# Liver Functions Physiology

> Liver functions in MBBS Physiology: dual blood supply, albumin and clotting factor synthesis, urea cycle, bilirubin conjugation, storage and CYP450 metabolism.

- Canonical URL: https://prepelephant.com/topics/mbbs/physiology/liver-functions-physiology
- Exam / course: MBBS · Subject: Physiology
- 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: "Liver Functions Physiology", PrepElephant, https://prepelephant.com/topics/mbbs/physiology/liver-functions-physiology

## Direct answer

The 1.5 kg liver — 2 per cent of body weight — receives about 25 per cent of cardiac output through a dual inflow: the portal vein supplies roughly 75 per cent of flow, the hepatic artery 25 per cent but half the oxygen. Its functions span metabolism (glycogen storage of 75-100 g, gluconeogenesis, lipoprotein and amino acid handling), synthesis (10-12 g of albumin daily, all clotting factors except most factor VIII, transferrin, and bile at 600-1000 mL/day), detoxification (ammonia to urea via the Krebs-Henseleit cycle, bilirubin glucuronidation, phase I CYP450 oxidation and phase II conjugation of drugs), storage (glycogen, vitamins A, D and B12, iron as ferritin), and filtration (Kupffer cells clearing gut-borne bacteria and endotoxin). It is also the only human internal organ that regenerates substantial mass.

## What you must remember

- **Haemodynamic numbers:** total hepatic flow near 1.5 L/min (25 per cent of cardiac output); portal vein 1000-1100 mL/min, hepatic artery 300-400 mL/min; the artery autoregulates to keep total flow constant when portal flow falls.
- **Albumin:** 10-12 g synthesized daily, half-life about 20 days — a chronic, not acute, marker of liver function; also transports bilirubin, calcium and drugs.
- **Clotting factors:** the liver makes fibrinogen and factors II, V, VII, IX, X, XI, XII and XIII; factor VIII is largely extrahepatic (endothelium) — factor VII's 4-6 hour half-life makes prothrombin time the earliest synthetic marker to fail.
- **Vitamin K distinction:** II, VII, IX and X need vitamin K for gamma-carboxylation; cholestatic jaundice causes a PT that corrects with vitamin K, hepatocellular jaundice a PT that does not — a favourite short-case question.
- **Ammonia handling:** the urea cycle converts toxic ammonia to excretable urea; in failure, ammonia and mercaptans cross the blood-brain barrier, and treatment (lactulose, rifaximin) works by acidifying the colon and reducing ammonia absorption.
- **Bilirubin:** UDP-glucuronosyltransferase conjugates bilirubin; its absence (Crigler-Najjar) or reduction (Gilbert syndrome, affecting up to 5-7 per cent of Indians) causes unconjugated hyperbilirubinaemia.
- **Drug metabolism:** phase I oxidation (CYP3A4 the workhorse) followed by phase II conjugation (glucuronidation, sulphation); first-pass extraction explains why cirrhosis doubles or triples oral bioavailability of flow-limited drugs.
- **Storage and others:** 75-100 g glycogen, several years of B12, iron as ferritin; plus IGF-1, angiotensinogen and thrombopoietin — the reason platelets fall and bruising appears in cirrhosis.
- **Regeneration:** up to 70 per cent resection is survivable, restored in weeks to months driven by HGF and IL-6 — the biological licence for living-donor donation.

## A worked case: reading a cirrhotic's function panel

A patient with cirrhosis has INR 1.9, albumin 28 g/L, platelets 80,000, bilirubin 3 mg/dL and mild encephalopathy — every value decodes one hepatic job. The INR reflects factor synthesis (VII's short half-life making it the sentinel), and it fails to correct with vitamin K, confirming hepatocellular rather than cholestatic disease. The low albumin reduces plasma oncotic pressure, joining portal hypertension in producing ascites. Thrombopoietin failure plus hypersplenism explains the platelet count, and shunted ammonia explains the flapping tremor and asterixis; lactulose acidifies the colon (trapping ammonia as ammonium) while rifaximin cuts ammonia-producing bacteria. Notice what transaminases do not tell you: they are leak markers of injury, nearly normal in burnt-out cirrhosis even as the synthetic panel screams failure — function tests measure function, transaminases measure damage.

## Where students slip

The factor VIII exception is the classic single-best-answer: all other clotting factors fall in liver failure, VIII stays normal or rises (endothelial origin, and an acute-phase reactant). The second slip is the vitamin K logic — the liver must synthesize the proteins; vitamin K only modifies them, so a failing liver cannot be rescued by the vitamin while an obstructed biliary tree (no bile, no fat, no vitamin K absorption) can. Third, in shock the hepatic artery cannot fully compensate for falling portal flow, and the centrilobular zone, farthest from arterial inflow, necroses first.

## Frequently asked questions

### What is the liver's dual blood supply and its proportions?

Portal vein about 75 per cent of flow (oxygen-poor, nutrient-rich) and hepatic artery about 25 per cent of flow but roughly half the oxygen supply, together near 1.5 L/min.

### Why is prothrombin time the earliest clotting abnormality in liver failure?

Factor VII has the shortest half-life of the hepatic clotting factors (4-6 hours), so its synthesis fails first and prolongs the prothrombin time before other factors fall.

### Why does hepatocellular jaundice not correct its PT with vitamin K?

Vitamin K only gamma-carboxylates factors the liver has already synthesized; in hepatocellular disease the factory itself is failing, unlike in cholestasis where bile-less malabsorption of vitamin K is the problem.

### How does the liver detoxify ammonia?

Through the Krebs-Henseleit urea cycle, converting ammonia to urea for renal excretion; failure leads to hepatic encephalopathy treated with lactulose and rifaximin.

### Which is the odd-one-out clotting factor in liver disease, and why?

Factor VIII — synthesized mainly by endothelial cells, it remains normal or rises in liver failure while factors II, V, VII, IX, X, XI, XII and XIII fall.