Download H pylori template - PBL-J-2015

Outline of Key Learning Areas related to PBL Case AHMEN 32y.o REFUGEE
Presenting Symptoms
Epigastric pain, waking him at night (=red flag)
Other Significant History
Refugee prev. in refugee camp (poor dietary, sanitary + physical & mental abuse). Had pain 3 years ago- relieved by antacids. Pain relieved by food and worse when
hasn't eaten for awhile.
Examination and Signs
Anxious, distressed.
Weight/height normal
Afebrile (therefore probably doesn't have a systemic acute infection)
Abdomen tender in epigastrium
Voluntary guarding
Endoscopy revealed duodenal ulcer with chronic antral gastritis
Biopsy taken from antrum + for CLO urease test (H pylori infection confirmed)
Principal Hypothesis
Differential Diagnoses
H pylori infected duodenal ulcer
Gastro-oesophageal reflux disease (GORD)
Risk Factors and Aetiology
Poor diet, unsanitary, physical and mental abuse experienced in refugee camp.
Potential previous ulcer (3 years ago)
Key Basic Science Learning Issues
1) Anatomy
See anatomy lectures/tutorials on abdominal organs.
2) Pathophysiology
3) Microbiology
Sequence of events in ulceration
Copyright UTS, 2012
H pylori infection: (see appendix 1)
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 H pylori is gram-negative has multiple flagella – motile.
 It burrows and lives deep beneath the mucus layer closely adherentCopyright
to theUTS, 2012
epithelial surface.
 Uses adhesion molecule to bind to surface antigen on epithelial cells.
 Here surface pH is close to neutral and any acidity is buffered by the organisms
production of the enzyme urease.
 Produces ammonia from urea to raise the pH around the bacterium and
between its 2 cell membrane layers.
 The bacteria spread by person-to-person contact via gastric reflexate or vomit.
 H pylori exclusively colonises gastric-type epithelium, in close association in
patches of gastric metaplasia.
 The bacterium stimulates chronic gastritis by provoking local inflammatory
response in the underlying epithelium.
 H pylori often causes antral gastritis associated with depletion of somatostatin
(from D cells) and increased gastrin (from G cells).
 The subsequent hypergastrinaemia stimulates acid production by parietal cells,
in the minority of patients this effect is exaggerated and leads to duodenal
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Ability to stay in a hostile acidic environment because it creates
urease, an enzyme which converts urea to ammonia, making
immediate
5 environment more basic.
4) Pathology
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ulceration.
 Believed that H pylori infection acts by reducing gastric mucosal resistance to
attack from acid and pepsin.
Investigations
1) Bloods
Results
1) Bloods
2) Imaging
Full blood count (FBC):
Ordered if Px seems clinically anaemic or has evidence of gastrointestinal bleeding.
Does not aid in diagnoses.
Upper gastrointestinal endoscopy
⁃ the most specific and sensitive test.
⁃ Histology and urease testing are performed on stomach biopsies obtained during
endoscopy.
Both tests can detect H pylori; however, the histology determines if the ulcer is neoplastic
(rare) and/or if there is evidence of an NSAID being the likely cause.
2) Imaging
3) Other
Stool heme test:
Often performed, but usually negative in the presence of peptic ulcer disease.
3) Other
Helicobacter pylori breath test or stool antigen test
+ test confirms H pylori present.
Management Plan
Problem
Goal/desired outcome
Method
Resources/health professional
H pylori infection
Eradicate H pylori infection
Antibiotics (double Tx)
GP
Chronic antral gastritis
Reduce inflammation, reduce secretion
of gastric acid.
Increase mucosal resistance.
Triple Tx (A, A + PPI)
GP
Duodenal ulcer
Repair/rebuild mucosa, heal ulcer.
reduce secretion of gastric acid.
Increase mucosal resistance.
Triple therapy (A, A + PPI)
Improve nutrition, improve sanitation
Refugee camps improve conditions,
Ahmed more informed re
diet/sanitation
Social workers, GP, dieticians,
Medications
Mode of action
Side effects
Any specific monitoring required?
Triple Therapy includes:
Proton Pump Inhibitor (PPI)
eg. Omeprazole
PPI: Bind to the H+/K+ - ATPase (proton pump)
Use ofofPPIsparietal
concerns
cells, suppressing
about long-term
action
safety
of H+(carcinoid
into gastric
tumours?)
lumen-> 90% inhibit ion.
Poor nutrition and sanitation
GP
Ahmed was given H2 Receptor antagonist
(this is not gold standard Tx anymore)
Poor English
Antibiotics x2
eg. amioxollin, metronidazole, bismuth,
clarithromycine, tetracycline.
A: eradication of h pylori - rapid healing
and low recurrence rate.
Standard triple Tx involves bismuth,
metronidazole and tetracycline for
2 weeks (90% eradication rate)
Antacids
Raise the luminal pH of the stomach
(More so treating the symptoms
not cause)
Histamine2 (H2) receptor antagonist
eg. cimetidine, ranitidine
Block action of histamine (H2 receptor)
on the parietal cells and thus reduce
acid secretion.
A: common side effects include: diarrhoea (30-50% Px), flushing and vomiting when taken w alcohol,
nausea, vomiting, abdominal cramps, headache, rash.
PPI:
A: Ensure Px takes full course (7-14
days). Tx with only single antimcrobial
drug is less effective (20-40%
eradication rate).
High use may be assoc w systemic
alkalosis, diarrhoea, constipation.
Usually minor: headache, dizziness,
diarrhea, muscle pain, confusion.
Full course is 6 weeks. Recurrence is
common after Tx is stopped (60-100%).
Other Psychosocial/ethical/legal considerations
Refugee camps- poor dietary and sanitary conditions.
Cultural issues- patient beliefs, importance of family involvement in healthcare (language facilitators, information interpreters)
Communication barriers can result in confused, feeling powerless in their treatment.
PPH/PPD implications
Language difficulties:
Valid consent (effectively communicated?) Cultural issues- patient beliefs, importance of family involvement in healthcare (language facilitators, information
interpreters), communication barriers can result in confused, feeling powerless in their treatment.
Resources
Davidsons Principles and Practices of Medicine,
Lecture notes
Resource Page:




Peptic Ulcer - refers to an ulcer in the lower oesophagus, stomach or duodenum
Ulcers develop when there is an imbalance between mucosal defensive factors & aggressive factors (see figure 1)
Maj. defensive factors are mucus, bicarbonate, prostaglandin, NO, and growth factors; Major aggressive: H. pylori, NSAID, gastric acid & pepsin
Release of hydrochloric acid (HCL) from the parietal cells of the stomach influenced by histamine, gastrin & acetylcholine
Figure 1: Relationship of mucosal defenses and aggressive factors

90% of duodenal ulcer patients and 70% of gastric ulcer patients are infected with H. pylori, the remaining 30% of gastric ulcers are due to NSAIDs.

Prevalence of H. pylori infection in the general population is 50% -90%
Relationship ofDuodenal
mucosal
andthan
aggressive
factors
ulcersdefenses
10X more frequent
gastric, esophageal.
Duodenal ulcers usually occur just distal to the pyloric sphincter.
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Risk factors for gastric ulcer include:
 Long term use of NSAIDs (aspirin, ibuprofen)
 H pylori infection of the gastric &/or duodenal mucosa
 Alcohol
 Smoking
 Chronic diseases (emphysema, rheumatoid arthritis, cirrhosis, diabetes)
Appendix 1:
l
ze
or
5
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CELLS OF THE STOMACH:
G CELLS- GASTRIN
Parietal Cells- H+ for hydrochloric acid
Chief cells- pepsinogen to convert pepsin (protein breakdown)
Enterendocrine cells- histamine.
Secretion of Hydrocholirc acid by the gastric parietal cells:
secretion of hydrochloric acid by
the gastric parietal cell
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HORMONES OF GIT:
Gastrin- gastrin causes an increase in secretion of HCL from parietal cells and increase pepsinogen from chief cells in the stomach. Released from G-cells in
stomach in response to distension of the antrum and presence of digestive products. Gastrin is inhibited by somatostatin.
Histamine- increases acid secretion. Released from enterochromaffin cells.
CCK (Cholecystokinin)- has most effect on gallbladder, decreases gastric emptying and increases release of pancreatic juice which is alkaline and neutralises
and chyme.
Seretin- produced in SI, mostly affects pancreas, increases pancreatic fluids and bicarbonate secretion. Secretin will also diminish acid secretion in the
stomach and reduce stomach emptying.
Gastric inhibitory peptide- GIP decreases both gastric acid release and motility. Increases insulin secretion.
Acetylcholine- increases acid secretion, increases blood flow, increases mucus secretion and increases bicarbonate secretion.
If have excess acidity, somatostatin, CCK, GIP are decreased.
How do NSAIDs contribute to increased risk of gastric ulcer?
NSAIDs reduce prostaglandin synthesis. However, PGs stimulate bicarbonate and gastric mucus secretion and increase mucosal blood flow. Bicarbonate
ions are secreted into the unstirred mucus layer, neutralizing hydrogen ions as they back- diffuse towards the epithelium. Rapid cell turnover and a rich
mucosal blood supply are important protective elements.
However, high NSAIDs use alters the gastric mucosal barrier:


↓ prostaglandin synthesis
↓ mucus and bicarbonate secretion




↓ submucosal blood flow
↓ mucosal ATP
↓ cell turnover
↓ platelet function (irreversible)
Gs and mucosal protection
mulate bicarbonate and mucus secretion and increase
blood flow. Bicarbonate ions are secreted into the
mucus layer, neutralising hydrogen ions as they backowards the epithelium. Rapid cell turnover and a rich
blood supply are important protective elements.
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