Cat. Pathology: Acute Inflammation, OmpathStudy

MOUNT KENYA UNIVERSITY ACADEMIC YEAR 2025/2026 SCHOOL OF MEDICINE PATHOLOGY DEPARTMENT BACHELOR OF MEDICINE AND BACHELOR OF SURGERY — YEAR 3 CONTINUOUS ASSESSMENT TEST 2 UNIT CODE: MBPA 3411 — INTRODUCTION TO PATHOLOGY --- 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. Model Answer: Acute inflammation is orchestrated by a cascade of chemical mediators released from plasma and cells (mast cells, platelets, neutrophils, macrophages, endothelium) at the site of injury. They act on vessels and leukocytes to produce the cardinal signs of inflammation — redness, heat, swelling, pain, loss of function. Vascular mediators: Histamine (from mast cell granules) — released within seconds of injury. Causes arteriolar vasodilation and increased venular permeability (endothelial gap formation), producing redness and oedema. The immediate mediator. Bradykinin (kinin system) — increases vascular permeability, causes pain, and contributes to vasodilation. Chemotactic mediators (directing cell traffic): C5a (complement) and IL-8/CXCL8 (chemokine) — establish a concentration gradient that recruits neutrophils first (within hours), guiding them from the vessel lumen to the site of injury (chemotaxis). Arachidonic acid metabolites: Prostaglandins (e.g. PGE2) — vasodilation, potentiate pain, fever. Leukotrienes (e.g. LTB4) — potent neutrophil chemoattractant, increases vascular permeability; LTC4/D4/E4 cause vasoconstriction and bronchospasm. Cellular sequence: Neutrophils are the first cells recruited in acute inflammation (peak 6–24h), clearing bacteria and debris via phagocytosis. Macrophages follow later (24–48h+), clearing remaining debris and apoptotic neutrophils, and — together with cytokines like IL-1 and TNF-α — bridging into the repair phase by stimulating fibroblast proliferation and angiogenesis (via growth factors such as VEGF). Two specific examples illustrated: Histamine (immediate vascular response) and C5a (chemotactic recruitment of neutrophils) — together demonstrating how mediators couple the vascular and cellular arms of acute inflammation. --- Question 2 Describe the sequence of pathological changes that occur in pulmonary embolism starting from thrombus formation to the development of shock. Model Answer: 1. Thrombus formation: A deep vein thrombosis (DVT) forms most commonly in the deep veins of the lower limb (femoral, popliteal, or iliac veins), favoured by Virchow's triad — stasis, hypercoagulability, endothelial injury. 2. Embolization: Part or all of the thrombus dislodges (becomes an embolus) and travels via the inferior vena cava → right atrium → right ventricle → pulmonary artery . 3. Lodgement: The embolus lodges in a pulmonary artery or its branches, mechanically obstructing blood flow. (Note: a paradoxical embolism reaching systemic circulation would require a septal defect — not the typical pathway.) 4. Haemodynamic consequence: Obstruction → increased pulmonary vascular resistance → impaired gas exchange and hypoperfusion of lung parenchyma distal to the clot → hypoxaemia. 5. Right heart strain: The right ventricle must pump against a sudden rise in afterload → acute right ventricular strain ("acute cor pulmonale") → reduced right ventricular output. 6. Shock: Reduced right ventricular output → reduced left ventricular filling → decreased cardiac output → obstructive shock , with hypotension, tachycardia, and tissue hypoperfusion. If massive, this can be rapidly fatal. --- 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. Model Answer: Protein deficiency: Protein is essential for fibroblast proliferation, collagen synthesis, and production of acute-phase proteins, enzymes, and clotting factors (e.g. thrombin) needed for tissue repair. Hypoalbuminaemia reduces oncotic pressure (contributing to oedema) and impairs transport of iron and other nutrients to healing tissue. Protein is also required to build antibodies and immune cell components, so deficiency directly impairs both repair and immunity — explaining recurrent infections. Vitamin C: Vitamin C is a cofactor for prolyl and lysyl hydroxylase , enzymes required to hydroxylate proline and lysine residues during collagen synthesis. Without this, collagen is structurally weak and cannot cross-link properly, leading to fragile, slow-healing wounds. Severe deficiency causes scurvy — manifesting as poor wound healing, bleeding gums, and easy bruising (not night blindness, wh