Medicine — Gastroenterology and Hepatology, NMC MBBS licence examination syllabus (Nepal Medical Council).
Chronic liver disease: two failures, and everything else
Ask of any complication — is the liver not working, or is blood not getting through it?
Cirrhosis produces a long list of complications: ascites, varices, encephalopathy, jaundice, bruising, an enlarged spleen, a low platelet count, swollen legs, gynaecomastia. Taught as a list it is unmemorable, and it collapses the moment an exam question describes a patient rather than a diagnosis.
Underneath, there are only two problems. Scarring destroys working hepatocytes, so the liver stops doing its jobs. And that same scarring obstructs blood flowing through the organ, so pressure rises behind it. Every complication in the list belongs to one of those two, or — in the case of ascites — to both at once.
🩺 Where this lives: A cirrhotic patient admitted with confusion is frequently treated for encephalopathy alone, with lactulose started and the matter considered closed. But decompensation is nearly always precipitated, and the commonest precipitant is infection — often spontaneous bacterial peritonitis, which in a cirrhotic can present with no abdominal pain, no fever, and nothing but altered mental state or a creeping creatinine. The confusion is a symptom. The infection is the diagnosis, and it is found by tapping the ascites rather than by treating the symptom.
The two failures
Use that division as a diagnostic reflex. A cirrhotic with a prolonged INR has a synthetic problem — the liver is not manufacturing clotting factors. A cirrhotic with a low platelet count has a portal problem — hypersplenism from a congested spleen is consuming them. Same patient, same disease, two entirely different mechanisms, and telling them apart is what the question is usually testing.
WHY THE INR IS NOT A BLEEDING RISK SCORE HERE
In cirrhosis the liver makes less of BOTH procoagulant
factors and anticoagulant proteins (protein C, protein S,
antithrombin). The result is a REBALANCED haemostatic
system that happens to be fragile in both directions.
So a raised INR in cirrhosis does NOT reliably predict
bleeding, and these patients can and do develop
THROMBOSIS — portal vein thrombosis is common.
Practical consequence: do not transfuse plasma to
"correct" an INR in a non-bleeding cirrhotic. You are
treating a number that is not measuring what it measures
in other patients.
Causes
🔍 What scars a liver
AlcoholProgresses through steatosis and alcoholic hepatitis to cirrhosis. The early stages are reversible with abstinence, which is why identifying it early matters.
Viral hepatitisChronic hepatitis B and C. Both are treatable, and both are major causes worldwide — so serology belongs in the work-up of every new cirrhosis.
Metabolic / fatty liverAssociated with obesity, type 2 diabetes and the metabolic syndrome. Increasingly the commonest cause in many populations, and it links back to the diabetes chapter.
AutoimmuneAutoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis — worth considering particularly in younger patients and women.
Inherited and otherHaemochromatosis (iron), Wilson disease (copper), alpha-1 antitrypsin deficiency, chronic venous congestion, drugs.
💡 Exam angle: Wilson disease is asked disproportionately because it is treatable and easily missed — suspect it in a young person with liver disease plus neurological or psychiatric features, look for Kayser–Fleischer rings, and check caeruloplasmin and urinary copper. Haemochromatosis similarly pairs liver disease with diabetes and skin pigmentation. Both are questions about noticing that the liver is not the only organ involved.
Recognising it
SIGNS, GROUPED BY MECHANISM
SYNTHETIC FAILURE
Jaundice · leuconychia (low albumin) · bruising
Peripheral oedema · asterixis (flapping tremor)
PORTAL HYPERTENSION
Ascites · splenomegaly · caput medusae
Dilated abdominal veins
ALTERED OESTROGEN HANDLING
Spider naevi · palmar erythema · gynaecomastia
Testicular atrophy · loss of body hair
(the liver normally metabolises oestrogens)
OTHER
Dupuytren contracture · clubbing · parotid enlargement
Fetor hepaticus
A firm, irregular, sometimes SHRUNKEN liver — cirrhosis
is not always hepatomegaly, and a small liver is a late
and ominous sign.
Compensated and decompensated
Investigating
WHAT THE TESTS ACTUALLY TELL YOU
"LIVER FUNCTION TESTS" mostly do not measure function
ALT / AST hepatocyte INJURY, not function
ALP / GGT cholestasis
BILIRUBIN handling capacity — this one is functional
TRUE MARKERS OF SYNTHETIC FUNCTION
ALBUMIN long half-life, so it falls in CHRONIC
disease
PROTHROMBIN TIME / INR
short half-life, so it rises EARLY in
acute failure — the more sensitive
acute marker
IMAGING
Ultrasound: nodular contour, splenomegaly, ascites,
portal flow. Also the surveillance tool for
hepatocellular carcinoma.
ESTABLISHING THE CAUSE
Viral serology · autoantibodies and immunoglobulins ·
ferritin and transferrin saturation · caeruloplasmin ·
alpha-1 antitrypsin · alcohol history
ENDOSCOPY
To screen for varices once cirrhosis is diagnosed —
before they bleed.
The albumin/INR distinction repays attention. Albumin has a half-life of around three weeks, so it cannot fall quickly — a normal albumin does not exclude acute liver failure. The prothrombin time reflects factors with half-lives measured in hours, so it rises within a day. In an acutely unwell jaundiced patient, the INR is the number that tells you how bad things are.
Ascites
MANAGING ASCITES
SALT RESTRICTION the foundation, and routinely
neglected
DIURETICS spironolactone first — aldosterone
is high in cirrhosis, so an
aldosterone antagonist is the
rational choice; a loop diuretic
is added if needed
LARGE-VOLUME PARACENTESIS
for tense ascites, WITH albumin
replacement to prevent circulatory
dysfunction
AVOID NSAIDs (precipitate renal failure)
and be cautious with ACE inhibitors
SBP PROPHYLAXIS long-term antibiotics after an
episode, or in high-risk patients
Hepatic encephalopathy
🔍 Mechanism, grading and treatment
MechanismNitrogenous products from the gut — ammonia among them — bypass the liver through portosystemic shunting and reach the brain. The failing liver cannot clear them.
GradingFrom mild inversion of the sleep pattern and subtle personality change, through confusion and asterixis, to somnolence and coma.
TreatmentLactulose — acidifies the colon, traps ammonia as ammonium and speeds transit. Rifaximin — a poorly absorbed antibiotic that reduces ammonia-producing gut flora, used for recurrence.
The real workFind the precipitant: infection, GI bleed (a large protein load in the gut), constipation, dehydration, electrolyte disturbance, sedatives. Treating the trigger is treating the encephalopathy.
Ammonia levelsCorrelate poorly with grade and are not needed to diagnose or manage it. This is a clinical diagnosis.
Variceal bleeding
💡 Exam angle: two points are examined repeatedly. Antibiotics for every cirrhotic with a GI bleed — prophylactically, whether or not infection is suspected, because they reduce both infection and mortality. And restrictive transfusion: over-transfusing raises portal pressure and can worsen the bleeding you are trying to stop. Both are counter-intuitive, which is precisely why they appear.
Other complications
HEPATORENAL SYNDROME
Progressive renal failure caused by intense renal
vasoconstriction in advanced cirrhosis. The kidneys
themselves are structurally NORMAL — which is why it can
reverse with liver transplantation. A diagnosis of
exclusion: hypovolaemia, sepsis and nephrotoxins must be
excluded first, and NSAIDs are a classic precipitant.
HEPATOCELLULAR CARCINOMA
Cirrhosis of any cause is the major risk factor, which is
why these patients enter ULTRASOUND SURVEILLANCE.
Suspect it if a stable patient decompensates without an
obvious trigger.
HEPATOPULMONARY SYNDROME
Intrapulmonary vasodilation → hypoxaemia, classically
worse when upright (platypnoea, orthodeoxia).
COAGULOPATHY AND THROMBOSIS
Rebalanced haemostasis — bleeding AND clotting risk,
including portal vein thrombosis.
Clinical reasoning: four presentations
🔍 Case 1 — the silent infection
PresentationA 54-year-old with known alcoholic cirrhosis and ascites is brought in confused. No fever, no abdominal pain, abdomen soft. Creatinine has risen from 82 to 148.
The distractorConfusion in a cirrhotic invites lactulose and nothing more.
ReasoningEncephalopathy is a symptom of decompensation, and decompensation is nearly always precipitated. SBP in cirrhosis frequently presents without pain or fever — confusion and a rising creatinine may be the only clues.
AnswerDiagnostic paracentesis. Ascitic neutrophils ≥ 250/mm³ diagnose SBP and antibiotics start immediately, without waiting for culture. Treat the encephalopathy too, but the infection is the diagnosis.
🔍 Case 2 — the number that misleads
PresentationA cirrhotic patient with an INR of 1.9 is not bleeding and needs an ascitic tap. A colleague proposes fresh frozen plasma first to "cover" the coagulopathy.
TrapTreating the INR as though it measured bleeding risk.
ReasoningCirrhosis reduces both procoagulant and anticoagulant proteins, giving a rebalanced system. The INR reflects only one side of that balance, so it over-states bleeding risk — and these patients also thrombose.
AnswerProceed without routine plasma. Correcting an INR in a non-bleeding cirrhotic exposes the patient to transfusion risk and volume load for no measured benefit.
🔍 Case 3 — the forgotten drug
PresentationA 60-year-old cirrhotic presents with haematemesis. Resuscitation is underway, terlipressin given, endoscopy arranged. The team reviews the plan.
Key clueSomething standard is missing from an otherwise correct plan.
ReasoningEvery cirrhotic with a gastrointestinal bleed should receive prophylactic antibiotics. Bacterial translocation is common in this setting, and antibiotics reduce infection, rebleeding and mortality.
AnswerAdd prophylactic antibiotics. Also transfuse to a restrictive threshold — over-transfusion raises portal pressure and can worsen the bleed.
🔍 Case 4 — the precipitated renal failure
PresentationA cirrhotic with ascites takes ibuprofen for a week for back pain. Creatinine rises from 90 to 260. Urine output falls. He is not hypovolaemic and has no sepsis; urinalysis is bland.
Key clueAn NSAID in a patient whose renal perfusion depends on prostaglandins.
ReasoningIn advanced cirrhosis, splanchnic vasodilation reduces effective circulating volume and the kidneys maintain perfusion partly through prostaglandin-mediated vasodilation. NSAIDs block exactly that, precipitating renal failure — and this is a classic route into hepatorenal syndrome.
AnswerStop the NSAID, stop diuretics, exclude infection and hypovolaemia with a fluid or albumin challenge. If renal failure persists with a bland urinalysis and no other cause, consider hepatorenal syndrome and involve specialists. NSAIDs should be avoided in cirrhosis.
Commonly confused
Confusion
The distinction
Why it matters
Synthetic failure vs portal hypertension
Not working versus blood not flowing through
Separates a raised INR from a low platelet count in the same patient.
Raised INR vs bleeding risk
Haemostasis is rebalanced in cirrhosis
Do not transfuse plasma to correct a number in a non-bleeding patient.
Albumin vs INR as a marker
Albumin falls slowly; INR rises fast
INR is the sensitive marker in acute deterioration.
"LFTs" vs liver function
ALT and ALP show injury and cholestasis, not function
Albumin, INR and bilirubin are the functional measures.
SAAG ≥ 11 vs < 11
Portal hypertension versus another cause
Directs the entire differential for ascites.
SBP vs secondary peritonitis
SBP is often painless with a soft abdomen
Waiting for peritonism means missing it.
Non-selective vs cardioselective beta-blocker
Only non-selective agents reduce portal pressure
Bisoprolol does not prevent variceal bleeding.
Rapid revision
MUST-KNOW FACTS
1. Cirrhosis = fibrosis + nodular regeneration, causing TWO problems.
2. Synthetic failure: ↓albumin, ↓clotting factors, ↓detoxification, jaundice.
3. Portal hypertension: varices, ascites, splenomegaly, caput medusae.
4. Ascites needs BOTH low albumin and high portal pressure.
5. Low platelets in cirrhosis = hypersplenism, a PORTAL problem.
6. Raised INR = a SYNTHETIC problem — and it is not a bleeding risk score.
7. Haemostasis is REBALANCED; these patients also thrombose.
8. Albumin has a long half-life; INR is the sensitive ACUTE marker.
9. ALT/AST show injury; ALP/GGT cholestasis — neither measures function.
10. Decompensation = jaundice, ascites, variceal bleed or encephalopathy.
11. Decompensation is nearly always PRECIPITATED — hunt the trigger.
12. New or worsening ascites → DIAGNOSTIC TAP. Always.
13. SAAG ≥ 11 g/L means portal hypertension.
14. SBP = ascitic neutrophils ≥ 250/mm³ — treat before culture returns.
15. SBP may present with confusion or a rising creatinine and nothing else.
16. Ascites: salt restriction, spironolactone first, then a loop diuretic.
17. Large-volume paracentesis needs albumin replacement.
18. AVOID NSAIDs in cirrhosis — they precipitate renal failure.
19. Encephalopathy: lactulose, rifaximin for recurrence, and find the trigger.
20. Ammonia levels correlate poorly and are not needed.
21. Variceal bleed: resuscitate, vasoactive drug, ANTIBIOTICS, endoscopy.
22. Prophylactic antibiotics for EVERY cirrhotic with a GI bleed.
23. Transfuse restrictively — over-transfusion raises portal pressure.
24. Secondary prevention: NON-SELECTIVE beta-blocker plus banding.
25. Hepatorenal syndrome: structurally normal kidneys, a diagnosis of exclusion.
26. Cirrhosis of any cause warrants HCC surveillance by ultrasound.
💡 Exam angle: the reliable threads are (a) sorting a complication into synthetic versus portal, (b) not correcting an INR in a non-bleeding cirrhotic, (c) tapping every new ascites and the 250 neutrophil threshold, (d) antibiotics in every cirrhotic GI bleed, and (e) NSAIDs precipitating renal failure. Notice that three of them are about not doing the obvious thing — which is the shape most cirrhosis questions take.
Syllabus points
The two failures: synthesis and portal flow
Why the INR is not a bleeding risk score in cirrhosis
Causes, including the inherited and autoimmune ones
Clinical signs grouped by mechanism
Compensated versus decompensated disease
Investigations and what each actually measures
Ascites, the SAAG and diagnostic paracentesis
Spontaneous bacterial peritonitis
Hepatic encephalopathy and its precipitants
Variceal bleeding and its prevention
Hepatorenal syndrome and hepatocellular carcinoma
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