Dyspepsia and PUD Flashcards
What is dyspepsia?
Epigastric pain or burning (epigastric pain syndrome) Postprandial fullness (postprandial distress syndrome) Early satiety (postprandial distress syndrome
What are the foregut structures?
Oesophagus, stomach, duodenum, pancreas and gallbladder
Cricopharyngeus to ampulla of Vater
When is dyspepsia more common?
In those infected with H pylori, those who used NSAIDs
Overlap with IBS/GORD.
No age sex,smoking, alcohol association
What are the organic causes of dyspepsia (25% of cases)?
PUD
Drugs (esp. NSAID, COX2 inhibators)
Gastric cancer
What is functional dyspepsia (75%)?
Idiopathic dyspepsia.
Same symptoms but with no evidence of structural disease. Associated with other functional gut disorders eg IBS
Can GORD coexist with dyspepsia?
Yes
You can have heart burn and indigestion. They are not the same thing
What would you find on examination of a patient with uncomplicated dyspepsia?
Epigastric tenderness only
What would you find on examination of a patient with complicated dyspepsia?
Cachexia
Mass
Evidence gastric outflow obstruction
Peritonism- symptom complex characterized by vomiting, pain or abdominal tenderness, and shock.
What are the alarm symptoms for dyspepsia?
Dysphagia Evidence of GI blood loss- haematemisis or melaena Persistent vomiting Unexplained weight loss Upper abdominal mass
How do you manage dyspepsia without alarm symptoms?
Non invasive test and treat.
CHeck H pylori status If positive, eradicate
If negative treat with antacids or histamine receptor antagonist
What is the Rome III classification of functional dyspepsia?
Epigastic pain, epigastric burning, early satiation and postprandial fullness
WITH no evidence of structural disease.
Criteria must be fulfilled for the last 3 months with symptom onset 6 months before diagnosis
WHat are the possible causes of functional dyspepsia?
Visceral hypersensitivity, altered brain gut interactions
Genetic factors
Psychosocial factors
Abnormal upper GI motor and reflex functions
Disrupted gut immune interactions
What is Peptic ulcer disease?
PUD is a common cause of organic dyspepsia associated with epigastic pain radiating to the back
If PUD a relapsing and remitting chronic illness?
Yes
What are the characteristic symptoms of of PUD?
Pain orse at night
Relapsing and remitting
Aggravated or relieved by eating
Family history common and more common in lower socio economic groups
What are the causes of PUD?
H pylori causes 90% of duodenal ulcers and 60% of gastric ulcers
NSAIDs (COX1, COX2, PGE) cause the majority of the rest. The ratio of NSAID: H pylori is rising
What type of bacteria is H pylori?
Gram negative microaerophilic flagellated bacillus
When is H pylori acquired and how is it spread?
Usually in infancy and oral-oral or faecal-oral spread. The consequences of infection do not arise until later in life
What are the consequences of H pylori infection?
1) No pathology- majority
2) PUD = 20-40%
3) Gastric cancer -1%
What are the most typical gastric cancers associted with H pylori infection?
Non- cardia gastric adenocarcinoma
Low grade B cell gastric lymphomas (Maltoma)
How does the prevalence of H pylori change in the developed and developing world?
Developed world = slowly increases with age
Developing world = the majority of people infected by age 15
There is greater H pylori infection and PUD in people of lower socioeconomic status?
True
Acid is produced by the parietal cells of the stomach and this signals to G cells of the stomach to do what?
Reduce gastrin release which intern signals to the parietal cells to reduce the acid secreted. Negative feedback.
What are the different outcome of H. pylori infection?
1) No clinical disease
2) Increased acid production => Gastrin production. No atrophy and duodenal ulcers in 20-40% of cases
3) Decased acid production => increased gastrin production. Atrophy and incidence of gastric cancer in 1% of cases
What is the pathophysiology of duodenal ulcers?
Increased acid secretion in the stomach which leaves. Decreased somatostatin leads to higher levels of gastrin which maintains acid production.
When acid enters the duodenum => Gastric metaplasia, h pylori collenisation and ulceration
What are the causes of duodenal ulceration?
H pylori infection
NSAIDs
Severe stress
How is H pylori diagnosed?
1) Gastric biopsy- urease test, histology and culture/sensitivity
2) Urease breath test
3) FAT= faecal antigen test
4) Serology (IgA antibodies)- not accurate with increasing patient age
H pylori increases the pH of its microenvironment. How does the body counter act this?
Urea is broken down with water and H+ to ammonium bicarbonate by the urease enzyme. It is the urease enzyme which you can test for the presence of .
What is the treatment for PUD?
1) All antisecretory therapy (PPI)
2) All tested for presence of H pylori and treated if positive
3) Lifestyleis difficult. no firm dietary recommendations.
4) Surgery infrequent
5) Non H pylori/non-NSAID ulcers. => Nutrition and optimse co morbidities.
What are teh types of antisecretory therapy?
Histamine receptor agonists (Cimetidine, ranitidine, famotidine and nizatidine)
Proton pump inhibatrs (omeprazole, lansoprazole, dexlansoprazole)
PPI inhibators are more effective for healing DU and also slightly better for GU
How are antacids used in therapy for DU/GU?
Help with symptoms but not as effective for healing.
Is misoprostol used in DU/GU treatment?
No- its less effective than PPIs or histamine receptor antagonists
How is H pylori infection treated in one week?
Triple therapy for 1 week (most common)
1) PPI + amoxycillin 1g bd + clarithromycin 500mg bd.
2) PPI + metronidazole 400mg bd + clarithromycin 250mg bd
Is two weeks of tripple therapy more effective for erradiaction of H pylori?
Yes- higher eradication rates but poorer complience
Why is complience poor for tripple therapy for H ylori?
Side effects are common (nausea and diahoea.
If they are still symptomatic after the course you must retest.
Dual therapy is not recommended for H pylori erradication. T or F?
True
What are the cmplications of PUD?
Anaemia, bleeding, perforation, gastric outlet/duodenal obstruction- fibrotic scar
Do duodenal ulcers adn gastric ulcers require a follow up?
Uncomplicated DU only requires follow up if ongoing symptoms.
Gastric ulcers require a follow up endoscopy at 6-8 weeks to check healing and check for malignancy
What may raise your suspicions of gastric cancer?
Dyspepsia + alarm symptoms (weight loss, anaemia, mass, recurrent vommiting)
Achlorhydria (due to pernicious anaemia or previous gastric surgery)
Family history
What is achlorhydria?
absence of hydrochloric acid in the gastric secretions.
What is the phenotype of gastric cancer?
Atrophy,
Intestinal metaplasia
H pylori disappear and mixed bacterial overgrowth takes over
Low acid secretion due to increased gastrin release
Those with H pylori infection with PUD are somehow protected from developing gastric cancer. T or F?
True
H pylori often inhibits gastric acid secretion. T or F?
True. Inflamation => IL-1 beta production which inhibits acid secretion
Are there genetci factors which may predispose an individual to hypochlorhydric response to h pylori?
Yes the IL-1B gene as IL-1beta production is increased which inhibits acid secretion
If your H pylori causes increased acid secretion what disease will you get?
If your H pylori causes decreased acid secretion what disease will you get?
NB: bodies response is down to genetics?
High acid => DU/GU
Low acid => Atrophy and cancer
What medications do you need to stop and when before a H pylori test?
Antibiotics- 4 weeks before
PPI 2 weeks before
Histamine receptor antagonists 24 hours before.
Where is alkaline phosphate found?
Liver and the bone
