FMGE 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 FMGE, 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 FMGE

24 of 63 cards from the Pathology deck — real questions with worked answers.

1. What are the two main patterns of reversible cell injury seen under light microscopy?

   Cellular (hydropic/vacuolar) swelling due to failure of energy-dependent ion pumps, and fatty change (steatosis), most often in liver, heart and kidney.

2. List the four cellular adaptations to stress with one example each.

   Hypertrophy (cardiac muscle in hypertension), hyperplasia (endometrium under estrogen), atrophy (disused skeletal muscle), and metaplasia (squamous metaplasia of bronchial epithelium in smokers).

3. What is the hallmark of irreversible cell injury at the morphological and molecular level?

   Severe mitochondrial dysfunction with inability to make ATP, plus profound membrane damage (including lysosomal); morphologically, irreversibility correlates with dense amorphous mitochondrial densities and membrane breaches.

4. Contrast the morphologic and biochemical features of necrosis versus apoptosis.

   Necrosis: cell swelling, membrane rupture, enzymatic digestion, leakage of contents, and inflammation; affects cell groups. Apoptosis: cell shrinkage, chromatin condensation, apoptotic bodies, intact membrane, no inflammation; ATP-dependent and usually single cells.

5. Name the types of necrosis and give a classic association for each.

   Coagulative (ischemic infarcts of solid organs), liquefactive (brain infarcts, abscesses), caseous (tuberculosis), fat necrosis (acute pancreatitis), fibrinoid (immune vasculitis, malignant hypertension), and gangrenous (limb ischemia).

6. Which intrinsic and extrinsic pathways trigger apoptosis, and what enzymes are the executioners?

   Intrinsic (mitochondrial) pathway via BAX/BAK and cytochrome c release (regulated by BCL-2 family); extrinsic via death receptors (Fas/FasL, TNFR). Both converge on executioner caspases 3 and 6.

7. What are the five cardinal signs of acute inflammation and their Latin terms?

   Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa).

8. List the sequential steps of leukocyte extravasation in acute inflammation.

   Margination and rolling (selectins), firm adhesion (integrins binding ICAM-1/VCAM-1), transmigration/diapedesis (PECAM-1/CD31), and chemotaxis toward the stimulus.

9. Name the principal chemical mediators of vasodilation, increased vascular permeability, and pain in inflammation.

   Vasodilation: histamine, prostaglandins (PGI2, PGE2), nitric oxide. Permeability: histamine, bradykinin, leukotrienes C4/D4/E4. Pain: prostaglandins (PGE2) and bradykinin.

10. What distinguishes chronic inflammation from acute inflammation in terms of cells and outcome?

    Chronic inflammation is dominated by macrophages, lymphocytes and plasma cells (not neutrophils), with concurrent tissue destruction, angiogenesis and fibrosis (healing by scarring) rather than resolution.

11. What is a granuloma and what are its two main types?

    A granuloma is a focal collection of activated (epithelioid) macrophages, often with multinucleate giant cells and a rim of lymphocytes. Types: caseating (e.g., TB) and non-caseating (e.g., sarcoidosis, Crohn disease).

12. What are the phases of cutaneous wound healing and their approximate timing?

    Hemostasis and inflammation (0-3 days), proliferation with granulation tissue, angiogenesis and re-epithelialization (3 days-2 weeks), and maturation/remodeling with collagen reorganization (weeks to months).

13. Differentiate healing by primary versus secondary intention.

    Primary intention: clean, apposed wound edges (sutured surgical wound) with minimal granulation tissue and small scar. Secondary intention: large open wound healing by abundant granulation tissue, wound contraction (myofibroblasts) and a larger scar.

14. What is the difference between a hypertrophic scar and a keloid?

    A hypertrophic scar has excess collagen confined to the original wound boundaries and may regress. A keloid extends beyond the original wound margins, does not regress, and is more common in darker-skinned individuals.

15. Define edema, transudate and exudate, including the protein and specific gravity criteria.

    Edema is excess interstitial fluid. Transudate: protein-poor (specific gravity <1.012), from hydrostatic/oncotic imbalance. Exudate: protein-rich (specific gravity >1.020), from increased vascular permeability in inflammation.

16. What is the difference between thrombosis and an embolus, and name the components of Virchow's triad.

    Thrombosis is in-situ formation of a blood clot in flowing blood; an embolus is a detached intravascular mass carried to a distant site. Virchow's triad: endothelial injury, abnormal (stasis/turbulent) blood flow, and hypercoagulability.

17. Contrast a red (hemorrhagic) infarct with a white (pale) infarct.

    Red infarcts occur in loose tissues with dual blood supply or venous occlusion (lung, intestine). White infarcts occur with arterial occlusion in solid organs with end-arterial supply (heart, spleen, kidney).

18. What are the lines of Zahn and what do they indicate?

    Lines of Zahn are alternating pale layers of platelets/fibrin and dark layers of red cells in a thrombus; they indicate the thrombus formed in flowing blood (antemortem) rather than postmortem clotting.

19. What is the difference between a benign and a malignant neoplasm in nomenclature and behavior?

    Benign tumors are well-differentiated, slow-growing, encapsulated, non-invasive and non-metastasizing (suffix -oma). Malignant tumors are poorly differentiated (anaplastic), invasive, metastasize, and are named carcinoma (epithelial) or sarcoma (mesenchymal).

20. List the cytological features of anaplasia (malignancy).

    Pleomorphism, hyperchromatic nuclei with high nuclear-to-cytoplasmic ratio, prominent nucleoli, abundant and atypical (tripolar) mitoses, loss of polarity, and tumor giant cells.

21. Define the difference between dysplasia, carcinoma in situ, and invasive carcinoma.

    Dysplasia is disordered, atypical growth that is reversible and does not breach the basement membrane. Carcinoma in situ is full-thickness dysplasia confined above the basement membrane. Invasive carcinoma penetrates the basement membrane.

22. What are the routes of metastatic spread and the typical route for carcinomas versus sarcomas?

    Routes: lymphatic, hematogenous, and transcoelomic (seeding of body cavities). Carcinomas classically spread first via lymphatics; sarcomas spread preferentially via the bloodstream (hematogenous).

23. Distinguish oncogenes from tumor suppressor genes, with a key example of each.

    Oncogenes are gain-of-function, dominant, promote growth (e.g., RAS, MYC, HER2). Tumor suppressor genes are loss-of-function, usually require both alleles inactivated (two-hit hypothesis), and brake growth (e.g., TP53, RB1).

24. List the four types of hypersensitivity reactions with the immune mechanism of each.

    Type I: IgE-mediated immediate (anaphylaxis). Type II: antibody-mediated cytotoxic (autoimmune hemolytic anemia). Type III: immune-complex mediated (SLE, serum sickness). Type IV: T-cell mediated delayed (TB, contact dermatitis).

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