Viva Prep: GI

Question 1

Definition

Acute liver failure

Answer 1

Rapid loss of liver function with coagulopathy (INR ≥1.5) and hepatic encephalopathy in a patient without pre-existing cirrhosis, developing within <26 weeks.

Question 2

Diagnostic Criteria ALF

Answer 2

INR ≥1.5

Any degree of hepatic encephalopathy

No pre-existing cirrhosis

Acute illness <26 weeks

Question 3

Core Pathophysiology ALF

Answer 3

Massive hepatocyte injury →
↓ detoxification → ammonia accumulation → cerebral oedema

↓ synthetic function →

coagulopathy

hypoglycaemia

↓ immune function →

infection risk

Systemic inflammatory response → vasodilation + shock

Question 4

Core Investigations – Diagnostic ALF

Answer 4

LFTs (ALT/AST)

INR / PT

Bilirubin

Serum ammonia

Viral hepatitis screen

Paracetamol level

Autoimmune markers

Question 5

Severity / Monitoring Investigations ALF

Answer 5

ABG + lactate

Renal function (AKI common)

CT head if reduced GCS

Continuous ICP concern if severe encephalopathy

Glucose monitoring

Question 6

Hallmark Findings ALF

Answer 6

Jaundice

Encephalopathy

Coagulopathy

Hypoglycaemia

Elevated transaminases

Question 7

Initial Management – What You Do ALF

Answer 7

Intubate if grade 3–4 encephalopathy

GCS monitoring

Check ammonia

Identify cause (paracetamol, viral, drug)

Specific therapies

N-acetylcysteine (NAC) if paracetamol or unknown cause

Treat hypoglycaemia

Early transplant centre referral

Question 8

Drug Card ALF

Answer 8

N-acetylcysteine

Mechanism
→ Replenishes glutathione → detoxifies paracetamol metabolites

Indication
→ Paracetamol toxicity or indeterminate ALF

Dose
→ 150 mg/kg IV loading → infusion protocol

Monitoring
→ LFTs, INR, clinical improvement

Adverse effects
→ Anaphylactoid reactions

Question 9

Complications ALF

Answer 9

Cerebral oedema

Sepsis

Renal failure

Coagulopathy

Hypoglycaemia

Question 10

When refer for transplant? ALF

Answer 10

King’s College Criteria

Example (paracetamol ALF)

pH <7.3 OR

INR >6.5 + creatinine >300 + encephalopathy

Question 11

Definition Hepatic Encephalopathy

Answer 11

Neuropsychiatric dysfunction due to liver failure, caused by accumulation of neurotoxins (mainly ammonia).

Question 12

Diagnostic Criteria HE

Answer 12

Clinical diagnosis in patient with liver disease:

altered mental status

elevated ammonia

exclusion of other causes

Question 13

Classification HE

Answer 13

West Haven grading

Grade Features
1 mild confusion
2 lethargy
3 stupor
4 coma

Question 14

Core Pathophysiology HE

Answer 14

Liver failure →
↓ ammonia detoxification

Ammonia crosses BBB →
astrocyte swelling → cerebral oedema

Question 15

Diagnostic Investigations HE

Answer 15

Serum ammonia

LFTs

Electrolytes

Infection screen

CT head if atypical

Question 16

Hallmark Findings HE

Answer 16

Confusion

Asterixis (flapping tremor)

Somnolence

Coma

Question 17

Initial Management HE

Answer 17

Specific therapy

Lactulose

traps ammonia in colon

Rifaximin

reduces ammonia-producing gut bacteria

Treat precipitant

Common triggers:

infection

GI bleed

constipation

renal failure

sedatives

Question 18

Drug Card HE

Answer 18

Lactulose

Mechanism
→ converts ammonia to ammonium in colon

Indication
→ hepatic encephalopathy

Dose
→ 20–30 g PO/NG every 1–2h until bowel movement

Monitoring
→ mental state, stool frequency

Adverse effects
→ diarrhoea, electrolyte loss

Question 19

Complications HE

Answer 19

cerebral oedema

aspiration pneumonia

coma

Question 20

Common precipitants? HE

Answer 20

infection

GI bleed

constipation

dehydration

sedatives

Question 21

Definition, Spontaneous Bacterial Peritonitis (SBP)

Answer 21

SBP: Infection of ascitic fluid without an intra-abdominal surgically treatable source, typically in patients with cirrhosis and ascites.

Question 22

Diagnostic Criteria SBP

Answer 22

Ascitic neutrophils ≥250 cells/mm³
± positive culture

👉 Culture can be negative — diagnosis is cell count-based

Question 23

Classification SBP

Answer 23

Classic SBP: neutrophils ≥250 + positive culture

Culture-negative neutrocytic ascites: neutrophils ≥250, culture negative

Bacterascites: culture positive, neutrophils <250 (may not need treatment unless symptomatic)

Question 24

Core Pathophysiology SBP

Answer 24

Cirrhosis → portal hypertension + gut oedema

Bacterial translocation from gut → ascitic fluid

Impaired immunity → infection develops

Question 25

Core Investigations – Diagnostic SBP

Answer 25

Diagnostic ascitic tap (essential) Cell count (PMNs) Culture (in blood culture bottles) Blood cultures FBC, CRP LFTs

Question 26

Core Investigations – Severity / Monitoring. SBP

Answer 26

Renal function (AKI risk high) Lactate Fluid balance Repeat ascitic tap if not improving

Question 27

Hallmark Findings SBP

Answer 27

Fever Abdominal pain or tenderness Worsening ascites Unexplained encephalopathy or AKI in cirrhosis

Question 28

Initial Management SBP

Answer 28

Ascitic tap BEFORE antibiotics (unless unstable) IV antibiotics 3rd gen cephalosporin (e.g. cefotaxime) IV albumin (critical exam point) Day 1: 1.5 g/kg Day 3: 1 g/kg → reduces hepatorenal syndrome + mortality Treat precipitating cause

Question 29

Drug Card SBP

Answer 29

Cefotaxime Mechanism → broad-spectrum cephalosporin (gram-negative cover) Indication → SBP Dose → 2 g IV q8h Monitoring → infection markers, renal function Adverse effects → allergy, C. difficile

Question 30

Complications SBP

Answer 30

Hepatorenal syndrome Sepsis / septic shock Recurrence

Question 31

When do you tap ascites? When give albumin? SBP

Answer 31

All cirrhotic patients with deterioration BP with AKI risk / all confirmed SBP (guideline-driven)

Question 32

Definition Upper GI Bleed (Non-variceal)

Answer 32

Bleeding proximal to the ligament of Treitz, presenting with haematemesis and/or melaena.

Question 33

Diagnostic Criteria UGIB

Answer 33

Clinical diagnosis: Haematemesis ± melaena Drop in Hb Endoscopy confirms source

Question 34

Classification UGIB

Answer 34

Non-variceal (most common) → ulcers, gastritis Variceal → portal hypertension (we’ll do separately next)

Question 35

Core Pathophysiology UGIB

Answer 35

Mucosal injury (e.g. ulcer) → vessel erosion → bleeding Hypovolaemia → shock Reduced oxygen delivery → organ dysfunction

Question 36

Core Investigations – Diagnostic UGIB

Answer 36

FBC (Hb) Urea (↑ in UGI bleed) LFTs Coagulation (INR) Group & save / crossmatch

Question 37

Core Investigations – Severity / Monitoring UGIB

Answer 37

Lactate ABG Continuous vitals Urine output

Question 38

Hallmark Findings UGIB

Answer 38

Haematemesis Melaena Tachycardia, hypotension Raised urea

Question 39

Initial Management – What You Do UGIB

Answer 39

2 large-bore IV lines Fluid resus (Hartmann’s) Blood transfusion if Hb <70 g/L (target 70–90) Look for liver disease signs Specific management IV PPI (e.g. omeprazole) Urgent OGD within 24h (earlier if unstable) Endoscopic therapy (clip, cautery, adrenaline)

Question 40

Drug Card UGIB

Answer 40

Omeprazole (IV PPI) Mechanism → inhibits gastric acid → stabilises clot Indication → suspected peptic ulcer bleed Dose → 80 mg IV bolus then infusion (or intermittent dosing depending local protocol) Monitoring → Hb, ongoing bleeding Adverse effects → minimal acutely

Question 41

Complications UGIB

Answer 41

Hypovolaemic shock Re-bleeding AKI Death

Question 42

Risk Stratification UGIB

Answer 42

Rockall / Glasgow-Blatchford scores