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
