MRCS Part A Pathology Flashcards

24 sample cards from the Pathology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Distinguish labile, stable, and permanent cells with examples relevant to tissue repair.

   Labile: continuously dividing (surface epithelia, bone marrow). Stable: quiescent, divide when stimulated (hepatocytes, renal tubular cells, fibroblasts). Permanent: non-dividing (neurons, cardiac and skeletal muscle) — heal by scar.

2. What are the steps of healing by primary vs secondary intention?

   Primary intention: clean, apposed wound edges (surgical incision) — minimal tissue loss, small scar. Secondary intention: large tissue defect — heals by granulation tissue, wound contraction (myofibroblasts), and larger scar.

3. Outline the components and sequence of granulation tissue formation.

   Angiogenesis (new capillaries), proliferation of fibroblasts, deposition of loose ECM/collagen, and infiltration by inflammatory cells. It appears soft, pink, and granular, and later matures into a fibrous scar.

4. Which growth factor drives angiogenesis and which drives fibroblast proliferation and collagen deposition in wound healing?

   Angiogenesis: VEGF (vascular endothelial growth factor). Fibroblast proliferation, collagen synthesis, and scar formation: TGF-β (also PDGF and FGF).

5. Which collagen predominates in early granulation tissue and which in the mature scar?

   Early wound/granulation tissue: type III collagen. Mature scar: type I collagen (via remodeling by matrix metalloproteinases, MMPs).

6. List local and systemic factors that impair wound healing.

   Local: infection, poor blood supply/ischemia, foreign bodies, mechanical stress, denervation. Systemic: diabetes, malnutrition (especially vitamin C and protein deficiency), glucocorticoids, zinc deficiency, old age, and smoking.

7. State Starling's forces and the equation governing fluid movement across capillaries.

   Net filtration depends on hydrostatic and oncotic pressure gradients: $$J_v = K_f\left[(P_c - P_i) - \sigma(\pi_c - \pi_i)\right]$$ where $P$ is hydrostatic pressure, $\pi$ is oncotic pressure, $K_f$ is the filtration coefficient, and $\sigma$ is the reflection coefficient.

8. List the four main pathophysiologic causes of edema.

   Increased hydrostatic pressure (venous obstruction, heart failure), reduced plasma oncotic pressure (hypoalbuminemia — nephrotic syndrome, liver disease, malnutrition), lymphatic obstruction (lymphedema), and increased vascular permeability/sodium retention (inflammation, renal disease).

9. Define hematoma, petechiae, purpura, and ecchymosis by size.

   Hematoma: accumulation of blood within tissue. Petechiae: 1–2 mm hemorrhages. Purpura: 3–10 mm (≥3 mm). Ecchymosis: >1–2 cm subcutaneous bruise.

10. State Virchow's triad for thrombosis.

    Endothelial injury, abnormal blood flow (stasis or turbulence), and hypercoagulability (thrombophilia).

11. How do arterial and venous thrombi differ in composition and appearance?

    Arterial thrombi: form under high flow, platelet-rich ('white'), grow retrograde, and show lines of Zahn. Venous thrombi: form in stasis, red/RBC-rich ('red'), grow in the direction of blood flow, and almost always occlusive.

12. What are the lines of Zahn and their significance?

    Lines of Zahn are alternating pale layers of platelets/fibrin and darker layers of red cells in a thrombus. They indicate the thrombus formed in flowing blood ante-mortem, distinguishing it from a post-mortem clot.

13. List the possible fates of a thrombus.

    Propagation, embolization, dissolution (fibrinolysis), and organization with recanalization.

14. Name the major inherited (primary) causes of hypercoagulability.

    Factor V Leiden (activated protein C resistance), prothrombin G20210A mutation, antithrombin III deficiency, protein C deficiency, and protein S deficiency.

15. Define embolism and list the main types.

    An embolus is a detached intravascular solid, liquid, or gas mass carried to a distant site. Types: thromboembolism (most common), fat, air/gas, amniotic fluid, tumor, septic, and foreign-body emboli.

16. Where do most pulmonary emboli originate, and what is a saddle embolus?

    Most pulmonary emboli arise from deep vein thromboses of the lower extremities (especially popliteal and larger proximal veins). A saddle embolus lodges at the bifurcation of the main pulmonary artery and can cause sudden death.

17. What is a paradoxical embolus?

    A paradoxical embolus is a venous (systemic) thrombus that passes into the arterial circulation through a right-to-left cardiac shunt (e.g. patent foramen ovale or atrial/ventricular septal defect), reaching systemic sites such as the brain.

18. Define shock and list its three major categories.

    Shock is systemic hypoperfusion causing inadequate tissue oxygenation and cellular hypoxia. Categories: hypovolemic (blood/fluid loss), cardiogenic (pump failure), and distributive (septic, anaphylactic, neurogenic — vasodilation).

19. Describe the three clinical stages of shock.

    Nonprogressive (compensated): reflex mechanisms (tachycardia, vasoconstriction) maintain perfusion. Progressive: tissue hypoperfusion, metabolic (lactic) acidosis, worsening circulation. Irreversible: cellular/organ injury so severe that survival is impossible even if hemodynamics are corrected.

20. What is the pathophysiology of septic shock?

    Most often gram-negative or gram-positive bacterial infection; microbial products (e.g. LPS/endotoxin) trigger massive cytokine release (TNF, IL-1), causing systemic vasodilation, increased vascular permeability, DIC, myocardial depression, and multi-organ failure — a hyperdynamic, warm, high-cardiac-output early state.

21. Explain the difference between autosomal dominant and autosomal recessive inheritance patterns.

    Autosomal dominant: one mutant allele suffices; affects both sexes, vertical transmission through generations, often structural proteins/receptors (e.g. Marfan, familial hypercholesterolemia). Autosomal recessive: two mutant alleles needed; often enzyme defects, may skip generations, associated with consanguinity (e.g. cystic fibrosis).

22. What are the karyotype and key features of Down syndrome, Klinefelter syndrome, and Turner syndrome?

    Down syndrome: trisomy 21 (47,XX or XY,+21) — intellectual disability, flat facies, cardiac defects. Klinefelter: 47,XXY — male hypogonadism, tall, infertility. Turner: 45,X — short stature, webbed neck, ovarian dysgenesis, coarctation of aorta.

23. What is the two-hit hypothesis (Knudson) in cancer genetics?

    For tumor suppressor genes, both alleles must be inactivated ('two hits') for tumorigenesis. In hereditary cancers the first hit is inherited (germline) and only one somatic hit is needed; in sporadic cancers both hits are somatic, hence later onset. Classic example: retinoblastoma (RB gene).

24. Define neoplasia and distinguish the essential features of benign vs malignant tumors.

    Neoplasia is autonomous, uncoordinated new tissue growth persisting after the stimulus stops. Benign: well-differentiated, slow-growing, encapsulated, non-invasive, do NOT metastasize. Malignant: poorly differentiated (anaplastic), rapid growth, invasive, and metastasize.

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