NEET PG Internal Medicine Syllabus

Internal Medicine syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Internal Medicine in NEET PG, not a summary of it.

1. 1

   Ischemic heart disease

   3 topics

   • Acute coronary syndrome
     • STEMI
     • NSTEMI
     • Unstable angina
   • Stable angina
   • Chronic ischemic heart disease
2. 2

   Asthma

   4 topics

   • Pathophysiology
   • Clinical Features
   • Diagnosis
   • Management
     • Inhaled Corticosteroids
     • Bronchodilators
     • Biologics
3. 3

   Gastroenterology

   5 topics

   • Gastrointestinal bleeding
     • Upper gastrointestinal bleeding (peptic ulcer disease, esophageal varices)
     • Lower gastrointestinal bleeding (diverticulosis, colorectal cancer)
   • Liver diseases
     • Hepatitis (viral hepatitis, alcoholic hepatitis)
     • Cirrhosis
     • Non-alcoholic fatty liver disease (NAFLD)
     • Hepatocellular carcinoma
   • Inflammatory bowel disease (IBD)
     • Crohn's disease
     • Ulcerative colitis
   • Gastrointestinal infections
     • Gastroenteritis (viral, bacterial)
     • Clostridium difficile infection
     • Parasitic infections
   • Pancreatic diseases
     • Acute pancreatitis
     • Chronic pancreatitis
     • Pancreatic cancer
4. 4

   Acute kidney injury (AKI)

   6 topics

   • Prerenal causes of AKI
   • Intrinsic causes of AKI
   • Postrenal causes of AKI
   • Clinical features of AKI
   • Diagnosis of AKI
   • Management of AKI
5. 5

   Diabetes mellitus

   5 topics

   • Type 1 diabetes
   • Type 2 diabetes
   • Diabetic ketoacidosis (DKA)
   • Hyperosmolar hyperglycemic state (HHS)
   • Diabetic complications
     • Retinopathy
     • Nephropathy
     • Neuropathy
6. 6

   Anemia

   4 topics

   • Iron deficiency anemia
   • Megaloblastic anemia
     • Vitamin B12 deficiency
     • Folate deficiency
   • Hemolytic anemia
     • Autoimmune hemolytic anemia
     • Hereditary spherocytosis
   • Aplastic anemia
7. 7

   Infectious Diseases

   5 topics

   • Bacterial Infections
     • Sepsis
     • Pneumonia (community-acquired)
     • Pneumonia (hospital-acquired)
     • Urinary Tract Infection (UTI)
     • Skin and Soft Tissue Infections
     • Tuberculosis
   • Viral Infections
     • Human Immunodeficiency Virus (HIV)
     • Viral Hepatitis (Hepatitis B)
     • Viral Hepatitis (Hepatitis C)
     • Influenza
     • Herpes Simplex Virus (HSV)
     • Varicella-Zoster Virus (VZV)
   • Fungal Infections
     • Candidiasis
     • Aspergillosis
     • Cryptococcosis
     • Histoplasmosis
   • Parasitic Infections
     • Malaria
     • Leishmaniasis
     • Toxoplasmosis
     • Schistosomiasis
   • Antimicrobial Therapy
     • Antibiotics (Penicillins)
     • Antibiotics (Cephalosporins)
     • Antibiotics (Fluoroquinolones)
     • Antifungals
     • Antivirals
     • Antiparasitic Drugs
8. 8

   Rheumatology

   4 topics

   • Rheumatoid arthritis
     • Pathophysiology
     • Clinical features
     • Diagnosis (rheumatoid factor, anti-CCP antibodies)
     • Management (disease-modifying antirheumatic drugs, biologics)
   • Systemic lupus erythematosus (SLE)
     • Clinical features
     • Diagnosis (antinuclear antibodies, anti-dsDNA antibodies)
     • Management (corticosteroids, immunosuppressants)
   • Spondyloarthropathies
     • Ankylosing spondylitis
     • Psoriatic arthritis
     • Reactive arthritis
     • Enteropathic arthritis
   • Vasculitis
     • Giant cell arteritis
     • Takayasu arteritis
     • Polyarteritis nodosa
     • Granulomatosis with polyangiitis (Wegener's granulomatosis)
9. 9

   Geriatrics

   3 topics

   • Geriatric syndromes
     • Falls
     • Delirium
     • Dementia
     • Urinary incontinence
     • Frailty
   • Polypharmacy
     • Rational prescribing in elderly patients
     • Drug interactions
     • Adverse drug reactions
   • Geriatric assessment
     • Comprehensive geriatric assessment (CGA)
     • Functional assessment
     • Cognitive assessment
10. 10

    Vaccinations

    3 topics

    • Childhood vaccinations
      • DTaP
      • MMR
      • Varicella
    • Adult vaccinations
      • Influenza
      • Pneumococcal
      • Herpes Zoster
    • Travel vaccinations

Internal Medicine flashcards for NEET PG

19 of 50 cards from the Internal Medicine deck — real questions with worked answers.

1. What ECG and biomarker findings distinguish STEMI, NSTEMI, and unstable angina in acute coronary syndrome (ACS)?

   STEMI: persistent ST-elevation (or new LBBB) with elevated troponin (transmural ischemia). NSTEMI: ST-depression/T-inversion or no ECG change WITH elevated troponin (subendocardial infarct). Unstable angina: ischemic symptoms at rest/crescendo with possible ST-depression but NORMAL troponin (no necrosis).

2. What is the pathophysiologic basis of acute coronary syndrome versus stable angina?

   ACS is caused by acute disruption (rupture/erosion) of an atherosclerotic plaque triggering thrombus formation and abrupt reduction in coronary flow. Stable angina results from a fixed atherosclerotic stenosis causing demand-supply mismatch only on exertion, without acute plaque rupture or thrombosis.

3. How are stable angina and unstable angina clinically distinguished?

   Stable angina: predictable chest discomfort provoked by a consistent level of exertion/stress, relieved within minutes by rest or nitroglycerin. Unstable angina: new-onset angina, angina at rest, or angina that is increasing in frequency/severity/duration (crescendo) — it is part of ACS and signals an unstable plaque.

4. What is the first-line antianginal therapy and key prognostic medications for chronic stable ischemic heart disease?

   Symptom relief: beta-blockers (first-line), plus nitrates and calcium-channel blockers. Prognosis-improving (mortality reduction): aspirin (antiplatelet), high-intensity statin, ACE inhibitors (esp. with LV dysfunction/diabetes), and risk-factor control. Revascularization for refractory symptoms or high-risk anatomy.

5. What is the immediate medical management ('MONA-BASH') of acute STEMI plus the definitive reperfusion strategy?

   Aspirin + a P2Y12 inhibitor (dual antiplatelet), anticoagulation (heparin), nitrates, oxygen if hypoxic, beta-blocker, statin, and morphine for pain. Definitive: primary PCI within 90 minutes (preferred); if unavailable, fibrinolysis within 30 minutes (door-to-needle) when no contraindication.

6. What are the most common causes of upper versus lower gastrointestinal bleeding?

   Upper GI bleed (proximal to ligament of Treitz): peptic ulcer disease (most common), esophageal varices, Mallory-Weiss tear, gastritis/esophagitis. Lower GI bleed: diverticulosis (most common in adults), angiodysplasia, colorectal cancer, hemorrhoids, ischemic colitis, IBD.

7. How do melena and hematochezia help localize a GI bleed?

   Melena (black, tarry, foul stool) indicates blood that has been digested — usually an UPPER GI source (or slow right colon bleed). Hematochezia (fresh/maroon blood per rectum) usually indicates a LOWER GI source, but can occur with a brisk, massive upper GI bleed causing hemodynamic instability.

8. What is the management priority and key risk-stratification tool in acute upper GI bleeding?

   Priority is resuscitation: two large-bore IV lines, fluids/blood transfusion, restrictive transfusion target (Hb ~7 g/dL). Then urgent endoscopy (within 24 h) for diagnosis and therapy. Glasgow-Blatchford score risk-stratifies need for intervention; give IV PPI for ulcers and IV octreotide + antibiotics for variceal bleeds.

9. What are the classic causes and stigmata of cirrhosis (chronic liver disease)?

   Causes: alcohol, chronic viral hepatitis (B, C), non-alcoholic fatty liver disease (NAFLD/NASH), autoimmune, hemochromatosis, Wilson disease. Stigmata: jaundice, spider angiomata, palmar erythema, gynecomastia, caput medusae, ascites, splenomegaly, asterixis, and clubbing.

10. What pattern of liver function tests distinguishes hepatocellular from cholestatic liver injury?

    Hepatocellular pattern: predominant rise in AST/ALT (transaminases) with relatively mild ALP elevation (e.g. viral/toxic hepatitis). Cholestatic pattern: predominant rise in alkaline phosphatase and GGT with mild transaminase rise and conjugated hyperbilirubinemia (e.g. biliary obstruction, PBC).

11. How is hepatic encephalopathy managed?

    Treat precipitants (GI bleed, infection/SBP, constipation, electrolyte disturbance, sedatives). Lactulose (reduces ammonia absorption, titrate to 2-3 soft stools/day) is first-line; rifaximin (non-absorbable antibiotic) is added for recurrent episodes.

12. What are the key differences between Crohn disease and ulcerative colitis in inflammatory bowel disease?

    Crohn: any site mouth-to-anus (esp. terminal ileum), skip lesions, transmural inflammation, fistulae/strictures, non-caseating granulomas, 'cobblestoning'. Ulcerative colitis: continuous involvement from rectum proximally (colon only), mucosal/submucosal inflammation, no granulomas, bloody diarrhea, risk of toxic megacolon and colorectal cancer.

13. What is the stepwise medical therapy for moderate-to-severe inflammatory bowel disease?

    5-ASA (aminosalicylates, mainly for mild UC), corticosteroids for acute flares (not maintenance), immunomodulators (azathioprine, methotrexate), and biologics (anti-TNF like infliximab/adalimumab, anti-integrin vedolizumab, anti-IL-12/23 ustekinumab) for moderate-severe/steroid-dependent disease.

14. What are the common bacterial causes of gastrointestinal infection and their hallmark features?

    Inflammatory/invasive (bloody, fever): Shigella, Salmonella, Campylobacter, enteroinvasive/enterohemorrhagic E. coli (EHEC O157:H7 → HUS). Non-inflammatory (watery): Vibrio cholerae (rice-water stools), enterotoxigenic E. coli (traveler's diarrhea), Staph aureus toxin (rapid onset). Campylobacter is linked to Guillain-Barre syndrome.

15. What is the diagnostic criterion and management of Clostridioides difficile colitis?

    Diagnosis: stool test for C. difficile toxin/PCR in a patient with recent antibiotics and diarrhea (pseudomembranes on colonoscopy). Management: stop the offending antibiotic; oral vancomycin or fidaxomicin first-line; fecal microbiota transplant for recurrent disease. Metronidazole only if others unavailable.

16. How are acute and chronic pancreatitis distinguished, and what are the main causes?

    Acute pancreatitis: sudden epigastric pain radiating to back, raised lipase/amylase (>3x normal); main causes GALLSTONES and ALCOHOL (also hypertriglyceridemia, ERCP, drugs). Chronic pancreatitis: irreversible fibrosis → exocrine (steatorrhea) and endocrine (diabetes) insufficiency, pancreatic calcifications; main cause is chronic alcohol use.

17. What scoring/criteria assess severity in acute pancreatitis and what is initial management?

    Severity: Ranson criteria, APACHE II, BISAP, or CT severity index; persistent organ failure defines severe disease. Management: aggressive IV fluid resuscitation, analgesia, early enteral nutrition, treat the cause (ERCP for gallstone pancreatitis with cholangitis); antibiotics only for infected necrosis.

18. What are the prerenal causes of acute kidney injury (AKI) and the characteristic urine findings?

    Prerenal AKI = renal hypoperfusion with intact tubules: hypovolemia (hemorrhage, diarrhea, vomiting), hypotension/sepsis, heart failure, hepatorenal syndrome, renal artery stenosis, and NSAIDs/ACE inhibitors. Findings: BUN:Cr >20:1, FENa <1%, urine osmolality >500, low urine sodium (<20), bland sediment.

19. What are the intrinsic (renal) causes of AKI?

    Acute tubular necrosis (most common — ischemic or nephrotoxic from aminoglycosides, contrast, rhabdomyolysis), acute interstitial nephritis (drug allergy → eosinophiluria), glomerulonephritis, and vascular causes (TTP/HUS, vasculitis, atheroemboli). ATN shows FENa >2% and muddy-brown granular casts.

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