GI & Hepatology JC059: Upper Abdominal Pain: Peptic Ulcer, Pancreatitis And Gallstone Flashcards
Epigastric pain
Structures:
1. Stomach
2. Duodenum
3. Pancreas
4. Liver
5. Gallbladder
6. Transverse colon (occasionally, mostly central / lower abdominal pain)
7. Abdominal aorta
8. Spine, Skin, Muscle
***DDx of Epigastric pain
- Gastroduodenal
- Peptic ulcer (~10%)
- Atypical GERD
- Gastric cancer (rare)
(- Gastritis) - Hepatobiliary
- Pancreatitis
- Pancreatic cancer
- Gallstone - **Functional dyspepsia (aka **Non-ulcer dyspepsia, about 60%, majority)
- Drugs
- NSAIDs
- Aspirin
- Alendronate
- etc. - Non-GI causes
- Cardiac: MI, myocarditis
- Chest: pneumothorax, PE
- Haematological: acute leukaemia, haemolytic anaemia
- Metabolic: uraemia, DM (***DKA), porphyria, Addison’s
- Toxins: hypersensitivity, chronic lead poisoning
- Infections: herpes zoster
- Neurological: radiculitis, tabes dorsalis (neurosyphilis)
- Miscellaneous: muscular contusion, narcotic withdrawal, psychiatric disorder, heat stroke
History taking of Upper abdominal pain
- Location (epigastric / retrosternal / lower abdominal pain)
- Referral
- Character (diffuse / localised)
- Severity
- Duration
- Onset (sudden / gradual)
- Frequency
- Aggravating / Alleviating factors
- Associated symptoms
- bleeding, melena, weight loss
Important considerations:
1. Duration
2. Age
3. ***Presence of alarming symptoms
4. Drug history: NSAID, Aspirin use
5. Family history: Ca stomach
6. Alternative diagnosis (Non-GI causes)
***Pain severity
Ulcer:
- ***Static, Steady
Intestinal, Renal colic:
- ***Fluctuating
Biliary colic, Pancreatic:
- Last much longer than intestinal / renal colic
- ***No fluctuating cycles
Referral of pain
Acute epigastric pain referring to back:
1. Posteriorly penetrating peptic ulcer
2. Biliary pain
3. **Acute pancreatitis
4. **Dissecting aneurysm / AAA
Associated symptoms
Epigastric pain + Repeated vomiting (記: Stomach, Intestine, Pancreas, HBP):
1. Food poisoning / **GE / Gastritis
2. **Acute pancreatitis
3. **Gastric outlet obstruction
4. **Gallstone
Agonising pain but insignificant signs:
1. Acute pancreatitis
2. ***Mesenteric thrombosis / infarct at early stage
Alarming features
- > =45 yo (***new onset)
- Anaemia / ***Bleeding
- LOW (>10% of BW)
- ***Anorexia / Early satiety
- ***Persistent vomiting
- ***Abdominal mass / Lymphadenopathy
- ***Dysphagia / Odynophagia —> Proximal cardiac region / Esophageal lesions
- Family history of Upper GI cancer
- Previous gastric surgery / malignancy
- Previous history of ulcer
- Jaundice
Physical examination
- General
- appearance, posture
- in pain
- vitals
- fever
- jaundice
- lymphadenopathy - Abdominal
- mass
- location + degree of tenderness
- rebound tenderness, guarding, rigidity - Genital, rectal, pelvic
- PR exam
- hernia orifices
***Peptic ulcer
- Gastric ulcer
- Duodenal ulcer
- Esophageal ulcer (Reflux ulcer)
- Meckel’s diverticulum (in ileum)
- Anastomotic ulcer
Clinical features:
1. Asymptomatic (mostly)
2. **Pain (duodenal ulcer: **hunger pain vs gastric ulcer: aggravated by eating)
3. **Bleeding (when ulcer erode into vessels —> melena / haematemesis)
4. **Perforation (more common in duodenal ulcers > gastric ulcers)
5. ***Gastric outlet obstruction (ulcer in pyloric region / duodenum ∵ scarring / edema / fibrosis)
(6. Penetration into adjacent organs —> fistula)
Causes:
1. **H. pylori infection (Duodenal ulcer, Gastric ulcer)
2. *NSAID, Aspirin (Gastric ulcer)
3. **Stress (typically ICU patients, duodenal ulcers usually)
4. **Zollinger Ellison syndrome (Gastrinoma)
5. Crohn’s disease (upper GI ulcers as well, refractory to treatment, tend to recur)
Pharmacological treatment:
1. Acid suppression
2. Eradication of H. pylori
3. Avoid ulcerogenic drugs
H. pylori
Bacteriology:
- **Gram -ve bacilli
- spiral
- unipolar flagella
- **slow growing
Prevalence:
- around ***50% adults in HK, ↓ worldwide
- developing countries 50-80%, developed countries 10-30%
- ↑ with age, poor socioeconomic status, poor hygiene, overcrowding
Transmission:
- unknown
- probably **oral-oral / **faecal-oral route —> close person-to-person spread
—> water supply, poor sanitary condition, crowded environmental, low socioeconomic status
- NOT present in environmental sources (e.g. water, food)
Colonisation:
- strong ***urease activity —> hydrolyse urea —> NH3 + HCO3 —> ↑ resistance to low pH of stomach
***H. pylori associated diseases
Gastroduodenal:
1. **Chronic gastritis (everyone)
2. **Dyspepsia
3. **Duodenal ulcer (92% associated with H. pylori, ∵ acid production by antral-predominant gastritis)
4. **Gastric ulcer (70% associated with H. pylori, ∵ weakened mucosal defence from suppressed acid production in corpus-predominant gastritis)
5. **Gastric adenocarcinoma
6. **Gastric MALT lymphoma
—> Eradication of H. pylori results in long term remission of peptic ulcer disease
Extra-GI system (not well-documented):
- ITP
- Anaemia (B12 folate deficiency)
Diagnosis of H. pylori
- Invasive (Endoscopy + Biopsy)
- ***Rapid urease test / CLO (Campylobacter-like organism) test
- Culture (lowest sensitivity, lowest yield): Antibiotic susceptibility testing
- Histology: H/E stain, Special stains ↑ sensitivity - Non-invasive
- Serology: whole blood / serum test (Ab: **IgG Ab (but can still be elevated even after eradication —> **NOT good for monitoring treatment response))
- **Urea breath test (urease activity) —> good for monitoring treatment response
- **Stool Ag test —> good for monitoring treatment response
- Urine Ab
Rapid urease test, Urea breath test
Rapid urease test:
pH indicator
- If have urease activity —> hydrolyse urea —> NH3 + HCO3
—> negative: yellow
—> ***positive: red
- instantaneous result of H. pylori when doing endoscopy
Urea breath test (most commonly available non-invasive test):
- 13C-urea
—> NH4 + ***13-CO2
—> 13-CO2 absorbed into systemic circulation
—> exhaled in lung
—> measure change in 13-CO2 in breath (baseline breath vs breath after taking 13C-urea)
SpC Medicine:
- False positive very unlikely
- False negative:
1. Drugs in past 2 weeks
- PPI: H pylori moves proximally to body / fundus
- Bismuth
- Antibiotics
2. Acute upper GI bleeding —> should not do rapid urease test as blood will interfere with urease
3. Technical issue (for young children only)
—> Retesting If the above causes are present
***H. pylori eradication regimen
記: PAC, PMC, PAM, PBTM, PACM
- PPI-based triple therapy (**PAC) (combination of 2 antibiotics ∵ not very susceptible to 1 antibiotic only):
- **PPI (standard dose) (↑ gastric pH —> ↑ bioavailability of antibiotics)
- **Amoxicillin (1000mg)
- **Clarithromycin (500mg)
—> **BD for **1 week
If allergic to Amoxicillin (**PMC):
PPI (standard dose) + **Metronidazole (400mg) + Clarithromycin (250mg)
- BD for 1 week
- Problem: antibiotic resistance to Metronidazole / Clarithromycin
Other regimen (***PAM):
PPI (standard dose) + Amoxicillin (1000mg) + Metronidazole (400mg)
- BD for 1 week / TDS for 1 week
- Bismuth-containing quadruple therapy
- PPI + Bismuth + Tetracycline + Metronidazole (PMBT)
—> Advantage: Little resistance to Tetracycline, Bismuth
—> Problem: Many SE for Bismuth (black stool) + Tetracycline + Metronidazole - Non-bismuth-containing quadruple therapy
- PPI + Amoxicillin + Clarithromycin + Metronidazole (***PACM)
Maastricht V Consensus (ALL regimens: ***2 weeks):
High Clarithromycin resistance (>15%)
—> High Metronidazole resistance as well —> Bismuth-containing quadruple therapy (PBTM)
—> Low Metronidazole resistance —> PPI (standard dose) + Amoxicillin (1000mg) + Metronidazole triple therapy
Both Clarithromycin / Metronidazole resistance low (<15%)
—> Bismuth-containing quadruple therapy / Non-bismuth-containing quadruple therapy
***NSAIDs and Aspirin
- Another important causal factor of peptic ulcer disease
- Major cause of ***gastric ulcer
Pathophysiology to ulcer:
- ***Blockage of Prostaglandin + Bicarbonate + Mucus production
Relative NSAID toxicity (high to low):
- **Aspirin
- **>1 NSAIDs
- Ketoprofen
- Etodolac
- Ibuprofen
- Naproxen (low)
- Diclofenac (low)
Risk factors for upper GI complications with NSAIDs:
Patient-related factors:
- >60 yo
- history of peptic ulcer disease / upper GI complications
Drug-related factors:
- use of relatively toxic NSAID
- use of high dose NSAID / >1 NSAIDs
- **concurrent use of anticoagulant
- **concurrent use of corticosteroid
Preventing NSAID-associated upper GI SE
Gastric mucosal damage by NSAID is ***pH dependent
- ↑ gastric pH —> ↓ gastric mucosal damage —> ∴ PPI prevent + protect against NSAID damage
- Review indications of NSAID
- Switch to less ulcerogenic NSAID / COX-2 inhibitor
- H. pylori eradication
- Co-therapy
- PPI
- H2RA (less potent than PPI)
- Misoprostol (PGE analogue)
Preventing Aspirin related GI complications:
1. H. pylori eradication
2. PPI / H2RA / Misoprostol
3. Replace with ***Clopidogrel in selected patients
***Gallstones
- 10% population above 40
3 types:
1. Cholesterol stone
2. Bile pigment (Bilirubin) stone
3. Mixed stone
Causes:
1. High concentration of cholesterol / bile salt
2. Stasis
3. Infection
**Risk factors:
1. **4Fs: Female, Middle age, Obesity, Fertile
2. **Estrogen (↑ cholesterol production in the liver)
3. OC pills
4. **Pregnancy (∵ hormonal changes, impair hormonal control of GB contraction)
5. Rapid weight loss in obese patient (∵ liver releases extra cholesterol into the bile)
6. **Use of Fibrates (↓ synthesis of bile acid —> easier for cholesterol to precipitate)
7. **Prolonged TPN (∵ induce cholestasis —> precipitation of bile)
8. **Ileal resection / jejunoileal bypass (induces enterohepatic circulation of bilirubin and doubles the secretion rate of bilirubin into the bile) (web: increased spillage of malabsorbed bile acids into the colon where they solubilize unconjugated bilirubin and promote its absorption and thereby increase the rate of bilirubin secretion into the bile)
9. Ileal disease (Crohn’s disease)
10. Spinal cord injury
11. Vagotomy / Previous gastrectomy (∵ dissection in surgery divide nerve supplying GB)
12. **DM (∵ peripheral neuropathy affect contractility of GB)
13. **Haemolytic anaemia, Haemolytic disorders e.g. **Thalassaemia (∵ ↑ Bilirubin deposition)
14. ***Cirrhosis
15. BM transplant / Solid organ transplant
Pathogenesis of Gallstones
Disturbed equilibrium between phospholipid, cholesterol, bile salt in Bile
Symptoms, Investigations and Treatment of Gallstone
Clinical features:
1. Asymptomatic (mostly)
2. **Biliary colic
3. **N+V
4. Dyspepsia (non-ulcer dyspepsic-like symptoms)
Complications (depend on location of gallstones):
- **Acute cholecystitis
- **Gangrenous
- **Empyema
- **Perforation
- **Cholangitis
- **Pancreatitis
- Gallstone ileus
Investigations:
- ***USG (model of choice: echogenic with acoustic tail)
- AXR
Treatment:
- No treatment for asymptomatic except DM
- Acute cholecystitis: 90% settled with **Bed rest, **Antibiotics, ***Elective cholecystectomy (some require urgent surgery if acute gangrenous cholecystitis, empyema, perforation)
***Acute pancreatitis: Causes
GET SMASHED
- Obstructive (***Biliary stones (Gallstones in CBD —> Pancreatic duct obstruction), others)
- ***Alcohol (esp. chronic pancreatitis)
- Infection
- mumps, coxsackie, CMV, Hep A, Hep B, mycoplasma, legionella, TB - ***Drugs
- steroids, azathioprine, 6-MP, thiazide, tetracycline, valproate, furosemide, sulfonamide, sulindac (NSAID), paracetamol, salicylate, erythromycin - Iatrogenic
- post-surgery
- ***post-ERCP - Toxins, trauma, pancreatic tumours
- ***Hypertriglyceridaemia
- ***Idiopathic (majority)
***Diagnosis of Acute pancreatitis
Mainly clinical + blood tests:
1. Acute abdominal pain
2. **3x ↑ Serum **Amylase / Lipase
Imaging:
3. **USG for biliary pathology (biliary dilatation + presence of stones)
4. **CT scan (usually in late phase): assess severity, necrosis, complications e.g. **pseudocysts, **abscess
5. ERCP only for biliary / pancreatic duct pathology —> take out biliary stones
***Prognostic scores of Acute pancreatitis
Clinical (Multi-organ failure):
- Respiratory failure
- **Peritonitis
- **Shock
- Renal failure
- ***GI bleeding
—> more likely to have chronic disease
***Local complications:
- Pseudocysts
- Abscess
- Necrosis
—> more likely to have worse prognosis
- ***Ranson’s criteria
On admission
- Age >55
- WCC >16
- Glucose >10
- LDH >350
- AST >250
During initial 48 hours
- Hct ↓ >10%
- BUN ↑ >1.79
- Ca <2 (∵ autodigestion of mesenteric fat by pancreatic enzyme —> release of free fatty acids —> precipitate Ca salts, other mechanisms: transient hypoparathyroidism, hypoMg)
- PaO2 <60 mmHg
- Base deficit (24-HCO3) >4
Fluid needs >6L
Score 0-2: 2% mortality
Score 3-4: 15% mortality
Score 5-6: 40% mortality
Score 7-8: 100% mortality
- ***APACHE-2 (acute pancreatitis requiring ICU care)
- age
- acute physiology score: vitals, ABG, electrolytes, GCS
- chronic health points: cirrhosis, COPD, on dialysis, CHF, immunocompromised
Treatment of Acute pancreatitis
- Mild
- Supportive
- **Hydration
- Analgesic
- **NG suction for ileus / vomiting - Severe
- **Antibiotics
- **Surgical debridement for infected necrotising pancreatitis (E. coli etc.)
- Surgical endoscopic drainage - ERCP (if biliary pancreatitis)
- perform early for ***removal of biliary stones may ↓ mortality - Manage complications of organ failure
Chronic pancreatitis
Causes:
- **Alcoholic (major cause)
- Hypercalcaemia
- **Cystic fibrosis
- ***Pancreatic duct disruption (tumours, surgery —> residual duct injury)
- Ampullary / Duodenal diseases —> obstructing chronic pancreatitis
- Hereditary
- Autoimmune
- Idiopathic
**Classification
1. **Obstructive
- fibrosis
- ductal changes with dilatation
- ***Calcifying
- fibrosis
- intraductal stone
- associated with alcohol - Inflammatory
- not the above 2
Clinical features of Chronic pancreatitis
- Chronic epigastric pain
- ***Exocrine insufficiency
- weight loss
- anorexia
- steatorrhoea
- malabsorption - ***Endocrine insufficiency
- DM - Jaundice (∵ bile duct obstruction)
Investigations of Chronic pancreatitis
- AXR
- ***calcification of pancreatic duct - USG
- ***pancreatic duct dilatation
- parenchymal changes of ↑ echogenicity with irregular gland contour - CT scan
- **pancreatic duct dilatation
- **calcification
- cystic lesions - ERCP (relieve pancreatic strictures, remove stones, stenting)
- ductal irregularity
- **dilatation
- **stenosis
- stones
Treatment of Chronic pancreatitis
- ***Stop drinking
- Pain control (maybe difficult)
- Surgery in some
Steatorrhoea:
- Low-fat diet
- ***Pancreatic supplements e.g. Pancreatin (commercial mixtures of amylase, lipase, protease)
DM:
- Diet control
- **Drugs / **Insulin
- Difficult control because patients also lack glucagon
(Liver abscess (from JC Microbiology))
Pyogenic / Amoebic
Pyogenic (Bacterial):
1. **Cholangitic (e.g. from RPC)
- E. coli
- Enterococcus
- Streptococcus anginosus
- Clostridium perfringens
2. **Haematogenous (e.g. from infective endocarditis)
- Viridans streptococci
- Staphylococcus aureus
- Enterococci
- HACEK group of bacteria
3. Iatrogenic (e.g. from TACE)
4. Trauma
5. ***Cryptogenic
- Klebsiella pneumoniae
Amoebic:
1. Entamoeba histolytica
Other causes:
1. Clonorchis sinensis (RPC)
2. Fasciola hepatica
3. Mycobacterium tuberculosis
4. Bartonella
5. Echinococcus etc.
