Peptic Disease and Gastritis Flashcards
Gastric glands and what they secrete
- Parietal Cells: found throughout the gastric complex and secrete HCL
- Chief Cells: Secrete pepsinogen
- Mucous cells: Found in neck. Bicarbonate rich mucous
- G cells: only found in antrum and they secrete gastrin
What are the three receptors on the serosal side of the parietal cell?
Acetylcholine receptor- receive Ach which comes from the vagus nerve (parasympathetic) which is stimulated by eating. Increases intracellular calcium
Gastrin receptor- Increases intracellular calcium
Histamine Receptor- Receives histamine. activates adenylate cyclase which increases cAMP levels which aids in acid secretion
Basically, high intracellular calcium concentrations trigger the H/K ATPase to pump hydrogen out and potassium in
What is the significance of the protaglandin receptor on the serosal surface of the parietal cell
Allows negative feedback as prostaglandin binding leads to low cAMP.
What stimulates Ach release via the Vagus nerve?
Taste, smell, chewing
Three phases of acid secretion
1) Cephalic- taste, smell, chewing
2) Gastric- chemical effects of food and distension of teh stomach stimulate gastrin release by G cells
3) Intestinal- Food and acid in small bowel causes release of CCk and secretin which inhibit acid production
Duodenal ulcer and acid secretion
Pts with duodenal ulcer=
- Basal acid output twice as high in pts with duodenal ulcer
- Peak acid output higher in pts with duodenal ulcer
- Serum gastrin is higher in pts with duodenal ulcer
Mucous secretion in the stomach creates a bicarbonate layer which makes a pH gradient that prevents autodigestion
ok….pts with peptic ulcer disease may have decreased bicarb
Most common symptoms of peptic ulcer
abdominal pain in 80%
- may be nocturnal or relieved by food
Nausea
Risk factors for PUD
- Heliobacter Pylori gastritis
- Medicines like NSAIDS
- Smoking
- genetics
PUD in chrinic diseases such as
- ICU pts on ventillators
- those with cirrhosis
- organ transplant pts
- COPD
These pts usualy get prophylactic PPI’s while in ICU
Morphology of Heliobacter Pyloris
spiral shaped gram neg organism with 4-6 flagella
H. Pylori makes what substance which makes it resistant to gastric acid
Urease
H. Pylori resides where?
In the mucous layer overlying the gastric epithelium.
H. Pylori and inflammation?
H. Pylori releases a Peptide and Lipopolysaccharide which are chemotactic for neutrophils and monocytes. These inflammatory cells release oxygen radicals, prostaglandins, IL-1 and TNF which then promote addittional inflammation
Slide 19 is a good summary
ok
H Pylori is most likely trasnsmitted how?
Person to person
High risk for NSAID GI Toxicity?
two criteria:
- History of complicated ulcer in the past OR…
- more than one of the moderate risk factors which are (over the age of 65, high dose NSAID therapy, previous uncomplicated ulcer, concurrent use of aspirin, gluccocorticoids, or corticosteroid)
Dx of H. Pylori
Barium x ray of stomach
Endoscopy (this also allows for biopsy for H. Pylori testing)
Complications of PUD
- Bleeding: hematemesis, melena, anemia
- Perforation; need surgery
- Penetration- may penetrate into adjacent organ
- Gastric outlet obstruction
Treatment of PUD
- Anti-secretory agents (H2 blockers) or PPIs for 6-8 wks
- Treat H. Pylori
- Avoid smoking, NSAIDS.
Gastritis
Pathological diagnosis of gastric inflammation of mucosa
- may be acute or chronic
Causes of Gastritis
NSAIDS, H. Pylori, Alcohol, ischemia, extreme stress
Endoscopic erosive gastritis
multiple erosive and hemorrhagic lesions on endoscopy
Alcoholic hemorrhagic gastritis
multiple subepithelial hemorrhages without without any visible breaks in the mucosa (blood under plastic wrap)
