The lecture emphasises that functional dyspepsia accounts for ~60% of cases, while peptic ulcer accounts for only ~10%. Always consider non-GI causes. ^[1]

Key teaching point: Epigastric pain ≠ Peptic ulcer. ^[1]

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 with characteristic waveform patterns: ^[1]
  • Ulcer pain — steady, low-grade (nearly flat line above baseline).
  • Intestinal / renal colic — undulating, with repeated rises and falls (true colicky pattern).
  • Biliary colic / pancreatic pain — rises to a broad peak then gradually declines (the most severe).
• 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]

Duration of symptoms, Age, Presence of alarming symptoms, Drug history (NSAID/aspirin), Family history of CA stomach, Alternative non-GI diagnoses. ^[1]

The slide-era list uses age ≥45 years, anaemia or bleeding, weight loss, anorexia/early satiety, persistent vomiting, mass or lymphadenopathy, dysphagia/odynophagia, family history of upper-GI cancer, previous gastric surgery or malignancy, previous ulcer and jaundice. ^[1]

Current interpretation: A fixed age threshold is not universal. The ACG/CAG dyspepsia guideline uses ≥60 years for routine endoscopy, but explicitly supports younger endoscopy when gastric-cancer risk is higher (for example, childhood in a high-incidence region or positive family history). Alarm features in a younger patient require case-by-case assessment rather than an automatic “scope everyone” or “scope nobody” rule. Dysphagia, overt bleeding, iron-deficiency anaemia, progressive weight loss, persistent vomiting, a mass or jaundice require prompt directed investigation. ^[12]

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.

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).

Reading the endoscopy images: The ulcers appear as discrete mucosal craters with a pale fibrinous base and surrounding erythema. Location distinguishes a gastric from a duodenal ulcer; appearance alone cannot reliably exclude malignancy, so a gastric ulcer is biopsied and followed according to local endoscopy guidance. ^[1]

Pain, Bleeding, Perforation, Gastric outlet obstruction. ^[1]

The bleeding-ulcer image shows a crater with a focal vessel/haemorrhagic stigma rather than a simple clean base. Active bleeding or a non-bleeding visible vessel is a high-risk endoscopic finding that requires endoscopic haemostasis; an adherent clot is managed according to the clinical/endoscopic context. ^[13]

H. pylori infection, NSAID, Aspirin, Stress (ICU), Zollinger-Ellison syndrome (Gastrinoma), Crohn's disease. ^[1]

• H. pylori: ~92% of DU, ~70% of GU. ^[1]
• NSAID: ~25% of GU, ~5% of DU. ^[1]
• Stress-related mucosal disease: acid-suppression prophylaxis is for critically ill patients with important bleeding risk factors, not every ICU admission; reassess and stop when the indication resolves. ^[21]
• Zollinger-Ellison: Gastrin-secreting tumour → massive acid hypersecretion → refractory/multiple ulcers, diarrhoea (acid inactivates lipase). Part of MEN1.

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 (for example, famotidine): Less potent than a PPI. Ranitidine has been withdrawn in many jurisdictions because of NDMA contamination and should not be presented as a routine option. ^[14]
• Always test and treat H. pylori. Always review NSAID/aspirin need.

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]

These pie charts describe 1994 cohorts. The durable teaching point is that H. pylori and NSAIDs are the dominant causes; the exact proportions vary by population, calendar period, testing method and medication exposure.

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.

Reading the urease-testing diagrams: ^[1]

• In the ¹³C urea breath test, bacterial urease splits labelled urea; labelled CO₂ is absorbed and then measured in exhaled breath.
• In the rapid urease/CLO test, a gastric biopsy is placed in a urea-containing indicator medium; urease-generated ammonia raises pH and changes the medium from yellow toward red/pink.
• Stool antigen and urea breath testing detect active infection; serology may remain positive after cure.

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]

Maastricht VI slide algorithm (only where clarithromycin resistance is low): ^[1]

• BQT duration: 14 days (unless a 10-day regimen has proven equally effective locally).
• The diagram places rifabutin triple therapy at fourth line, but this is not a universal sequencing rule; regimen choice after failure depends on prior antibiotics, penicillin allergy, local susceptibility and access to susceptibility testing.

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? Raising intragastric pH improves the stability/activity of key antibiotics and encourages H. pylori to enter a replicative state that is more antibiotic-susceptible. Adequate PPI or PCAB dosing is therefore an important component of an eradication regimen. ^[1][15]

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]

The lecture presents resistance trend data (Hong TZ et al., Lancet Gastroenterol Hepatol 2023) showing rising resistance across the region: ^[1]

• Metronidazole has the highest resistance at every time point.
• Clarithromycin resistance has risen from 7% to 30%, exceeding the 15% threshold that triggers a switch away from clarithromycin-based triple therapy.
• Amoxicillin and tetracycline resistance remains low (≤ 6%), supporting their continued use in quadruple regimens.

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:

1. Stimulating mucus secretion
2. Stimulating bicarbonate secretion
3. Maintaining mucosal blood flow
4. 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]

The lecture cites experimental data (Elliott et al. 1996) demonstrating that NSAID-induced haemorrhagic mucosal area is greatest at gastric luminal pH 2.0–4.0 (~3.4–3.5%) and drops markedly at pH 5.5–7.0 (~0.4–0.75%), confirming the rationale for PPI co-therapy to raise intragastric pH. ^[1]

Prevalence of ulceration depends on relative NSAID toxicity. ^[1]

The lecture presents historical endoscopic-ulcer data (Cheatum et al. 1999) showing substantial variation by NSAID: ^[1]

The chart's exact ranking should not be used as a current comparative-prescribing table: it reflects a specific older cohort and endoscopic-ulcer outcome. The transferable points are that GI harm is dose- and drug-dependent, and concurrent NSAIDs substantially increase risk. Aspirin also increases bleeding risk, but its cardiovascular indication must be weighed before alteration.

Patient-related: Age > 60, History of peptic ulcer disease / upper GI complications. ^[1]

Drug-related: Relatively toxic NSAID, High dose (or two NSAIDs concurrently), Concurrent anticoagulant, Concurrent corticosteroid. ^[1]

For NSAID users: ^[1]

1. Review indications of NSAID (do they actually need it?)
2. Switch to COX-2 inhibitor (celecoxib, etoricoxib — spare COX-1 in the stomach)
3. H. pylori eradication (removes additive risk)
4. Co-therapy: PPI, H2RA, or Misoprostol (PGE analogue)

How to use the prevention diagram safely: use the lowest effective dose for the shortest necessary duration, avoid combining NSAIDs, assess both GI and cardiovascular/renal risk, test and eradicate H. pylori when appropriate, and use PPI gastroprotection for patients at increased GI risk who must continue an NSAID. A COX-2 selective drug may reduce upper-GI injury but is not automatically safer overall; cardiovascular and renal risks still matter. Standard-dose H2RAs are less reliable than PPIs for preventing NSAID-related gastric ulcers, and misoprostol is limited by diarrhoea/cramping and is contraindicated in pregnancy. ^[17]

For Aspirin users: ^[1]

1. H. pylori eradication
2. H2 receptor antagonists
3. Proton Pump Inhibitor
4. Misoprostol
5. 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.)

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]

Reading the bile-composition triangle: The three axes are cholesterol, bile acids and phosphatidylcholine. Within the micellar zone, bile acids and phospholipid keep cholesterol soluble. As bile becomes cholesterol-rich or relatively deficient in bile acids/phospholipid, it moves into the vesicle/liquid-crystal zone and then the solid-crystal zone; nucleated cholesterol crystals can grow into stones, especially when gallbladder emptying is poor. ^[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]

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]

This is lecture-era management. For a surgically suitable patient, current guidance recommends early laparoscopic cholecystectomy during the index admission, as soon as practical; antibiotics and supportive care do not replace source control. Percutaneous cholecystostomy is reserved for selected patients who are severely ill or not suitable for surgery, with definitive planning after stabilisation. ^[18]

The lecture ultrasound shows an echogenic intraluminal focus with clean posterior acoustic shadowing in the anechoic gallbladder. Demonstrating mobility with patient repositioning supports a stone; a stone impacted at the neck may not move. In acute cholecystitis also seek wall thickening, distension, pericholecystic fluid and a sonographic Murphy sign. ^[1]

The lecture illustrates this progression as stones migrate from the gallbladder to the cystic duct, common bile duct, and ampulla. ^[1]

The lecture diagram maps stone location to complication: ^[1]

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]

Gallstones and alcohol account for most cases. Check triglycerides and calcium when the cause is not evident, review recent ERCP/trauma and medicines, and consider tumour in an older patient with unexplained pancreatitis. Evidence linking individual medicines varies; diagnose drug-induced pancreatitis cautiously after excluding more likely causes. ^[19]

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]

The slide highlights acute abdominal pain plus ≥3× elevation of serum amylase and/or lipase. ^[1]

The diagnosis requires at least 2 of 3 criteria: (1) characteristic acute epigastric pain, often radiating to the back; (2) serum lipase or amylase ≥3× the upper limit of normal; (3) characteristic imaging. Imaging is not mandatory when the pain and enzyme criteria are already met. ^[19]

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.
• Contrast CT abdomen: Do not perform routinely at admission solely to grade severity. Reserve it for diagnostic uncertainty or failure to improve after about 48–72 hours; later contrast imaging better delineates necrosis. Look for enlargement, heterogeneous enhancement, peripancreatic fat stranding/fluid, non-enhancing parenchyma suggesting necrosis, and gas within a collection suggesting infection. ^[19]
• 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 and/or a local or systemic complication without persistent organ failure
• Severe: Persistent organ failure > 48h

Reading the acute-pancreatitis CT: The labelled pancreas is enlarged and ill-defined, with inflammatory change and fluid tracking in the surrounding fat. Compare pancreatic enhancement with adjacent organs: patchy or absent enhancement raises concern for necrosis. ^[1]

Reading the collection images: The arrows indicate mature, encapsulated peripancreatic collections. Under Revised Atlanta terminology, a pseudocyst is an encapsulated, predominantly fluid collection arising after interstitial oedematous pancreatitis, usually after ≥4 weeks, with no solid necrotic component and no epithelial lining. A mature collection containing necrotic debris after necrotising pancreatitis is walled-off necrosis, not a pseudocyst; this distinction affects drainage and debridement planning. ^[1][19]

The slide-era treatment summary lists hydration/analgesia, antibiotics and debridement for infected necrosis, and early ERCP for biliary stones. ^[1]

Manage complications or organ failures. ^[1]

Details on management:

• Moderately aggressive, goal-directed IV fluid resuscitation, preferably lactated Ringer's, with frequent reassessment of haemodynamics, urine output, BUN/haematocrit and signs of overload. Avoid reflexively “aggressive” large-volume hydration, especially in cardiac/renal comorbidity. ^[19]
• Analgesia: Titrate multimodal analgesia to need; opioids may be used when required. The old claim that morphine is absolutely contraindicated because of sphincter-of-Oddi spasm is not supported, and pethidine has no routine advantage.
• NG tube: Only if vomiting/ileus, NOT routine.
• Early oral feeding: in mild disease, start a low-fat solid diet within 24–48 hours as tolerated rather than keeping the patient nil by mouth until enzymes normalise. If oral intake is not possible, enteral feeding is preferred over parenteral nutrition. ^[19]
• Antibiotics: NOT routine prophylaxis and not indicated for sterile necrosis. Suspect infected necrosis with clinical deterioration/sepsis, bacteraemia or gas in a necrotic collection; routine CT-guided FNA is usually unnecessary. ^[19]
• ERCP: Perform within 24 hours for gallstone pancreatitis with acute cholangitis. Do not perform routine early ERCP in biliary pancreatitis without cholangitis; if a retained CBD stone is suspected without cholangitis, use EUS or MRCP to screen and select patients for therapeutic ERCP. ^[19]
• Cholecystectomy: Perform during the same admission for mild gallstone pancreatitis once clinically improving, to prevent recurrence; severe/necrotising disease requires individualised timing. ^[19]
• Infected necrosis: Use antibiotics that penetrate necrotic tissue. In a stable patient, delay drainage/necrosectomy for about 4 weeks so the collection can wall off, and use a minimally invasive step-up approach rather than immediate open surgery. ^[19]

Alcoholic (major cause), Hypercalcaemia, Cystic fibrosis, Trauma with residual duct injury, Ampullary/duodenal diseases causing obstruction, Hereditary, Autoimmune, Idiopathic. ^[1]

Obstructive: Fibrosis, ductal changes with dilatation. ^[1] Calcifying: Fibrosis, intraductal stones, associated with alcohol. ^[1] Inflammatory: Not the above two. ^[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]

The ERCP appearance is useful conceptually, but ERCP is now primarily therapeutic, not a first-line diagnostic test for chronic pancreatitis. Cross-sectional CT or MRI is first line; EUS or secretin-enhanced MRCP can clarify suspected early disease when cross-sectional imaging is inconclusive. ^[20]

The lecture shows imaging examples of chronic pancreatitis: a CT image with coarse and punctate high-density calcifications following the pancreatic bed/duct, and a plain AXR with irregular calcific densities projected transversely across the upper central abdomen. CT localises the calcification to the pancreas and can also show duct dilatation, atrophy, stones or a complication; the plain film is less sensitive and less specific. ^[1]

The slide recommends alcohol cessation, pain control, selected endoscopic/surgical therapy, pancreatic enzyme replacement for steatorrhoea, and diabetes treatment. ^[1]

Also stop smoking, which accelerates chronic-pancreatitis progression. Pancreatic enzyme replacement is taken with meals/snacks and titrated to symptoms and nutrition. Routine severe fat restriction can worsen malnutrition; use an adequate balanced diet and restrict fat only if steatorrhoea persists despite optimised enzymes and dietetic review. ^[20]