GC092 Upper Abdominal Pain: Peptic Ulcer; Pancreatitis And Gallstone
Upper abdominal pain caused by peptic ulcer disease, pancreatitis, or gallstones encompasses a spectrum of conditions involving mucosal erosion of the gastroduodenal lining, inflammation of the pancreas, or obstruction of the biliary tract by calculi, each presenting with distinct but sometimes overlapping epigastric or right upper quadrant pain patterns.
Upper Abdominal Pain: Peptic Ulcer, Pancreatitis, and Gallstone
This GC lecture (GC 092) is delivered by Prof. Wai Keung Leung and forms a cornerstone of the General Clerkship gastrointestinal curriculum. It covers three of the most common and most examined causes of upper abdominal pain: peptic ulcer disease (PUD), gallstone disease, and pancreatitis (acute and chronic). The lecture also deeply covers H. pylori biology, diagnosis, and eradication, as well as NSAID/aspirin-related ulcer pathogenesis and prevention — both of which are perennial favourites in MCQ, SAQ, and minicase formats. [1]
Learning objectives (derived from the lecture outline and Block A notes):
- Systematically approach upper abdominal pain — differential diagnosis, history, examination, investigations.
- Understand the aetiology, pathophysiology, diagnosis, and management of peptic ulcer disease.
- Master H. pylori: microbiology, epidemiology, associated diseases, diagnostic methods, eradication regimens.
- Understand NSAID/aspirin mucosal injury and strategies for prevention.
- Know the aetiology, diagnosis, severity scoring, and management of acute and chronic pancreatitis.
- Understand gallstone disease: types, risk factors, presentations, complications, and management.
How this fits into exams: Past papers (2018–2025) consistently test acute pancreatitis investigation and severity assessment, peptic ulcer complications and perforation, H. pylori eradication, NSAID ulcer prevention, and biliary colic vs. cholecystitis vs. cholangitis vs. pancreatitis differentiation. [3][4][5][6]
Part 1: Approach to Upper Abdominal Pain
The lecture emphasises that functional dyspepsia accounts for ~60% of cases, while peptic ulcer accounts for only ~10%. Always consider non-GI causes. [1]
| Category | Conditions |
|---|---|
| Gastroduodenal | Peptic ulcer (~10%), Atypical GERD, Gastric cancer (rare) |
| Hepatobiliary | Pancreatitis, Ca pancreas, Gallstone |
| Functional | Functional dyspepsia (~60%) |
| Drug-related | NSAID, aspirin, alendronate |
| Cardiac | MI, myocarditis |
| Chest | Pneumothorax, pulmonary embolism |
| Haematological | Acute leukaemia, haemolytic anaemia |
| Metabolic | Uraemia, DKA, porphyria, Addison's disease |
| Toxins | Hypersensitivity, lead poisoning |
| Infections | Herpes zoster |
| Neurological | Radiculitis, tabes dorsalis |
| Miscellaneous | Muscular contusion, narcotic withdrawal, psychiatric disorder, heat stroke |
The lecture explicitly lists 10 questions: Location, Referral, Character (diffuse/localized), Severity, Duration, Onset (sudden/gradual), Frequency, Aggravating factors, Relieving factors, Associated symptoms. [1]
Why each matters:
- Location: Epigastric → PUD, pancreatitis, GERD; RUQ → biliary; LUQ → splenic, pancreatic tail.
- Referral/radiation: Back → pancreatitis, posteriorly penetrating ulcer, biliary colic, dissecting aneurysm. Right shoulder → cholecystitis (phrenic nerve irritation).
- Character: Visceral (dull, vague, poorly localized) vs. somatic (sharp, well-localized) vs. colicky (waves).
- Severity: The lecture provides a severity hierarchy: Ulcer pain is the mildest; intestinal and renal colic are moderate; biliary colic and pancreatic pain are the most severe. [1]
- Onset: Sudden → perforation, mesenteric ischaemia; gradual → inflammation, obstruction.
- Aggravating/relieving factors: Eating worsens gastric ulcer (↑acid secretion on food); eating relieves duodenal ulcer (food buffers acid reaching DU). Leaning forward relieves pancreatic pain (takes pressure off retroperitoneal pancreas). NSAID use aggravates PUD.
- Associated symptoms: Vomiting, haematemesis, melaena, weight loss, jaundice, fever.
1. Acute epigastric pain referring to the back → Posteriorly penetrating peptic ulcer, Biliary pain, Acute pancreatitis, Dissecting aneurysm [1]
2. Epigastric pain + repeated vomiting → Food poisoning/gastroenteritis, Acute pancreatitis, Gastric outlet obstruction [1]
3. Agonizing pain but insignificant signs → Acute pancreatitis, Mesenteric thrombosis at early stage [1]
Exam Discriminator
Duration of symptoms, Age, Presence of alarming symptoms, Drug history (NSAID/aspirin), Family history of CA stomach, Alternative non-GI diagnoses. [1]
≥45 years (new onset), Anaemia or bleeding, Weight loss ( > 10% BW), Anorexia/early satiety, Persistent vomiting, Abdominal mass or lymphadenopathy, Dysphagia or odynophagia, Family history of upper GI cancer, Previous gastric surgery or malignancy, Previous history of ulcer, Jaundice. [1]
Why these matter: Any of these warrant urgent OGD (oesophagogastroduodenoscopy) to exclude malignancy or complicated PUD. In patients < 45 without alarm features, a non-invasive "test-and-treat" approach for H. pylori is reasonable. [1][8]
General: Appearance, posture, in pain, vital signs, Fever, jaundice. Abdominal: Location and degree of tenderness, Rebound tenderness, guarding, rigidity. Genital, rectal, and pelvic: PR exam, hernia orifices. [1]
- Guarding/rigidity: Suggests peritonitis (e.g., perforated ulcer → board-like rigidity).
- Murphy's sign: RUQ tenderness on inspiration → acute cholecystitis.
- Cullen's sign / Grey Turner's sign: Periumbilical / flank bruising → severe haemorrhagic pancreatitis (LATE signs).
- PR exam: Don't forget — melaena, masses, and hernias.
Part 2: Peptic Ulcer Disease
Gastric ulcer, Duodenal ulcer, Oesophageal ulcer, Meckel's diverticulum, Anastomotic ulcer. [1]
Why Meckel's? Contains ectopic gastric mucosa → acid secretion → ulceration of adjacent ileal mucosa.
Why anastomotic? Post-gastrectomy patients can develop ulcers at the surgical anastomosis (stomal ulcer).
Pain, Bleeding, Perforation, Gastric outlet obstruction. [1]
| Complication | Explanation |
|---|---|
| Pain | Epigastric; GU worse with eating (acid stimulated by food), DU worse when hungry / at night (acid unopposed by food) |
| Bleeding | Erosion into vessels — left gastric artery (lesser curve GU), gastroduodenal artery (posterior DU). Presents as haematemesis or melaena. [9] |
| Perforation | Anterior DU/GU → peritonitis → board-like rigidity → free gas under diaphragm on erect CXR |
| Gastric outlet obstruction | Chronic fibrotic scarring at pylorus/duodenum → vomiting of undigested food, succussion splash, metabolic alkalosis (loss of HCl) |
Anatomical Bleeding Sites
Ulcers high on the lesser curve (left gastric artery) and in the postero-inferior wall of the duodenal bulb (gastroduodenal artery) bleed more easily because these are the sites where major arterial supply runs closest to the mucosal surface. [9]
H. pylori infection, NSAID, Aspirin, Stress (ICU), Zollinger-Ellison syndrome (Gastrinoma), Crohn's disease. [1]
Acid suppression, Eradication of H. pylori, Avoid ulcerogenic drugs. [1]
- PPI is the mainstay of acid suppression (omeprazole, esomeprazole, pantoprazole, etc.). Works by irreversibly blocking H+/K+ ATPase (proton pump) on parietal cells.
- H2RA (ranitidine, famotidine): Less potent but useful adjunct.
- Always test and treat H. pylori. Always review NSAID/aspirin need.
Part 3: Helicobacter pylori
Gram-negative, rod-shaped, spiral with unipolar flagella. Discovered in 1982 by Drs Barry Marshall and Robin Warren (Nobel laureates). [1]
Colonization mechanism:
Strong urease activity → hydrolyses urea to ammonia and bicarbonate → increases resistance to the low pH of the stomach. [1]
This is the fundamental survival trick. The ammonia creates a local alkaline microenvironment around the bacterium, protecting it from gastric acid. The flagella allow motility through the mucus layer to reach the epithelial surface. [1]
~50% prevalence in HK adults, but decreasing worldwide. Developing countries 50–80%, Developed countries 10–30%. Increases with age, poor socioeconomic status, poor hygiene. [1]
Transmission: Unknown, probably oral-oral route; water supply, poor sanitary condition, crowded environment, low socio-economic status. [1]
The global trend shows decreasing prevalence over recent decades (1980–2022 data from Lancet Gastroenterol Hepatol 2023). [1]
Gastroduodenal: Chronic gastritis, Dyspepsia, Duodenal ulcer, Gastric ulcer, Gastric cancer (adenocarcinoma), Gastric MALT lymphoma. [1]
Extra-GI: ? ITP, Anaemia (B12 and Fe deficiency). [1]
Why gastric cancer? Chronic H. pylori infection → chronic active gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → adenocarcinoma (Correa cascade). WHO classifies H. pylori as a Group 1 carcinogen.
Why MALT lymphoma? Chronic antigenic stimulation by H. pylori drives clonal B-cell proliferation in gastric MALT. Early-stage MALT lymphoma can regress with H. pylori eradication alone.
Duodenal ulcer: H. pylori 92%, NSAID 5%, Zollinger-Ellison 1%, Other 2%. [1]
Gastric ulcer: H. pylori 70%, NSAID 25%, Cancer 3%, Other 2%. [1]
High Yield
Eradication of H. pylori results in long-term remission of peptic ulcer disease — both DU and GU recurrence rates plummet after successful eradication, confirming the causal role. If H. pylori is not eradicated, ulcer relapse rates remain high (~60–80% within 1 year). [1]
| Method | Invasive/Non-invasive | Principle | Notes |
|---|---|---|---|
| Rapid urease test (CLO test) | Invasive (biopsy) | Urease activity turns indicator | Fast, bedside; gold if doing OGD |
| Culture | Invasive (biopsy) | Grow organism | Allows antibiotic sensitivity testing |
| Histology | Invasive (biopsy) | H&E + special stains | Special stains (Giemsa, Warthin-Starry) increase sensitivity |
| Serology | Non-invasive | Detects IgG antibodies | Cannot distinguish active from past infection; not for post-treatment |
| Urea breath test (UBT) | Non-invasive | Labelled urea → if HP urease present → labelled CO₂ in breath | Useful for monitoring after treatment |
| Stool antigen test | Non-invasive | Detects HP antigens in stool | Useful for monitoring after treatment |
UBT and stool antigen are useful for monitoring after treatment (confirming eradication). Serology is NOT useful for monitoring. [1]
Why serology is not for monitoring: IgG antibodies persist for months to years after eradication, so a positive serology does not confirm active infection post-treatment.
PPI-based triple therapy: PPI + Amoxicillin + Clarithromycin/Metronidazole [1]
Bismuth-containing quadruple therapy: PPI + Bismuth + Tetracycline + Metronidazole [1]
Non-bismuth-containing quadruple therapy (Concomitant therapy): PPI + Amoxicillin + Clarithromycin + Metronidazole [1]
Duration:
HK Consensus (Leung WK et al, HKMJ 2023): Triple therapy with PPI + Clarithromycin + Amoxicillin for 14 days; OR Bismuth quadruple therapy with PPI + Tetracycline + Metronidazole + Bismuth salt for 10–14 days. [1]
Maastricht VI Consensus: If local clarithromycin resistance < 15%, use CLA triple × 14 days. If ≥ 15%, use BQT × 14 days. [1]
Patient factors: Allergic history, Non-compliance, Previous antibiotics use. [1]
HP factors: Antibiotic resistance (especially clarithromycin resistance — rising globally and in Asia Pacific). [1]
Regime factors: Choice of antibiotics, Degree of acid suppression, Length of therapy. [1]
Why does acid suppression matter? Most antibiotics (amoxicillin, clarithromycin) are acid-labile — their efficacy increases at higher pH. A higher-dose PPI or potassium-competitive acid blocker (PCAB, e.g. vonoprazan) improves antibiotic efficacy. [1]
The lecture shows data on falling efficacy of standard triple therapy over time, largely driven by rising clarithromycin resistance. This is why 14-day courses and quadruple therapies are now preferred. [1]
Part 4: NSAID and Aspirin-Related Ulcer Disease
NSAIDs inhibit COX → decrease prostaglandin production → decreased mucosal bicarbonate production, decreased mucus production, decreased mucosal blood supply → mucosal barrier breakdown → acid/pepsin-mediated injury. [1]
The lecture slide illustrates the gastric mucosal defence: surface epithelial cells produce a mucus layer and a bicarbonate layer that create an ionic gradient — the luminal side is acidic while the mucosal surface is near-neutral. Prostaglandins (PGE₂, PGI₂) maintain this defence by:
- Stimulating mucus secretion
- Stimulating bicarbonate secretion
- Maintaining mucosal blood flow
- Promoting epithelial cell turnover
NSAIDs block COX-1 (constitutive) → prostaglandin synthesis drops → all four mechanisms fail → mucosal erosion and ulceration. [1]
Gastric mucosal damage by NSAID is pH-dependent — meaning that injury is worse in a more acidic environment. This is why co-prescribing a PPI is protective. [1]
Prevalence of ulceration depends on relative NSAID toxicity. Indomethacin, piroxicam, and aspirin are among the most ulcerogenic; ibuprofen and etodolac are less so. [1]
For NSAID users: [1]
- Review indications of NSAID (do they actually need it?)
- Switch to COX-2 inhibitor (celecoxib, etoricoxib — spare COX-1 in the stomach)
- H. pylori eradication (removes additive risk)
- Co-therapy: PPI, H2RA, or Misoprostol (PGE analogue)
For Aspirin users: [1]
- H. pylori eradication
- H2 receptor antagonists
- Proton Pump Inhibitor
- Misoprostol
- Substitution with Clopidogrel? (The lecture puts a question mark — because clopidogrel alone is NOT proven to be safer than aspirin + PPI for GI bleeding prevention in high-risk patients.)
Exam Trap — Clopidogrel as GI-Sparing Alternative
A common MCQ distractor claims that switching from aspirin to clopidogrel reduces GI bleeding risk. Evidence shows that aspirin + PPI is superior to clopidogrel alone in preventing recurrent GI bleeding. The lecture deliberately marks this with a question mark. [1]
Part 5: Gallstone Disease
10% of population above 40. Mnemonic: Fat, Female, Forty. [1]
3 types: Cholesterol, Bile pigment, Mixed. [1]
Causes: High concentration of cholesterol/bile salt, Stasis, Infection. [1]
Risk factors: Estrogen, OC pills, Pregnancy, Rapid weight loss in obese patients, Use of fibrates, Prolonged TPN, Ileal resection or jejunoileal bypass, Ileal disease (Crohn's disease), Spinal cord injury, Vagotomy, DM, Thalassaemia, Cirrhosis. [1]
Why these risk factors?
- Oestrogen/pregnancy/OC pills: Increase hepatic cholesterol secretion and decrease gallbladder motility → cholesterol supersaturation and stasis.
- Rapid weight loss: Mobilises body fat → liver excretes excess cholesterol into bile → supersaturation.
- Ileal disease/resection: Interrupts enterohepatic circulation of bile salts → bile salt depletion → cholesterol-rich bile.
- Thalassaemia/haemolytic anaemia: Chronic haemolysis → excess bilirubin → pigment stones.
- TPN: Gallbladder stasis from no oral intake.
- Fibrates: Increase biliary cholesterol excretion.
- Cirrhosis: Impaired bile salt synthesis.
Three factors converge: cholesterol supersaturation of bile → nucleation → gallbladder stasis → stone formation. [1]
Most asymptomatic. [1] Symptomatic: Biliary colic, nausea, vomiting, dyspepsia. [1]
Biliary colic: Constant (not truly "colicky") RUQ or epigastric pain, often after fatty meals, lasting 30 min to several hours, sometimes radiating to the right shoulder or back. Subsides spontaneously or with analgesics. No fever, no jaundice in simple biliary colic.
Acute cholecystitis, Gangrenous gallbladder, Empyema, Perforation, Cholangitis, Pancreatitis, Gallstone ileus. [1]
| Complication | Mechanism | Key Features |
|---|---|---|
| Acute cholecystitis | Stone impacted in cystic duct → distension → chemical inflammation → secondary bacterial infection | RUQ pain > 6h, fever, Murphy's sign positive, leukocytosis |
| Gangrenous GB | Vascular compromise of GB wall | Systemic toxicity, risk of perforation |
| Empyema | Purulent infection in obstructed GB | High fever, sepsis |
| Cholangitis | Stone in CBD → obstruction → ascending biliary infection | Charcot's triad: Fever + Jaundice + Abdominal pain → Reynold's pentad adds: confusion + shock |
| Gallstone pancreatitis | Stone impacted at ampulla of Vater → pancreatic duct obstruction → premature enzyme activation | Epigastric pain radiating to back, raised amylase/lipase |
| Gallstone ileus | Large stone erodes into duodenum via cholecystoduodenal fistula → lodges at ileocaecal valve → mechanical SBO | AXR: pneumobilia + SBO + ectopic gallstone (Rigler's triad) |
Ultrasound (first line), MRI/MRCP. [1]
- USG: Demonstrates stones (echogenic foci with posterior acoustic shadowing), GB wall thickening, pericholecystic fluid, dilated CBD.
- MRCP: Non-invasive visualisation of biliary tree; indicated when USG is inconclusive or CBD stones suspected.
- ERCP: Therapeutic — sphincterotomy + stone extraction for CBD stones.
Asymptomatic gallstone: No treatment. [1]
Acute cholecystitis: 90% settle with bed rest, antibiotics, elective cholecystectomy. Some require urgent surgery. [1]
High Yield — Asymptomatic Gallstones
Asymptomatic gallstones do NOT require treatment. This is a common MCQ distractor — do not recommend prophylactic cholecystectomy for incidental gallstones unless special circumstances (e.g., porcelain gallbladder, very large stones > 3 cm). [1]
The lecture shows an ultrasound image demonstrating echogenic focus with posterior acoustic shadowing within the gallbladder — the classic appearance of a gallstone. [1]
The lecture illustrates this progression as stones migrate from the gallbladder to the cystic duct, common bile duct, and ampulla. [1]
Part 6: Acute Pancreatitis
Obstructive (biliary stones, others), Alcohol, Infection (mumps, coxsackie, CMV, hepatitis A/B, mycoplasma, Legionella, Mycobacterium tuberculosis), Drugs (steroids, azathioprine, 6-MP, thiazide, tetracycline, valproic acid, furosemide, sulfonamide, sulindac, acetaminophen, salicylates, erythromycin), Iatrogenic (post-surgery, post-ERCP), Toxins, Trauma, Pancreatic tumours, Hypertriglyceridaemia, Idiopathic. [1]
Mnemonic: "GET SMASHED" — Gallstones, Ethanol, Trauma, Steroids, Mumps/Malignancy, Autoimmune, Scorpion venom, Hyperlipidaemia/Hypercalcaemia/Hypothermia, ERCP, Drugs.
Alternatively from Maksim's notes: GAME ID — Gallstone (MC), Alcohol, Metabolic (hyperTG, hyperCa), ERCP, Idiopathic, Drugs. [10]
Premature activation of pancreatic enzymes (especially trypsinogen → trypsin) within acinar cells → autodigestion of pancreatic tissue → necrosis → release of inflammatory mediators (TNF-α, IL-1, IL-6) → SIRS → multiorgan failure. [10][11]
Fat necrosis occurs as lipase digests peripancreatic fat → fatty acids released bind calcium → saponification → transient hypocalcaemia (can cause tetany). [10]
Acute abdominal pain + ≥3× increase in serum amylase and/or lipase. [1]
Ultrasound for biliary pathology. [1]
CT scan: Assess severity, necrosis, or complications (pseudocysts, abscess). [1]
ERCP: Only for biliary and pancreatic duct pathology. [1]
Details on investigations:
- Serum amylase: Rises within 6–12h, normalises in 3–5 days. Cut-off is 3× upper limit of normal (NOT indicative of severity). [10]
- Serum lipase: More specific than amylase; stays elevated longer.
- AXR: Sentinel loop sign (localised ileus), colon cut-off sign (paucity of gas distal to splenic flexure), obliteration of psoas shadow.
- CT abdomen with contrast: Gold standard. Best performed at 72–96h after admission (early CT may underestimate necrosis). Look for: focal/diffuse enlargement, heterogeneous enhancement, peripancreatic fat stranding, non-enhancing areas = necrosis, gas in necrosis = infected necrosis. [10][11]
- MRCP: For suspected biliary cause; avoids radiation.
Clinical indicators of severe disease: Respiratory failure, Peritonitis, Shock, Renal failure, GI bleeding. [1]
Local complications: Pseudocyst, Abscess, Necrosis. [1]
Revised Atlanta Classification: [1]
- Mild: No organ failure, no local or systemic complications
- Moderately severe: Transient organ failure < 48h
- Severe: Persistent organ failure > 48h
| Scoring System | Key Points |
|---|---|
| Revised Atlanta | Based on organ failure (respiratory, cardiovascular, renal) and duration |
| Ranson's score | 0h ("GALAW": Glucose, Age, LDH, AST, WBC) + 48h ("CHOBBS": Ca, Hct drop, O₂ (PaO₂), Base deficit, BUN increase, Sequestered fluid) → ≥ 3 = severe [10] |
| Glasgow (Imrie) score | ≥ 3/8 in first 48h = severe |
| APACHE II | ≥ 8 = severe; calculated on admission then daily |
| Balthazar CT severity index | Grade of pancreatitis (0–4) + percentage of necrosis (0–6); score 7–10 = morbidity 92%, mortality 17% [11] |
| CRP > 150 at 48h | Predicts severe attack [10] |
The lecture shows CT images of pancreatitis with a swollen, heterogeneously enhancing pancreas and peripancreatic fluid collections, as well as a pseudocyst — a walled-off fluid collection that develops ≥ 4 weeks after onset, lacks an epithelial lining (hence "pseudo"), and contains enzyme-rich fluid. [1]
Mild: Supportive, hydration, analgesics, NG suction for ileus or vomiting. [1]
Severe: Antibiotics, endoscopic or surgical debridement for infected necrotising pancreatitis. [1]
ERCP: Perform early for removal of biliary stones — may decrease mortality. [1]
Manage complications or organ failures. [1]
Details on management:
- Aggressive IV fluid resuscitation (Ringer's lactate preferred) — pancreatic inflammation causes massive third-space fluid loss.
- Analgesics: Opioids (morphine, pethidine) — the old teaching that morphine is contraindicated (sphincter of Oddi spasm) is NOT well supported, but examiners may still reference it.
- NG tube: Only if vomiting/ileus, NOT routine.
- Enteral nutrition preferred over parenteral — maintains gut barrier, reduces infection.
- Antibiotics: NOT routine prophylaxis; indicated only for infected pancreatic necrosis (diagnosed by clinical deterioration, gas on CT, or CT-guided FNA with Gram stain/culture).
- ERCP: For gallstone pancreatitis with concurrent cholangitis or persistent biliary obstruction — early ERCP (within 24–72h) reduces morbidity. [1][5][6]
- Cholecystectomy: Should be performed during the same admission (index cholecystectomy) for gallstone pancreatitis once recovered, to prevent recurrence. [10]
Part 7: Chronic Pancreatitis
Alcoholic (major cause), Hypercalcaemia, Cystic fibrosis, Trauma with residual duct injury, Ampullary/duodenal diseases causing obstruction, Hereditary, Autoimmune, Idiopathic. [1]
Symptoms: Epigastric pain, Weight loss, Anorexia, Steatorrhoea, DM, Jaundice. [1]
Why steatorrhoea? Exocrine insufficiency → inadequate lipase → fat malabsorption → bulky, foul-smelling, pale, floating stools.
Why DM? Endocrine insufficiency → loss of beta cells (↓insulin) AND alpha cells (↓glucagon). This "type 3c" diabetes is particularly difficult to control because counter-regulation by glucagon is impaired → risk of severe hypoglycaemia. [1]
AXR: Calcification. USG: Pancreatic duct dilatation, parenchymal changes (increased echogenicity, irregular contour). CT: PD dilatation, calcification, cystic lesions. ERCP: Ductal irregularity, dilatation, stenosis, stones. [1]
Stop drinking. Pain control (may be difficult — may need opioids, coeliac plexus block). Surgery in some (drainage procedures like Puestow/Frey, or resection). Steatorrhoea: Low-fat diet, pancreatic enzyme supplements (e.g. pancreatin/Creon). DM: Diet, drugs, or insulin — difficult control because patients also lack glucagon. [1]
Exam Intelligence
| Year/Paper | Topic | Key Points |
|---|---|---|
| 2019 SAQ Q5 | Acute pancreatitis: diagnosis, investigations, causes, mortality indicators [4] | Dx = acute pancreatitis; Ix = USG HBS, CT, LFT, Ca, glucose, lipids; Causes = gallstones, alcohol, drugs; Mortality indicators = old age, organ failure |
| 2019 SAQ Q7 | Perforated peptic ulcer [4] | Free gas under diaphragm + board-like rigidity + NSAID use → perforated DU/GU |
| 2023 MCQ Q35 | Epigastric pain worse early morning, relieved by eating, smoker [5] | DU (hunger pain, relieved by food) |
| 2023 SAQ Q1 | Alcoholism + upper abdominal pain + diffusely swollen pancreas on imaging [5] | Dx = acute pancreatitis; First line Ix = USG abdomen (pancreas + biliary); If suboptimal → CT; Cause = alcohol; Marker = amylase or lipase |
| 2024 MCQ Q56 | Acute cholecystitis: Murphy's sign + GB wall thickening + pericholecystic fluid [6] | Laparoscopic cholecystectomy (not ERCP — CBD not dilated, no stones in CBD) |
| 2024 SAQ Q5 | Acute pancreatitis: blood tests for other causes, USG features of biliary cause, instruments for ERCP [6] | Other causes: Ca, triglycerides; USG: gallstones, dilated CBD; ERCP instruments: basket, balloon |
| 2018 Minicase | Epigastric pain + melaena + NSAID for migraine + gallstones [3] | Pathophysiology = NSAID-induced peptic ulcer with bleeding; Signs = peritonism if perforated |
| Trap | Correct Understanding |
|---|---|
| Serology for post-eradication monitoring | Wrong — Use UBT or stool antigen |
| Clopidogrel is safer than aspirin for GI | Wrong — Aspirin + PPI is superior to clopidogrel alone |
| Amylase level correlates with severity | Wrong — 3× ULN is diagnostic, but level does NOT predict severity |
| Prophylactic antibiotics for all pancreatitis | Wrong — Only for infected pancreatic necrosis |
| Routine ERCP for all acute pancreatitis | Wrong — Only if biliary aetiology with cholangitis or persistent obstruction |
| CT within first 24h for pancreatitis | May miss necrosis — Best at 72–96h |
| Asymptomatic gallstones need cholecystectomy | Wrong — Observe unless special indications |
| Morphine is absolutely contraindicated in pancreatitis | Outdated — No strong evidence; can use with caution |
1. SAQ: A 55-year-old woman presents with acute epigastric pain and vomiting. Amylase is 1250 U/L. What is the diagnosis? What investigations would you perform? Name 3 common causes.
- Markscheme: Acute pancreatitis. Ix: USG HBS (gallstones, CBD), CT abdomen with contrast (72–96h or if severe), LFT, Ca, triglycerides, glucose, CRP. Causes: Gallstones, alcohol, drugs, hypertriglyceridaemia, post-ERCP, idiopathic.
2. MCQ: A 45-year-old man has epigastric pain worse in early morning, relieved by eating, no weight loss. Most likely diagnosis?
- Markscheme: Duodenal ulcer. (Hunger pain / night pain, relieved by food = classic DU.)
3. SAQ: List 4 alarming features in a patient with dyspepsia that warrant urgent OGD.
- Markscheme: Age ≥ 45 new onset, anaemia/bleeding, weight loss > 10% BW, dysphagia, abdominal mass, persistent vomiting, FHx upper GI cancer.
4. MCQ: Which non-invasive H. pylori test is NOT useful for confirming eradication?
- Markscheme: Serology. (IgG persists after eradication; UBT and stool antigen detect active infection.)
5. SAQ: Name the first-line and second-line H. pylori eradication regimens per HK Consensus.
- Markscheme: 1st line: PPI + clarithromycin + amoxicillin × 14 days OR BQT (PPI + bismuth + tetracycline + metronidazole) × 10–14 days.
6. SAQ: How do you prevent NSAID-associated upper GI complications? List 4 strategies.
- Markscheme: Review NSAID indication, switch to COX-2 inhibitor, eradicate H. pylori, co-prescribe PPI or misoprostol.
7. SAQ: What is the Revised Atlanta Classification of acute pancreatitis severity?
- Markscheme: Mild (no organ failure, no complications), Moderately severe (transient organ failure < 48h), Severe (persistent organ failure > 48h).
8. MCQ: A patient with known gallstones presents with fever, jaundice, and RUQ pain. What is the diagnosis?
- Markscheme: Ascending cholangitis (Charcot's triad).
High Yield Summary
Peptic Ulcer: H. pylori (~92% DU, ~70% GU) and NSAIDs are the two major causes. Complications = pain, bleeding, perforation, GOO. Treatment = PPI + H. pylori eradication + stop NSAIDs. Always test for H. pylori and confirm eradication with UBT/stool antigen (NOT serology). HK Consensus 1st line: PPI + amoxicillin + clarithromycin × 14 days.
Gallstones: Fat/Female/Forty. Three types (cholesterol, pigment, mixed). Most asymptomatic → no treatment. Complications: cholecystitis, cholangitis, pancreatitis, gallstone ileus. Investigation: USG first line. Treatment: cholecystectomy if symptomatic.
Acute Pancreatitis: Gallstones (MC) and alcohol are the top causes. Diagnose with pain + amylase/lipase ≥ 3× ULN. USG to assess biliary cause; CT at 72–96h for severity/necrosis. Revised Atlanta: mild/moderately severe/severe based on organ failure duration. Treatment: IV fluids, analgesia, enteral nutrition; ERCP for biliary cause with cholangitis; antibiotics only for infected necrosis.
Chronic Pancreatitis: Alcohol is the major cause. Triad: pain, steatorrhoea, DM. AXR calcification is suggestive. Treatment: stop alcohol, pancreatic enzyme supplements, pain control, manage brittle DM (lack of glucagon → hypoglycaemia risk).
Active Recall - Upper Abdominal Pain: Peptic Ulcer, Pancreatitis, Gallstone
[1] Lecture slides: GC 092. Upper abdominal pain_ peptic ulcer; pancreatitis and gallstone.pdf [2] Senior notes: Block A - Upper abdominal pain_ peptic ulcer; pancreatitis and gallstone.pdf [3] Past papers: 2018 Fourth Summative Minicase.pdf (Section 2, Q3-4) [4] Past papers: 2019 Fourth Summative SAQ.pdf (Q5, Q7) [5] Past papers: 2023 Fourth Summative MCQ.pdf (Q35); 2023 Fourth Summative SAQ.pdf (Q1) [6] Past papers: 2024 Fourth Summative MCQ.pdf (Q56); 2024 Fourth Summative SAQ.pdf (Q5) [7] Senior notes: Maksim Medicine Notes.pdf (p119) [8] Lecture slides: Gastroenterology - Two cases of dyspepsia.pdf [9] Senior notes: Block A - Coffee ground vomitus tarry stool upper GI bleeding.pdf (p20) [10] Senior notes: Maksim Surgery Notes.pdf (p142-143) [11] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p582-585)
GC091 Unsteady Gait Cerebellar Lesions; Movement Disorders; Parkinsonism
Unsteady gait is a disturbance in walking stability that can arise from cerebellar lesions causing ataxia, movement disorders such as dystonia or chorea, or parkinsonism characterized by shuffling steps, festination, and postural instability.
GC093 Urticaria, Angioedema And Anaphylaxis
Urticaria, angioedema, and anaphylaxis represent a spectrum of hypersensitivity reactions ranging from localized mast cell–mediated wheals and submucosal swelling to a severe, systemic, life-threatening allergic response involving multiorgan dysfunction.