour window for alteplase is the standard answer. The 3-hour window is for certain high-risk subgroups (age >80, diabetics with prior stroke, on anticoagulants, severe stroke).

GASTROENTEROLOGY / HEPATOLOGY

Q14. A 45-year-old chronic alcoholic presents with sudden massive hematemesis. On exam he has jaundice, spider angiomas, palmar erythema, and splenomegaly. Endoscopy shows large esophageal varices with active bleeding.
The drug used for vasoconstriction of splanchnic circulation to reduce portal pressure in acute variceal bleeding is:
A) Propranolol B) Vasopressin / Terlipressin C) Omeprazole D) Metoprolol
Answer: B
Explanation: Acute variceal bleeding management - "ABCDE" approach:
  1. Resuscitation + airway protection (intubate if needed)
  2. Vasoconstrictors - Terlipressin (preferred, reduces mortality) or octreotide/somatostatin - reduce splanchnic blood flow and portal pressure; start BEFORE endoscopy
  3. Antibiotics - prophylactic ciprofloxacin/norfloxacin (reduces bacterial translocation, improves survival)
  4. Endoscopy - Band ligation (preferred) or sclerotherapy within 12 hours
  5. TIPS (Transjugular Intrahepatic Portosystemic Shunt) - for refractory bleeding
Non-selective beta-blockers (propranolol, carvedilol) are used for primary and secondary prophylaxis of variceal bleeding (reduce portal pressure by decreasing cardiac output and splanchnic vasoconstriction via beta-2 blockade), NOT for acute management.
Q15. A 40-year-old man presents with progressive jaundice, fatigue, and pruritus. He has elevated alkaline phosphatase (5x normal), mildly elevated AST/ALT, and total bilirubin of 8 mg/dL. ERCP shows "beads on a string" appearance of the biliary tree. He has a history of ulcerative colitis.
The most likely diagnosis is:
A) Primary biliary cholangitis (PBC) B) Primary sclerosing cholangitis (PSC) C) Choledocholithiasis D) Autoimmune hepatitis
Answer: B
Explanation: Primary Sclerosing Cholangitis (PSC):
  • Fibro-inflammatory disease of both intra- and extrahepatic bile ducts
  • "Beads on a string" or "pruned tree" appearance on ERCP/MRCP (alternating strictures and dilatations)
  • Strongly associated with Inflammatory Bowel Disease (especially Ulcerative Colitis - in ~80% of PSC patients)
  • Predominantly affects young men
  • pANCA positive in many cases
  • High risk of cholangiocarcinoma (lifetime risk ~10-15%)
  • No effective medical treatment; liver transplant for end-stage disease
Contrast with PBC (Primary Biliary Cholangitis):
  • Middle-aged women
  • Intrahepatic bile ducts only
  • Anti-mitochondrial antibody (AMA) positive (M2 antigen)
  • Treated with ursodeoxycholic acid

RESPIRATORY MEDICINE

Q16. A 60-year-old male smoker presents with progressive dyspnea, chronic productive cough, and barrel-shaped chest. Spirometry shows FEV1/FVC = 0.55 (post-bronchodilator). FEV1 = 45% of predicted. CXR shows hyperinflation.
According to GOLD classification, this patient's COPD severity is:
A) GOLD 1 (Mild) B) GOLD 2 (Moderate) C) GOLD 3 (Severe) D) GOLD 4 (Very Severe)
Answer: C
Explanation: COPD diagnosis: Post-bronchodilator FEV1/FVC < 0.70 confirms airflow obstruction.
GOLD Spirometric Severity (based on % predicted FEV1):
StageFEV1 % predicted
GOLD 1 (Mild)≥80%
GOLD 2 (Moderate)50-79%
GOLD 3 (Severe)30-49%
GOLD 4 (Very Severe)<30%
This patient's FEV1 = 45% → GOLD 3 (Severe).
Key management by stage:
  • All: smoking cessation, LABA or LAMA
  • GOLD 2-4 with exacerbations: ICS + LABA combination
  • Severe/Very severe: pulmonary rehabilitation, long-term O2 if PaO2 ≤55 mmHg
Q17. A 35-year-old non-smoker woman presents with progressive dyspnea and bilateral hilar lymphadenopathy on CXR. She has erythema nodosum on her shins and anterior uveitis. Serum ACE level is elevated. Biopsy shows non-caseating granulomas.
The most characteristic laboratory finding in this condition is:
A) Positive Mantoux test B) Elevated serum calcium + elevated ACE C) Positive ANA D) Elevated IgE
Answer: B
Explanation: This is Sarcoidosis - multi-system granulomatous disease of unknown etiology, most common in young African-American women and Northern Europeans.
Key features:
  • Bilateral hilar lymphadenopathy (BHL) - most common chest finding
  • Non-caseating granulomas - the histological hallmark (vs. caseating granulomas in TB)
  • Elevated serum ACE - produced by macrophages in granulomas (marker of disease activity but not specific)
  • Hypercalcemia/hypercalciuria - due to 1-alpha-hydroxylase activity in granuloma macrophages converting vitamin D to active form
  • Extrapulmonary: uveitis (most common eye manifestation), erythema nodosum, Lofgren syndrome (BHL + erythema nodosum + polyarthritis - good prognosis)
  • Löfgren syndrome carries excellent prognosis
Mantoux (tuberculin) test is often negative in sarcoidosis due to anergy (cutaneous anergy).
Treatment: Systemic corticosteroids when indicated (symptomatic pulmonary disease, eye disease, hypercalcemia, cardiac/neuro involvement).

INFECTIOUS DISEASES

Q18. A 25-year-old returns from sub-Saharan Africa with high-grade fever, chills, headache, and rigors occurring every 48 hours. Blood smear shows ring forms and banana-shaped (crescent-shaped) gametocytes inside RBCs. He has severe thrombocytopenia.
The drug of choice for severe malaria caused by this parasite is:
A) Chloroquine B) IV Artesunate C) Primaquine D) Mefloquine
Answer: B
Explanation: The banana-shaped (crescent) gametocytes are pathognomonic for Plasmodium falciparum - the most dangerous form of malaria, responsible for severe/cerebral malaria.
Drug of choice for severe falciparum malaria: IV Artesunate (replaced quinine as first-line per WHO guidelines).
Malaria drug summary:
ParasiteFeatureTreatment
P. vivax / P. ovaleHypnozoites (relapse)Chloroquine + Primaquine (radical cure)
P. malariaeQuartan fever (72 hrs)Chloroquine
P. falciparum (uncomplicated)Chloroquine-resistant mostlyACT (Artemether-Lumefantrine)
P. falciparum (severe)Cerebral malariaIV Artesunate
Primaquine eliminates liver hypnozoites (radical cure for vivax/ovale) - contraindicated in G6PD deficiency (causes hemolysis).
Q19. A 30-year-old HIV-positive man (CD4 count 50 cells/µL) presents with confusion, fever, and headache. CSF shows: opening pressure 28 cm H2O, lymphocytosis, elevated protein, low glucose. India ink preparation of CSF is positive for encapsulated yeast.
The treatment of choice is:
A) Fluconazole alone B) Amphotericin B + Flucytosine (induction), then fluconazole (consolidation/maintenance) C) Voriconazole D) Caspofungin
Answer: B
Explanation: This is Cryptococcal meningitis - caused by Cryptococcus neoformans (encapsulated yeast). Most common in HIV patients with CD4 <100.
Diagnosis: India ink prep (negative stain shows capsule as clear halo), cryptococcal antigen (CrAg - most sensitive), CSF culture.
Treatment (IDSA guidelines):
  1. Induction (2 weeks): IV Amphotericin B + Flucytosine (5-FC) - most effective, reduces fungal burden rapidly
  2. Consolidation (8 weeks): Oral Fluconazole 400 mg/day
  3. Maintenance (≥1 year): Oral Fluconazole 200 mg/day
Key management point: Therapeutic lumbar punctures to reduce intracranial pressure (ICP) are critical - elevated ICP is the main cause of early mortality. Do NOT use steroids routinely.

HEMATOLOGY

Q20. A 55-year-old woman is incidentally found to have WBC 95,000/µL on a routine CBC. Differential shows predominantly mature lymphocytes. Peripheral smear shows "smudge cells" (basket cells). She has no lymphadenopathy or splenomegaly. She is asymptomatic.
The most likely diagnosis is:
A) Acute lymphoblastic leukemia (ALL) B) Chronic myeloid leukemia (CML) C) Chronic lymphocytic leukemia (CLL) D) Multiple myeloma
Answer: C
Explanation: This is Chronic Lymphocytic Leukemia (CLL) - the most common leukemia in adults in the Western world.
Key features:
  • Predominantly mature-appearing small lymphocytes (not blasts)
  • Smudge cells / basket cells - fragile CLL lymphocytes crushed during smear preparation - pathognomonic
  • Often found incidentally; indolent course
  • Hypogammaglobulinemia - increased susceptibility to infections
  • Positive for CD5, CD19, CD23 by flow cytometry (CD5 on B-cells is the hallmark)
  • Autoimmune hemolytic anemia (warm AIHA) can complicate
Rai staging (simplified):
  • Stage 0: lymphocytosis only (best prognosis)
  • Stage I/II: + lymphadenopathy / + splenomegaly or hepatomegaly
  • Stage III/IV: + anemia / + thrombocytopenia (worst prognosis)
Treatment: Asymptomatic early disease - watch and wait. Treatment when symptomatic: BTK inhibitors (ibrutinib), venetoclax, chemoimmunotherapy.
Compare CML: Mature granulocytes + basophilia + eosinophilia + low LAP score + Philadelphia chromosome (BCR-ABL) + splenomegaly - treated with imatinib (TKI).

Quick Reference Summary Table

QTopicKey Teaching Point
1Infective EndocarditisDuke criteria - 2 major = definite IE
2Dressler syndromePost-MI pericarditis at 2-10 weeks
3Aortic dissectionBeta-blocker first, never vasodilator alone
4Nephrotic syndrome - childMinimal change disease most common in children
5FSGSFocal segmental sclerosis; steroid-resistant
6PSGN2-3 weeks post-strep; low C3, normal C4
7HypothyroidismHashimoto's (India); delayed DTR relaxation
8DKAIV fluids FIRST, then insulin
9PheochromocytomaAlpha-block first, THEN beta-block
10SLESOAP BRAIN MD; anti-dsDNA highest weight
11SclerodermadcSSc (anti-Scl-70) → ILD; lcSSc (ACA) → PAH
12Parkinson's diseaseLewy bodies (alpha-synuclein) in substantia nigra
13Acute ischemic stroketPA window 4.5 hours; thrombectomy 24 hours
14Variceal bleedingTerlipressin + antibiotics + band ligation
15PSCBeads on a string; associated with UC
16COPDGOLD 3 = FEV1 30-49%
17SarcoidosisNon-caseating granuloma; elevated ACE; hypercalcemia
18MalariaP. falciparum (crescent gametocytes); IV artesunate for severe
19Cryptococcal meningitisAmB + flucytosine induction; monitor ICP
20CLLSmudge cells; CD5+CD19+CD23; watch and wait
Sources: Goldman-Cecil Medicine, Harrison's Principles of Internal Medicine 22E (2025), Robbins & Kumar Pathologic Basis of Disease, Tintinalli's Emergency Medicine, Rheumatology (Elsevier), Frameworks for Internal Medicine
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