UGI Flashcards
Definition of peptic ulcer disease
Erosions in gastric or duodenal mucosa that extend through the muscularis mucosae
Pathophysiology of peptic ulcer disease
• Increased aggressive factors and/or decreased defensive factors
o Protective factors
▪ Mucosal bicarbonate secretion
▪ Mucus
▪ Blood flow
▪ Growth factors
▪ Cell renewal
▪ Endogenous prostaglandins
o Damaging factors
▪ HCl secretion
▪ Pepsins
▪ Ethanol
▪ Smoking
▪ Duodenal bile reflux
▪ Ischaemia, hypoxia
▪ NSAIDs
▪ H. Pylori infection
Helicobacter pylori
Involved in 80% duodenal and 60% gastric ulcers
Flagella manouveres the bacteria through mucus into epithelium
Curved gram neg rod, adheres to gastric epithelium inantrum (to avoid acid producing parietal cells), buries under mucous layer with flagella
Releases enzymes and toxins that directly injury cells, incite inflammatory response and disrupts the mucous layer rendering mucosa vulnerable to acid damage
Inflammation causes antral G cells to release gastrin -> stimulates parietal cells to proliferate and secrete acid -> causes chronic gastritis, atrophy, ulcers
Enzymes
Urease - neutralises acid around bacteria, converts urea to ammonium chloride
Catalase - antioxidant, protects organism from toxic oxygen metabolites from activated neutrophils
Bacterial phospholipases - alters gastric mucosal barrier
Bacterial proteolytic enzymes - degrades mucous
Cytotoxin associated gene A (CagA) positive - more virulent strain, increased inflammatory response, higher risk of ulcers and malignancy
A/w gastric metaplasia in duodenum
Aspirin/NSAIDscausing peptic ulcer disease
Local effects - carboxylic acids absorbed across gastric mucosa, ionized in the pH neutral mucosa, trapped temporarily in mucosal cells where they can cause damage
Systemic effect - inhibition of COX (enzyme in prostaglandin synthesis) activity. PGs reduce acid secretion, stimulate glycoprotein, bicarbonate and phospholipid secretion by epithelial cells, enhance blood flow and oxygen delivery by local vasodilation and enhanced epithelial cell migration and proliferation
COX-1 expressed in most cells, COX-2 expressed in cells when endotoxins, proinflammatory cytokines or growth factors induce its expression
Selective COX2 inhibitors (+ PPI) reduce ulcer risk
Smoking and steroids causing PUD
Smoking
Exacerbates H. Pylori disease
Impairs mucosal blood flow, inhibits prostaglandin secretion, increases production of free radicals
Steroids
Suppresses PG synthesis and impair healing
Endoscopic findings of PUD
Endoscopy
90% sensitive
Smooth, regular, rounded edges
Round or oval, sharply punched out defect
Flat, smooth base
Bx suspicious ulcers
Ulcerated mass protruding into lumen
Mucosal folds surrounding ulcer are nodular, clubbed, fused or stop short of ulcer margin
All gastric ulcers should be biopsied -> 4 biopsies from edge of ulcer
Antral biopsies for H. Pylori testing
Testing for helicobacter pylori
o Invasive testing (Endoscopic)
▪ Biopsy during endoscopy for rapid urease assay (CLO - Campylobacter liked organism)
• Sensitivity 90%, specificity 95-100% • Accuracy lowered if taking PPIs or antibiotics
▪ Biopsy during endoscopy for histology
• Gold standard
• Sensitivity 95%, specificity 99%
▪ Culture of biopsies taken during endoscopy
• Sensitivity 80%, specificity 100%
• Takes 3-5 days
• Can be used to test for antibiotic sensitivities
o Non-invasive tests
▪ Serology
• Enzyme-linked immunosorbent assay
• Sensitivity 90%, specificity 76-96%
o Stays positive after treatment and eradication (~1 year)
▪ Urea breath test
• Carbon-labelled
• Sensitivity and specificity 95%
• Utilises h pylori ability to hydrolyse labelled urea
o Cease antibiotics 4 weeks prior and PPIs 2 weeks prior to test
▪ Stool antigen
• Monoclonal antibody antigen
• Sensitivity 90%, specificity 90%
Managementof PUD
General principles
Antisecretory therapy - PPI
Cease precipitants (NSAID, smoking, steroid)
Re-scope
H. Pylori eradication - heals >90% ulcers
First line (20% fail initial eradication - compliance and resistance)
Omperazole 20mg bd
Clarithromycin 500mg bd
Amoxicillin 1g bd
If allergic to penicilin
Omperazole 20mg bd
Clarithromycin 500mg bd
Metronidazole 500mg bd
Second line Treatment
Omeprazole 20mg bd
Levofloxacin 500mg bd
Amoxicillin 1g bd
Quadruple
Bismuth 120mg qid PO
PPI
Tetracycline 500mg qid
Metronidazole 400 tds
Long term PPI (>8 weeks)
Indicated for
large or complicated ulcers
gastric ulcers
high risk patients
NSAID ulcers
those continuing on NSAIDs
Post treatment testing
Wait >4 weeks
Urea breath testing, faecal antigen or gastroscopy
Follow up endoscopy
For all gastric ulcers -exclude malignancy and document healing
Not routine forduodenal ulcersunless complicated or symptoms persist or recur
Refractory ulcers defined as an endoscopically proven ulcer >5mm that does not heal after 12 weeks of treatment with a PPI
Surgery
Rarely needed in elective treatment
Indications
Failure of non-operative management of an ulcer complication
Suspicion of malignancy
Usually in a gastric ulcer
Failure to heal after 12 weeks of medical therapy
Refractory or recurrent PUD
Procedures revolve around concept of acid reduction
Resection of most of parietal cell mass
Vagal denervation of parietal cells
Resection of antral gastrin-producing cells
Vagotomy
Elimination of direct cholinergic stimulation to acid secretion
Options:
Truncal
Selective
Highly selective
Subtotal gastrectomy
Eliminates major portion of parietal cells and gastrin-producing cells in the antrum
Complicated by dumping syndrome and reflux of intestinal contents into stomach
Side effects of PPI
• C diff
• Pneumonia
• Osteoporosis
• CKD
Urease breath test
Radiolabelled urea-C14 ingested
Presence of H pylori will result in breakdown of urea -> ammonium chloride and radiolabelled C02
C14 will be absorbed and eventually expired out as radiolabelled CO2
Tested for presence of C14
Common site for bleeding PUD
Most common site for a bleeding duodenal ulcer is posterior wall
Most common site for a bleeding gastric ulcer is in antrum or at incisura
Management of PUD
▪ Resuscitate
• Large bore IV access
• NG lavage (?role – lavage stomach in preparation for endoscopy, predict upper gi vs lower gi bleed)
• IV PPI
o Bolus then infusion or intermittent dosing IV for 72h
• ICU for 24h if high risk
▪ Upper GI endoscopy
• <24h from presentation
• Forrest classification
o No bleeding, clean base, no visible vessel [IIc, III] – no treatment required
o Any of above [Ia, Ib, IIa] → intervention required [IIb controversial]
• Test for H pylori
• Interventions
o Dual therapy recommended
▪ Adrenaline injection (1:10 000 in 1ml bolus) with either thermal therapy or clips
Forrest classification of bleeding PUD
1a - active bleed, risk of rebleeding 90-100%
1b - ooze, risk of rebleeding 10-30%
2a - non bleeding visible vessel, risk of rebleeding 50%
2b - adherent clot, risk of rebleeding 25%
2c - pigmented spot, risk of rebleeding 10%
3 - clean ulcer base, risk of rebleeding 5%
Indications for surgery for bleeding PUD
Failure of endoscopic therapy
Continued bleeding with haemodynamic instability despite appropriate resus
Recurrent haemorrhage after 2nd attempt at endoscopic haemostasis
Unable to identify source of bleeding
Continued slow bleeding with ongoing transfusion requirement
Surgical intervention for bleeding PUD
• Approach
o Upper midline laparotomy. Kocher manoeuvre
o Anterior longitudinal duodenotomy – extending to pylorus
o Oversew GDA with 3-point U-stitch technique [Avoid picking up CBD]
o Close duodenotomy transversely (HeinekeMikulicz or Finney pyloroplasty)
• Anterior gastrotomy
o Most ulcers are at the incisura or antrum
o Consider simple underrunning of ulcer
• Partial gastrectomy
o If proximal ulcer (high on lesser curve into left gastric artery → total gastrectomy vs local excision of lesser curvature (Pauchets manoeuvre)
