NEET PG Pathology Syllabus

Define neoplasia and contrast benign versus malignant tumors on key features.

Neoplasia = abnormal autonomous tissue growth. Benign: well-differentiated, slow, encapsulated, non-invasive, no metastasis. Malignant: poorly differentiated/anaplastic, rapid, infiltrative, metastasizes.

What is the classic naming rule for benign and malignant tumors of epithelial vs mesenchymal origin?

Benign: tissue + '-oma' (e.g., adenoma, lipoma). Malignant epithelial = carcinoma (adenocarcinoma); malignant mesenchymal = sarcoma (osteosarcoma, leiomyosarcoma).

List the hallmarks of malignancy (Hanahan & Weinberg).

Sustained proliferative signaling, evading growth suppressors, resisting apoptosis, replicative immortality, inducing angiogenesis, activating invasion/metastasis, deregulated metabolism, evading immune destruction; enabled by genome instability and tumor-promoting inflammation.

Differentiate tumor grading from staging.

Grading = degree of differentiation/anaplasia (histologic; low to high grade). Staging = extent of spread (TNM: Tumor size, Node involvement, Metastasis). Staging has greater prognostic value.

Name the major steps of the metastatic cascade.

Loosening of intercellular junctions (E-cadherin loss) -> ECM degradation (matrix metalloproteinases) -> migration/invasion -> intravasation -> survival in circulation -> arrest/extravasation -> colonization at distant site.

Give two examples each of oncogenes and tumor suppressor genes with their associated cancers.

Oncogenes: RAS (many carcinomas), MYC (Burkitt lymphoma), HER2/neu (breast). Tumor suppressors: TP53 (Li-Fraumeni, many), RB (retinoblastoma), APC (FAP/colon), BRCA1/2 (breast-ovarian).

Classify hypersensitivity reactions I-IV with mechanism and one example each.

I: IgE/mast cell -> anaphylaxis/atopy. II: antibody (IgG/IgM) vs cell antigen -> hemolytic anemia, Goodpasture. III: immune complex -> SLE, serum sickness. IV: T-cell mediated (delayed) -> contact dermatitis, TB granuloma.

What is amyloid, and which stain confirms it with what birefringence?

Amyloid = misfolded protein in beta-pleated sheet, extracellular. Stained with Congo red, showing apple-green birefringence under polarized light.

Match amyloid types: AL, AA, A-beta, ATTR.

AL = immunoglobulin light chains (plasma cell dyscrasias/myeloma); AA = serum amyloid A (chronic inflammation); A-beta = Alzheimer disease; ATTR = transthyretin (familial/senile cardiac amyloid).

Define autoimmune central versus peripheral tolerance mechanisms.

Central: clonal deletion of self-reactive lymphocytes in thymus (AIRE-mediated) and bone marrow. Peripheral: anergy, suppression by regulatory T cells (Tregs), and activation-induced apoptosis.

Provide the morphologic classification of anemia by MCV with examples.

Microcytic (MCV <80): iron deficiency, thalassemia, anemia of chronic disease, sideroblastic. Normocytic: acute blood loss, hemolysis, aplastic. Macrocytic (MCV >100): B12/folate deficiency, liver disease, alcohol.

Contrast iron deficiency anemia and anemia of chronic disease on iron studies.

IDA: low serum iron, high TIBC, low ferritin, low transferrin saturation. ACD: low serum iron, low TIBC, high/normal ferritin (iron sequestered, hepcidin high).

What peripheral smear and lab findings characterize megaloblastic anemia?

Macro-ovalocytes, hypersegmented neutrophils (>5 lobes), pancytopenia, high LDH, high indirect bilirubin; due to B12 or folate deficiency impairing DNA synthesis.

List key features distinguishing intravascular from extravascular hemolysis.

Intravascular: hemoglobinemia, hemoglobinuria, hemosiderinuria, low haptoglobin, schistocytes. Extravascular: splenomegaly, jaundice, spherocytes, increased indirect bilirubin, less hemoglobinuria.

What defines acute leukemia, and how do AML and ALL differ on key markers?

Acute leukemia: >20% blasts in marrow. AML: myeloid blasts, Auer rods, MPO+, occurs in adults. ALL: lymphoid blasts, TdT+, occurs in children, CD10/CD19 (B-ALL) or CD3 (T-ALL).

Name the diagnostic genetic abnormality and treatment of CML.

t(9;22) Philadelphia chromosome producing BCR-ABL1 fusion (constitutive tyrosine kinase). Treated with tyrosine kinase inhibitors (imatinib).

What is the diagnostic cell of Hodgkin lymphoma and its classic immunophenotype?

Reed-Sternberg cell ('owl-eye' binucleate). Classic HL: CD15+ and CD30+, CD45-, CD20- (usually).

Differentiate Hodgkin from non-Hodgkin lymphoma on spread and B symptoms.

Hodgkin: contiguous/orderly nodal spread, localized, B symptoms common, Reed-Sternberg cells. Non-Hodgkin: non-contiguous spread, often extranodal/disseminated, more frequently leukemic, diverse B/T cell origins.

Give the translocation associated with Burkitt lymphoma and its histologic appearance.

t(8;14) MYC-IgH translocation. Histology: 'starry sky' pattern from tingible-body macrophages amid sheets of intermediate B cells; very high proliferation index.

Outline the coagulation cascade's intrinsic, extrinsic and common pathways with the test for each.

Intrinsic (XII, XI, IX, VIII) -> measured by aPTT. Extrinsic (VII + tissue factor) -> measured by PT/INR. Common (X, V, II/prothrombin, fibrinogen) -> affects both PT and aPTT.

Distinguish hemophilia A and B, and von Willebrand disease.

Hemophilia A: factor VIII deficiency, X-linked, prolonged aPTT. Hemophilia B: factor IX deficiency, X-linked, prolonged aPTT. vWD: vWF deficiency, autosomal dominant, prolonged bleeding time/PFA + variable aPTT.

What lab pattern characterizes disseminated intravascular coagulation (DIC)?

Prolonged PT and aPTT, low platelets, low fibrinogen, elevated D-dimer/fibrin degradation products, schistocytes on smear (microangiopathic hemolysis).

Compare ITP and TTP on mechanism and key features.

ITP: anti-platelet antibodies (anti-GPIIb/IIIa), isolated thrombocytopenia, normal coagulation. TTP: ADAMTS13 deficiency -> microthrombi; pentad of fever, thrombocytopenia, MAHA, renal dysfunction, neurologic signs.

List ABO blood group antigens and naturally occurring antibodies for each group.

Group A: A antigen, anti-B antibody. Group B: B antigen, anti-A. Group AB: A+B antigens, no antibody (universal recipient). Group O: no antigen, anti-A+anti-B (universal donor).

What is the difference between major and minor crossmatch in transfusion?

Major crossmatch: donor RBCs vs recipient serum (most important). Minor crossmatch: donor serum vs recipient RBCs (less significant, largely obsolete with component therapy).

Differentiate acute hemolytic transfusion reaction from febrile non-hemolytic reaction.

Acute hemolytic: ABO incompatibility, IgM-mediated intravascular hemolysis, fever, hypotension, hemoglobinuria, DIC. Febrile non-hemolytic: recipient antibodies vs donor leukocyte cytokines, fever/chills only, benign.

Which blood products carry the highest risk of bacterial contamination and why?

Platelet concentrates, because they are stored at room temperature (20-24C) to maintain function, favoring bacterial growth.

Describe the morphologic stages of atherosclerosis.

Fatty streak (lipid-laden macrophages/foam cells) -> fibrous plaque/atheroma (lipid core with fibrous cap, smooth muscle, cholesterol clefts) -> complicated plaque (calcification, ulceration, hemorrhage, thrombosis, aneurysm).

What are the major modifiable risk factors for atherosclerosis?

Hyperlipidemia (high LDL/low HDL), hypertension, smoking, and diabetes mellitus.

Give the time-line of gross and microscopic changes after a myocardial infarction.

0-4 h: none. 4-12 h: early coagulative necrosis, wavy fibers. 1-3 d: neutrophils. 3-7 d: macrophages, soft yellow center (risk of rupture). 1-2 wk: granulation tissue. >2 mo: dense collagenous scar.

List COPD components and contrast emphysema with chronic bronchitis.

Emphysema: permanent alveolar wall destruction (loss of elastic recoil), 'pink puffer', dyspnea. Chronic bronchitis: productive cough >=3 months/2 yrs, mucus gland hyperplasia (Reid index increased), 'blue bloater'.

Differentiate lobar pneumonia from bronchopneumonia.

Lobar: consolidation of an entire lobe, typically Streptococcus pneumoniae, four stages (congestion, red hepatization, gray hepatization, resolution). Bronchopneumonia: patchy consolidation around bronchi, often elderly/debilitated, mixed organisms.

Compare the main types of lung carcinoma: small cell vs non-small cell features.

Small cell (SCLC): central, neuroendocrine, paraneoplastic (ADH/ACTH), aggressive, not surgical. NSCLC: adenocarcinoma (peripheral, non-smokers, EGFR/ALK), squamous cell (central, hypercalcemia/PTHrP), large cell (anaplastic).

Distinguish ulcerative colitis from Crohn disease on key pathology.

UC: continuous, rectum-to-proximal, mucosa/submucosa only, crypt abscesses, pseudopolyps, no granulomas. Crohn: skip lesions, mouth-to-anus, transmural, granulomas, fistulae, 'cobblestone' mucosa, fat wrapping.

List the histologic types of cirrhosis end-stage features and a hepatocellular carcinoma marker.

Cirrhosis: diffuse bridging fibrosis with regenerative nodules disrupting architecture (micronodular/macronodular). Hepatocellular carcinoma tumor marker: alpha-fetoprotein (AFP).

Match viral hepatitis: which are RNA, which DNA, and routes of transmission.

HAV (RNA, fecal-oral), HBV (DNA, parenteral/sexual/vertical), HCV (RNA, parenteral), HDV (RNA, needs HBV), HEV (RNA, fecal-oral, severe in pregnancy).

Differentiate nephritic from nephrotic syndrome.

Nephritic: hematuria, RBC casts, hypertension, mild proteinuria, oliguria, azotemia (inflammatory GN). Nephrotic: heavy proteinuria (>3.5 g/day), hypoalbuminemia, edema, hyperlipidemia, lipiduria.

Match glomerular diseases: minimal change, membranous, post-strep, IgA nephropathy.

Minimal change: effacement of foot processes (children, nephrotic). Membranous: subepithelial 'spike and dome' deposits (adult nephrotic). Post-strep: subepithelial humps, low C3 (nephritic). IgA (Berger): mesangial IgA, recurrent hematuria post-infection.

What is the most common renal stone type and its predisposing condition?

Calcium oxalate stones (~75-80%); associated with hypercalciuria/hypercalcemia. Radiopaque on X-ray.

Name the classic histology and a key feature of clear cell renal cell carcinoma.

Clear cytoplasm (lipid/glycogen) cells in nests; arises from proximal tubule; associated with VHL gene; tends to invade renal vein; paraneoplastic polycythemia (EPO).

Compare type 1 and type 2 diabetes mellitus pathogenesis.

Type 1: autoimmune T-cell destruction of beta cells -> absolute insulin deficiency, HLA-DR3/DR4, autoantibodies, ketosis-prone. Type 2: insulin resistance + relative deficiency, obesity-related, amyloid in islets, not autoimmune.

Describe papillary thyroid carcinoma's diagnostic nuclear features.

'Orphan Annie eye' nuclei (optically clear/empty), nuclear grooves, intranuclear inclusions, and psammoma bodies. Best prognosis; spreads via lymphatics.

Differentiate fibroadenoma from invasive ductal carcinoma of breast.

Fibroadenoma: benign, young women, well-circumscribed mobile mass, proliferation of stroma + glands. Invasive ductal carcinoma: malignant, hard fixed mass, desmoplastic stroma, infiltrating duct cells; most common breast cancer.

What receptors are tested in breast cancer and why?

Estrogen receptor (ER), progesterone receptor (PR), and HER2/neu. They guide therapy (hormonal therapy for ER+, trastuzumab for HER2+) and prognosis; triple-negative has worst prognosis.

Match CNS tumors: glioblastoma, meningioma, medulloblastoma to feature.

Glioblastoma multiforme: pseudopalisading necrosis + microvascular proliferation, GFAP+, adults, poor prognosis. Meningioma: psammoma bodies, whorls, dural-based, women. Medulloblastoma: cerebellum, children, small blue cells, Homer-Wright rosettes.

Distinguish osteosarcoma from Ewing sarcoma on age, site and genetics.

Osteosarcoma: adolescents, metaphysis of long bones (knee), Codman triangle/sunburst, malignant osteoid, RB/p53 mutation. Ewing sarcoma: children, diaphysis, 'onion-skin' periosteum, small round blue cells, t(11;22) EWS-FLI1, CD99+.

What is the classic radiographic and histologic feature of giant cell tumor of bone?

'Soap-bubble' lytic lesion at the epiphysis of long bones (around the knee) in young adults; histology shows multinucleated osteoclast-type giant cells in a background of mononuclear stromal cells.