Renal, Liver, Cardiac & Adrenal Function OmpathStudy

MONDAY 14TH JULY — FULL REVISION PACK Chemical Pathology (8–11 AM) + Haematology & Blood Transfusion (2–5 PM) --- PART A: CHEMICAL PATHOLOGY (MBPA 3600) --- A1. RENAL FUNCTION Tests used: Urea, creatinine, eGFR, electrolytes (Na⁺, K⁺, HCO3⁻), urinalysis (protein, blood, casts) Acute Kidney Injury (AKI) — classify by cause: Pre-renal — reduced perfusion (dehydration, hypotension, haemorrhage, heart failure) Renal/intrinsic — direct damage (acute tubular necrosis, glomerulonephritis, nephrotoxins) Post-renal — obstruction (stones, BPH, tumour) AKI lab pattern: ↑Urea, ↑creatinine (rapid rise over hours–days) ↑K⁺ — risk of arrhythmia Oliguria Urea:creatinine ratio 20:1 → pre-renal cause Chronic Kidney Disease (CKD) lab pattern: Persistently ↑urea/creatinine (weeks–months) Anaemia — from ↓erythropoietin production Hypocalcaemia + hyperphosphataemia — from ↓active vitamin D ↓eGFR (calculated from creatinine + age + gender + race) Nephritic vs Nephrotic syndrome (commonly confused — know cold): Feature Nephritic Nephrotic --- --- --- Proteinuria Mild Heavy ( 3.5g/day) Haematuria Prominent Minimal Blood pressure ↑ Normal/↑ Oedema Mild Marked Albumin Normal ↓ Lipids Normal ↑ Casts RBC casts Fatty/oval fat bodies Other renal points: ADH acts on V2 receptors in the collecting duct Thick ascending limb = "diluting segment" ATN = commonest cause of intrinsic AKI --- A2. LIVER FUNCTION TESTS (LFTs) Components and what each shows: ALT, AST → hepatocellular injury ALP, GGT → cholestasis (bile flow obstruction) Albumin, PT/INR → synthetic function Bilirubin (total, conjugated/unconjugated) → excretory function Pattern recognition: ALT/AST ALP → hepatocellular (viral hepatitis, alcohol, drugs) ALP/GGT ALT/AST → obstructive/cholestatic (gallstones, pancreatic head Ca) AST:ALT ratio 2 → suggests alcoholic liver disease Jaundice work-up: Ultrasound — dilated ducts = obstructive; normal ducts = hepatocellular Viral serology (HBsAg, anti-HCV) PT/INR — doesn't correct with vitamin K in hepatocellular disease; corrects in obstructive disease Split bilirubin — conjugated fraction dominant in obstruction Bilirubin metabolism disorders: Gilbert syndrome — mild ↓UGT activity, unconjugated hyperbilirubinaemia, benign Crigler-Najjar type II — reduced (not absent) UGT Crigler-Najjar type I — absent UGT, severe, fatal if untreated Dubin-Johnson syndrome — conjugated hyperbilirubinaemia, black liver pigmentation Rotor syndrome — conjugated hyperbilirubinaemia, no pigmentation --- A3. CARDIAC MARKERS Markers used to assess cardiac injury, in order of rise/fall: Marker Rises Peaks Returns to normal --- --- --- --- Myoglobin 1–2h 6–12h 24h CK-MB 3–6h 12–24h 48–72h Troponin I/T 3–6h 12–24h 7–14 days LDH 6–12h 24–48h 7–10 days Troponin — most sensitive and specific for MI, gold standard CK-MB — useful for detecting re-infarction, since troponin stays elevated too long Myoglobin — earliest to rise, but not cardiac-specific (also from skeletal muscle) LDH — historically used; LDH1 LDH2 ("flipped pattern") in MI, rarely used now Total CK also rises in skeletal muscle damage — CK-MB is the cardiac-specific fraction --- A4. ADRENAL DISORDERS Cushing's syndrome (↑cortisol): Causes: pituitary adenoma (Cushing's disease), adrenal adenoma, ectopic ACTH (small cell lung Ca), exogenous steroids Cortisol synthesis occurs in the zona fasciculata of the adrenal cortex Diagnostic tests: 24h urinary free cortisol, low-dose dexamethasone suppression test, late-night salivary cortisol Causes secondary diabetes via ↑gluconeogenesis + insulin resistance Addison's disease (adrenal insufficiency): ↓Cortisol, ↓aldosterone Hyponatraemia, hyperkalaemia, hypoglycaemia, hypotension ACTH stimulation (Synacthen) test — cortisol fails to rise Phaeochromocytoma: Tumour of adrenal medulla chromaffin cells, secretes catecholamines Key enzyme: Phenylethanolamine N-methyltransferase (PNMT) — converts noradrenaline to adrenaline, only found in the adrenal medulla Diagnostic test: 24h urinary metanephrines/catecholamines, plasma free metanephrines Causes secondary diabetes via glycogenolysis + inhibited insulin release Classic triad: episodic headache, sweating, palpitations (with hypertension) Congenital Adrenal Hyperplasia: Most common cause: 21-hydroxylase deficiency Leads to ↓cortisol, ↓aldosterone, ↑androgens (virilisation) Salt-wasting crisis in neonates (hyponatraemia, hyperkalaemia) --- A5. THYROID FUNCTION TESTS Primary hyperthyroidism — ↑T3/T4, ↓TSH (e.g. Graves' disease) Primary hypothyroidism — ↓T3/T4, ↑TSH (e.g. Hashimoto's thyroiditis) Secondary hypothyroidism — ↓T3/T4, ↓TSH (pituitary cause) Subclinical hypothyroidism — normal T3/T4, ↑TSH Graves' disease — TSH receptor antibodies (TRAb) stimulate the gland Hashimoto's — anti-TPO and anti-thyroglobulin antibodies --- A6. CALCIUM, PHOSPHATE & BONE Hypercalcaemia work-up: Serum calcium (ionised + total) PTH — ↑ in primary hyperparathyroidism, suppressed in malignancy Phosphate — ↓ in hyperparathyroidism PTHrP — ↑ in hum