General & Systemic Pathology SAQ — Paper II OmpathStudy

MOUNT KENYA UNIVERSITY School of Medicine Department of Pathology Bachelor of Medicine and Bachelor of Surgery — Year 3 Unit Code: MBPA3500 General & Systemic Pathology SAQ — Paper II Date: 15th July 2025 Time: 3 Hours Main Exam --- SECTION A: SHORT ANSWER QUESTIONS (10 marks each)--- Q1. Give an outline of the various congenital neural tube defects mentioning their distinguishing features. Anencephaly — failure of rostral neuropore closure; absence of cerebral hemispheres; incompatible with life Encephalocele — herniation of brain tissue through a skull defect; usually occipital Meningocele — meninges herniate through vertebral defect; cord intact; better prognosis Meningomyelocele — meninges + spinal cord herniate; causes motor/sensory deficits below lesion Spina bifida occulta — vertebral arch defect only; no herniation; skin-covered; often asymptomatic Syringomyelia — cavitation within the spinal cord; progressive sensorimotor loss --- Q2. Classify chemical carcinogenic agents giving examples and types of cancers caused. Polycyclic aromatic hydrocarbons (e.g. benzo[a]pyrene in cigarette smoke) → lung, skin cancer Aromatic amines (e.g. beta-naphthylamine) → bladder cancer Alkylating agents (e.g. cyclophosphamide, chemotherapy drugs) → leukaemia, lymphoma Nitrosamines (e.g. in processed meats) → gastric, oesophageal cancer Aflatoxin B1 (fungal toxin, Aspergillus ) → hepatocellular carcinoma Asbestos → mesothelioma, lung cancer Benzene → acute myeloid leukaemia --- Q3. Compare and contrast autosomal dominant and autosomal recessive disorders focusing on mode of transmission and clinical manifestation. Feature Autosomal Dominant Autosomal Recessive --- --- --- Copies needed 1 mutant allele sufficient 2 mutant alleles required Carrier state No silent carriers Carriers exist (heterozygotes) Generation skipping No Yes (can skip generations) Penetrance Variable Usually complete Expressivity Variable More uniform Examples Marfan's, Huntington's, Neurofibromatosis Cystic fibrosis, Sickle cell, PKU, Tay-Sachs Onset Often adult-onset Often childhood/early onset Enzyme defects Structural proteins usually Enzyme deficiencies usually --- Q4. Discuss the different pathophysiological categories of oedema giving two examples for each. Increased hydrostatic pressure → fluid pushed out of vessels; e.g. CCF, portal hypertension Decreased oncotic pressure → reduced plasma proteins; e.g. nephrotic syndrome, liver cirrhosis (hypoalbuminaemia) Lymphatic obstruction → impaired drainage; e.g. filariasis, post-mastectomy lymphoedema Increased vascular permeability → inflammatory leakage; e.g. sepsis, acute inflammation Sodium/water retention → e.g. renal failure, Cushing's syndrome Pitting oedema — leaves a pit on pressure (systemic causes); Non-pitting — lymphoedema/myxoedema --- Q5. Describe the immune mechanisms of glomerular injury. Type II hypersensitivity — anti-GBM antibodies (e.g. Goodpasture's syndrome); linear IgG deposits on GBM Type III hypersensitivity — immune complex deposition (e.g. post-streptococcal GN, SLE); granular deposits T-cell mediated — podocyte injury; e.g. minimal change disease (cytokine-mediated foot process effacement) IgA nephropathy — mesangial IgA deposits; haematuria after mucosal infections FSGS — focal segmental sclerosis; podocyte loss; heavy proteinuria Complement activation → membrane attack complex → GBM damage → proteinuria/haematuria --- Q6. Give an outline of the major risk factors for atherosclerosis. Non-modifiable: Age, male sex, family history, genetic predisposition Modifiable: Hypertension → endothelial injury Hyperlipidaemia (increased LDL, decreased HDL) → foam cell formation Diabetes mellitus → glycation of vessel walls Smoking → oxidative stress, endothelial dysfunction Obesity → dyslipidaemia, inflammation Sedentary lifestyle, stress Pathological basis: Endothelial injury → lipid accumulation → macrophage infiltration → foam cells → fatty streak → fibrous plaque --- Q7. Discuss the aetiology, pathogenesis and morphology of liver cirrhosis. Aetiology: Alcohol (commonest in West) — direct hepatotoxicity Viral hepatitis B and C — chronic inflammation Non-alcoholic fatty liver disease (NAFLD) Autoimmune hepatitis, primary biliary cirrhosis Wilson's disease, haemochromatosis Cryptogenic (unknown) Pathogenesis: Repeated hepatocyte injury → activation of stellate cells (Ito cells) → fibrosis TGF-β drives collagen deposition → disruption of normal lobular architecture Regenerative nodules form but lack normal function Morphology: Micronodular (alcohol) — nodules <3mm, uniform Macronodular (viral) — nodules 3mm, variable Bridging fibrosis → bands of fibrous tissue crossing lobules Grossly: shrunken, hard, nodular liver --- Q8. Compare Type 1 and Type 2 Diabetes Mellitus focusing on aetiology, pathogenesis and clinical features. Feature Type 1 DM Type 2 DM --- --- --- Onset Childhood/young Adult ( 40, now younger) Aetiology Autoimmune destruction of β-cells Insulin resistance + relative