When the gatekeepers go on strike…
In pre-hepatic jaundice, the liver was overworked but otherwise innocent.
But in this Kingdom, the liver itself is the problem.
Hepatocellular jaundice occurs when hepatocytes are damaged or dysfunctional, meaning they can’t:
- Take up bilirubin properly
- Conjugate it efficiently
- Excrete it into bile canaliculi
So bilirubin piles up on both sides of the workflow:
Conjugated and unconjugated bilirubin rise
Urine becomes dark (water-soluble conjugated bilirubin sneaks out via kidneys)
Stool colour becomes variable (bile flow unpredictable)
The liver is trying, but it’s failing.
So, who wages war on hepatocytes?
There are four major enemy armies:
| Cause Category | Common Examples | Mechanism |
| Viruses | Hepatitis A, B, C, EBV | Direct hepatocyte injury |
| Alcohol & toxins | Alcoholic hepatitis, Paracetamol overdose | Inflammation + necrosis |
| Metabolic diseases | NAFLD/NASH, Wilson’s disease, Hemochromatosis | Fat → fibrosis, metal accumulation |
| Autoimmune | Autoimmune hepatitis | Antibodies attack hepatocytes |
On exam day, hepatocellular jaundice = think hepatitis first, then alcohol, then autoimmune/metabolic based on context.
The clinical picture has its own personality
Symptoms are more systemic here:
Fever (if viral)
Nausea & vomiting
Scleral icterus
Right upper quadrant tenderness
Fatigue and malaise
Signs of acute liver failure in bad cases:
– confusion (hepatic encephalopathy)
– coagulopathy (INR ↑)
If jaundice + tender hepatomegaly + fever → hepatitis until proven otherwise.
And remember:
Alcoholic hepatitis loves to present with RUQ pain + jaundice + high AST/ALT ratio >2
Blood tests, the Second Kingdom has a pattern
| Test | What happens | Why |
| ALT/AST ↑ (esp. ALT) | Skyrockets | Hepatocyte injury releases enzymes |
| Bilirubin ↑ (mixed) | Elevated | Impaired uptake + excretion |
| Albumin ↓ | Low | Reduced synthetic function |
| INR ↑ | High | Liver failing to make clotting factors |
| Alkaline phosphatase | Normal or mildly ↑ | Bile ducts not primarily obstructed |
Sing this to yourself on the ward:
“High ALT? Hepatocyte!”
A quick word about acute liver failure
This is the lava pit in the middle of this Kingdom, you cannot ignore it.
Danger signs:
- Confusion or personality changes
- Rapidly rising bilirubin
- INR > 1.5 and worsening
- Hypoglycaemia
- Asterixis (flapping tremor)
This is a critical care emergency.
Call for help early, even the bravest junior does not fight this beast alone.
Imaging & further tests: when to escalate
If the diagnosis isn’t obvious:
- Ultrasound → assess liver texture, rule out obstruction
- Hepatitis serology
- Autoimmune screen
- Ferritin, ceruloplasmin (in younger patients)
- Acetaminophen level (never forget!)
Liver biopsy only if the fog refuses to clear.
Management, protect the liver at all costs
| Cause | Action |
| Paracetamol toxicity | N-acetylcysteine ASAP |
| Viral hepatitis | Supportive ± antivirals depending on type |
| Alcoholic hepatitis | Steroids in selected cases + abstinence |
| Autoimmune | Corticosteroids / immunosuppression |
| NAFLD/NASH | Weight loss + metabolic control |
Always:
- Optimise fluids
- Correct coagulopathy
- Monitor neuro status
- Avoid hepatotoxic drugs
And if liver failure spirals, consider transplant early.
A clinical pearl to carry forever
Dark urine always means conjugated bilirubin → the liver has processed it but cannot send it onward.
Hepatocellular or obstructive
Not pre-hepatic
That tiny observation will save you in OSCEs.
In summary, the Kingdom in one breath
“Mixed bilirubin rise + high ALT/AST + dark urine + tender hepatomegaly = hepatocellular jaundice.”
If you can say that while palpating the abdomen confidently, congratulations, you’ve conquered the Second Kingdom.
