138b/139b - Pathology of Gastric Disorders, PUD, H. Pylori Flashcards
Do benign gastric ulcers occur in pernicious anemia?
No!
- Pernicious anemia is often caused by autoimmune destruction of parietal cells
- => decreased gastric acid
- Any ulcer that forms in the setting of pernicious anemia should be considered for malignancy
Which stimulants of parietal cell gastric acid secretion act through the IP3/Ca2+ pathway?
- ACh
- Released when we think about food (cephalic phase) or secondary to antral distention (gastric phase)
- Gastrin
![](https://s3.amazonaws.com/brainscape-prod/system/cm/363/540/429/a_image_thumb.png?1605021254)
Which part of the stomach is affected by H. pylori gastritis?
Antrum
Describe the pathophysiology of diarrhea in patinets with Zollinger-Ellison syndrome
ZE = gastrin-secreting tumor
- Increased HCl secretion
- HCL spills into duodenum
- Denatures pancreatic enzymes
- Maldigestion of fat and protein
- Diarrhea
- Directly damages the small intestinal epithelium
- Secretory diarrhea
- Denatures pancreatic enzymes
What is the treatment for Zollinger-Ellison Syndrome?
High dose PPI
- Resect tumor if you can, but they can be hard to find!
Describe the pathophysiology of chronic autoimmune gastritis
- Antibodies against parietal cells and intrinsic factor
- -> Destruction of parietal cells
- -> Hypochlorhydria, high serum gastrin
How does H. pylori cause an increase in gastric acid release?
H. Pylori preferentially destroys D cells
- D cells normally secrete somatostatin
- Normally inhibits gastrin secretion from G cells
- Results in decreased gastric acid release
-
No D cells = no brakes on gastrin secretion
- Lots of gatrin -> lots of gastric acid
![](https://s3.amazonaws.com/brainscape-prod/system/cm/363/540/436/a_image_thumb.png?1605022191)
Describe the pathophysiology of H. pylori infection in the gastric epithelium
(Starting with ingestion of H. pylori)
- Ingestion of H. pylori
- H. pylori lodges into the mucus using adhesins
- Protected from acid by urease (Urea -> CO2 + NH3)
- NH3 is converted to NH4+ in the acidic stomach; NH4+ cloud protcts H. pylori
- H. pylori multiplies
- Immune response
- Cytokine release
- Damage to mucosa
- H. pylori internalizes in the epithelium
Describe the pathophysiology of a Curling ulcer
Severe burns/trauma -> hypovolemia -> ischemia
What is the eradication rate for H. pylori after antibiotic treatment?
~75% and decreasing due to abx resistance
What is the most common cause of benign peptic ulcer disease?
H. pylori
![](https://s3.amazonaws.com/brainscape-prod/system/cm/363/540/450/a_image_thumb.png?1605021655)
What are the two subtypes of gastric adenocarcinoma?
How do you tell them apart?
- Intestinal
- Ulcer with raised borders
- Composed of glands
- Diffuse
- Diffusely thickened gastric wall
- Signet ring cells are present
![](https://s3.amazonaws.com/brainscape-prod/system/cm/363/540/453/a_image_thumb.png?1604981009)
List two hypertrophic gastropaties
How do you tell them apart histologically?
- Menetrier disease (excess TGF-alpha)
- Foveolar hyperplasia
- Zollinger-Ellison syndrome (gastrin-secreting tumor)
- Parietal cell hyperplasia
Endoscopically, both will have enlarged folds
![](https://s3.amazonaws.com/brainscape-prod/system/cm/363/540/455/a_image_thumb.png?1604980311)
H. pylori typically colonizes in gastric epithelium
How, then, does it caue duodenal ulcers?
- H. pylori colonization in the stomach results in increased post-prandial gastrin release, resulting in increased gastric acid
- Due to destruction of D cells (no brakes on gastrin release)
- Gastric acid spills into the duodenum
- -> Gastric metaplasia
- -> H. pylori colonizes in the gastric metaplasia in the duodenum
What is the effect of somatostatin on gastric acid secretion?
Somatostatin inhibits gastric acid secretion
- Inhibits gastrin secretion from G cells, histamine secretion from HCL cells
Describe the pathophysiology of a Cushing ulcer
- Increased intracranial pressure
- -> Vagal stimulation
- -> Acid production
- -> Ulcer formation
Which of the following mechanisms plays an important role in the development of a gastric ulcer in a 32 year old patient with rheumatoid arthritis taking ibuprofen 800 mg three times daily for one month?
- Reduction in blood flow to the gastric mucosa
- Ion trapping and low pKa of ibuprofen
- Excessive production of acid induced by ibuprofen
- Concomitant infection with H.pylori
- Autoimmune damage to the gastric epithelium
a. Reduction in blood flow to the gastric mucosa
- Ibuprofen is a nonselective COX inhibitor
- -> Decreased prostaglandins production
- -> Decreased blood flow
Ishcemic damage = nidus for ulcer