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
Compare the pathological changes in acute and chronic gastritis
See slide
What is poetic ulcer disease
Defects in gastric/duodenal mucosa
◦ Must extend through muscularis mucosa
◦ Most common in first part of duodenum
◦ Commonly affects lesser curve/antrum of stomach
Describe the pathogeniss in peptic locker disease
Note- normal defence mechanisms
• Mucus
• Bicarbonate
• Adequate mucosal blood flow
• Can remove acid that diffuses through injured mucosa
• Prostaglandins (stimulate above)
• Epithelial renewal
Breakdown of normal defences more important than excessive acid
• Ulcers can develop in people with normal or low levels of acid
• Rapid gastric emptying/inadequate acid neutralisation (from bile/pancreas)
has been implicated in duodenum ulcers
What are the causes of poetic ulcer disease
Caused by mucosal injury
◦ Stomach acid
◦ H-pylori
◦ NSAIDS
◦ Smoking (really only contributes to relapse of ulcer disease)
◦ Stress (only massive physiological stress)
◦ Burns
Compare acute and chronic peptic ulcers
Acute ulcers
•Develop as part of acute gastritis
Chronic ulcers
•Occur most frequently at mucosal junctions
• Where antrum meets body (on lesser curve)
•/ In duodenum where antrum meets small intestine
Decsribe the morphology of peptic ulcers
Morphology
•Generally less than 2cm diameter (but can be 10cm)
•Base of ulcer is necrotic tissue/granulation tissue
•Muscularis propria can be replaced by scar tissue- scar tissue an contract down stomach - reduce ability to distend - rugae - of cat expand - early satiety
Pyloric stenosis - projectile vomiting
What re teh clinical consequences of peptic ulcer diesease
Clinical consequences •Scar tissue shrinking can narrow stomach lumen or cause pyloric stenosis - projectile vomiting
•Perforation causing peritonitis - inflammation of lining
•Erosion into adjacent structure (liver or pancreas)
•Haemorrhage from vessel in base of ulcer - bleed into duodenum.- name of vessel????
Oesophageal varices
•Malignancy (rare) - if a ulcer is found - biopsy around ulcer to test if malignancy
What are teh symptoms of peptic ulcer disease
Symptoms • Epigastric pain (sometimes back pain) • Burning/gnawing • Follows meal times - when you eat, pyloric sphincter contracts, not pain immediately - tends to be a few hours after • Often at night (especially Duodenal) Serious symptoms • Bleeding/anaemia (haematemesis or malaena (dark black stool from upper gi bleed - haem component digested by gut bacteria ) • Satiety (early) • Weight loss
What is the management for peptic ulcer disease
•Lifestyle modification •Stopping any exacerbating medications •Testing for H-pylori (if present- eradicate) •PPIs •Endoscopy
What is functional dyspepsia
Have symptoms of ulcer disease
◦ No physical evidence of organic disease
Diagnosis of exclusion!
How are gi pathologies diagnosed
Upper GI endoscopy
• Biopsies
• Benign/malignant ulceration • H-pylori
Urease breath test
Erect chest X-ray
- air or gas in peritoneal cavity underneath diaphragm
• Perforation
Blood test
• anaemia
What are teh pharmacological interventions
-directly affect proton pump - histamine modulates acid releas e- h2 blockers
H2 blockers • Cimetidine • Ranitidine
Proton pump inhibitors
• Omeprazole???
What is zollinger-elison syndrome
Non beta islet cell gastrin secreting tumour of the pancreas Proliferation of parietal cells
• Lots of acid production
• Severe ulceration of the stomach and small bowel
• Abdominal pain, diarrhoea
What si stress ulceration
Symptoms of gastritis/ulceration Following • Severe burns • Raised intracranial pressure • Sepsis • Severe trauma • Multiple organ failure
Decsribe stomach cance
Third most common cancer in the world Usually presents late
• Has to be quite large before symptoms
• Dysphagia • Loss of appetite • Malaena • Weight loss • Nausea/vomiting/ • Virchows nodes
Describe the risk factors for stomach cancer
Huge geographical variation around the world • High rates • Chile/Japan/South America • Have screening programs Risk factors • Male • H-pylori • Dietary factors • Smoking
