Page 1 of 6

BI11.1-2 | Organ Function tests and Hormones — SDL Guide

Learning Objectives

  • Interpret a Liver Function Test (LFT) panel and identify patterns of hepatocellular vs cholestatic liver disease
  • Interpret a Renal Function Test (RFT) panel and recognise markers of glomerular and tubular dysfunction
  • Interpret a Thyroid Function Test (TFT) panel and diagnose primary vs secondary hypo/hyperthyroidism
  • Describe the biochemical basis of each test and explain why specific analytes are measured
  • Correlate common clinical scenarios in India (jaundice, nephrotic syndrome, hypothyroidism) with biochemical findings

INSTRUCTIONS

Work through each section in order. The clinical scenarios are built around real district hospital situations. Attempt each self-check question before revealing the answer. Estimated time: 50 minutes.

References


CLINICAL SCENARIO

A 38-year-old man from a village near Puducherry arrives at the MGMCRI outpatient with yellowish discolouration of the eyes for 5 days, fatigue, and mild upper abdominal discomfort. His urine is dark. He has no history of alcohol use. The RMO orders a "Liver Profile." The results come back:

Total Bilirubin: 8.2 mg/dL (N: <1.2)
Direct Bilirubin: 6.1 mg/dL
ALT (SGPT): 820 U/L (N: 7–56)
AST (SGOT): 680 U/L (N: 10–40)
ALP: 190 U/L (N: 44–147)
Albumin: 3.6 g/dL (N: 3.5–5.0)
Total Protein: 6.8 g/dL
Prothrombin Time: 14.2 sec (N: 11–13.5)

What is happening in his liver — and can you explain each abnormal value biochemically?

WHY THIS MATTERS

Organ function tests are the most ordered biochemistry panels in any hospital — from PHC to tertiary care. As a first-year student, you will be expected to:

  • Order the right panel for the right clinical question
  • Understand why each test is included (not just the normal range)
  • Distinguish between patterns of disease (hepatocellular vs cholestatic, pre-renal vs renal vs post-renal, primary vs secondary endocrine dysfunction)

These tests also underpin BI11 competencies, which assess your ability to correlate biochemistry with clinical medicine — a core CBME skill.

RECALL

Before proceeding, quickly recall:

  • The basic structure of the liver lobule (from Anatomy) — hepatocytes, portal triad, central vein
  • The role of the kidneys in filtration and reabsorption (from Physiology)
  • The thyroid gland anatomy and the HPT axis overview (from Physiology)
  • General enzyme kinetics: what does enzyme elevation in plasma tell you about cellular damage?

These foundations make this module much easier to understand.

Liver Function Tests — The Panel and Its Logic

Liver Function Tests (LFT) is a panel of biochemical markers that assess different aspects of hepatic function. No single test tells the whole story — interpretation requires looking at the pattern.

What the LFT panel measures:

ComponentWhat It MeasuresRises in
Total BilirubinBilirubin load (conjugated + unconjugated)All liver disease, haemolysis
Direct (Conjugated) BilirubinConjugated by hepatocytes, excreted in bileHepatocellular injury, cholestasis
ALT (Alanine Aminotransferase)Cytoplasmic enzyme — hepatocyte-specificHepatocellular necrosis
AST (Aspartate Aminotransferase)Cytoplasmic + mitochondrial — liver + muscle + heartHepatocellular, MI, myopathy
ALP (Alkaline Phosphatase)Bound to bile canalicular membraneCholestasis, bone disease
GGT (Gamma-GT)Canalicular enzyme, alcohol-sensitiveCholestasis, alcohol use
AlbuminSynthesised by hepatocytes (reflects synthetic function)Falls in chronic liver disease
Total ProteinAlbumin + globulinsComplex interpretation
PT/INRClotting factor synthesis (all factors except VIII)Impaired hepatic synthesis

Key concept — ALT vs AST: ALT is cytoplasmic only and almost entirely hepatocyte-specific. AST is in both cytoplasm and mitochondria, and is present in heart, skeletal muscle, and kidney too. ALT elevation is a more specific indicator of liver cell injury. The AST:ALT ratio >2:1 suggests alcoholic hepatitis (alcohol depletes pyridoxal phosphate, needed more by ALT than AST).

Liver Function Tests — The Panel and Its Logic

Figure: Liver Function Tests — The Panel and Its Logic

Multi-panel illustration of liver function tests: liver lobule anatomy with enzyme locations, cellular localisation of ALT/AST/ALP/GGT, bilirubin metabolism pathway, and hepatic synthetic function markers (albumin, PT/INR)
What the LFT panel measures:

Figure: What the LFT panel measures:

Multi-panel illustration of LFT biochemistry: ALT and AST transamination reactions, ALP structure and isoforms, AST:ALT ratio in different liver diseases, and albumin binding functions with clinical timeline
Blanks

LFT Patterns — Hepatocellular vs Cholestatic

Hepatocellular pattern: Severe rise in ALT and AST (often 10–100× normal) with modest rise in ALP. Seen in viral hepatitis (hepatitis A, B, E — the latter very common in India during monsoon), drug-induced liver injury, and ischaemic hepatitis.

Cholestatic pattern: Marked rise in ALP and GGT with modest rise in aminotransferases. Seen in bile duct obstruction (stones, stricture, carcinoma of the head of pancreas), primary biliary cholangitis, or intrahepatic cholestasis of pregnancy.

Direct vs indirect bilirubin:
- Unconjugated (indirect) hyperbilirubinaemia = problem before hepatocytes: haemolysis (malaria — highly prevalent in India), Gilbert's syndrome, crigler-Najjar syndrome
- Conjugated (direct) hyperbilirubinaemia = problem at or after hepatocytes: liver cell damage, bile duct obstruction, Dubin-Johnson syndrome

Interpreting the clinical scenario: ALT 820 + AST 680 = severe hepatocellular injury. ALP only mildly elevated → not primary cholestasis. Direct bili > indirect → conjugated hyperbilirubinaemia (hepatocyte unable to excrete conjugated bilirubin). Albumin normal + PT mildly prolonged → acute injury, synthetic function partly preserved. Diagnosis: acute viral hepatitis (likely hepatitis E in rural Tamil Nadu/Puducherry context).

LFT Patterns — Hepatocellular vs Cholestatic

Figure: LFT Patterns — Hepatocellular vs Cholestatic

Multi-panel illustration of LFT patterns: hepatocellular injury pattern with enzyme release, cholestatic pattern with biliary obstruction, bilirubin differential diagnosis flowchart, and clinical case interpretation for acute viral hepatitis
Branching

CLINICAL PEARL

Hepatitis E is the commonest cause of epidemic jaundice in India — especially in rural areas and pregnant women. It is spread by contaminated water (faeco-oral route), peaks during and after monsoon flooding, and is usually self-limiting. However, in pregnant women (especially third trimester), it can cause fulminant hepatic failure with mortality up to 20%. This is why hepatitis E serology (IgM anti-HEV) should always be included in workup of jaundice in rural India and in any pregnant patient with liver disease.

SELF-CHECK — : LFT Interpretation

A 52-year-old man has LFT: ALT 45 U/L (normal), AST 48 U/L (mildly elevated), ALP 420 U/L (markedly elevated), Total Bilirubin 3.2 mg/dL, Albumin 3.8 g/dL. Which pattern does this represent?

A. Hepatocellular pattern — severe viral hepatitis

B. Cholestatic pattern — likely bile duct obstruction

C. Gilbert's syndrome — unconjugated hyperbilirubinaemia

D. Alcoholic hepatitis — AST:ALT ratio >2

Reveal Answer

Answer: B. Cholestatic pattern — likely bile duct obstruction


Which LFT parameter best reflects the liver's synthetic function (i.e., how well hepatocytes are working metabolically)?

A. ALT

B. ALP

C. Serum albumin

D. Total bilirubin

Reveal Answer

Answer: C. Serum albumin

Renal Function Tests — Assessing the Kidney

Renal Function Tests (RFT) assess glomerular filtration, tubular function, and electrolyte homeostasis.

The standard RFT panel:

TestNormal RangeInterpretation
Serum Creatinine0.6–1.2 mg/dL (M); 0.5–1.0 (F)GFR surrogate — rises when GFR falls >50%
Blood Urea Nitrogen (BUN)7–20 mg/dLRises in renal failure, high protein catabolism, GI bleed
BUN:Creatinine Ratio10–20:1>20 suggests pre-renal cause; <10 suggests renal/tubular
eGFR (CKD-EPI equation)>60 mL/min/1.73m²Calculated from creatinine, age, sex — stages CKD 1–5
Uric Acid3.5–7.2 mg/dLRises in gout, CKD, tumour lysis
Electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻)See normal rangesElectrolyte and acid-base balance

Creatinine as a GFR marker: Creatinine is the waste product of creatine phosphate breakdown in muscle. It is freely filtered at the glomerulus and minimally secreted by tubules. Unlike urea, it is not significantly reabsorbed — making it a better GFR surrogate. However, it is a late marker: creatinine rises noticeably only when GFR has fallen by ~50%. Cystatin C is a newer, more sensitive marker available in tertiary centres.

BUN:Creatinine ratio:
- Pre-renal (reduced blood flow — dehydration, heart failure, haemorrhage): both BUN and creatinine rise, but urea rises proportionally more → ratio >20:1
- Renal (intrinsic kidney disease — glomerulonephritis, ATN): both rise but ratio stays 10–20:1
- Post-renal (obstruction — BPH, stones, ureteric obstruction): ratio usually normal initially, then rises

Renal Function Tests — Assessing the Kidney

Figure: Renal Function Tests — Assessing the Kidney

Multi-panel illustration of renal function tests: nephron anatomy with analyte handling sites, creatinine-GFR relationship with the creatinine-blind range, BUN:creatinine ratio diagnostic algorithm, and CKD staging by eGFR
The standard RFT panel:

Figure: The standard RFT panel:

Multi-panel illustration of RFT biochemistry: creatinine metabolism from creatine, urea cycle summary, pre-renal vs renal vs post-renal failure comparison, and cystatin C as alternative GFR marker
Crossword
Fill in the Blanks BI11.1-2 | Organ Function tests and Hormones — Blanks