medicineneet pghigh yieldcardiologyendocrinologynephrologyhematology
Master every high-yield medicine topic for NEET PG 2026: cardiology, endocrinology, nephrology, hematology, neurology, gastroenterology, infectious disease, and rheumatology with real exam patterns and study strategies.
Version 1.0 — Published April 2026
Medicine contributes 35–45 questions to NEET PG — the highest of any clinical subject. Focus on these 8 high-yield systems:
This guide covers each system with the clinical facts that NBE tests, the diagnostic criteria you need to recall under pressure, and the drug-of-choice tables that convert knowledge into marks.
Medicine is the subject where clinical reasoning meets pattern recognition. Unlike Anatomy, where spatial relationships are fixed, or Pharmacology, where mechanism chains are predictable, Medicine demands that you integrate findings across history, examination, labs, and imaging into a single diagnosis — often from a 4-line vignette with one critical clue buried in the middle. The exam does not reward the student who knows the most. It rewards the student who recognizes the pattern fastest.
That recognition comes from two sources: understanding the pathophysiology deeply enough to predict the clinical picture, and drilling enough vignettes that the pattern becomes automatic. This guide provides the first source — the high-yield clinical content for each of the eight systems that dominate NEET PG. For the second source, pair this with daily MCQ practice on the Medicine subject hub and apply the 5-step MCQ strategy to every vignette you encounter.
This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
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Join on Telegram →Cardiology is the branch of medicine dealing with disorders of the heart and cardiovascular system — and it contributes 8–12 questions per NEET PG paper, more than any other medicine subsystem. The testable core is concentrated in four areas: heart failure, acute coronary syndromes, arrhythmias, and hypertension.
NYHA functional classification is the most frequently tested staging system in cardiology:
| Class | Symptoms | Exercise tolerance | Clinical implication |
|---|---|---|---|
| I | No limitation | Ordinary activity asymptomatic | Lifestyle modification, monitor |
| II | Slight limitation | Comfortable at rest, symptomatic with ordinary activity | ACE inhibitor + beta-blocker |
| III | Marked limitation | Comfortable at rest, symptomatic with less than ordinary activity | Add diuretic, consider device therapy |
| IV | Unable to carry out any activity without discomfort | Symptomatic at rest | Inotropes, transplant evaluation |
Heart failure treatment ladder (as tested by NBE):
Key NBE trap: Diuretics relieve symptoms but do NOT reduce mortality in heart failure. ACE inhibitors, beta-blockers, MRAs, and sacubitril-valsartan reduce mortality. If the question asks "which drug reduces mortality," never pick furosemide.
STEMI vs NSTEMI differentiation:
| Feature | STEMI | NSTEMI |
|---|---|---|
| ECG | ST elevation in contiguous leads | ST depression, T-wave inversion, or no changes |
| Troponin | Elevated | Elevated |
| Management | Primary PCI within 90 min (or thrombolysis within 12 hours if PCI unavailable) | Antiplatelet + anticoagulant; PCI if high-risk |
| Thrombolysis agents | Streptokinase, tenecteplase, alteplase | NOT indicated |
| Door-to-balloon | <90 minutes | Not applicable |
Thrombolysis contraindications (tested as a standalone question): active internal bleeding, history of hemorrhagic stroke, ischemic stroke within 3 months, intracranial neoplasm, suspected aortic dissection, significant head trauma within 3 months.
Secondary hypertension clues — NBE loves presenting a young patient with hypertension and asking for the cause:
| Clue in the stem | Diagnosis | Confirmatory test |
|---|---|---|
| Young woman, renal bruit | Renal artery stenosis (fibromuscular dysplasia) | CT angiography / MR angiography |
| Paroxysmal HTN, headache, sweating, palpitations | Pheochromocytoma | 24-hour urine metanephrines |
| Hypokalemia, alkalosis, low renin | Primary hyperaldosteronism (Conn syndrome) | Aldosterone-renin ratio |
| Truncal obesity, striae, buffalo hump | Cushing syndrome | Overnight dexamethasone suppression |
| Radiofemoral delay, rib notching on CXR | Coarctation of aorta | CT angiography / echocardiography |
Endocrinology is the study of hormone-producing glands and their disorders — contributing 5–8 questions per NEET PG paper, with diabetes mellitus alone accounting for 3–4 of those.
DKA vs HHS differentiation — a perennial NBE favorite:
| Feature | DKA | HHS |
|---|---|---|
| Type of diabetes | Usually Type 1 | Usually Type 2 |
| Onset | Rapid (hours to 1-2 days) | Gradual (days to weeks) |
| Blood glucose | Usually 300–800 mg/dL | Usually >600 mg/dL, often >1000 |
| pH | <7.3 (metabolic acidosis) | >7.3 (no significant acidosis) |
| Bicarbonate | <18 mEq/L | >18 mEq/L |
| Ketones | Strongly positive | Absent or trace |
| Serum osmolality | Variable | >320 mOsm/kg |
| Mental status | Alert to obtunded | Often comatose |
| Mortality | ~1-5% | ~5-20% (higher) |
| Key treatment | Insulin drip + fluids + K+ replacement | Aggressive fluid resuscitation first |
Critical NBE point: In DKA, always check and replace potassium BEFORE starting insulin. Insulin drives K+ intracellularly and can cause fatal hypokalemia if serum K+ is already low.
Graves disease vs Hashimoto thyroiditis:
| Feature | Graves disease | Hashimoto thyroiditis |
|---|---|---|
| Function | Hyperthyroidism | Hypothyroidism (may have initial thyrotoxic phase) |
| Antibody | TSI (thyroid-stimulating immunoglobulin) | Anti-TPO, anti-thyroglobulin |
| Radioiodine uptake | Diffusely increased | Decreased (or patchy) |
| Eye signs | Exophthalmos, lid retraction, lid lag | None |
| Treatment | Antithyroid drugs (carbimazole/methimazole), RAI, or surgery | Levothyroxine replacement |
Thyroid storm — a clinical emergency: fever >40°C, tachycardia, altered sensorium, heart failure. Management sequence: propylthiouracil/PTU (block synthesis — give FIRST) + propranolol concurrently (symptom control) → Lugol's iodine ≥1 hour AFTER PTU (block release — giving iodine before antithyroid drug can worsen storm via Jod-Basedow) → hydrocortisone (prevent peripheral T4→T3 conversion + adrenal support). NBE tests the principle: block synthesis before blocking release.
Cushing syndrome workup algorithm: 24-hour urine cortisol or overnight dexamethasone suppression test → if positive, ACTH level → high ACTH: pituitary (Cushing disease) vs ectopic → high-dose dexamethasone suppression test → suppresses: pituitary; does not suppress: ectopic.
Addisonian crisis — acute adrenal insufficiency: hypotension, hyponatremia, hyperkalemia, hypoglycemia. Treatment: IV hydrocortisone 100mg stat + IV saline. Do not delay steroids for confirmatory tests.
Nephrology is the specialty dealing with kidney diseases and electrolyte/acid-base homeostasis — contributing 5–7 questions per NEET PG, with acid-base and electrolyte questions appearing almost every year.
| Stage | GFR (mL/min/1.73m²) | Description | Action |
|---|---|---|---|
| G1 | ≥90 | Normal or high | Diagnose and treat cause, reduce risk |
| G2 | 60–89 | Mildly decreased | Estimate progression |
| G3a | 45–59 | Mild-moderate decrease | Monitor, manage complications |
| G3b | 30–44 | Moderate-severe decrease | Nephrology referral |
| G4 | 15–29 | Severely decreased | Prepare for RRT |
| G5 | <15 | Kidney failure | Dialysis or transplant |
Hyperkalemia ECG progression (most tested electrolyte-ECG correlation):
Emergency management: IV calcium gluconate (cardioprotection, does NOT lower K+) → insulin + glucose (shifts K+ intracellularly) → salbutamol nebulization → sodium bicarbonate if acidotic → kayexalate/patiromer for elimination → dialysis if refractory.
Anion gap metabolic acidosis causes (MUDPILES): Methanol, Uremia, DKA, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates.
| Type | Classic presentation | Key finding | Complement | Common cause |
|---|---|---|---|---|
| Minimal change | Nephrotic syndrome in children | Podocyte foot process effacement on EM | Normal | Idiopathic |
| Membranous | Nephrotic syndrome in adults | Spike and dome pattern on EM | Normal (primary); Low in lupus-associated | PLA2R antibody (primary); SLE Class V, hepatitis B (secondary) |
| MPGN | Mixed nephrotic-nephritic | Tram-track appearance | Low C3 | Hepatitis C, cryoglobulinemia |
| IgA nephropathy | Gross hematuria after URI | Mesangial IgA deposits on IF | Normal | Most common GN worldwide |
| Post-streptococcal | Nephritic syndrome 2-3 weeks after pharyngitis | Subepithelial humps on EM | Low C3 (transient) | Group A strep |
| RPGN/Crescentic | Rapidly progressive renal failure | Crescents on light microscopy | Variable | Anti-GBM, ANCA, immune complex |
Hematology is the study of blood and blood-forming organs — contributing 4–6 questions per NEET PG with anemia classification, leukemia differentiation, and coagulation disorders as the reliable test targets.
| Type | MCV | Common causes | Key lab finding |
|---|---|---|---|
| Microcytic (<80 fL) | Low | Iron deficiency, thalassemia, chronic disease, sideroblastic | Low ferritin (IDA), high HbA2 (beta-thal trait) |
| Normocytic (80-100 fL) | Normal | Acute blood loss, chronic disease, renal failure, aplastic | Reticulocyte count differentiates |
| Macrocytic (>100 fL) | High | B12 deficiency, folate deficiency, hypothyroidism, liver disease, MDS | Hypersegmented neutrophils (megaloblastic) |
Iron deficiency vs thalassemia trait — a classic NBE differentiator:
| Parameter | Iron deficiency | Beta-thalassemia trait |
|---|---|---|
| Serum iron | Low | Normal |
| TIBC | High | Normal |
| Ferritin | Low | Normal or high |
| HbA2 | Normal or low | Elevated (>3.5%) |
| RDW | High | Normal |
| Mentzer index (MCV/RBC) | >13 | <13 |
| Feature | ALL | AML | CLL | CML |
|---|---|---|---|---|
| Age | Children (peak 2-5 years) | Adults (median 65) | Elderly (>60) | Adults (40-60) |
| Cell | Lymphoblast | Myeloblast | Mature B-lymphocyte | Granulocyte series |
| Marker | TdT+, CD10+ (B-ALL) | MPO+, Auer rods | CD5+, CD23+, smudge cells | BCR-ABL (Philadelphia chromosome) |
| Treatment | Multi-agent chemo, CNS prophylaxis | Induction with 7+3 (cytarabine + daunorubicin) | Watch-and-wait or ibrutinib | Imatinib (TKI) |
| Prognosis | >85% cure in children | Variable (30-40% cure) | Indolent, median survival 10+ years | Excellent with TKI |
DIC (Disseminated Intravascular Coagulation) — simultaneous clotting and bleeding: prolonged PT, PTT, low fibrinogen, elevated D-dimer, low platelets, schistocytes on smear. Treatment: treat the underlying cause + supportive (FFP, cryoprecipitate, platelets).
ITP vs TTP — critical differentiation:
| Feature | ITP | TTP |
|---|---|---|
| Mechanism | Antiplatelet antibodies | ADAMTS13 deficiency, vWF multimer aggregation |
| Pentad | Isolated thrombocytopenia | Thrombocytopenia, MAHA, fever, renal failure, neurological symptoms |
| Smear | Large platelets, otherwise normal | Schistocytes (MAHA) |
| Treatment | Steroids → IVIG → splenectomy | Plasma exchange (emergency) |
| Platelet transfusion | Safe | CONTRAINDICATED (worsens thrombosis) |
Neurology is the medical specialty concerned with disorders of the nervous system — contributing 3–5 questions per NEET PG, with stroke management, epilepsy drug-of-choice, and neuromuscular differentiation as the most predictable targets.
| Feature | Ischemic stroke | Hemorrhagic stroke |
|---|---|---|
| Frequency | ~85% of all strokes | ~15% |
| CT scan | Hypodense area (may be normal <6 hours) | Hyperdense area (blood appears white) |
| Thrombolysis | IV alteplase within 4.5 hours of onset | Contraindicated |
| BP management | Permissive (do not lower acutely unless >220/120) | Target SBP <140 mmHg |
| Common cause | AF (cardioembolic), carotid atherosclerosis | Hypertension (basal ganglia), aneurysm (SAH) |
| Seizure type | First-line drug | Alternative | Key consideration |
|---|---|---|---|
| Generalized tonic-clonic | Valproate | Levetiracetam, lamotrigine | Valproate is teratogenic — avoid in women of childbearing age |
| Absence | Ethosuximide | Valproate | Ethosuximide ONLY for absence — does not treat GTCS |
| Myoclonic | Valproate | Levetiracetam | Avoid carbamazepine (worsens myoclonus) |
| Focal/partial | Carbamazepine | Oxcarbazepine, levetiracetam | Check HLA-B*1502 in Asian populations (SJS risk) |
| Status epilepticus | IV diazepam (Indian practice) or IV lorazepam (international) → IV phenytoin/fosphenytoin | Midazolam, levetiracetam | Diazepam is standard first-line in Indian formulary; lorazepam preferred internationally but not universally available in India |
| Feature | Myasthenia gravis | Guillain-Barré syndrome |
|---|---|---|
| Onset | Gradual | Acute (ascending weakness over days) |
| Pattern | Fatigable weakness, worse with activity | Ascending symmetric paralysis |
| Reflexes | Normal | Areflexia |
| Eye involvement | Ptosis, diplopia (common initial presentation) | Facial diplegia (bilateral facial weakness) |
| CSF | Normal | Albumino-cytological dissociation (high protein, normal cells) |
| Diagnosis | Anti-AChR antibodies, edrophonium test | Nerve conduction (demyelinating pattern) |
| Treatment | Pyridostigmine, immunosuppression, thymectomy | IVIG or plasmapheresis |
Gastroenterology is the branch of medicine focused on the digestive system and its disorders — contributing 3–5 NEET PG questions, with liver cirrhosis scoring, hepatitis markers, and IBD differentiation as the reliable test targets.
| Parameter | 1 point | 2 points | 3 points |
|---|---|---|---|
| Bilirubin (mg/dL) | <2 | 2–3 | >3 |
| Albumin (g/dL) | >3.5 | 2.8–3.5 | <2.8 |
| INR | <1.7 | 1.7–2.3 | >2.3 |
| Ascites | None | Mild (controlled) | Moderate-severe |
| Encephalopathy | None | Grade I–II | Grade III–IV |
Class A: 5–6 points (well-compensated). Class B: 7–9 (significant compromise). Class C: 10–15 (decompensated, consider transplant).
| Feature | Crohn disease | Ulcerative colitis |
|---|---|---|
| Location | Any part of GI tract (mouth to anus); terminal ileum most common | Colon only; starts at rectum, extends proximally |
| Distribution | Skip lesions | Continuous involvement |
| Depth | Transmural (all layers) | Mucosal and submucosal only |
| Complications | Fistulae, strictures, abscesses | Toxic megacolon, colorectal cancer |
| Pathology | Non-caseating granulomas, cobblestone mucosa | Crypt abscesses, pseudopolyps |
| Smoking | Worsens disease | Protective (cessation may trigger flare) |
| Surgery | Not curative (recurrence at anastomosis) | Curative (total proctocolectomy) |
| Marker | Significance |
|---|---|
| HBsAg | Active infection (acute or chronic) |
| Anti-HBs | Immunity (from vaccination or past infection) |
| HBeAg | High infectivity, active viral replication |
| Anti-HBe | Low infectivity, seroconversion |
| Anti-HBc IgM | Acute infection |
| Anti-HBc IgG | Past infection (with or without immunity) |
| HBsAg+ Anti-HBc IgM+ | Acute hepatitis B |
| HBsAg+ Anti-HBc IgG+ HBeAg+ | Chronic active hepatitis B |
| Anti-HBs+ Anti-HBc IgG+ | Recovered from past infection |
| Anti-HBs+ only | Vaccinated |
Infectious disease is the specialty dealing with infections caused by bacteria, viruses, fungi, and parasites — contributing 3–5 NEET PG questions with HIV staging, TB management, and malaria treatment as the most frequently tested topics.
| Stage | Defining conditions | CD4 correlation |
|---|---|---|
| 1 | Asymptomatic, persistent generalized lymphadenopathy | >500 |
| 2 | Weight loss <10%, minor mucocutaneous, recurrent URI | 350–499 |
| 3 | Weight loss >10%, chronic diarrhea >1 month, oral candidiasis, pulmonary TB, severe bacterial infections | 200–349 |
| 4 | HIV wasting, PCP, cerebral toxoplasmosis, extrapulmonary TB, CMV retinitis, Kaposi sarcoma, CNS lymphoma | <200 |
Important: WHO clinical staging is based on clinical criteria only, NOT CD4 count. The CD4 values shown are typical epidemiological associations, not diagnostic thresholds. A patient can have Stage 3 disease with CD4 >500 if they develop oral candidiasis or pulmonary TB. CD4 <200 defines AIDS by CDC criteria (separate from WHO staging). NBE tests this distinction — do not conflate the two systems.
Note: Pulmonary TB = WHO Stage 3; Extrapulmonary TB = WHO Stage 4. This is a frequently tested differentiation.
First-line ART (NACO India guidelines): TDF + 3TC (or FTC) + DTG (dolutegravir). Dolutegravir replaced efavirenz as the preferred NNRTI/INSTI in current Indian guidelines due to better efficacy, fewer side effects, and higher genetic barrier to resistance.
Category I (new cases): 2 months intensive (HRZE) + 4 months continuation (HR) — daily regimen under revised NTEP (2019 onward). Ethambutol is NOT continued in the continuation phase under the revised daily NTEP regimen (the old thrice-weekly RNTCP used HRE in continuation — do not confuse the two). Pyridoxine given with isoniazid to prevent peripheral neuropathy.
MDR-TB: resistance to at least isoniazid AND rifampicin. Treated with longer regimens including bedaquiline, linezolid, fluoroquinolones. Duration: 9-18 months.
Key drug ADRs: Rifampicin (hepatotoxicity, orange secretions, CYP induction), Isoniazid (peripheral neuropathy, hepatotoxicity, SLE-like syndrome), Pyrazinamide (hyperuricemia, hepatotoxicity), Ethambutol (optic neuritis — test visual acuity before starting), Streptomycin (ototoxicity, nephrotoxicity).
| Species | RBC preference | Periodicity | Severe malaria | Treatment |
|---|---|---|---|---|
| P. falciparum | All ages of RBCs | 48 hours (malignant tertian) | Yes (cerebral, severe anemia, ARDS) | ACT (artemether + lumefantrine); IV artesunate for severe malaria |
| P. vivax | Reticulocytes | 48 hours (benign tertian) | Rare | Chloroquine + primaquine (14 days for radical cure) |
| P. malariae | Older RBCs | 72 hours (quartan) | No | Chloroquine |
| P. ovale | Reticulocytes | 48 hours | No | Chloroquine + primaquine |
Critical point: Primaquine is given for P. vivax and P. ovale to eliminate hypnozoites in the liver (radical cure). Check G6PD status before prescribing — primaquine causes hemolytic anemia in G6PD-deficient patients.
Rheumatology is the medical specialty focused on autoimmune and inflammatory diseases of the joints, muscles, and connective tissue — contributing 2–4 questions per NEET PG with SLE criteria, RA management, and vasculitis classification as the tested core.
The 2019 EULAR/ACR criteria use a weighted scoring system with ANA as entry criterion. Key domains tested by NBE:
| Domain | Criteria | Points |
|---|---|---|
| Hematologic | Leukopenia, thrombocytopenia, autoimmune hemolysis | 2-4 |
| Renal | Proteinuria >0.5g/day, Class III/IV lupus nephritis on biopsy | 4-10 |
| Musculoskeletal | Inflammatory arthritis (≥2 joints) | 6 |
| Serosal | Pleural or pericardial effusion | 5-6 |
| Skin | Malar rash, discoid lesion, oral ulcers, alopecia | 2-6 |
| Neuropsychiatric | Seizures, psychosis | 2-5 |
| Immunological | Anti-dsDNA, anti-Smith, antiphospholipid, low complement | 2-6 |
Drug-induced lupus — tested as a differential: Hydralazine, procainamide, isoniazid, minocycline. Key differentiators: anti-histone antibodies positive, anti-dsDNA usually negative, no renal or CNS involvement, resolves on stopping the drug.
| Vessel size | Disease | Key feature |
|---|---|---|
| Large | Takayasu arteritis | Young Asian female, pulseless disease, aortic arch involvement |
| Large | Giant cell arteritis | Age >50, temporal headache, jaw claudication, risk of blindness |
| Medium | Polyarteritis nodosa | Hepatitis B association, spares lungs, microaneurysms |
| Medium | Kawasaki disease | Child <5 years, coronary artery aneurysms, strawberry tongue |
| Small (ANCA+) | Granulomatosis with polyangiitis (Wegener) | c-ANCA (PR3), upper + lower respiratory + renal |
| Small (ANCA+) | Microscopic polyangiitis | p-ANCA (MPO), renal + pulmonary, no granulomas |
| Small (ANCA+) | Eosinophilic granulomatosis (Churg-Strauss) | p-ANCA, asthma, eosinophilia, neuropathy |
| Small (immune complex) | Henoch-Schönlein purpura (IgA vasculitis) | Children, palpable purpura, abdominal pain, IgA nephropathy |
Study strategy for medicine is the systematic approach to converting clinical knowledge into reliable exam performance — and it differs from other subjects because Medicine rewards integration, not isolation.
Phase 1 — System-by-system foundation (3 weeks). One system every 2–3 days. For each system, read the high-yield content from this guide or Harrison's selectively. Build one-page summary tables for diagnostic criteria, classifications, and drug-of-choice. Solve 15 MCQs daily on the system you studied.
Phase 2 — Clinical vignette drilling (2 weeks). Stop re-reading. Drill 40 mixed-topic medicine vignettes daily. Apply the 5-step MCQ approach from our Pharmacology MCQ strategy guide — it works identically for Medicine vignettes. Audit wrong answers weekly: diagnosis error vs management error vs investigation error.
Phase 3 — Revision and mocks (1 week). Revise tables in reverse order. Take 2 timed medicine mini-mocks (50 questions, 60 minutes). Build a spaced repetition deck of drug-of-choice tables, diagnostic criteria, and ECG patterns. Final day: review only NYHA, CKD staging, DKA vs HHS, and the anemia classification table.
For the complete preparation framework across all subjects, read our comprehensive NEET PG Surgery high-yield guide and build cross-subject connections.
Medicine typically contributes 35-45 questions to NEET PG, making it the single highest-weighted clinical subject. Cardiology and endocrinology alone account for 10-15 questions most years. The subject's weight makes it the highest-ROI clinical subject for focused preparation.
Cardiology (heart failure, MI, arrhythmias, hypertension), endocrinology (diabetes, thyroid, adrenal), nephrology (AKI, CKD, acid-base, electrolytes), hematology (anemias, leukemias, coagulation), and infectious disease (HIV, TB, malaria) dominate consistently across recent papers.
No. Harrison's is a reference, not a prep book. Use it selectively for mechanism depth on high-yield topics — heart failure pathophysiology, diabetic complications, CKD staging. For day-to-day prep, use a concise guide and reserve Harrison for concepts where understanding the 'why' is weak.
Read the last line first to identify what is being asked. Then scan for the clinical clue — the one finding that narrows the differential. Medicine vignettes test pattern recognition: specific lab values, imaging findings, or symptom clusters that point to one diagnosis. Practice 30-40 vignettes daily to build speed.
Yes, heavily. Drug-of-choice questions for hypertension, diabetes, heart failure, infections, and autoimmune diseases are tagged as Medicine but test Pharmacology knowledge. Study drug tables alongside disease management protocols — they are tested as integrated clinical decisions.
Build the ABG interpretation algorithm once and practice applying it to 20 clinical scenarios. For electrolytes, master the ECG changes of hypo/hyperkalemia and hypo/hypercalcemia — these are the most tested correlations. Use tables for normal ranges and clinical features.
In the final two weeks, revise classification tables — NYHA for heart failure, CKD staging, WHO classification of lymphomas, DM complications. Solve 40 medicine MCQs daily under timed conditions. Focus on drug-of-choice tables and diagnostic criteria rather than pathophysiology narratives.
Medicine deserves 25-30% of your total clinical subject time. For a 6-month plan, that is roughly 4-5 weeks of dedicated medicine study plus ongoing integration through clinical vignettes. The breadth is wide but the high-yield core is concentrated in 8 systems.
Start your medicine prep today. Open the Medicine subject page and solve your first 15 MCQs — the clinical patterns you drill now are the patterns you will recognize on exam day.
See our pricing plans for unlimited practice across all 19 subjects.
Written by: NEETPGAI Editorial Team Reviewed by: Dr. SME Agent, NEETPGAI Medical Advisory Board Last reviewed: April 2026
This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.