L4- GIT Pathology II (stomach) Flashcards
(47 cards)
discuss the distribution of cells in different areas of the gastric mucosa
Cardia, Antrum: mucus secreting cells
Corpus, Fundus (oxyntic): chief cells (pepsinogen) and parietal cells (acid, IF)
list the causes of Pyloric Stenosis
Congenital
Acquired: chronic antral gastritis, peptic ulcers, malignancies
Congenital hypertrophic pyloric stenosis:
- (1) defect/definition
- (2) associated Syndromes
- affects (males/females) more
1- concentric hypertrophy of circular muscle coat
2- Turner syndrome, Trisomy 18, Esophageal atresia
3- males (3:1)
Congenital hypertrophic pyloric stenosis:
- (1) clinical presentation
- (2) Tx
1- regurgitation, projectile vomiting, palpable epigastric mass, visible peristalsis
2- surgery: myotomy
list the categories of gastritis
Erosive:
- acute gastritis
- NSAID injury, EtOH gastritis, oral Fe, KCl
Chronic, non-erosive:
- H. pylori
- pernious anemia
describe acute gastritis (what occurs, how long it occurs, occurs in response to what)
- acute mucosal process transient nature
- occurs in severe stress (burns, shock)
-inflammation associated with hemorrhage, in severe cases erosion => GI bleed
how does EtOH affect the stomach
- direct injury
- inc acid secretion
-may lead to acute gastritis
list the clinical features (and complications) of gastritis
-maybe asymptomatic
- epigastric pain, n/v
- hematemesis, melena
-bleeding may be fatal
list some causes of Acute Gastritis
- NSAIDs
- excess EtOH
- heavy smoking
- ischemia, shock
- severe stress (burns, surgery)
- chemotherapy drugs
- systemic infections
- uremia
Acute Gastritis:
- can either be (1) or (2) type
- (3) is obvious on endoscopy, and they can lead to (4)
1- superficial mucosal injury = erosions (loss of surface epithelium)
2- full thickness mucosal injury = ulcer
3- erosions and hemorrhage
4- hyperemia, punctate areas of hemorrhage
Acute Gastritis, on histology:
- (1) in lamina propria
- (2) in epithelium, glands
1- edema, congestion (lamina propria)
2- neutrophil infiltration (surface epithelium, glands)
Chronic Gastritis:
- (1) definition
- (2) are the common causes
- (3) are the less common causes
1- chronic inflammation of gastric mucosa associated with epithelial injury, mucosal atrophy, or epithelial metaplasia
2- H. pylori, autoimmune disease
3- chronic bile reflux, post-surgical (antrectomy), Crohn’s, sarcoidosis, radiation
Chronic Gastritis appearance on endoscopy
- variable: from normal to patchy/diffuse erythema
- w/ or w/o hemorrhage to boggy with thick mucosal folds
Chronic Gastritis appearance on microscopy
- inflammatory infiltrates in lamina propria: lymphocytes, plasma cells
- PMNs / neutrophils in surface epithelium, glandular lumen
- reactive lymphoid aggregates (mainly superficial, marks H. pylori infections)
- intestinal metaplasia, glandular atrophy, dysplasia
H. pylori: classic bacterial features (hint- 5 important distinguishing features)
Gram- curvilinear shape motile: flagella non-invasive urease+
list the diseases associated with H. pylori
-Chronic gastritis: diffuse antral, multifocal atrophic
- peptic ulcer
- gastric adenocarcinoma
- gastric lymphoma
describe the basic progression of H. pylori infections into its associated diseases
1:
- enzymes: proteases, ureases, phospholipases
- -> direct mucosal damage
- -> induces inflammatory response (+ attraction of inflammatory cells)
- -> chronic gastritis, peptic ulcer
2:
- attracts PMNs + other inflammatory cells
- uncontrolled B cell proliferation
- lymphoma
list the diagnostic testing for H. pylori, indicate the most commonly used test
Non-Invasive:
- **urea breath test
- serology: IgG, IgA
- PCR in saliva, feces
Endoscopic based invasive:
- rapid urease test
- histopathology + culture
- PCR
Autoimmune gastritis:
- (1) definition
- destruction of (2), leading to (3) changes
- inc risk for (4), (5)
1- Ig’s against parietal cell Ags/IF
2- oxyntic glands
3- achlorhydria (dec HCl in stomach) + inc gastrin levels
4- gastric carcinoma
5- neuroendocrine tumors / carcinoids
Autoimmune gastritis has the presence of (1) to cause gland destruction and (2) in the (3) part of the stomach. As a result of the destruction / (2), there is a loss of (4) and a loss of (5), where (5) leads to (6).
1- Ig's against parietal cells +/- Ig against IF 2- atrophy 3- stomach body, fundus 4- acid production (= achlorhydria) 5- Intrinsic Factor 6- vitB12 def --> pernicious anemia
Autoimmune gastritis histology:
-list the 3 main features and describe their individual presentations
- chronic inflammation: deep inflammatory infiltrates composed of lymphocytes
- gastric atrophy
- intestinal metaplasia: goblet cells in foveolar pits
Gastric Ulcers:
- (1) definition
- (2) common locations
- heals (better/worse) than an erosion
1- loss of mucosa that extends thru muscularis mucosa or deeper
2- antrum (gastric), duodenal
3- worse, longer healing time
Acute gastric ulcers:
- (1) major causes
- Curling ulcers via (2)
- Cushing ulcers via (3)
- can develop while in (4), 5-10% of the time
1- severe trauma, major surgeries
2- extensive burns
3- head injury, intracranial lesions
4- ICU
Acute gastric ulcers:
-usually presents with (1), although can present as (2)
-pathogenesis is related to (3) and (4)
1- multiple ulcers, asymptomatic
2- massive upper GI bleed
3- systemic acidosis, hypoxia (trauma, burns)
4- vagal stimulation (intracranial lesions)