🇮🇳 NEET PG · subject

NEET PG Internal Medicine Syllabus

The Internal Medicine syllabus for NEET PG in full: 10 chapters, 42 topics and 85 sub-topics, every one listed below, plus 50 Internal Medicine flashcards with answers.

10Chapters
42Topics
85Sub-topics
50Flashcards

Internal Medicine syllabus: all 10 chapters

Expand any chapter to see its topics and sub-topics.

  1. Ischemic heart disease

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

    4 topics
    • Pathophysiology
    • Clinical Features
    • Diagnosis
    • Management
      • Inhaled Corticosteroids
      • Bronchodilators
      • Biologics
  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. 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. Diabetes mellitus

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

    4 topics
    • Iron deficiency anemia
    • Megaloblastic anemia
      • Vitamin B12 deficiency
      • Folate deficiency
    • Hemolytic anemia
      • Autoimmune hemolytic anemia
      • Hereditary spherocytosis
    • Aplastic anemia
  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. 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. 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. Vaccinations

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

NEET PG Internal Medicine flashcards — 50 questions with 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.

  20. What are the postrenal causes of AKI and the key diagnostic test?

    Postrenal AKI = obstruction to urine flow: bladder outlet obstruction (BPH, prostate cancer), bilateral ureteric obstruction (stones, tumor, retroperitoneal fibrosis), neurogenic bladder. Bilateral obstruction (or unilateral in a solitary kidney) is needed for AKI. Diagnose with renal ultrasound showing hydronephrosis; relieve with catheter/nephrostomy.

Show the other 30 Internal Medicine flashcards
  1. What are the clinical features and complications of acute kidney injury?

    Often oliguria (<400 mL/day) or anuria, rising creatinine/urea. Complications: fluid overload/pulmonary edema, HYPERKALEMIA (most dangerous), metabolic acidosis, hyperphosphatemia/hypocalcemia, uremia (encephalopathy, pericarditis, platelet dysfunction).

  2. What are the indications for emergency dialysis in AKI (mnemonic AEIOU)?

    A — severe metabolic Acidosis refractory to therapy; E — Electrolyte disturbance, especially refractory Hyperkalemia; I — Intoxication (dialyzable poisons: salicylates, lithium, methanol, ethylene glycol); O — fluid Overload refractory to diuretics; U — Uremic complications (pericarditis, encephalopathy, bleeding).

  3. What is the general supportive management of AKI?

    Identify and treat the cause; optimize volume status and renal perfusion; STOP nephrotoxic drugs (NSAIDs, ACEi/ARB, aminoglycosides, contrast); adjust drug doses to renal function; correct hyperkalemia and acidosis; treat hyperkalemia urgently; and initiate dialysis for AEIOU indications.

  4. How is the pathophysiology of type 1 diabetes different from type 2 diabetes?

    Type 1: autoimmune destruction of pancreatic beta cells → ABSOLUTE insulin deficiency (anti-GAD/islet antibodies, HLA-associated, ketosis-prone). Type 2: insulin resistance with relative insulin deficiency and progressive beta-cell dysfunction, strongly linked to obesity and metabolic syndrome; not autoimmune and less ketosis-prone.

  5. What are the diagnostic glycemic thresholds for diabetes mellitus?

    Any one: fasting plasma glucose >=126 mg/dL (7.0 mmol/L); 2-hour OGTT glucose >=200 mg/dL (11.1 mmol/L); HbA1c >=6.5%; or random glucose >=200 mg/dL with classic symptoms. Asymptomatic results need confirmation on a repeat test.

  6. What is the first-line and stepwise pharmacologic management of type 2 diabetes?

    Lifestyle modification plus METFORMIN first-line. Add agents with cardio-renal benefit: SGLT2 inhibitors (heart failure/CKD) and GLP-1 agonists (ASCVD, weight loss). Other agents: sulfonylureas, DPP-4 inhibitors, pioglitazone; insulin when other agents fail or glucose is very high.

  7. What are the diagnostic criteria and key management steps for diabetic ketoacidosis (DKA)?

    Triad: hyperglycemia (>250 mg/dL), high anion-gap metabolic acidosis (pH <7.3, HCO3 <18), and ketonemia/ketonuria. Management: aggressive IV fluids first, then IV regular insulin infusion, and POTASSIUM replacement (insulin drives K+ into cells). Find and treat the precipitant (infection, missed insulin).

  8. How does hyperosmolar hyperglycemic state (HHS) differ from DKA?

    HHS occurs in type 2 diabetes: profound hyperglycemia (often >600 mg/dL), severe hyperosmolarity (>320 mOsm/kg), and marked dehydration with altered mental status, but MINIMAL or NO ketosis/acidosis (residual insulin prevents ketogenesis). It has higher mortality; treatment is aggressive fluids, insulin, and electrolyte correction.

  9. What are the microvascular and macrovascular complications of diabetes?

    Microvascular: retinopathy, nephropathy (microalbuminuria → CKD), and neuropathy (peripheral sensory, autonomic). Macrovascular: coronary artery disease, stroke, and peripheral arterial disease. Also diabetic foot ulcers and increased infection risk. Tight glycemic and BP control plus ACEi/ARB and statins reduce complications.

  10. What are the laboratory findings and causes of iron deficiency anemia?

    Microcytic, hypochromic anemia with LOW ferritin, low serum iron, HIGH total iron-binding capacity (TIBC), and low transferrin saturation. Causes: chronic blood loss (GI bleeding, menorrhagia), inadequate intake, malabsorption, increased demand (pregnancy). In older adults, occult GI malignancy must be excluded.

  11. What distinguishes vitamin B12 deficiency from folate deficiency in megaloblastic anemia?

    Both cause macrocytic anemia with hypersegmented neutrophils and high MCV. B12 (cobalamin) deficiency ALSO causes neurological signs (subacute combined degeneration of the cord, paresthesias) and methylmalonic acid is elevated. Folate deficiency has no neuro signs and normal methylmalonic acid; both have elevated homocysteine.

  12. What laboratory findings indicate hemolytic anemia and how are causes classified?

    Findings: elevated indirect (unconjugated) bilirubin, raised LDH, LOW haptoglobin, reticulocytosis. Intravascular hemolysis adds hemoglobinuria. Classification: intrinsic (hereditary — G6PD deficiency, hereditary spherocytosis, sickle cell, thalassemia) vs extrinsic/acquired (autoimmune — positive direct Coombs test, microangiopathic, infections).

  13. What is the pathophysiology and characteristic finding of aplastic anemia?

    Aplastic anemia is bone marrow failure from stem-cell injury (idiopathic/autoimmune, drugs, radiation, viruses, benzene) causing PANCYTOPENIA (anemia, leukopenia, thrombocytopenia) with reticulocytopenia. Bone marrow biopsy shows a HYPOCELLULAR marrow replaced by fat, with no infiltration or fibrosis.

  14. Give examples of bacteria classified by Gram stain and oxygen requirement that are high-yield in internal medicine.

    Gram-positive cocci: Staphylococcus (catalase+), Streptococcus/Enterococcus (catalase-). Gram-negative rods: E. coli, Klebsiella, Pseudomonas (aerobe). Anaerobes: Clostridium, Bacteroides. Atypicals (no cell wall/intracellular): Mycoplasma, Chlamydia, Legionella. Acid-fast: Mycobacterium tuberculosis.

  15. What are the key features of viral hepatitis B versus hepatitis C?

    Hepatitis B: DNA virus, transmitted parenterally/sexually/perinatally; HBsAg = active infection, anti-HBs = immunity, HBeAg = high infectivity; vaccine available. Hepatitis C: RNA virus, mainly bloodborne (IV drug use); high rate of CHRONIC infection and cirrhosis/HCC; NO vaccine but curable with direct-acting antivirals.

  16. What are common fungal infections and their first-line treatments?

    Candidiasis (oral/esophageal/invasive) — fluconazole or echinocandin for invasive disease. Aspergillosis — voriconazole. Cryptococcal meningitis (HIV) — amphotericin B + flucytosine then fluconazole. Pneumocystis jirovecii pneumonia (immunocompromised) — TMP-SMX. Dermatophytes — topical/oral azoles or terbinafine.

  17. What are major parasitic infections relevant to internal medicine and their hallmark features?

    Malaria (Plasmodium, cyclical fever, thick/thin smear) — artemisinin-based therapy. Amebiasis (Entamoeba histolytica) — bloody dysentery + liver abscess, metronidazole. Giardiasis — foul fatty diarrhea, metronidazole. Helminths cause eosinophilia. Visceral leishmaniasis (kala-azar) — fever, splenomegaly, pancytopenia.

  18. What principles guide rational antimicrobial therapy?

    Use empiric therapy based on likely organisms and local resistance, then DE-ESCALATE to targeted therapy once cultures/sensitivities return. Choose narrowest effective spectrum, correct dose/route/duration, consider tissue penetration and organ function, obtain cultures BEFORE antibiotics when possible, and practice stewardship to limit resistance.

  19. What are the diagnostic and clinical features of rheumatoid arthritis?

    Chronic symmetric inflammatory polyarthritis of small joints (MCP, PIP, wrists) with prolonged morning stiffness (>1 hour), sparing the DIP joints. Serology: rheumatoid factor and anti-CCP (more specific). Deformities: ulnar deviation, swan-neck, boutonniere. Treated with DMARDs (methotrexate first-line) and biologics.

  20. What are the classic clinical and serologic features of systemic lupus erythematosus (SLE)?

    Multisystem autoimmune disease: malar (butterfly) rash, photosensitivity, oral ulcers, arthritis, serositis, lupus nephritis, cytopenias, neuropsychiatric features. Serology: ANA (sensitive, screening), anti-dsDNA and anti-Smith (specific). Anti-dsDNA and low complement (C3/C4) track disease/nephritis activity.

  21. What defines the spondyloarthropathies and their shared features?

    A group including ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and IBD-associated arthritis. Shared features: HLA-B27 association, SERONEGATIVE (RF-negative), axial/sacroiliac involvement, enthesitis, dactylitis, and extra-articular features (uveitis, mucocutaneous lesions). AS shows 'bamboo spine' on imaging.

  22. How are the vasculitides classified by vessel size with key examples?

    Large-vessel: giant cell (temporal) arteritis, Takayasu arteritis. Medium-vessel: polyarteritis nodosa, Kawasaki disease. Small-vessel ANCA-associated: granulomatosis with polyangiitis (c-ANCA/PR3), eosinophilic GPA and microscopic polyangiitis (p-ANCA/MPO). Immune-complex small-vessel: IgA vasculitis (Henoch-Schonlein).

  23. What are the common geriatric syndromes ('the geriatric giants')?

    Multifactorial conditions in the elderly: falls, frailty, delirium (acute confusion), dementia, urinary incontinence, immobility, pressure ulcers, polypharmacy, sensory impairment, and malnutrition. They share multiple contributing causes and require comprehensive rather than single-disease management.

  24. What is polypharmacy and what tools help reduce inappropriate prescribing in the elderly?

    Polypharmacy is the concurrent use of multiple medications (commonly >=5), raising risks of adverse drug events, interactions, falls, and non-adherence. Tools: the BEERS Criteria (potentially inappropriate medications in older adults) and STOPP/START criteria (drugs to stop and beneficial drugs to start) guide deprescribing.

  25. What is comprehensive geriatric assessment (CGA)?

    A multidimensional, interdisciplinary evaluation of an older person's medical, functional (ADLs/IADLs), cognitive (e.g. MMSE/MoCA), psychological (mood/depression), nutritional, and social/environmental domains. It produces a coordinated care plan to maximize function and independence, reducing hospitalization and institutionalization.

  26. What are the live versus inactivated vaccines important in the childhood schedule?

    Live attenuated: BCG, oral polio (OPV), MMR, varicella, rotavirus, yellow fever (contraindicated in pregnancy and significant immunocompromise). Inactivated/subunit/toxoid: DPT, inactivated polio (IPV), hepatitis B, Hib, pneumococcal conjugate, inactivated influenza, and HPV.

  27. What are the key recommended adult vaccinations?

    Influenza (annual), Td/Tdap (tetanus booster every 10 years, one Tdap), pneumococcal (PCV/PPSV23 for elderly and high-risk), hepatitis B, HPV (up to recommended age), zoster (shingles) vaccine for older adults, and MMR/varicella catch-up if non-immune.

  28. Which vaccines are commonly required or recommended for international travelers?

    Yellow fever (mandatory for endemic regions, certificate required), typhoid, hepatitis A and B, oral cholera, rabies (pre-exposure for high-risk), Japanese encephalitis, and meningococcal (mandatory for Hajj pilgrims). Routine vaccines should also be up to date; malaria needs chemoprophylaxis, not a vaccine routinely.

  29. What ECG leads localize an inferior wall myocardial infarction and which coronary artery is usually involved?

    Inferior MI shows ST changes in leads II, III, and aVF, most commonly from occlusion of the RIGHT CORONARY ARTERY. It may be associated with right ventricular infarction (so avoid nitrates/preload reduction) and with bradyarrhythmias/heart block.

  30. What is the calculation for the fractional excretion of sodium (FENa) and how is it interpreted in AKI?

    FENa (%) = (urine Na x plasma creatinine) / (plasma Na x urine creatinine) x 100. FENa <1% suggests PRERENAL AKI (avid sodium retention with intact tubules); FENa >2% suggests intrinsic AKI such as acute tubular necrosis. (Unreliable if the patient is on diuretics.)

Same Internal Medicine syllabus in other exams

The Internal Medicine outline above is identical in these 3 exams:

NEET PG Internal Medicine FAQ

What is in the NEET PG Internal Medicine syllabus?

NEET PG Internal Medicine is split into 10 chapters: Ischemic heart disease, Asthma, Gastroenterology, Acute kidney injury (AKI), Diabetes mellitus, Anemia, Infectious Diseases, Rheumatology, Geriatrics and Vaccinations. Together they contain 42 topics and 85 sub-topics.

How many chapters are in NEET PG Internal Medicine?

10 chapters, containing 42 topics and 85 sub-topics. The largest chapter is Acute kidney injury (AKI), with 6 topics.

Are there flashcards for NEET PG Internal Medicine?

Yes — a 50-card Internal Medicine deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.