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Explain in detail about each topics given in the pic and provide details as much to understand and clear neet pg

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Given the large scope (5 subjects with many sub-topics each), I'll organize this into a detailed, NEET PG-focused masterclass. Let me search the medical library for the highest-yield topics across all 5 subjects simultaneously.
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I now have excellent material from authoritative textbooks. Let me compile the comprehensive NEET PG masterclass.Here is your complete NEET PG masterclass covering all 5 high-yield subjects from the images. Each section is written to give you conceptual clarity + exam-ready facts.

NEET PG HIGH-YIELD MASTERCLASS


1. SURGERY (30-32 Questions)

Surgery is the single largest contributor to NEET PG. Integrate with radiology for image-based MCQs.

TRAUMA

ATLS Primary Survey - ABCDE:
  • Airway with C-spine protection
  • Breathing and ventilation
  • Circulation with hemorrhage control
  • Disability (neurological)
  • Exposure
Shock Classification (Most tested):
ClassBlood LossHRBPUrine Output
I<750 mL (<15%)<100Normal>30 mL/hr
II750-1500 mL (15-30%)100-120Normal20-30 mL/hr
III1500-2000 mL (30-40%)120-140Decreased5-15 mL/hr
IV>2000 mL (>40%)>140Very lowNegligible
Key trauma MCQ facts:
  • Damage control resuscitation = permissive hypotension + massive transfusion protocol (1:1:1 ratio - PRBCs : FFP : Platelets)
  • FAST exam: fluid in Morrison's pouch, perisplenic, pericardial, pelvic
  • Tension pneumothorax: needle decompression at 2nd ICS midclavicular line BEFORE chest X-ray
  • Flail chest = paradoxical breathing, requires positive pressure ventilation
  • Splenic injury: Grade I-II can be observed; Grade III-V needs intervention
  • Zone I neck injury (below cricoid): always explore surgically
  • FAST-negative + hemodynamically unstable = laparotomy
Burns:
  • Rule of Nines: Head 9%, each arm 9%, each leg 18%, anterior trunk 18%, posterior trunk 18%, perineum 1%
  • Parkland formula: 4 mL x body weight (kg) x %BSA burned (Ringer's lactate - half in first 8 hrs, half in next 16 hrs)
  • Full thickness (3rd degree): dry, leathery, painless, requires grafting
  • Curling's ulcer = stress ulcer after burns (gastric)

HERNIA

Types and key features:
TypeLocationKey fact
Indirect inguinalLateral to inferior epigastric vessels, through deep ringMost common hernia overall; congenital patent processus vaginalis
Direct inguinalMedial to inferior epigastric vessels, through Hesselbach's triangleAcquired, weakness of posterior wall
FemoralBelow inguinal ligament, medial to femoral veinMost common in women; highest strangulation risk
UmbilicalThrough umbilicusMost common hernia in infants
ParaumbilicalBeside umbilicusAdults, obese women
Hesselbach's triangle boundaries:
  • Medial: lateral border of rectus abdominis
  • Lateral: inferior epigastric vessels
  • Inferior: inguinal ligament
Complications of hernia (in order of seriousness):
  1. Reducible - can be pushed back
  2. Irreducible (incarcerated) - cannot be reduced, no vascular compromise yet
  3. Obstructed - bowel contents cannot pass
  4. Strangulated - blood supply cut off = EMERGENCY (most feared)
Richter's hernia: Only one wall of bowel herniates - can strangulate WITHOUT obstruction (no distension!)
Littre's hernia: Contains Meckel's diverticulum
Maydl's hernia (W hernia): Double loop in sac - middle loop inside abdomen is the first to strangulate
Surgical repair:
  • Lichtenstein (tension-free mesh repair) = gold standard for adults
  • Laparoscopic (TEP/TAPP) = bilateral hernias, recurrent hernias
  • Bassini / Shouldice = tissue repair (no mesh)

GENITOURINARY SYSTEM

Renal Trauma (AAST Classification):
  • Grade I: contusion/subcapsular hematoma - observe
  • Grade II: laceration <1 cm - observe
  • Grade III: laceration >1 cm - observe
  • Grade IV: collecting system involved - may need intervention
  • Grade V: shattered kidney or renal pedicle - surgery
BPH (Benign Prostatic Hyperplasia):
  • Zone involved: Transitional zone
  • Prostate cancer: Peripheral zone
  • PSA >4 ng/mL = suspicious
  • Medical treatment: Alpha-1 blockers (tamsulosin) + 5-alpha reductase inhibitors (finasteride)
  • Surgical: TURP (gold standard); open prostatectomy if >80g
Bladder Cancer:
  • Most common histology: Transitional cell carcinoma (TCC/urothelial)
  • Painless hematuria = most common presentation
  • Risk factors: Smoking (most common), aniline dyes, cyclophosphamide, schistosomiasis (squamous cell)
  • Diagnosis: Cystoscopy + biopsy
Testicular Cancer:
  • Painless testicular swelling in young males
  • Most common type: Seminoma (most common) vs. Non-seminoma (NSGCT - teratoma, embryonal, yolk sac, choriocarcinoma)
  • Seminoma = radiosensitive
  • AFP elevated in yolk sac tumor, NOT in pure seminoma
  • hCG elevated in choriocarcinoma

ARTERIES & VEINS

Buerger's Disease (Thromboangiitis Obliterans):
  • Young male smokers
  • Affects small/medium vessels
  • Presents with claudication, rest pain, digital gangrene
  • Treatment: Absolute smoking cessation
Varicose Veins:
  • Long saphenous vein most common
  • Trendelenburg test: identifies saphenofemoral incompetence
  • Complications: DVT, bleeding, lipodermatosclerosis, venous ulcer (gaiter area = medial lower 1/3 leg)
  • Treatment: EVLA (endovenous laser ablation), sclerotherapy, surgery (Trendelenburg operation + stripping)
DVT - Virchow's Triad:
  • Stasis + Endothelial damage + Hypercoagulability
  • Homan's sign: calf pain on dorsiflexion (unreliable)
  • Investigation: Doppler USS (first line), D-dimer, venography
  • Treatment: LMWH/DOAC; thrombolysis for massive PE
Aortic Aneurysm:
  • AAA >3 cm = aneurysm; >5.5 cm = repair
  • Risk: smoking, hypertension, male, family history
  • Rupture triad: sudden severe back/abdominal pain + hypotension + pulsatile abdominal mass
  • Endovascular repair (EVAR) preferred in unfit patients; open repair in fit patients

HEPATOBILIARY SURGERY

Gallstones (Cholelithiasis):
  • Types: Cholesterol (80%, radiolucent), Pigment (black = hemolysis; brown = infection)
  • Murphy's sign: pain on inspiration with pressure at gallbladder fossa
  • Mirizzi syndrome: common hepatic duct compressed by stone in Hartmann's pouch
  • Courvoisier's law: Palpable gallbladder + jaundice = NOT gallstones (likely malignancy)
  • Treatment: Laparoscopic cholecystectomy; ERCP for CBD stones
Gallbladder Cancer:
  • Most common type: Adenocarcinoma
  • Porcelain gallbladder = risk factor
  • Most common site: fundus
  • Spread: direct to liver (most common)
Liver Tumors:
  • HCC: Associated with cirrhosis, HBV, HCV; AFP raised; arterial enhancement + washout on CT
  • Hepatic hemangioma: Most common benign tumor; "fill-in" on delayed CT
  • FNH: Central scar on imaging; no malignant potential
Pancreatitis:
  • Most common cause worldwide: Gallstones; in India: alcohol
  • Ranson criteria (at admission): Age >55, WBC >16,000, glucose >200, LDH >350, AST >250
  • At 48 hrs: Hematocrit fall >10%, BUN rise >5, Ca <8 mg/dL, PaO2 <60, base deficit >4, fluid sequestration >6L
  • Modified Glasgow (BISAP) also used
  • Pseudocyst: collection of pancreatic juice - treat if symptomatic (>6 weeks)
  • Necrotizing pancreatitis: most feared complication; infected necrosis = surgery/drainage

GIT SURGERY

Appendicitis:
  • McBurney's point: 1/3rd from ASIS on line to umbilicus
  • Rovsing's sign: RIF pain on pressing LIF
  • Psoas sign: pain on extending right thigh (retrocecal appendix)
  • Obturator sign: pain on internal rotation of flexed right thigh (pelvic appendix)
  • Alvarado score: >7 = appendicitis likely
  • Treatment: Laparoscopic appendicectomy
Colorectal Cancer:
  • Right-sided colon: bleeding + anemia + weight loss (no obstruction early)
  • Left-sided colon: obstruction + change in bowel habits + "apple-core" on barium enema
  • Staging (Duke's/TNM): T staging determines surgical approach
  • Screening: Colonoscopy at 50 years (average risk)
  • FAP: APC gene mutation, >100 polyps, 100% malignancy risk, prophylactic colectomy
  • HNPCC (Lynch syndrome): MLH1, MSH2 mutation; right-sided colon Ca; most common hereditary CRC
Peptic Ulcer Disease:
  • Duodenal ulcer (DU): H. pylori >90%; pain relieved by food (night pain); more common
  • Gastric ulcer (GU): NSAIDs, H. pylori; pain worsened by food
  • Complications: Bleeding (most common), perforation, obstruction
  • Perforation: Air under diaphragm on X-ray; emergency laparotomy
  • Triple therapy: PPI + Amoxicillin + Clarithromycin

BARIATRIC SURGERY (Recent Favorite)

Indications:
  • BMI ≥40 kg/m²
  • BMI ≥35 kg/m² with obesity-related comorbidities (T2DM, HTN, OSA, etc.)
  • BMI ≥30 kg/m² with uncontrolled T2DM (metabolic surgery)
Procedures:
ProcedureMechanismKey fact
Sleeve gastrectomyRestrictiveRemoves fundus; reduces ghrelin
Roux-en-Y Gastric BypassRestrictive + MalabsorptiveGold standard; best for T2DM remission
Laparoscopic Adjustable Gastric BandRestrictiveReversible
Biliopancreatic DiversionMalabsorptiveMaximum weight loss
Complications post-bariatric surgery:
  • Dumping syndrome (early/late)
  • Nutritional deficiencies: Iron, B12, Folate, Vitamin D, Calcium
  • Wernicke's encephalopathy (B1 deficiency)

TRANSPLANT SURGERY (Recent Favorite)

Types of rejection:
TypeTimingMechanismTreatment
HyperacuteMinutes to hoursPre-formed antibodiesNo treatment; prevention only
AcuteDays to weeksT-cell mediatedHigh-dose steroids, anti-thymocyte globulin
ChronicMonths to yearsAntibody + T-cellNo effective treatment; re-transplant
Immunosuppression protocol:
  • Induction: Basiliximab (anti-IL-2R) or Anti-thymocyte globulin
  • Maintenance triple therapy: Tacrolimus + Mycophenolate mofetil + Prednisolone
  • Cyclosporine: Nephrotoxicity, gingival hyperplasia, hirsutism
  • Tacrolimus: More potent; neurotoxicity + nephrotoxicity; does NOT cause gingival hyperplasia
Brain death criteria (for cadaveric donation):
  • Fixed dilated pupils
  • Absent brainstem reflexes (corneal, gag, oculocephalic)
  • Apnea test positive
  • Two consultants, minimum 6 hours apart

2. MICROBIOLOGY (20-22 Questions)


MYCOLOGY (4-5 Questions)

Classification of Fungi:
  • Yeast: unicellular (Candida, Cryptococcus)
  • Mold: multicellular filamentous (Aspergillus, Mucor, Rhizopus)
  • Dimorphic: yeast in body (37°C), mold in environment (25°C) - "Body heat makes them yeast"
Dimorphic fungi mnemonic - "CHBS MBP":
  • Coccidioides immitis
  • Histoplasma capsulatum
  • Blastomyces dermatitidis
  • Sporothrix schenckii
  • Malassezia furfur (partially)
  • Paracoccidioides brasiliensis
  • Penicillium marneffei
Key Fungi for NEET PG:
FungusDiseaseStain/Lab FindingKey feature
Candida albicansThrush, esophagitis, vaginitis, invasiveGerm tube positiveMost common opportunistic fungus
Cryptococcus neoformansMeningitis in HIVIndia ink = capsule; Mucicarmine stain"Soap bubble" lesions in brain
Aspergillus fumigatusInvasive aspergillosis, ABPA, aspergilloma45° angle branchingGalactomannan antigen test
Mucor/RhizopusMucormycosis90° angle, non-septate hyphaeDiabetic ketoacidosis; Rhino-orbital-cerebral
DermatophytesTinea (ringworm)KOH mountTrichophyton, Microsporum, Epidermophyton
Sporothrix schenckiiSporotrichosisCigar-shaped yeast"Thorn prick" disease; rose gardener
Histoplasma capsulatumHistoplasmosisIntracellular yeast in macrophagesOhio/Mississippi valley; bird/bat droppings
Pneumocystis jiroveciiPCP pneumoniaSilver methenamine stain; Gomori stainCD4 <200; "ground glass" on CT
Opportunistic mycoses - predisposing factors (from Medical Microbiology 9e):
  • Neutropenia → Aspergillus, Candida, Mucor
  • HIV/AIDS → Cryptococcus, PCP, Candida
  • Corticosteroids → Aspergillus, Mucor, Cryptococcus
  • IV catheters → Candida
  • DKA → Mucormycosis (Rhizopus)
Antifungal drugs:
  • Amphotericin B: Gold standard for serious infections; binds ergosterol; nephrotoxicity
  • Azoles (Fluconazole, Itraconazole, Voriconazole): Inhibit ergosterol synthesis (CYP450)
  • Voriconazole: Drug of choice for invasive Aspergillus
  • Caspofungin (Echinocandin): Inhibits beta-1,3 glucan synthesis; for Candida and Aspergillus
  • Flucytosine: Used with Ampho-B for Cryptococcal meningitis
  • Griseofulvin: Dermatophytes only; disrupts microtubule assembly

PARASITOLOGY (4-5 Questions)

Malaria - Most tested topic:
FeatureP. falciparumP. vivaxP. malariaeP. ovale
Fever cycle48 hrs (tertian)48 hrs (tertian)72 hrs (quartan)48 hrs (tertian)
RBC affectedAny size, multipleEnlargedNormal/smallEnlarged
HypnozoitesNoYesNoYes
Severe malariaYes (most)RarelyNoNo
Schuffner's dotsNoYesNoYes
Banana gametocyteYesNoNoNo
Cerebral malaria: P. falciparum; altered consciousness, seizures; sequestration of parasitized RBCs in cerebral vessels
Treatment:
  • Uncomplicated falciparum: Artemisinin Combination Therapy (ACT) - Artemether+Lumefantrine
  • P. vivax/ovale: Chloroquine + Primaquine (to kill hypnozoites; check G6PD first)
  • Severe malaria: IV Artesunate (drug of choice); IV Quinine if artesunate unavailable
Amoebiasis:
  • Entamoeba histolytica
  • Cyst = infective form (4 nuclei); Trophozoite = pathogenic (has RBCs inside = pathognomonic)
  • Flask-shaped ulcers in colon
  • Amebic liver abscess: RUQ pain + fever + tender hepatomegaly; chocolate-brown "anchovy sauce" pus
  • Diagnosis: Serology (best for liver abscess), microscopy for intestinal
  • Treatment: Metronidazole + Lumefantrine (diloxanide furoate for cyst passers)
Leishmaniasis:
  • Kala-azar (visceral): L. donovani; vector = Phlebotomus sandfly; fever, splenomegaly, pancytopenia
  • LD bodies (amastigotes) in macrophages
  • rK39 test: quick diagnostic
  • Treatment: Liposomal Amphotericin B (first line in India now); Miltefosine (oral)
  • PKDL (Post Kala-azar Dermal Leishmaniasis): after treatment, skin manifestations
Filariasis:
  • W. bancrofti: lymphedema, elephantiasis; microfilariae in blood at night (nocturnal periodicity)
  • Treatment: DEC (Diethylcarbamazine) + Albendazole (MDA program in India)
  • Microfilariae seen in thick blood film at midnight
Tapeworms:
TapewormDefinitive hostIntermediate hostDisease
T. soliumHumans (adult worm)Pig/HumansCysticercosis (humans are accidental intermediate)
T. saginataHumansCattleNo cysticercosis in humans
E. granulosusDogSheep/HumansHydatid cyst
Cysticercosis: Neurocysticercosis = most common cause of acquired epilepsy in India; CT shows ring-enhancing lesions; Treatment: Albendazole/Praziquantel + steroids
Toxoplasma gondii:
  • Definitive host: Cat; Oocysts in cat feces
  • TORCH infection: causes congenital toxoplasmosis
  • Triad: Chorioretinitis + Hydrocephalus + Intracranial calcifications
  • Ring-enhancing lesions in HIV patients (CD4 <100)
  • Treatment: Pyrimethamine + Sulfadiazine + Folinic acid
Hydatid Cyst:
  • Echinococcus granulosus
  • Most common site: Liver (65%) > Lung (25%)
  • Daughter cysts inside; hydatid sand (scolices + brood capsules)
  • Casoni test (intradermal), IHA serology
  • Treatment: PAIR (Puncture-Aspiration-Injection-Reaspiration) or surgery; ALBENDAZOLE pre-op
  • Never aspirate without coverage (anaphylaxis risk)

VIROLOGY (2-3 Questions)

Hepatitis Viruses:
FeatureHAVHBVHCVHDVHEV
TypessRNAdsDNAssRNAssRNA (defective)ssRNA
TransmissionFecal-oralBlood/Sexual/VerticalBloodBlood (needs HBV)Fecal-oral
ChronicNoYes (5-10%)Yes (80%)YesNo
VaccineYesYesNo(HBV vaccine covers)Yes (limited)
Most severe acute----Pregnant (20% mortality)
HBV Serology (most tested):
  • HBsAg: Active infection (appears first)
  • Anti-HBs: Recovery/immunity after vaccination
  • HBeAg: High infectivity, active replication
  • Anti-HBc IgM: Acute infection marker
  • Anti-HBc IgG: Past infection or current chronic
  • Window period: HBsAg disappears, Anti-HBs not yet detectable - ONLY Anti-HBc IgM positive
HIV:
  • Retrovirus (ssRNA); infects CD4+ T cells, macrophages, dendritic cells
  • CD4 <200 = AIDS-defining
  • Diagnosis: ELISA (screening) → Western blot (confirmatory)
  • Window period for ELISA: 3-4 weeks
  • Treatment: cART (Tenofovir + Lamivudine + Efavirenz = first line in India)
  • Opportunistic infections by CD4 count:
    • <500: Oral thrush, HSV
    • <200: PCP, Toxoplasma, Cryptosporidium
    • <100: Cryptococcus, CMV, MAC, Microsporidiosis
Herpes Viruses:
VirusDiseaseKey feature
HSV-1Oral herpes, encephalitisTemporal lobe encephalitis
HSV-2Genital herpes, neonatal herpesAcyclovir treatment
VZVChickenpox, ShinglesRamsay Hunt = geniculate ganglion
EBVInfectious mononucleosisHeterophile antibodies (Monospot test)
CMVCongenital CMV, retinitis in HIV"Owl-eye" inclusions
HHV-8Kaposi sarcomaIn HIV patients
Influenza:
  • Antigenic drift: minor changes in H/N antigens - causes epidemics
  • Antigenic shift: major reassortment - causes pandemics
  • H1N1 (Swine flu): treatment with Oseltamivir (Tamiflu)
  • M2 inhibitors (Amantadine): only for Influenza A
Rabies:
  • Rhabdovirus; transmitted by animal bite
  • Negri bodies: eosinophilic inclusions in Purkinje cells (cerebellum) and hippocampus
  • Incubation: 1-3 months
  • Post-exposure: wound washing + HRIG (rabies immunoglobulin at bite site) + 4 doses vaccine
  • Pre-exposure: 3 doses on days 0, 7, 21/28

IMMUNOLOGY (2-3 Questions)

Hypersensitivity Reactions (Gell & Coombs):
TypeMediatorMechanismExamples
Type I (Immediate)IgE + Mast cellsAllergen cross-links IgE on mast cells → histamine releaseAnaphylaxis, asthma, urticaria, hay fever
Type II (Cytotoxic)IgG/IgM + ComplementAntibody binds cell surface antigenHemolytic anemia, Goodpasture's, ABO transfusion reactions
Type III (Immune Complex)IgG/IgM + ComplementImmune complexes deposit in tissuesSLE, serum sickness, post-streptococcal GN, Arthus reaction
Type IV (Delayed/Cell-mediated)T-cells (no antibody)Sensitized T-cells + macrophagesTB (Mantoux), contact dermatitis, graft rejection
Complement System:
  • Classical pathway: activated by IgG/IgM antibody-antigen complexes
  • Alternative pathway: activated by bacterial cell walls (LPS)
  • Lectin pathway: MBL binds mannose on pathogens
  • C3b: opsonization
  • C5a: chemotaxis + anaphylatoxin (most potent)
  • C5b-C9: Membrane Attack Complex (MAC) - kills bacteria
  • C1q deficiency → increased SLE risk
  • C3 deficiency → recurrent pyogenic infections
  • C5-C9 deficiency → recurrent Neisseria infections
Immunoglobulins:
IgKey role
IgGMost abundant; crosses placenta; secondary response; opsonization
IgAMucosal immunity; secretory dimer; found in colostrum, tears, saliva
IgMFirst antibody produced (primary response); pentamer; best complement activator
IgEAllergy and parasitic infections; lowest serum concentration
IgDB-cell receptor; activates naive B cells
Cytokines:
  • IL-1, IL-6, TNF-α: Pro-inflammatory, fever, acute phase response
  • IL-2: T-cell proliferation
  • IL-4, IL-5: IgE class switching; eosinophil activation (allergy/parasites)
  • IL-10: Anti-inflammatory (produced by Treg)
  • IL-12: Activates NK cells, promotes Th1 differentiation
  • IFN-γ: Activates macrophages; Th1 response; anti-viral
  • TGF-β: Anti-inflammatory; promotes Treg; fibrosis
Primary Immunodeficiencies:
DiseaseDefectFeatures
X-linked Agammaglobulinemia (Bruton's)Btk kinase; no B cellsRecurrent bacterial infections after 6 months
SCIDBoth T and B cell defectRecurrent ALL infections from birth
DiGeorge syndromeThymic aplasia; no T cellsTetany (hypoCa), conotruncal heart defects, 22q11 deletion
Wiskott-AldrichWASp proteinTriad: eczema + thrombocytopenia + recurrent infections
Chronic Granulomatous DiseaseNADPH oxidase defectRecurrent catalase-positive organism infections (Staph, Aspergillus, Nocardia)

3. BIOCHEMISTRY (10-15 Questions)


CARBOHYDRATE METABOLISM

Glycolysis (Embden-Meyerhof pathway):
  • Location: Cytoplasm; occurs in ALL cells
  • Net gain: 2 ATP + 2 NADH per glucose
  • Rate-limiting enzyme: Phosphofructokinase-1 (PFK-1)
    • Activated by: AMP, ADP, Fructose-2,6-bisphosphate, Pi
    • Inhibited by: ATP, citrate, H+
  • Other key enzymes: Hexokinase (inhibited by glucose-6-P), Pyruvate kinase
TCA Cycle (Krebs Cycle):
  • Location: Mitochondrial matrix
  • Starts with: Acetyl-CoA + Oxaloacetate → Citrate
  • Rate-limiting enzyme: Isocitrate dehydrogenase
  • Produces per turn: 3 NADH + 1 FADH2 + 1 GTP
  • Substrate-level phosphorylation: Succinyl-CoA → Succinate
Pyruvate fates:
  • Aerobic: Pyruvate → Acetyl-CoA (Pyruvate dehydrogenase complex; requires B1-thiamine)
  • Anaerobic: Pyruvate → Lactate (LDH)
  • Gluconeogenesis: Pyruvate → OAA → Glucose
Gluconeogenesis:
  • Occurs in: Liver (main), kidney cortex
  • Precursors: Lactate, Alanine, Glycerol, Odd-chain fatty acids
  • Key enzymes (bypass glycolysis): Pyruvate carboxylase, PEPCK, Fructose-1,6-bisphosphatase, Glucose-6-phosphatase
  • Fructose-1,6-bisphosphatase deficiency → cannot do gluconeogenesis → hypoglycemia after fasting
Glycogen Storage Diseases (GSD):
DiseaseEnzyme deficientOrganKey feature
Von Gierke (Type I)Glucose-6-phosphataseLiver/KidneySevere hypoglycemia, lactic acidosis, hypertriglyceridemia, "doll face"
Pompe (Type II)Acid alpha-glucosidase (lysosomal)Heart + MuscleCardiomegaly, hypotonia; most severe
Cori (Type III)Debranching enzymeLiver + MuscleMild Von Gierke-like
Anderson (Type IV)Branching enzymeLiverCirrhosis
McArdle (Type V)Muscle phosphorylaseMuscleExercise intolerance, myoglobinuria
Hers (Type VI)Liver phosphorylaseLiverMild hypoglycemia

LIPID METABOLISM

Fatty acid synthesis:
  • Location: Cytoplasm (liver, adipose)
  • Key enzyme: Acetyl-CoA carboxylase (rate-limiting; activated by citrate, insulin; inhibited by fatty acyl-CoA, glucagon)
  • Biotin required
  • NADPH required (from HMP shunt)
Beta-oxidation:
  • Location: Mitochondrial matrix
  • Each cycle: 1 Acetyl-CoA + 1 FADH2 + 1 NADH
  • Carnitine shuttle: transports long-chain fatty acids into mitochondria
  • Carnitine deficiency → cannot oxidize long-chain FA → myopathy + hypoglycemia
Ketogenesis:
  • Location: Liver mitochondria (but liver CANNOT USE ketones!)
  • Rate-limiting enzyme: HMG-CoA synthase
  • Occurs when: fasting, DKA, starvation
  • Ketone bodies: Acetoacetate, Beta-hydroxybutyrate (predominant in DKA), Acetone
Cholesterol metabolism:
  • Rate-limiting enzyme: HMG-CoA reductase (inhibited by statins)
  • Activated by: insulin, thyroxine
  • Inhibited by: glucagon, statins, cholesterol
Lipoproteins:
LipoproteinMade inFunctionKey apoprotein
ChylomicronIntestineDietary TG transportApoB-48
VLDLLiverEndogenous TG transportApoB-100
IDLFrom VLDLIntermediateApoB-100, ApoE
LDLFrom IDLCholesterol to tissuesApoB-100
HDLLiver/IntestineReverse cholesterol transportApoA-I

UREA CYCLE

  • Location: Liver (both mitochondria and cytosol)
  • Purpose: Detoxify ammonia → urea
  • Enzymes in order:
    1. Carbamoyl phosphate synthetase I (CPS-I) - mitochondria, rate-limiting; requires N-acetylglutamate as cofactor
    2. OTC (Ornithine transcarbamylase) - mitochondria; most common urea cycle defect; X-linked
    3. Argininosuccinate synthetase - cytosol
    4. Argininosuccinate lyase (ASL) - cytosol
    5. Arginase - cytosol; produces urea + ornithine
Urea Cycle Defects (from Harrison's 22e):
  • All defects except OTC: Autosomal recessive; OTC = X-linked
  • OTC deficiency = most common urea cycle defect
  • Present at 1-4 days of life: refusal to feed, lethargy → coma
  • Key lab: High ammonia + High glutamine; Elevated OROTIC ACID (in OTC deficiency)
  • CPS-1 deficiency: High ammonia, NORMAL orotic acid (differentiates from OTC)
  • Treatment: Low protein diet, sodium benzoate/phenylbutyrate (to excrete nitrogen), arginine supplementation, liver transplant (definitive)

ELECTRON TRANSPORT CHAIN (ETC)

Components:
  • Complex I: NADH dehydrogenase (NADH → ubiquinone; pumps 4H+)
  • Complex II: Succinate dehydrogenase (FADH2 → ubiquinone; NO H+ pumping)
  • Complex III: Cytochrome bc1 complex (ubiquinol → cyt c; pumps 4H+)
  • Complex IV: Cytochrome c oxidase (cyt c → O2; pumps 4H+)
  • Complex V: ATP synthase (uses H+ gradient to make ATP)
ATP yield from glucose (modern estimate):
  • 1 NADH = ~2.5 ATP; 1 FADH2 = ~1.5 ATP
  • Total from glucose: ~30-32 ATP
ETC Inhibitors (NEET PG favorites):
InhibitorSite of action
Rotenone, Amytal (barbiturates)Complex I
MalonateComplex II
Antimycin AComplex III
CO, Cyanide, H2S, AzideComplex IV
OligomycinComplex V (ATP synthase)
Uncouplers: Dissipate H+ gradient as heat without making ATP
  • 2,4-Dinitrophenol (DNP) - used illegally for weight loss
  • Thermogenin (UCP-1): In brown adipose tissue (BAT); for non-shivering thermogenesis in newborns

VITAMINS

Fat-soluble vitamins (A, D, E, K):
VitaminFunctionDeficiencyToxicity
A (Retinol)Vision (rhodopsin), epithelial integrity, immune functionNight blindness → Xerophthalmia → KeratomalaciaPseudotumor cerebri, teratogenic
D (Calciferol)Ca/P absorption; bone mineralizationRickets (children), Osteomalacia (adults)Hypercalcemia, metastatic calcification
E (Tocopherol)Antioxidant; protects RBC membranesHemolytic anemia, spinocerebellar ataxiaRare
K (Phylloquinone)Clotting factors (II, VII, IX, X), Protein C, SBleeding (prolonged PT > PTT)Hemolytic anemia in G6PD-deficient infants
Water-soluble vitamins:
VitaminFunctionDeficiencyKey enzyme
B1 (Thiamine)Pyruvate dehydrogenase, alpha-KG dehydrogenase, TransketolaseBeriberi (wet = cardiac; dry = peripheral neuropathy), Wernicke-KorsakoffTPP (cofactor)
B2 (Riboflavin)FAD, FMN - ETCAngular stomatitis, cheilosis, corneal vascularization-
B3 (Niacin)NAD, NADPPellagra: 3 Ds - Dermatitis + Diarrhea + DementiaFlushing, hepatotoxicity
B5 (Pantothenic acid)CoA, fatty acid synthesis"Burning feet" syndrome-
B6 (Pyridoxine)Amino acid transamination, heme synthesisSideroblastic anemia, peripheral neuropathyPLP (cofactor)
B7 (Biotin)Carboxylation reactionsDermatitis, alopecia, neurological (raw egg white - avidin binds biotin)-
B9 (Folate)One-carbon transfer; nucleotide synthesisMegaloblastic anemia; Neural tube defects (no neurological symptoms)THFA
B12 (Cobalamin)Methylmalonyl-CoA mutase, methionine synthaseMegaloblastic anemia + SUBACUTE COMBINED DEGENERATION of cord-
C (Ascorbic acid)Collagen synthesis (hydroxylation of Pro, Lys)Scurvy: perifollicular hemorrhage, bleeding gums, corkscrew hairsRenal oxalate stones

PROTEIN METABOLISM

Amino acid classification:
  • Essential (not synthesized): PVT TIM HALL (Phe, Val, Thr, Trp, Ile, Met, His, Arg*, Lys, Leu)
  • Glucogenic: can be converted to glucose
  • Ketogenic only: Leucine, Lysine
  • Both: Phe, Tyr, Trp, Ile
Phenylketonuria (PKU):
  • Phenylalanine hydroxylase deficiency
  • Phenylalanine accumulates → Phenylacetate, Phenyllactate, Phenylpyruvate in urine
  • Features: Musty odor, intellectual disability, fair skin/hair (reduced melanin), eczema
  • Treatment: Low phenylalanine diet; avoid aspartame
Homocystinuria:
  • Cystathionine beta-synthase deficiency (most common) or B12/Folate deficiency
  • Features: Marfanoid habitus, lens dislocation (DOWNWARD, unlike Marfan - upward), intellectual disability, thromboembolism
  • Treatment: B6 (if responsive), low methionine diet
Alkaptonuria:
  • Homogentisate oxidase deficiency
  • Ochronosis: dark pigmentation of cartilage/sclerae
  • Dark urine on standing
  • Ochronotic arthropathy

4. OBSTETRICS & GYNECOLOGY (25-30 Questions)


PLACENTA PREVIA

Definition (from Creasy & Resnik's Maternal-Fetal Medicine): Implantation that covers the internal os of the cervix. A leading cause of antepartum hemorrhage.
Low-lying placenta: Placental edge within 2 cm of internal os (but not covering it)
Classification (modern): Old terms (complete/partial/marginal) are no longer recommended. Now:
  • Placenta previa = covers internal os
  • Low-lying placenta = edge within 20 mm but not covering os
  • Normal = placental edge >20 mm from internal os
Risk factors: Prior cesarean section (most important), prior uterine surgery, multiparity, previous placenta previa, smoking, IVF pregnancy
Clinical features:
  • Painless, bright red vaginal bleeding (hallmark) - usually at 28-32 weeks
  • Soft, non-tender uterus
  • Abnormal fetal lie (20% have malpresentation)
  • No warning sign - bleeding can be sudden and severe
Diagnosis: Transvaginal ultrasound (most accurate; safer than abdominal for this purpose)
Management:
  • Stable + preterm: Conservative - hospitalize, steroids for lung maturity, blood transfusion if needed
  • Major hemorrhage / term: Cesarean section (method of delivery)
  • Placenta accreta must be excluded (risk with prior CS + placenta previa)
Associated condition - Placenta Accreta Spectrum:
  • Accreta: Placenta attaches to myometrium (no decidua basalis)
  • Increta: Invades into myometrium
  • Percreta: Penetrates through myometrium (may invade bladder)
  • Risk: #1 cause of peripartum hysterectomy

HYDATIDIFORM MOLE

Definition: Abnormal trophoblastic proliferation with hydropic degeneration of chorionic villi
Complete vs Partial Mole:
FeatureComplete MolePartial Mole
Karyotype46,XX (90%) or 46,XY (all paternal)69,XXY or 69,XXX (triploid)
OriginNo maternal chromosomes; 2 sperm fertilize enucleate egg1 egg + 2 sperm
Fetal partsAbsentMay be present
hCGVery high (>100,000 mIU/mL)Moderately raised
Risk of malignancy15-20% → Choriocarcinoma2-3%
Theca lutein cystsPresent (50%)Less common
Ultrasound"Snowstorm" appearanceSwiss-cheese placenta
Presentation:
  • Vaginal bleeding (most common)
  • Uterus large for dates
  • Hyperemesis gravidarum
  • Pre-eclampsia <20 weeks (pathognomonic of mole)
  • Hyperthyroidism (hCG cross-reacts with TSH receptors)
Management:
  • Suction evacuation (method of choice)
  • Oxytocin after suction starts
  • Follow-up with serial hCG levels (should return to normal in 8 weeks for partial, 12 weeks for complete)
  • Contraception for at least 6 months (OCP preferred - does not affect hCG levels)
Gestational Trophoblastic Neoplasia (GTN):
  • Includes: Invasive mole, Choriocarcinoma, PSTT, ETT
  • Diagnosed by: Rising/plateauing hCG after mole evacuation
  • Choriocarcinoma: Highly vascular; hematogenous spread to lung ("cannonball" metastases); extremely chemosensitive
  • Treatment: Methotrexate (low risk); EMA-CO regimen (high risk)

PREECLAMPSIA & ECLAMPSIA

Definition (ACOG): New-onset hypertension (≥140/90 mmHg on two occasions ≥4 hours apart) at ≥20 weeks gestation PLUS one of:
  • Proteinuria ≥300 mg/24 hrs
  • Thrombocytopenia <100,000
  • Renal insufficiency (Creatinine >1.1)
  • Impaired liver function (LFTs doubled)
  • Pulmonary edema
  • New-onset headache or visual disturbances
Pathogenesis (from Robbins Pathology): Abnormal placentation - failure of trophoblastic invasion of spiral arteries → these vessels remain narrow and high-resistance → placental hypoxia → release of antiangiogenic factors (sFlt-1, endoglin) → endothelial dysfunction → systemic manifestations
Severity features (Severe preeclampsia):
  • BP ≥160/110 mmHg
  • Platelets <100,000
  • Creatinine >1.1
  • LFTs >2x normal
  • Severe headache, visual changes
  • Pulmonary edema
HELLP Syndrome (~10% of severe preeclampsia):
  • H = Hemolysis (microangiopathic)
  • EL = Elevated Liver enzymes
  • LP = Low Platelets
  • Can occur WITHOUT hypertension/proteinuria
  • LDH >600, AST/ALT elevated, platelets <100,000
  • Management: Delivery (definitive)
Eclampsia: Preeclampsia + Convulsions (tonic-clonic)
  • Treatment of acute convulsions: MgSO4 (Pritchard regimen: 4g IV loading + 1g/hr maintenance)
  • Anti-seizure: MgSO4 (not diazepam)
  • Antihypertensive: Hydralazine (IV), Labetalol (IV), Nifedipine (oral) for acute BP control
  • Antidote for MgSO4 toxicity: Calcium gluconate (10 mL of 10% IV)
  • Monitor: patellar reflexes (first lost in toxicity), respiratory rate, urine output
Definitive treatment: Delivery (the only cure)

DIABETES IN PREGNANCY (GDM)

Screening:
  • 24-28 weeks with 75g OGTT (WHO criteria)
  • Diagnosis: Fasting ≥92 mg/dL, 1-hr ≥180 mg/dL, 2-hr ≥153 mg/dL
Maternal complications: Pre-eclampsia, polyhydramnios, infections, operative delivery, future T2DM
Fetal complications:
  • Macrosomia (most common) → Shoulder dystocia
  • Congenital malformations (most important in pre-gestational DM, especially cardiac and neural tube)
  • Neonatal hypoglycemia (baby is hyperinsulinemic - maternal hyperglycemia → fetal hyperinsulinemia → after birth, glucose supply cut → hypoglycemia)
  • Respiratory distress syndrome (insulin inhibits surfactant synthesis)
  • Polycythemia, hypocalcemia, hyperbilirubinemia
Management:
  • Diet control first; if not adequate → Insulin (safest in pregnancy)
  • Metformin and Glibenclamide used in some centers
  • Target: Fasting <95, 1-hr postprandial <140, 2-hr postprandial <120

ANEMIA IN PREGNANCY

Physiological changes: Plasma volume increases by 50%, RBC mass increases by 25% → dilutional anemia (hemoglobin <11 g/dL = anemia in pregnancy; <10 = moderate; <7 = severe)
Iron Deficiency Anemia (most common in pregnancy):
  • Hypochromic microcytic anemia
  • Serum ferritin = most sensitive marker (decreases first)
  • Treatment: Ferrous sulfate 200 mg TDS; IV iron if severe or non-compliance
Megaloblastic Anemia:
  • Most common cause: Folate deficiency (folate requirement doubles in pregnancy)
  • B12 deficiency: Also causes megaloblastic + subacute combined degeneration
  • Folate supplementation: 400 mcg/day pre-conception + first trimester; 5 mg/day if high-risk
Sickle Cell Disease in Pregnancy:
  • Increased risk of crisis, infections, maternal mortality
  • Hydroxyurea contraindicated in pregnancy
  • Folic acid + vaccinations + prophylactic transfusions in severe disease

CONTRACEPTION

Hormonal methods:
  • Combined OCP: Estrogen + Progesterone; inhibits ovulation (most effective mechanism)
  • Progesterone-only pill (Mini-pill): Thickens cervical mucus; suitable for breastfeeding
  • Depot Medroxyprogesterone Acetate (DMPA/Depo-Provera): 3-monthly injection; causes amenorrhea
  • Emergency contraception: Levonorgestrel 1.5 mg within 72 hours; Cu-IUD within 5 days
Intrauterine Devices (IUDs):
  • Copper IUD: Non-hormonal; spermicidal; lasts 10 years; DOC for emergency contraception
  • Levonorgestrel IUD (Mirena): Hormonal; reduces menorrhagia; lasts 5 years
Barrier methods: Condom (only method that protects against STIs)
Permanent methods: Tubectomy (modified Pomeroy = most common; during cesarean = Parkland method); Vasectomy (failure rate lower than tubectomy)

UTEROVAGINAL PROLAPSE

Degrees:
  • 1st degree: Cervix within vagina
  • 2nd degree: Cervix at introitus
  • 3rd degree (Procidentia): Entire uterus outside vagina
Supporting structures (lost in prolapse):
  • Cardinal (Mackenrodt's) ligaments: Most important for cervical support
  • Uterosacral ligaments
  • Pubocervical fascia (anterior wall/cystocele)
  • Rectovaginal fascia (posterior wall/rectocele)
Management:
  • Conservative: Pelvic floor exercises (Kegel), ring pessary (for unfit patients)
  • Surgical: Vaginal hysterectomy + repair (gold standard for most); Manchester operation (amputation of cervix + repair; fertility preserving)

5. PSM - PREVENTIVE & SOCIAL MEDICINE (20+ Questions)


NATIONAL HEALTH PROGRAMS

Key programs and targets:
ProgramTargetKey drug/intervention
RNTCP → NTPEliminate TB by 2025 (incidence <44/lakh; End TB by 2030)DOTS: 2HRZE/4HR; Bedaquiline for MDR-TB
National Malaria Eradication Program (NMEP)Eliminate malariaACT, DDT spraying
Pulse Polio ProgramEradicationOPV (bivalent); IPV in routine schedule
National Vector Borne Disease Control (NVBDCP)Malaria, Dengue, Filaria, Kala-azar, JEDEC in MDA for filaria
Rashtriya Bal Swasthya Karyakram (RBSK)0-18 yrs screening4 Ds: Defects, Deficiencies, Diseases, Developmental delays
National Immunization ProgramUniversal ImmunizationBCG, OPV, DPT, Measles, MMR, Hepatitis B, IPV, PCV, Rotavirus
AYUSHMAN BHARAT - PMJAY5 lakh coverage/family/yearPoorest 40% of India
NHP 2017 targetLife expectancy ≥70 by 2025; IMR <28 by 2019-
Universal Immunization Programme (UIP) schedule:
  • Birth: BCG + OPV0 + Hepatitis B (birth dose)
  • 6 weeks: OPV1 + DPT1 + HepB2 + IPV1 + PCV1 + Rotavirus1
  • 10 weeks: OPV2 + DPT2 + PCV2 + Rotavirus2
  • 14 weeks: OPV3 + DPT3 + IPV2 + PCV3 + Rotavirus3
  • 9 months: Measles/MR1 + Vitamin A (1st dose)
  • 16-24 months: DPT booster1 + OPV booster + MR2 + Vitamin A (2nd dose)

NUTRITION

Protein-Energy Malnutrition (PEM):
FeatureKwashiorkorMarasmus
Age1-3 years<1 year
CaloriesAdequate calories, low proteinBoth protein + calories deficient
EdemaYes (pitting pedal edema - hallmark)No
Appearance"Moon face", skin lesions (flaky paint), hair changesWasted, "old man" appearance, "skin and bones"
Fatty liverYes (hepatomegaly)No
Serum albuminLowMay be low
MUACUsed for screening (<11.5 cm = SAM)
Vitamin A deficiency (most common nutritional cause of preventable blindness):
  • Night blindness (first symptom)
  • Bitot's spots: Triangular, foamy, silver-gray spots on conjunctiva
  • Xerophthalmia → Keratomalacia (corneal melting = irreversible blindness)
  • Prophylaxis: 200,000 IU at 9 months, 16-24 months, then 6 monthly till 5 years
Iodine Deficiency:
  • Goiter (most common sign), cretinism (most serious effect)
  • Iodized salt: ≥15 ppm at consumer level
  • Universal Salt Iodization (USI) policy in India
Iron Deficiency:
  • Anemia (most common nutritional deficiency worldwide)
  • NNMB surveys in India: Most common deficiency
  • Weekly Iron and Folic Acid Supplementation (WIFS): School-age children and adolescents
Fluorosis:
  • Excess fluoride (>1.5 ppm): Dental fluorosis → Skeletal fluorosis
  • Deficiency (<0.5 ppm): Dental caries

EPIDEMIOLOGY

Key study designs (from most to least evidence):
LevelStudy typeKey feature
ISystematic review/Meta-analysisHighest evidence
IIRCTGold standard for causation
IIICohort studyProspective; calculates Relative Risk (RR); best for incidence
IVCase-control studyRetrospective; calculates Odds Ratio (OR); best for rare diseases
VCross-sectional (prevalence) studySnapshot; calculates prevalence
Measures of disease frequency:
  • Incidence rate = New cases / Population at risk / Time
  • Prevalence = All existing cases / Total population
  • Attack rate = Cases / Those exposed (used in outbreak investigation)
  • CFR = Deaths / Cases × 100
Measures of association:
  • Relative Risk (RR): Used in cohort studies; RR >1 = increased risk
  • Odds Ratio (OR): Used in case-control; approximates RR when disease is rare
  • Attributable risk (AR) = Risk in exposed - Risk in unexposed
Screening tests:
ParameterFormulaMeaning
SensitivityTP / (TP + FN)Ability to detect true positives; "PID" - Positive in Disease
SpecificityTN / (TN + FP)Ability to correctly identify negatives
PPVTP / (TP + FP)Probability disease present when test positive
NPVTN / (TN + FN)Probability disease absent when test negative
Key points:
  • Sensitivity used when: disease is serious and must not be missed (e.g., HIV ELISA for screening)
  • Specificity used when: false positives are costly/dangerous (e.g., confirmatory test)
  • High sensitivity → low false negatives → used for screening
  • High specificity → low false positives → used for confirmation (Western blot)
  • Wilson's criteria for screening: Disease must be common, important, detectable at preclinical stage, effective treatment available, acceptable test
Bias:
  • Selection bias: Berkson's bias (hospital studies), Neyman (late-look) bias
  • Information bias: Observer bias, recall bias, Hawthorne effect
  • Confounding: third variable distorts association; controlled by randomization, matching, restriction

BIOMEDICAL WASTE MANAGEMENT

Biomedical Waste Management Rules 2016 (amended 2019):
Categories and color coding:
CategoryColorType of wasteTreatment
YellowYellow bagHuman anatomical waste, soiled items, expired medicines, chemical wasteIncineration or deep burial
RedRed bagRecyclable, contaminated non-sharps (IV tubing, bottles)Autoclave/Microwave → shredding/recycling
White (Translucent)White/Translucent puncture-proof containerSharps (needles, syringes, blades)Autoclaving → sharps pit or encapsulation
BlueBlue/WhiteGlassware, metallic itemsAutoclave → disposal
Key facts:
  • Common Bio-Medical Waste Treatment Facility (CBWTF) = facility authorized to treat BMW
  • Healthcare facilities must have BMW management plan
  • Bar-coded bags required
  • Segregation at source = most important step
  • Needle-stick injury rate = important occupational hazard; post-exposure prophylaxis (PEP) within 72 hours for HIV

DISASTER MANAGEMENT

Types of disasters:
  • Natural: Earthquake, floods, cyclone, drought, tsunami
  • Man-made: Industrial accidents, nuclear, biological, chemical (CBRN)
Disaster cycle:
  1. Mitigation → 2. Preparedness → 3. Response → 4. Recovery
Medical aspects:
  • Triage systems: START (Simple Triage And Rapid Treatment) - used in mass casualty
    • Red (Immediate): Life-threatening but salvageable
    • Yellow (Delayed): Serious but stable
    • Green (Minor): "Walking wounded"
    • Black (Expectant): Dead or unsurvivable injury
Key national frameworks:
  • National Disaster Management Act 2005
  • National Disaster Management Authority (NDMA) - Chairman = Prime Minister
  • State level: SDMA; District level: DDMA
  • National Policy on Disaster Management 2009

QUICK REVISION TABLE - HIGH-YIELD MNEMONICS

TopicMnemonic
Essential amino acidsPVT TIM HALL
ETC inhibitors at Complex IVCO, Cyanide, H2S, Azide
Preeclampsia vs EclampsiaSame disease + seizures
Hypersensitivity typesACID (Anaphylactic, Cytotoxic, Immune complex, Delayed)
HELLP syndromeHemolysis, Elevated Liver enzymes, Low Platelets
Dimorphic fungi rule"Body heat makes them yeast" (37°C = yeast form)
Urea cycle defect (most common)OTC deficiency - X-linked
Hernia with highest strangulation riskFemoral hernia

STUDY STRATEGY RECAP

  1. Surgery (30-32 Qs): Start with Trauma and GIT. Integrate with radiology (CT abdomen, X-rays of obstruction, perforation). Do maximum MCQs. Recent exams = Bariatric + Transplant.
  2. Microbiology (20-22 Qs): Prioritize Mycology (dimorphic fungi, Candida, Aspergillus, Mucor) and Parasitology (malaria, Entamoeba, Plasmodium). Immunology = Hypersensitivity + immunodeficiency.
  3. Biochemistry (10-15 Qs): Master Carbohydrate metabolism (glycolysis, TCA, GSD), Urea cycle (especially OTC deficiency), ETC inhibitors, and Vitamins table.
  4. OBG (25-30 Qs): Obstetrics > Gynecology. Focus on Placenta Previa, Mole, Preeclampsia/HELLP, GDM. Know HELLP criteria cold.
  5. PSM (20+ Qs): National programs (UIP schedule, RNTCP/NTP, RBSK), Epidemiology (study designs, sensitivity/specificity), BMW rules (color coding), and Nutrition (Kwashiorkor vs Marasmus).
Good luck with your NEET PG preparation!

*Sources: Robbins & Kumar Basic Pathology; Creasy & Resnik's Maternal-Fetal Medicine; Harrison's Principles of Internal Medicine 22e; Medical Microbiology 9e; Bailey & Love's Surgery 28e; Tietz Textbook of Laboratory Medicine.*The complete masterclass above covers all 5 subjects from your NEET PG priority list. Here's a quick summary of what was covered:

What You Got - Summary

1. Surgery (30-32 Qs)

  • Trauma: ATLS, shock classification table, burns (Parkland formula, Rule of 9s)
  • Hernia: Types with boundaries, Hesselbach's triangle, complications, surgical repairs
  • GU System: Renal trauma grading, BPH vs prostate cancer zones, bladder + testicular cancer
  • Arteries & Veins: Buerger's, DVT (Virchow's triad), varicose veins, AAA
  • Hepatobiliary: Gallstones, Courvoisier's law, HCC markers, pancreatitis (Ranson criteria)
  • GIT: Appendicitis signs, colorectal cancer (FAP/HNPCC genes), peptic ulcer
  • Bariatric: BMI criteria, procedure types + mechanisms
  • Transplant: Rejection types (timing + mechanism), immunosuppression drugs, brain death criteria

2. Microbiology (20-22 Qs)

  • Mycology: Dimorphic fungi rule, Candida/Aspergillus/Mucor/Crypto identification, antifungals
  • Parasitology: Malaria (complete species comparison table), Amoebiasis, Leishmaniasis, Filariasis, Tapeworms, Toxoplasma
  • Virology: Hepatitis serology window period, HIV CD4 thresholds, Herpes viruses, Rabies
  • Immunology: Hypersensitivity types I-IV, complement cascade, immunoglobulins, cytokines, primary immunodeficiencies

3. Biochemistry (10-15 Qs)

  • Carbohydrate Metabolism: Glycolysis, TCA, gluconeogenesis, Glycogen Storage Diseases table
  • Lipid Metabolism: FA synthesis, beta-oxidation, ketogenesis, cholesterol, lipoproteins
  • Urea Cycle: All 5 enzymes in order, OTC deficiency (X-linked + orotic acid marker)
  • ETC: All 5 complexes, inhibitors per complex, uncouplers
  • Vitamins: Both fat-soluble and water-soluble - complete table with deficiency diseases

4. OBG (25-30 Qs)

  • Placenta Previa (modern classification, management)
  • Hydatidiform Mole (complete vs partial - complete comparison table)
  • Preeclampsia/Eclampsia/HELLP (pathogenesis, MgSO4 protocol)
  • GDM (OGTT criteria, fetal complications)
  • Anemia in Pregnancy (iron, folate, B12)
  • Contraception + Uterovaginal Prolapse

5. PSM (20+ Qs)

  • National Health Programs + UIP schedule
  • Nutrition (Kwashiorkor vs Marasmus, Vitamin A, Iodine)
  • Epidemiology (study designs, sensitivity/specificity, bias types)
  • Biomedical Waste (color-coded categories)
  • Disaster Management (triage, NDMA)
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