INI CET Pathology Syllabus

Pathology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pathology in INI CET, not a summary of it.

1. 1

   General Pathology

   6 topics

   • Cellular adaptations
     • Hypertrophy
     • Hyperplasia
     • Atrophy
     • Metaplasia
     • Dysplasia
   • Cell injury and cell death
     • Necrosis
     • Apoptosis
     • Causes of cell injury
   • Inflammation
     • Acute vs. chronic inflammation
     • Cellular and chemical mediators
     • Outcomes
   • Healing and repair
     • Regeneration
     • Fibrosis
     • Wound healing
     • Factors affecting wound healing
   • Hemodynamic disorders
     • Edema
     • Congestion
     • Hemorrhage
     • Thrombosis
     • Embolism
   • Neoplasia
     • Classification
     • Benign vs. malignant tumors
     • Tumor nomenclature
     • Cancer metastasis
2. 2

   Systemic Pathology

   8 topics

   • Cardiovascular System Pathology
     • Ischemic heart disease
     • Hypertensive heart disease
     • Cardiomyopathies
     • Valvular heart diseases
     • Vascular diseases
   • Respiratory System Pathology
     • Acute respiratory infections
     • Chronic respiratory infections
     • Obstructive lung diseases
     • Restrictive lung diseases
     • Lung tumors
     • Pulmonary embolism
   • Gastrointestinal System Pathology
     • Peptic ulcer disease
     • Inflammatory bowel disease
     • Liver diseases (e.g., hepatitis, cirrhosis)
     • Gastrointestinal tumors
   • Renal Pathology
     • Acute kidney diseases
     • Chronic kidney diseases
     • Glomerulonephritis
     • Nephrotic syndrome
     • Renal tumors
   • Hematopoietic System Pathology
     • Anemia
     • Leukemia
     • Lymphoma
     • Myeloproliferative disorders
     • Coagulation disorders
   • Endocrine System Pathology
     • Thyroid diseases
     • Adrenal diseases
     • Diabetes mellitus
     • Pituitary disorders
   • Nervous System Pathology
     • Stroke
     • Neurodegenerative diseases (e.g., Alzheimer's disease, Parkinson's disease)
     • CNS tumors
     • Demyelinating diseases
   • Musculoskeletal System Pathology
     • Osteoarthritis
     • Rheumatoid arthritis
     • Osteoporosis
     • Bone tumors
     • Connective tissue disorders
3. 3

   Special Pathology

   5 topics

   • Infectious diseases
     • Bacterial
     • Viral
     • Fungal
     • Parasitic infections
   • Immunopathology
     • Autoimmune diseases
     • Hypersensitivity reactions
     • Immunodeficiency disorders
     • Transplantation immunology
   • Environmental and nutritional diseases
     • Nutritional deficiencies (e.g., vitamin deficiencies)
     • Chemical toxins
     • Environmental pollutants
   • Genetic and developmental diseases
     • Inherited disorders
     • Chromosomal abnormalities
     • Congenital malformations
   • Neoplastic diseases
     • Pathogenesis
     • Histological classification
     • Grading
     • Staging
     • Molecular diagnostics of tumors
4. 4

   Laboratory Investigations in Pathology

   4 topics

   • Hematological investigations
     • Complete blood count (CBC)
     • Peripheral blood smear
     • Bone marrow examination
     • Coagulation tests
   • Microbiological investigations
     • Microscopic examination
     • Culture
     • Sensitivity testing
   • Histopathological techniques
     • Gross examination
     • Tissue processing
     • Staining (H&E, special stains)
     • Interpretation of histopathology slides
   • Immunohistochemistry and molecular pathology
     • Applications in diagnosis
     • Applications in prognosis
     • Applications in targeted therapy of tumors

Pathology flashcards for INI CET

24 of 52 cards from the Pathology deck — real questions with worked answers.

1. Differentiate the four cellular adaptations: hypertrophy, hyperplasia, atrophy, and metaplasia.

   Hypertrophy = increased cell size (e.g., cardiac muscle in hypertension). Hyperplasia = increased cell number (e.g., endometrial hyperplasia). Atrophy = decreased cell size/number (e.g., disuse atrophy). Metaplasia = reversible replacement of one differentiated cell type by another (e.g., squamous metaplasia of bronchial epithelium in smokers; Barrett esophagus = squamous to columnar).

2. What is the key biochemical/morphologic distinction between reversible and irreversible cell injury?

   Reversible injury: ATP depletion, cellular and mitochondrial swelling, membrane blebbing, ribosomal detachment — all recoverable. Irreversibility hallmarks are severe mitochondrial dysfunction (cannot restore oxidative phosphorylation) and profound plasma membrane damage causing massive Ca2+ influx and enzyme leakage (e.g., elevated cardiac troponins).

3. Name and locate the five classic patterns of necrosis.

   Coagulative (ischemic infarcts of solid organs except brain; architecture preserved), liquefactive (brain infarcts, bacterial abscesses), caseous (TB; cheese-like granuloma center), fat necrosis (acute pancreatitis, breast trauma; saponification), and fibrinoid (immune vascular damage, malignant hypertension; pink amorphous wall deposits).

4. Compare apoptosis and necrosis (energy, membrane, inflammation, DNA).

   Apoptosis: ATP-dependent, single cells, intact membrane, no inflammation, internucleosomal DNA laddering, apoptotic bodies. Necrosis: ATP-independent, cell groups, membrane rupture with enzyme leakage, marked inflammation, random DNA breakdown. Apoptosis = programmed/regulated; necrosis = accidental.

5. Outline the intrinsic (mitochondrial) pathway of apoptosis.

   Cell injury/loss of survival signals shifts the BCL-2 family balance: pro-apoptotic BAX/BAK form pores releasing cytochrome c. Cytochrome c + APAF-1 + caspase-9 form the apoptosome, activating executioner caspases 3 and 6. Regulated by anti-apoptotic BCL-2/BCL-XL. p53 promotes this pathway after DNA damage.

6. List the five cardinal signs of acute inflammation and their Latin terms.

   Rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function). The first four were described by Celsus; functio laesa was added by Virchow.

7. What are the sequential steps of leukocyte extravasation in acute inflammation?

   Margination and rolling (selectins: E-, P-, L-selectin binding sialyl-Lewis X), firm adhesion (integrins binding ICAM-1/VCAM-1, upregulated by TNF/IL-1), transmigration/diapedesis (PECAM-1/CD31), and chemotaxis toward agents like C5a, LTB4, IL-8, and bacterial N-formyl peptides.

8. Distinguish transudate from exudate.

   Transudate: low protein (<3 g/dL), low specific gravity (<1.012), few cells; due to altered hydrostatic/oncotic pressure (e.g., CHF, nephrotic syndrome). Exudate: high protein (>3 g/dL), high specific gravity (>1.020), many cells; due to increased vascular permeability from inflammation/infection. Light's criteria distinguish pleural effusions.

9. What characterizes granulomatous inflammation and name caseating vs non-caseating causes.

   Chronic inflammation with epithelioid macrophages, often Langhans/foreign-body giant cells, surrounded by lymphocytes. Caseating: tuberculosis, some fungi. Non-caseating: sarcoidosis, Crohn disease, leprosy, foreign body, berylliosis, cat-scratch disease. Driven by Th1 cells and IFN-gamma/TNF.

10. Contrast healing by primary vs secondary intention.

    Primary intention: clean, approximated wound edges (surgical incision), minimal tissue loss, little granulation tissue, small scar. Secondary intention: large tissue defect, abundant granulation tissue, significant wound contraction (via myofibroblasts), larger scar, slower healing.

11. Outline the phases and timeline of cutaneous wound healing.

    Hemostasis/inflammation (0–3 days: clot, neutrophils then macrophages), proliferation (3–10 days: granulation tissue, angiogenesis, re-epithelialization, type III collagen), and maturation/remodeling (weeks–months: type III collagen replaced by type I, increasing tensile strength to ~70–80% by ~3 months).

12. What is the difference between a labile, stable, and permanent cell with regard to regeneration?

    Labile cells continuously divide (surface epithelia, hematopoietic, GI mucosa) — excellent regeneration. Stable cells are quiescent (G0) but can re-enter cycle when stimulated (hepatocytes, renal tubules, fibroblasts). Permanent cells cannot divide (neurons, cardiac/skeletal muscle) — heal by scarring.

13. Define the components of Virchow's triad in thrombosis.

    Endothelial injury (most important, e.g., atherosclerosis, vasculitis), abnormal blood flow (stasis or turbulence, e.g., atrial fibrillation, aneurysm), and hypercoagulability (e.g., Factor V Leiden, antiphospholipid syndrome, malignancy). Any combination promotes pathologic thrombus formation.

14. Distinguish lines of Zahn, red (venous) thrombi, and postmortem clots.

    Lines of Zahn = alternating pale platelet/fibrin and dark RBC layers, indicating a thrombus formed in flowing blood antemortem. Red thrombi form in veins with stasis (more RBCs). Postmortem clots are gelatinous 'chicken-fat' yellow over dark 'currant-jelly' red, lack lines of Zahn, and are not attached to the wall.

15. What are the four types of emboli besides thromboemboli, and a classic feature of each?

    Fat embolism (long-bone fractures; dyspnea, petechiae, neurologic changes). Air/gas embolism (decompression sickness — 'the bends', caisson disease). Amniotic fluid embolism (labor; DIC, sudden dyspnea). Septic/tumor emboli. Most pulmonary emboli arise from deep leg veins; saddle embolus lodges at the bifurcation.

16. Define the steps of the metastatic cascade.

    Invasion (loss of E-cadherin, matrix metalloproteinase degradation of basement membrane), intravasation into vessels, survival in circulation, arrest and extravasation at distant site, then colonization/growth of micrometastases. Requires epithelial-mesenchymal transition and angiogenesis.

17. Differentiate benign from malignant neoplasms across key features.

    Benign: well-differentiated, slow growth, no invasion (encapsulated), no metastasis, few/normal mitoses, '-oma' suffix. Malignant: variable differentiation/anaplasia, rapid growth, local invasion, metastasis, atypical mitoses, '-carcinoma/-sarcoma' suffix. Metastasis is the single most reliable sign of malignancy.

18. What features define anaplasia (markers of malignancy)?

    Pleomorphism (variation in size/shape), hyperchromatic nuclei with high nuclear-to-cytoplasmic ratio (~1:1), prominent nucleoli, abundant and atypical (tripolar) mitoses, loss of polarity, and tumor giant cells. Anaplasia means lack of differentiation.

19. Compare oncogenes and tumor suppressor genes with examples.

    Oncogenes: gain-of-function, dominant (one mutated allele suffices), promote growth — RAS, MYC, HER2/ERBB2, ABL. Tumor suppressors: loss-of-function, recessive (Knudson two-hit, both alleles inactivated), normally restrain growth — RB, TP53, APC, BRCA1/2, NF1. TP53 is the 'guardian of the genome.'

20. List important tumor markers and their associated tumors.

    AFP — hepatocellular carcinoma, yolk sac/nonseminomatous germ cell tumors. CEA — colorectal/pancreatic. CA-125 — ovarian. CA 19-9 — pancreatic. PSA — prostate. beta-hCG — choriocarcinoma, germ cell. Calcitonin — medullary thyroid carcinoma. Chromogranin — neuroendocrine tumors.

21. Define the stages of atherosclerosis development.

    Endothelial injury -> LDL accumulation and oxidation in intima -> monocyte adhesion and migration becoming foam cells (fatty streak) -> smooth muscle cell migration/proliferation and collagen deposition forming a fibrous cap over a lipid/necrotic core (atheroma). Plaque rupture triggers thrombosis -> acute events.

22. What is the temporal evolution of microscopic changes in myocardial infarction?

    0–4 h: none (or wavy fibers). 4–12 h: early coagulation necrosis, edema. 12–24 h: contraction bands, neutrophils. 1–3 days: dense neutrophils, loss of nuclei. 3–7 days: macrophages remove dead myocytes (softest, rupture risk). 1–2 wk: granulation tissue. >2 mo: dense collagenous scar.

23. Differentiate the major cardiomyopathies.

    Dilated (most common): systolic failure, dilated chambers — alcohol, viral myocarditis, peripartum, doxorubicin. Hypertrophic: diastolic dysfunction, asymmetric septal hypertrophy, myofiber disarray — beta-myosin heavy chain mutation, sudden death in athletes. Restrictive: decreased compliance — amyloidosis, sarcoidosis, endomyocardial fibrosis.

24. Contrast emphysema and chronic bronchitis (COPD subtypes).

    Emphysema ('pink puffer'): permanent airspace enlargement distal to terminal bronchiole with alveolar wall destruction; centriacinar (smoking, upper lobes), panacinar (alpha-1 antitrypsin deficiency, lower lobes). Chronic bronchitis ('blue bloater'): productive cough >=3 months/year for >=2 years, mucous gland hyperplasia (increased Reid index).

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