Cirrhosis is the late stage of liver fibrosis with distortion of liver architecture and formation of regenerative nodules. ^[1]

Why does this matter from first principles?

• The liver normally has an elegant lobular architecture that allows blood to flow from the portal triad through sinusoids to the central vein. Hepatocytes sit along these sinusoids and perform metabolic, synthetic, and detoxification functions.
• Chronic injury (viral, toxic, metabolic, immune) triggers hepatic stellate cells to produce collagen → fibrosis. Over time, fibrosis distorts the normal vascular channels and creates regenerative nodules (hepatocytes trying to regenerate but enclosed by fibrotic bands).
• This structural distortion increases resistance to portal blood flow → portal hypertension. It also reduces functioning hepatocyte mass → liver insufficiency (↓ albumin, ↓ clotting factors, ↓ bilirubin clearance).

What the fibrosis diagram shows (slide 3): progression is an architectural continuum: F1 portal fibrosis → F2 portal fibrosis with a few septa → F3 numerous bridging septa → F4 cirrhosis, where fibrous bands surround regenerative nodules. F4 is therefore not simply “more collagen”; it is remodelling of both liver structure and its vascular channels.

Compensation is defined clinically, not by Child-Pugh class. A first episode of ascites, variceal haemorrhage or overt hepatic encephalopathy marks decompensation. Child-Pugh A often overlaps with compensated disease and B/C with decompensated disease, but they are not interchangeable definitions. ^[17]

The lecture cites the following 2022 modelled aetiological estimates for Hong Kong: HBV 64%, HCV 10%, heavy alcohol 5%, MAFLD 18%. ^[1]

These percentages describe the cited dataset and should not be treated as fixed current prevalence. MAFLD is retained here only when reproducing the slide; the current nomenclature is metabolic dysfunction-associated steatotic liver disease (MASLD).

Why HBV dominates in HK: Vertical transmission (mother-to-child) was extremely common before universal neonatal vaccination (1988). Chronic HBV → ongoing immune-mediated hepatocyte destruction → fibrosis → cirrhosis.

Other causes to know (from senior notes and past papers ^[2][3]):

• Autoimmune hepatitis, PBC (Primary Biliary Cholangitis), PSC (Primary Sclerosing Cholangitis)
• Wilson's disease, haemochromatosis
• Drug-induced (e.g., methotrexate)
• Alpha-1 antitrypsin deficiency

Treating the underlying disease can lead to some degree of fibrosis regression. ^[1]

Key point from lecture: Treating underlying disease in Child's A/B → ↓ complications/hospitalisation. In Child's C → less impact. ^[1]

Why? In early cirrhosis the fibrotic scaffolding can be partially remodelled by matrix metalloproteinases once the injurious stimulus is removed. In advanced cirrhosis (Child C), the degree of architectural distortion, vascular remodelling, and hepatocyte loss is so extensive that reversal is minimal → liver transplant becomes the definitive option.

Portal hypertension = resistance to portal blood flow. ^[1]

Gold standard measurement:

HVPG (Hepatic Venous Pressure Gradient) = WHVP − FHVP ^[1]

• HVPG ≥ 10 mmHg = clinically significant portal hypertension (CSPH)
• HVPG ≥ 12 mmHg = risk of variceal bleeding

Normal HVPG is ≤ 5 mmHg ^[7]. The measurement involves catheterising a hepatic vein and comparing the wedged (occluded) pressure with the free (unoccluded) pressure. Not widely performed in practice.

Why does portal hypertension develop in cirrhosis?

1. Structural changes: Fibrosis, regenerative nodules, and angiogenesis physically compress and distort sinusoids → ↑ intrahepatic vascular resistance.
2. Dynamic changes: Imbalance of vasoactive substances within the liver — ↑ endothelin (vasoconstrictor), ↓ nitric oxide (vasodilator) in hepatic sinusoids → further vasoconstriction.
3. Splanchnic vasodilation: Paradoxically, in the splanchnic (gut) circulation, there is ↑ NO production → vasodilation → ↑ portal blood inflow → worsens portal hypertension further.

Pre-hepatic, Hepatic (most common = cirrhosis), Post-hepatic. ^[1]

Reading the anatomical diagram (slide 7): the lettered obstructions move along the portal-to-systemic path: A is prehepatic at the portal vein; B is presinusoidal in the portal tract; C is sinusoidal (the usual site in cirrhosis); D is postsinusoidal near the central/hepatic venules; and E is posthepatic at hepatic venous or cardiac outflow.

Ultrasound findings (not sensitive) ^[1]:

• Splenomegaly
• Nodular small liver
• ↑ Portal vein diameter
• ↓ Portal vein flow
• Varices

Other modalities: EUS-guided portal pressure measurement (not widely performed), HVPG (gold standard but invasive) ^[1].

Reading the pressure diagram (slide 8): an occlusion balloon wedges a hepatic vein so WHVP equilibrates with sinusoidal pressure; FHVP is the unoccluded systemic reference. Their difference is the HVPG. This reliably reflects sinusoidal portal hypertension, but can remain normal in prehepatic or presinusoidal disease.

When portal pressure rises (HVPG ≥ 10), blood seeks alternative routes back to the systemic circulation via portosystemic collaterals:

• Oesophageal varices (left gastric vein → oesophageal veins → azygos) — most clinically significant
• Gastric varices (short gastric veins / left gastric vein → fundus)
• Caput medusae (paraumbilical veins → superficial epigastric veins)
• Rectal varices (inferior mesenteric vein → rectal veins)
• Retroperitoneal collaterals

HVPG ≥ 12 mmHg required for variceal bleeding. ^[1] Prevalence of varices in cirrhosis: Child A = 40%, Child B/C = 70%. ^[1] Mortality of acute variceal bleed: 15–25%. ^[1]

This is one of the most feared GI emergencies. Varices only account for 5–10% of UGIB cases but 80% of UGIB mortality ^[9].

TIPSS (Transjugular Intrahepatic Portosystemic Shunt) ^[1]:

• Creates a shunt between hepatic vein and portal vein within the liver
• Other indications: refractory ascites, refractory hydrothorax
• Contraindications: right heart failure, pulmonary hypertension, hepatic encephalopathy (relative)
• Complications: acute (infection/bleeding/rupture), HE, stent occlusion/migration
• Limited availability in HK

Reading the TIPSS diagram (slide 13): the covered stent traverses liver parenchyma to connect a portal-vein branch to a hepatic vein, bypassing the high-resistance sinusoidal bed. This decompresses the portal system and can control bleeding or refractory ascites. The trade-off is that more blood bypasses hepatic detoxification, increasing the risk of hepatic encephalopathy.

In selected high-risk acute bleeds, pre-emptive TIPSS within 72 hours (ideally < 24 hours) improves control: Baveno VII criteria include Child-Pugh C < 14 or Child-Pugh B > 7 with active bleeding at initial endoscopy (or HVPG > 20 mmHg). Persistent bleeding despite drug plus endoscopic therapy is an indication for salvage covered TIPSS. ^[17]

Balloon tamponade — Sengstaken-Blakemore Tube ^[1]:

• Temporary measure only (bridge to definitive treatment)
• Requires intubation to prevent aspiration
• Complications: aspiration, rebleeding, oesophageal rupture
• "Try to avoid!" ^[1]

Reading the tamponade diagram (slide 14): the gastric balloon anchors at the gastro-oesophageal junction; traction plus an oesophageal balloon compresses the variceal columns. Separate gastric and oesophageal aspiration channels help drain blood and secretions. It is a skilled, airway-protected, temporary bridge only because aspiration, migration, pressure necrosis and perforation are serious risks.

The slide labels oesophageal stenting “experimental,” but this is now outdated. In refractory oesophageal variceal bleeding, a covered self-expanding metal stent (SEMS) or balloon tamponade may bridge to definitive therapy; SEMS is similarly effective and safer when available. Neither replaces definitive control such as covered TIPSS. Shunt surgery is now seldom required. ^[17]

Treated with cyanoacrylate (tissue glue) injection. ^[1] Other management similar to oesophageal variceal bleeding. ^[1]

Why tissue glue not banding? Gastric varices (especially fundal) are larger, higher-flow, and in a location where band ligation is technically difficult and less effective. Cyanoacrylate polymerises on contact with blood, physically occluding the varix.

Sarin classification shown on slide 16:

On endoscopy, fundal varices appear as large, smooth, bluish submucosal bulges; the slide sequence then shows needle injection of tissue glue into the varix.

Clinical pearl from senior notes ^[9]: Isolated gastric varices without oesophageal varices → think splenic vein thrombosis (e.g., from pancreatitis) causing localised portal hypertension → "sinistral/left-sided portal hypertension."

Current screening logic ^[17]:

• In compensated advanced chronic liver disease, LSM ≤15 kPa plus platelets ≥150 × 10⁹/L rules out CSPH with high negative predictive value; this is a CSPH rule-out criterion, not a universal definition of who never needs endoscopy.
• If a compensated patient is already receiving an NSBB to prevent decompensation, screening OGD is unnecessary because the result will not change management.
• If an NSBB cannot be used, perform screening OGD when LSM ≥20 kPa or platelets ≤150 × 10⁹/L. If OGD is deferred, repeat transient elastography and platelets annually.
• High-risk varices (large, red signs, or Child-Pugh C) require primary prophylaxis: an NSBB is generally preferred; EVL is used when NSBBs are contraindicated or not tolerated.

Prevention — Non-selective beta-blocker (NSBB) ^[1]:

• Oral carvedilol / propranolol / nadolol
• Side effects: hypotension, bradycardia
• Used for both primary and recurrence prevention
• Survival benefit

For secondary prophylaxis after a bleed, combine an NSBB with repeated EVL; recurrent bleeding despite both generally prompts TIPSS consideration. ^[17]

Why non-selective beta-blockers?

• β1 blockade → ↓ cardiac output → ↓ portal inflow
• β2 blockade → unopposed α1 activity in splanchnic vessels → splanchnic vasoconstriction → ↓ portal inflow
• Net effect: ↓ portal pressure

The pathogenesis of ascites links portal hypertension, splanchnic vasodilation, and neurohormonal activation. ^[1]

The forward flow / peripheral arterial vasodilation hypothesis:

1. Portal hypertension → ↑ NO and other vasodilators in splanchnic circulation → splanchnic vasodilation
2. Splanchnic vasodilation → ↓ effective arterial blood volume (arterial underfilling)
3. Baroreceptors detect underfilling → activate RAAS, AVP (arginine vasopressin), SNS (sympathetic nervous system)
4. RAAS/SNS drive renal sodium retention, while AVP drives disproportionate water retention → oedema/ascites and, when advanced, dilutional hyponatraemia
5. Progressive systemic and intrarenal vasoconstriction reduces renal perfusion and can culminate in HRS-AKI
6. Portal/sinusoidal hydrostatic pressure and excess hepatic lymph formation then exceed lymphatic drainage → ascites accumulates

This is the causal chain highlighted by the slide 18 flowchart. Hypoalbuminaemia can contribute to fluid distribution, but splanchnic vasodilation with effective arterial underfilling and renal sodium retention is the central driver; low serum albumin alone does not explain cirrhotic ascites.

Ascites is the MOST common complication of cirrhosis. ^[11]

Colour: straw, blood-stained, chylous ^[1] Protein concentration varies and must be interpreted with the clinical context WCC < 500/mm³ (< 250 PMN) in uncomplicated cirrhotic ascites ^[1]

Reading the specimens on slide 19: uncomplicated cirrhotic fluid is usually pale/straw-coloured; blood-staining raises traumatic tap, malignancy or haemorrhage; milky fluid suggests chylous ascites and should prompt triglyceride testing. Appearance is a clue, never a substitute for cell count and biochemical analysis.

Ascitic protein is not “without significance”: < 15 g/L identifies higher SBP risk in cirrhotic ascites, while a high-SAAG, high-protein pattern can suggest cardiac ascites. ^[18]

Generally indicated for all new-onset ascites. ^[1]

Tests to order on ascitic fluid:

Choosing the site (slide 20): the lower quadrant is common, but there is no universally “always LLQ” site. Use bedside ultrasound to identify an adequate pocket, mark the abdominal wall vessels where relevant, and choose a path that avoids bowel, bladder, scars and visible collateral veins. Ultrasound guidance reduces adverse events and is especially helpful with small or loculated collections. ^[18]

Moderate sodium restriction: approximately 2 g sodium/day, equivalent to about 5–6.5 g salt/day ^[18] Do not routinely fluid-restrict. Reserve about 1–1.5 L/day for clinically hypervolaemic severe hyponatraemia (serum Na < 125 mmol/L). ^[18] Diuretics: Potassium-sparing diuretics +/− Loop diuretics ^[1]

Avoid confusing sodium with salt: 2 g elemental sodium is about 5 g sodium chloride. Overly severe restriction can make food unpalatable and worsen malnutrition, so dietary counselling matters.

Loop-diuretic monotherapy is usually inappropriate for cirrhotic ascites. ^[1]

Why? Secondary hyperaldosteronism is the dominant sodium-retaining signal, so aldosterone antagonism directly targets the mechanism. Furosemide alone is less effective and can cause hypokalaemia and metabolic alkalosis. For a first moderate episode, spironolactone monotherapy is reasonable; recurrent/severe ascites or a need for faster diuresis favours spironolactone plus furosemide. ^[18]

Typical combination ratio: Spironolactone 100 mg : Furosemide 40 mg, adjusted to response, electrolytes and renal function. ^[7][18]

Be aware of overdiuresis / acute kidney injury. ^[1] After peripheral oedema has resolved, aim weight loss ≤0.5 kg/day; up to 1 kg/day may be acceptable while marked oedema persists. ^[18]

Monitoring: Daily weights, fluid balance, symptoms, blood pressure, electrolytes and renal function. If adherence/response is uncertain, a 24-hour urinary sodium > 78 mmol/day or a spot urine Na:K ratio > 1 supports adequate natriuresis. ^[18]

Therapeutic paracentesis ^[1]:

• For diuretic-refractory TENSE ascites
• Drain in a single session as clinically appropriate; there is no arbitrary 4–8 L ceiling
• If > 5 L is removed, give albumin 8 g per litre removed
• Use ultrasound-selected access; complications include bleeding, infection, visceral injury, leak and post-paracentesis circulatory dysfunction ^[18]

Why IV albumin? Large-volume paracentesis rapidly removes protein-rich fluid from the peritoneum. Without volume replacement, the already underfilled arterial circulation worsens → exaggerated neurohormonal activation → renal vasoconstriction → post-paracentesis circulatory dysfunction → AKI. Albumin is the preferred colloid because it stays intravascular and expands effective circulating volume.

Dose used in the BSG/BASL guideline: 8 g albumin per litre removed when > 5 L is drained; consider the same replacement after < 5 L in ACLF or patients at high risk of post-paracentesis AKI. ^[18]

Other options for refractory ascites ^[1]:

• TIPSS
• Experimental: long-term intermittent albumin administration, low-flow ascitic pump

Reading the low-flow pump diagram (slide 23): a subcutaneous pump draws ascites through a peritoneal catheter and transfers it through a second catheter into the urinary bladder, so the fluid is passed in urine. This is a specialised device for selected refractory cases, not routine first-line therapy; infection, catheter and renal complications limit its use.

Bacterial translocation from the gut lumen across the intestinal wall into ascitic fluid. ^[1]

In cirrhosis:

• Gut mucosal oedema (portal HTN) → ↑ intestinal permeability
• Impaired gut motility → bacterial overgrowth
• Reduced opsonin activity in ascitic fluid (low protein ascites)
• Impaired reticuloendothelial function (liver not clearing bacteria)
• Result: bacteria (usually a single Gram-negative organism, e.g., E. coli, Klebsiella) seed the ascitic fluid

Reading the pathogenesis diagram (slide 24): intestinal hypomotility and local immune dysfunction permit bacterial overgrowth; organisms cross the bowel wall, reach mesenteric lymph nodes, cause transient bacteraemia, and finally seed poorly opsonic ascitic fluid. The diagram also distinguishes two related culture/cell-count patterns:

• Culture-negative neutrocytic ascites: PMN ≥250/mm³ but culture negative — manage as SBP.
• Monomicrobial non-neutrocytic bacterascites: positive monomicrobial culture but PMN < 250/mm³ — interpret with symptoms and repeat sampling; symptomatic patients require treatment.

Typical: Fever, abdominal pain, new-onset ascites ^[1] Can have atypical symptoms or be asymptomatic ^[1] Need HIGH INDEX OF SUSPICION! ^[1]

Mortality: 90% (untreated); < 20% (early treatment) ^[1]

Why high index of suspicion? Cirrhotic patients may not mount a typical inflammatory response (impaired immune function, low complement, impaired opsonisation). They may present only with worsening encephalopathy, worsening renal function, or unexplained clinical deterioration without classic peritoneal signs. Any cirrhotic patient admitted to hospital with ascites should have a diagnostic paracentesis — this is the standard of care.

Ascitic PMN (neutrophil) count ≥ 250 cells/mm³ ^[1] Often culture-negative ^[1]

Important differentials: other causes of acute abdomen, bowel perforation. ^[1] Look out for: surgical signs, atypical presentation, polymicrobial culture growth, lack of treatment response. ^[1]

Why is this distinction critical? Missing secondary peritonitis (e.g., from a perforated viscus) and treating as SBP alone can be fatal — the patient needs surgical intervention, not just antibiotics.

If the clinical response is inadequate or secondary peritonitis/resistant infection is suspected, repeat paracentesis at about 48 hours. A PMN fall of less than 25% from baseline should prompt reassessment of antibiotic coverage and a search for a surgically treatable source rather than waiting five days. ^[18]

Treatment ^[1]:

• Empirical antibiotics — do not wait!
• Choose empiric therapy by community versus healthcare acquisition, illness severity and local resistance. A 3rd-generation cephalosporin is standard for uncomplicated community-acquired SBP; broader therapy is reserved for healthcare-associated infection, sepsis or resistant-organism risk. ^[18]
• Give IV albumin when renal dysfunction is present or developing: 1.5 g/kg within 6 hours of diagnosis, then 1 g/kg on day 3. ^[18]

Prophylaxis to prevent recurrence ^[1]:

• Offer long-term secondary prophylaxis after recovery, selecting an agent according to local susceptibility and stewardship policy (commonly ciprofloxacin or trimethoprim-sulfamethoxazole; norfloxacin where available). ^[18]

Why IV albumin in SBP? SBP triggers inflammation, further splanchnic vasodilation and renal hypoperfusion. Albumin reduces renal impairment and mortality in higher-risk patients, but it should be used with attention to volume status rather than as an unqualified fluid bolus for everyone.

Pathogenesis: Slowing of portal vein flow ^[1] > 10% of cirrhosis; ↑ during decompensation (~25%) ^[1]

Majority: clinically silent ^[1] Minority: abdominal pain when new-onset ^[1] When chronic (cavernous transformation): ↑ variceal bleeding, ↑ ascites, ↓ treatment options if HCC develops ^[1]

Cavernous transformation = the body forms a network of small collateral veins around the thrombosed portal vein. This restores some portal flow but is disorganised and maintains portal hypertension.

Diagnosis: Ultrasound Doppler or CT with contrast ^[1]

Consider other causes of PVT ^[1]:

• Malignancy (pancreatic, cholangiocarcinoma)
• Venous thrombosis / hypercoagulability causes
• Local inflammation or infection (e.g., pancreatitis or pylephlebitis)

Management ^[1]:

• Urgent anticoagulation if there is intestinal ischaemia
• Base other decisions on chronicity, percentage occlusion, vessel extent, progression and transplant candidacy ^[19]

Reading the CT (slide 29): the arrow points to a low-attenuation filling defect within the contrast-opacified portal vein. Doppler ultrasound can detect reduced/absent flow, but contrast CT or MRI confirms thrombus, defines extent and chronicity, and helps exclude malignant portal-vein invasion. ^[19]

Current decision framework ^[19]:

LMWH, vitamin K antagonists and direct oral anticoagulants are all possible options; selection is individualised by liver function, renal function, interactions, bleeding risk and patient preference. DOACs may be considered in compensated Child-Pugh A or B disease. If anticoagulated, repeat imaging every 3 months and continue until thrombus resolution or transplant, as appropriate. ^[19]

Why is PVT management tricky? Cirrhosis produces a rebalanced but fragile haemostatic state: both bleeding and thrombosis are possible. INR prolongation does not itself quantify procedural or spontaneous bleeding risk. Before anticoagulation, address high-risk varices without delaying indicated therapy; untreated progressive PVT can worsen portal hypertension and complicate liver transplantation. ^[17][19]

AKI: ↑ ≥ 50% creatinine in 7 days OR ↑ ≥ 26.5 μmol/L creatinine in 48 hours ^[1]

Causes of AKI in liver disease ^[1] — Hepatorenal syndrome is NOT the most common cause!

• Hypovolaemia — diuretics, GI bleeding
• Sepsis
• Nephrotoxic drugs/herbs
• Parenchymal renal disease
• Obstructive uropathy
• Hepatorenal syndrome

Always exclude other causes of AKI! ^[1]

Same haemodynamic mechanism as ascites, taken to the extreme ^[1]:

• Cirrhosis and portal hypertension → splanchnic arterial vasodilation and reduced systemic vascular resistance
• Effective arterial underfilling → escalating RAAS/SNS activation and AVP release
• RAAS/SNS increase tubular sodium retention and intrarenal vasoconstriction; AVP retains water
• Progressive renal vasoconstriction and impaired renal autoregulation → HRS-AKI

This is the three-branch flowchart on slide 32: neurohormonal activation produces sodium retention → ascites/oedema, water retention → dilutional hyponatraemia, and renal vasoconstriction → HRS. HRS-AKI is primarily a functional haemodynamic phenotype, but current criteria recognise that it can coexist with CKD, tubular injury or proteinuria; “structurally normal kidneys” is therefore an oversimplification. ^[20]

HRS-AKI (broadly replacing the old “type 1 HRS” concept): acute creatinine/urine-output deterioration, often precipitated by SBP or GI bleeding; mortality is high.

HRS without AKI is classified by duration as HRS-AKD (< 90 days) or HRS-CKD (≥90 days). This replaces the imprecise old “type 2 HRS” label, which usually described more gradual dysfunction with refractory ascites. ^[20]

Current HRS-AKI diagnostic criteria ^[20]:

1. Cirrhosis with ascites.
2. AKI: serum creatinine rise ≥26.5 μmol/L within 48 hours or ≥50% from baseline within 7 days, and/or urine output ≤0.5 mL/kg/hour for ≥6 hours.
3. No improvement within 24 hours after adequate volume resuscitation, when fluids are clinically indicated.
4. No strong evidence that another process is the primary cause (for example septic shock requiring vasopressors, obstruction, drug toxicity or glomerular disease).

The older algorithm reproduced on slide 33 requires routine diuretic withdrawal plus a two-day albumin challenge. The 2024 ICA–ADQI consensus no longer requires systematic albumin for 48 hours: in euvolaemic or overloaded patients this delays vasoconstrictor therapy and may cause pulmonary oedema. Assess volume promptly and give a targeted fluid challenge only if volume depletion is plausible. ^[20]

Simultaneous management ^[1]:

• Exclude other causes
• Stop nephrotoxins; hold or adjust diuretics and NSBBs according to haemodynamics and volume status
• Treat infection
• Once HRS-AKI is established, start terlipressin plus 20–25% albumin; reassess volume status daily and reduce/stop albumin if overloaded ^[20]

A spot urine sodium < 10 mmol/L is a lecture clue, not a diagnostic criterion Can recur after treatment discontinuation ^[1] RRT (renal replacement therapy) / LT (liver transplant) may be needed ^[1]

Why terlipressin? It is a V1 receptor agonist → causes splanchnic vasoconstriction → reverses the arterial underfilling → less compensatory renal vasoconstriction → improved renal perfusion.

Why spot urine sodium < 10 can occur: RAAS/SNS activation makes the kidney avidly retain sodium. However, low urine sodium and low fractional sodium excretion are also common in other AKI phenotypes in advanced cirrhosis and are affected by diuretics, so they do not distinguish HRS reliably on their own. Use the clinical course, urinalysis/sediment, imaging and evidence for alternative causes. ^[20]

• Aetiology: HBV/HCV status, alcohol history (amount, duration, pattern), obesity/metabolic syndrome (MASLD), autoimmune symptoms, drugs, family history (Wilson's, haemochromatosis, alpha-1 AT deficiency)
• Symptoms of CLD: Jaundice, pruritus, dark urine, bruising, ↓ libido (males), amenorrhoea (females) ^[11]
• Symptoms of complications: Abdominal distension (ascites), haematemesis/melaena (varices), fever/abdominal pain (SBP), confusion/sleep disturbance (HE), oedema
• Constitutional: Weight loss, fatigue, anorexia, muscle cramps ^[11]
• Red flags: Rapid deterioration, acute confusion, GI bleeding, oliguria

From CFB abdominal examination ^[13] and past papers ^[3]:

From 2021 SAQ Q5(e) ^[6]: "Suggest additional investigations which will aid further management."

"Known alcoholic cirrhosis admitted for increased confusion. Arterial ammonia 120. Which MOST LIKELY precipitates confusion?"

• A. Diagnostic paracentesis → Unlikely
• B. Duodenal ulcer bleeding → CORRECT (GI bleeding → ↑ protein load in gut → ↑ ammonia production → HE)
• C. Failure of alcohol abstinence → Less acute
• D. Recent HCC diagnosis → Less direct

2024 MCQ Q9 ^[10]: "Can occur after GI bleeding" → Answer: Hepatic Encephalopathy. 2024 MCQ Q10 ^[10]: "Can occur in non-cirrhotic chronic HBV" → Answer: HCC (HBV is directly carcinogenic even without cirrhosis).

• Splenomegaly in cirrhosis → congestive (portal hypertension) → leads to hypersplenism (↑ destruction of all cell lines → pancytopenia)
• 2022 Minicase Section 3 ^[3]: "Most likely cause for pancytopenia?" → Answer: Hypersplenism (secondary to portal hypertension/cirrhosis).

• MASLD is the rising cause of cirrhosis globally and in HK (18%)
• Alcohol: ↓ inflammation and ↓ fat with abstinence, but fibrosis reversal uncertain ^[1]