Pathology Of Gastric Disease Flashcards
What is dyspepsia
The term ‘dyspepsia’ is used to describe a complex of upper gastrointestinal tract symptoms which are typically present for four or more weeks, including upper abdominal pain or discomfort, heartburn, acid reflux, nausea and/or vomiting
What are some common gastric disorders
GORD Gastritis • Acute • Chronic - Bacterial - Autoimmune
Peptic ulcer disease
What is GORD
In North America approx. 40% of adults report suffering with GORD at least once a month
Pregnancy- 50-80% have had new or worse
GORD Symptoms:
Chest pain, acid taste in mouth, cough
Consequences of GORD: •Nothing •Oesophagitis •Strictures •Barrett’s oesophagus - precursor to dysplasia - increases risk of adenocarcinoma
Decsribe the structure of the lower oesophageal sphincter
LOS Consists of: •Muscular element - good tone
•Right crus of diaphragm -
•Angle of entry of oesophagus into stomach
•Intra-abdominal pressure - portion of oesophagus lies in abdomen - pressure keeps its shut. Stomach is more muscular so can resist
Relaxes when bolus entres
Failure to relax - (name_) can result in dysphagia,
Pierces diaphragm at level of t10
LOS consists of distal 4cm of oesophagus
•Resting pressures are 10-30mm Hg (only 5-10mm Hg required)
• At rest is tonically contracted •Pressures vary
• Lowest after meals
• Highest at night
What are the treatments for gord
Treatment
◦ Lifestyle modifications.- avoid certain food, eat earlier
◦ Pharmacological
◦ Antacids
◦H2 antagonists
◦ PPIs
◦ Surgery (rare) - wrap fungus around base ofoesophagus - but can result in dysphagia -last resort
Describe god and hiatus hernias
•Much higher rate of reflux oesophagitis with hiatal hernias - osce the bit of oesophagus in abdomen
•Mechanism slightly unclear
•Moving LOS into thorax reduces:
• basal tone
• The normal increase in LOS tone when straining
Reflux more common in ppl with hiatus hernias then without
What is gastritis
Slightly difficult to define? Inflammatory process of the stomach
• Symptom complex (pain, nausea, vomiting, bleeding)
• Endoscopic appearance
• Inflammation of the stomach mucosa
•!cute and chronic varieties…
Invasion with neutrophils into mucosal lining.
What is acute gastritis
Acute mucosal inflammatory process
◦ Heavy use of NSAIDS - Reduce prostaglandin synthesis - reduce blood flow - not repair epithelial cells of stomach as well
◦ Lots of alcohol - damage epithelial cells
◦ Chemotherapy
◦ Bile reflux - goes back thru pyloric sphincter into stomach - reacts with lining -
Exposure of mucosa to chemical injury results in damaged epithelial cells and a reduction in mucus production
Mucosa responds by vasodilatation/oedema and appearance of inflammatory cells (mainly neutrophils)
What are the symptoms of acute gastritis
Symptoms
•Asymptomatic
• Or abdominal pain, nausea, vomiting
• Occasionally bleeding (which can be fatal)
Treatment
•Removal of irritant
What is chronic gastritis
Bacterial
◦ H-pylori infection (most common cause)
Autoimmune
◦ Antibodies to gastric parietal cells - can producce HCl and intrinsic factors - atrophy in body of stomach
◦ Can lead to pernicious anaemia
Chemical/reactive (minimal inflammation)
◦ Chronic alcohol abuse, NSAIDS, reflux of bile
What are the symptoms of chronic gastritis
H-pylori
• Asymptomatic or similar to acute gastritis
• Symptoms may develop due to complications
• Peptic ulcers, adenocarcinoma, MALT lymphoma - malt lymphoma can be treated by getting rid of h pylori
Autoimmune • Symptoms of anaemia • Glossitis • Anorexia - no appetitive • Neurological symptoms - calcium restoration problems
What are the modes of action of h pylori
Problems
• Releases cytotoxins
• Direct epithelial injury - can degrade mucosal layer ?
- Expresses enzymes
- Urease
- Ammonia toxic to epithelia
- Possibly degrades mucus layer
- Promotes inflammatory response
- Self injury
What is h pylori
Helix shaped/gram negative/microaerophilic
Spread
• Oral to oral/faecal to oral Produces urease
• Converts urea to ammonium (basic in solution)
• Increases local pH Has a flagellum
• Good motility
• Lives in mucus layer/adheres to gastric epithelia
Where can h-pylori colonise
If in antrum (home of G cells)
• Increased Gastrin secretion (or decreased D cell activity)
• Increased parietal cell acid secretion - can lead to metaplasia of duodenal epithelia - allowing h pylori to colonise parts of duodenum its not sorted to.
• Duodenal epithelial metaplasia
• Colonisation of duodenum
• Duodenal ulceration likely
If in antrum and body
• Asymptomatic
If predominantly in body • Atrophic effect • Gastric ulcer • Leads to intestinal metaplasia • Dysplasia • cancer (in
What is teh diagnssi/treatment for h pylori
Diagnosis
•Urea breath test (using radio labelled carbon 13 on ammonia)
•Stool antigen test
•Blood test
Treatment
•Proton pump inhibitor
•Amoxicillin + (clarithromycin or metronidazole)
Most people with it dont have symptoms or severe problems
