Pathophysiology Of Gastric Disease Flashcards
What is dyspepsia? How common is it?
Dyspepsia- upper GI symptoms/ typically for 4+ weeks including upper abdo pain/ discomfort, heartburn, acid reflux, nausea, vomiting
Up to 40% adults suffer from dyspepsia/ year
What is GORD? What conditions does it encompass? How prevalent is it? Symptoms, consequences and risk factors.
Gastro-oesophageal reflux disease
Includes:
- acute/ chronic/ bacterial/ auto immune gastritis
- peptic ulcer disease
- Zollinger-Ellison disease (gastrinomas secrete gastrin)
- Cancer of the stomach
40% adults suffering at least one a month
In pregnancy 50-80% have new/worse GORD
Symptoms: chest pain, acid taste in mouth, cough
Consequences: nothing, oesophagitis, strictures (swallow-> vomit), Barrett’s oesophagus (metaplasia SS-> columnar-> adenocarcinoma)
Risk factors: anything that increases intra-abdo pressure e.g. obesity, pregnancy, hiatus hernia, chronic cough or LOS poor functioning, delayed gastric emptying
How do you treat GORD?
Lifestyle modification e.g. don’t eat before lying down, lose weight, antacids (many form layer over acid), smaller meals more often, H2 antagonist, proton pump inhibitor, surgery rare (fundoplication move fundus to wrap around lower oesophagus but can lead to dysphagia)
How do hiatus hernias increase the risk of GORD?
Stomach is higher now in thorax so:
Loss of diaphragmatic support for LOS
Loss of intra-abdo LOS segment
Retention of gastric fluid in hernial sac
Stretching and rupture of the phreno- oesophageal ligament
Widened diaphragmatic hiatus
Acute gastritis Pathology Causes Symptoms Treatment
Acute mucosal inflammatory process
Causes:
- heavy use NSAIDS (reduce prostaglandins)
- XS alcohol (dissolves mucus)
- Chemotherapy (kills rapidly dividing gut cells)
- bile reflux (pylorus sphincter prevents)
- > damaged epithelial cells and reduction in mucus production
- > mucosa rosins by vasodilation/ oedema and appearance of inflammatory cells (mainly neutrophils)
Treatment: remove irritant
Symptoms: asymptomatic, abdo pain, nausea, emesis , occasional bleeding
Chronic gastritis
Causes
Symptoms
Causes: H Pylori infection most common, autoimmune- antibodies to gastric parietal cells of fundus -> pernicious and iron deficient anaemia, chemical/ reactive minimal inflammation e.g. chronic alcohol abuse, NSAIDS chronic use, ongoing bile reflux
Symptoms of H-pylori: asymptomatic or abdo pain/ nausea/ emesis/ bleeding, due to complications like peptic ulcers/ adenocarcinoma/ MALT lymphoma (mucosa-associated lymphoid tissue)
Autoimmune symptoms: anaemia symptoms, glossitis, anorexia, neurological symptoms
Helicopter- pylori. Structure, location, spread, pathology including differences between infection of the antrum/ body/ both, diagnosis and treatment
structure: Helix shaped, gram negative, microaerophilic (stomach perfect small PO2), flagellum
location: Lives in mucus layer and adheres to gastric epithelia (resists peristalsis).
Spread: oral to oral, faecal to oral
Pathology: Produces urease convert urea to ammonia toxic to epithelia (alkaline cloud around bacteria), increases local PH. Releases cytotoxins, direct epithelial injury, degrades mucus layer,
Promotes inflammatory response
If in antrum (home G cells) increases gastrin secretion/ parietal acid secretion/ duodenal epithelia metaplasia colonisation of duodenum-> ulceration
If in body: atrophied effect, gastric ulcer, intestinal metaplasia, dysplasia, cancer
If in antrum and body asymptomatic (effects cancel out) as in body causes decreased acid secretion & gastric atrophy
Diagnosis: urea breath test, stool antigen gets, upper gastrointestinal endoscopy and mucosal biopsy
Treatment: proton pump inhibitor, amoxicillin + (clarythromycin OR metronidazole)
What is active chronic gastritis?
Acute and chronic pathology occurring simultaneously so
Acute: surface epithelia degeneration, regenerative hyperplasia of pit-link g epithelium, vasodilation/ congestion, neutrophil polymorph response
Chronic: lymphocyte and plasma cell response, glandular atrophy, lamina propria fibrosis, metaplasia
Peptic ulcer disease
Criteria
Common sites
Causes
Peptic = stomach and duodenum
Defects in gastric and duodenal mucosa must extend through muscularis mucosa
Most common in superior duodenum, lesser curve/ antrum
Causes: breakdown of normal defences more important than XS acid, can develop with normal/ low acid levels. Rapid gastric emptying/ inadequate acid neutralisation (from bile/ pancreas)
By mucosal injury e.g. H-pylori, NSAIDS, smoking (more for relapse), physiological stress, burns
Compare and contrast gastric and duodenal ulcers
Incidence
Gastric- 1
Duodenal- 3
Age
G- increases with age
D- increases up to 35
Social class
G - more in low socioeconomic
D- all
Blood group
G- A
D- O
Acid levels
G- normal or low
D- elevated or normal
Helicobacter Pylori gastritis
G- 70%
D- 95-100%
Differences between acute and chronic peptic ulcer disease
Acute- develop as part of acute gastritis
Chronic- occur most frequently at mucosal junctions where antrum meets body of lesser curve, in duodenum where antrum meets small intestine
Morphology of peptic ulcer disease and clinical consequences
Normally <2cm diameter but can be 10cm, base of ulcer is necrotic tissue/ granulation tissue, muscularis propria can be replaced by scar tissue
Clinical consequences: scar tissue shrinking can narrow stomach lumen/ pyloric stenosis,
perforation of gastroduodenal artery causing peritonitis (inflammation of peritoneum) or haematemesis,
erosion into adjacent structures (liver/ pancreas) causing a fistula (Erosion of one epithelia surface onto another) ,
haemorrhage from vessel in base of ulcer,
Malignancy rare (biopsy base ulcer)
Symptoms and management of peptic ulcer disease
Epigastric pain/ sometimes back, burning/ gnawing post meals (delayed off duodenal), often at night (duodenal especially)
Serious symptoms:
Haematemesis or malaena-bleeding/ anaemia (black tar stools), early satiety from repeated scarring, weight loss
Management: Lifestyle modification(eat less, change types of food), stop NSAIDs, test for h-pylori, PPI e.g. omeprazole (-increase risk infection), endoscopy (inject bleeding ulcer adrenaline), H2 blocker e.g. cimetidine/ ranitidine
What is functional dyspepsia?
Symptoms of ulcer disease but no physical evidence
Diagnosis of exclusion
What would you see on an erect chest x-ray if a gastric perforation was present? Why are these difficult o obtain usually?
Gap under diaphragm from gas that has escaped
Difficult for patient to be erect as often very sick
