Pathology Mechanisms: Inflammation, PE, & OmpathStudy

MOUNT KENYA UNIVERSITY Academic Year: 2025/2026 School of Medicine — Pathology Department Programme: Bachelor of Medicine and Bachelor of Surgery, Year 3 Assessment: Continuous Assessment Test 2 — End of Semester 1 Unit Code: MBPA 3411 Unit Title: Introduction to Pathology Date: 8th December, 2025 Time: 30 minutes Reg No: BMS/2023/.. --- SECTION 1: SHORT ANSWER QUESTIONS (10 marks each) Question 1: "Explain the role and significance of chemical mediators in the initiation and regulation of the acute inflammatory response. Illustrate your answer with two specific examples." Answer: Chemical mediators are molecules released by cells or plasma that trigger, amplify, and control the acute inflammatory response They act on vessels, leukocytes, and tissues to produce the cardinal signs of inflammation (redness, heat, swelling, pain, loss of function) Roles/significance: Vasodilation → increased blood flow (redness, heat) Increased vascular permeability → plasma leakage/oedema Chemotaxis → recruitment of leukocytes to injury site Pain induction (sensitise nerve endings) Regulation/resolution of the response, preventing excessive tissue damage Examples (any two): Histamine (from mast cells) — causes vasodilation and increased vascular permeability, acting early in the response Prostaglandins (from arachidonic acid via COX pathway) — cause vasodilation and potentiate pain/fever Other acceptable examples: bradykinin (pain, permeability), complement (C3a/C5a — chemotaxis, opsonisation), cytokines like TNF-α/IL-1 (systemic effects, fever, leukocyte activation) Question 2: "Describe the sequence of pathological changes that occur in pulmonary embolism starting from thrombus formation to the development of shock." Answer: Thrombus formation: usually originates as a deep vein thrombosis (DVT) in the lower limb veins, favoured by Virchow's triad (stasis, hypercoagulability, endothelial injury) Embolisation: part of the thrombus dislodges (embolus) and travels via the venous system → right heart → pulmonary arterial circulation Lodgement: embolus occludes a pulmonary artery or its branches, depending on size (saddle embolus in main pulmonary artery vs smaller peripheral occlusion) Pulmonary consequences: Obstruction → reduced perfusion to ventilated lung (V/Q mismatch) → hypoxaemia Release of vasoactive mediators (serotonin, thromboxane) → reflex vasoconstriction, bronchoconstriction Possible pulmonary infarction if collateral circulation is inadequate Cardiovascular consequences: Increased pulmonary vascular resistance → acute right ventricular strain/failure (cor pulmonale) Reduced left ventricular preload → falling cardiac output Progression to shock: Falling cardiac output + hypoxaemia → systemic hypotension Inadequate tissue perfusion → obstructive shock Can progress to cardiac arrest if massive embolism (saddle embolus) --- SECTION 2: LONG ESSAY QUESTION (20 marks) Question 1: "A 4-year-old child from a resource-limited setting presents with delayed wound healing, recurrent infections, and poor growth. Discuss the pathological mechanisms by which nutritional deficiencies impair tissue repair and immune function. Include the role of protein, vitamin C, and micronutrients in the healing process and explain the environmental factors that perpetuate malnutrition." Answer: A. Role of protein in healing/immunity Protein provides amino acids essential for collagen synthesis, fibroblast proliferation, and granulation tissue formation Deficiency (as in kwashiorkor) → reduced collagen deposition → weak, delayed wound healing Protein is also required for antibody (immunoglobulin) synthesis and immune cell proliferation → deficiency causes impaired humoral and cell-mediated immunity → recurrent infections B. Role of vitamin C Essential cofactor for prolyl and lysyl hydroxylase enzymes, which hydroxylate collagen precursors Deficiency → defective collagen cross-linking → fragile, poorly tensile scar tissue and delayed wound healing (classically seen in scurvy) Also supports neutrophil function and acts as an antioxidant, contributing to immune defence C. Role of micronutrients Zinc: cofactor for DNA/RNA polymerases and matrix metalloproteinases; deficiency impairs cell proliferation, epithelialisation, and immune cell function Iron: required for oxygen transport (haemoglobin) and collagen hydroxylation; deficiency causes tissue hypoxia and impaired healing Vitamin A: supports epithelial differentiation and immune function; deficiency impairs mucosal barriers, increasing infection risk D. Mechanisms linking malnutrition to poor growth and infection Reduced substrate availability impairs cell division, tissue regeneration, and thymic/lymphoid tissue development Immune compromise (reduced T-cell function, impaired phagocytosis, low antibody levels) → recurrent infections Infections further worsen nutrition (anorexia, increased catabolic demand) → vicious cycle of malnutrition–infection–poor growth E. Environmental factors perpetuatin