# Clinical Enzymology > Clinical enzymology for FMGE Biochemistry: Km and Vmax, inhibition types, cardiac and pancreatic enzyme timelines, De Ritis ratio and drug inhibitors. - Canonical URL: https://prepelephant.com/topics/fmge/biochemistry/enzyme-clinical-fmge - Exam / course: FMGE · Subject: Biochemistry - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Clinical Enzymology", PrepElephant, https://prepelephant.com/topics/fmge/biochemistry/enzyme-clinical-fmge ## Direct answer Plasma enzymes are measured because injured cells leak them, and the pattern — which enzyme, how high, in what company — localises the damaged organ. Michaelis–Menten kinetics supplies the two constants the exam tests: Km, the substrate concentration at half-maximal velocity and an inverse index of affinity, and Vmax, proportional to the amount of enzyme; competitive inhibitors raise the apparent Km with Vmax unchanged, while non-competitive inhibitors cut Vmax and leave Km alone. FMGE Biochemistry pairs this kinetics with named drugs — statins at HMG-CoA reductase, methotrexate at dihydrofolate reductase, allopurinol at xanthine oxidase — and with the serial cardiac, hepatic and pancreatic enzyme profiles. ## What you must remember - Competitive inhibition: Km rises, Vmax unchanged, and a high substrate concentration overcomes the block; non-competitive inhibition: Vmax falls, Km unchanged because the inhibitor binds the enzyme regardless of substrate. - Named competitive inhibitors worth memorising: statins on HMG-CoA reductase, methotrexate on dihydrofolate reductase, allopurinol on xanthine oxidase, sulphonamides as substrate mimics of PABA, and the active metabolite of 5-fluorouracil on thymidylate synthase. - Irreversible inhibitors: aspirin on cyclo-oxygenase, organophosphates on acetylcholinesterase, heavy metals on sulfhydryl-dependent enzymes. - Myocardial infarction timeline: myoglobin rises first (1–2 hours) but is non-specific; troponin I or T rises at 3–4 hours, peaks around 24–48 hours and stays up 7–10 days (troponin T up to about 14); CK-MB rises at 4–6 hours and normalises by 48–72 hours, making it the reinfarction marker; LDH-1 exceeding LDH-2 (the "flipped" pattern) appears at 3–5 days. - Pancreatitis: amylase rises at 6–12 hours and falls within 3–5 days; lipase peaks near 24 hours, persists 7–14 days and is more specific — a raised amylase with normal lipase points away from the pancreas. - De Ritis ratio: AST/ALT above 2, with neither enzyme usually crossing 300–500 U/L, suggests alcoholic hepatitis because pyridoxal phosphate depletion cripples both hepatic transaminases. - An isolated raised alkaline phosphatase needs GGT: parallel elevation means liver origin; normal GGT means bone (adolescent growth, Paget disease, osteoblastic metastases, vitamin D deficiency). - Zymogens (trypsinogen, pepsinogen, prothrombin) are synthesised as inactive precursors so protease-producing organs do not digest themselves; most water-soluble vitamins serve as coenzyme precursors. ## Seventy-two hours of chest pain, read enzymatically A 58-year-old diabetic reaches the emergency department 90 minutes after crushing central chest pain with ST elevation. The troponin sent on arrival may still be normal — the marker confirms necrosis but must never gate reperfusion, which is decided by the electrocardiogram and symptoms. The troponin peaks on day 1–2 and, because of its long tail, will still be high on day 3. At 60 hours the patient develops fresh pain with new ST elevation; the troponin is meaningless now, already elevated from the first event, whereas CK-MB, which should have normalised by 48–72 hours, has risen again — biochemical proof of reinfarction, and the reason CK-MB survived the troponin era. Had the patient presented silently on day 4, the flipped LDH pattern (LDH-1 greater than LDH-2) was the historical clue to a late infarct. Finally, if the same profile appeared with a soft abdomen and a liquor-heavy weekend, amylase at ten times normal with lipase matching it moves the diagnosis from myocardium to pancreas in a single arithmetic step. ## Where students slip Waiting for troponin before reperfusing a STEMI is the classic error — markers confirm, they do not triage. Second, reinfarction is read off troponin despite its 10-day tail; CK-MB is the only marker whose return to baseline makes a second rise visible. Third, Km direction under competitive inhibition gets inverted; write it as "affinity falls, so the number rises" to fix it. Fourth, prostate questions still expect acid phosphatase awareness, though PSA has replaced it in practice, and PSA monitors disease more dependably than it screens for it. Fifth, an isolated alkaline phosphatase is chased as liver disease without a GGT, forgetting that a growing adolescent or a pregnant woman has physiologically high bone or placental enzyme. And a genuinely non-specific myoglobin rise at 2 hours is over-read as myocardial when the patient ran a marathon or has rhabdomyolysis. ## Frequently asked questions ### Which cardiac marker diagnoses reinfarction three days after the first infarct? CK-MB, because it normalises within 48–72 hours; a fresh rise is unambiguous, unlike the prolonged elevation of troponin. ### Which enzyme is most specific for acute pancreatitis? Lipase; amylase rises earlier but falls within days and also rises in salivary disease, macroamylasaemia and perforated viscus. ### How do competitive and non-competitive inhibition affect Km and Vmax? Competitive inhibition raises apparent Km with Vmax unchanged; non-competitive inhibition lowers Vmax with Km unchanged. ### What does an AST:ALT ratio above 2 suggest? Alcoholic liver disease, aided by pyridoxal phosphate deficiency limiting hepatic transaminase synthesis; levels usually stay below about 500 U/L. ### Which enzyme separates bone from hepatic origin of a raised alkaline phosphatase? GGT, which rises in parallel with hepatic but not osseous alkaline phosphatase. ### Which vitamin deficiency can lower both AST and ALT? Pyridoxine (vitamin B6), the precursor of pyridoxal phosphate, the coenzyme of both transaminases.