Stomach Path I Flashcards
parietal cells
HCl and IF
chief cells
protelytic enzymes
stomach ulceration
smooth border - better
rough border - likely malignant
acute gastritis
acute mucosa inflammation
-neutros present - w/ or w/out ulceration
acute hemorrhagic gastritis
erosive with bleeding
- with NSAIDs, aspirin
- alcoholic
- heavy smoker
- stress
stress ulcer
tx with PPIs
-pt with shock, burns, sepsis, trauma, critically ill
curling - burns/trauma
cushings - intracranial bleed
erosion
stressed situation
-not an ulcer
h. pyloric
inhibition of gastric bicarb transporters
curling ulcer
severe stress situations
-burns, trauma, sepsis, etc.
cushing ulcer
intracranial injury - disrupted vagal activity
chronic gastritis
presence of chronic mucosal inflammatory changes
-atrophy and metaplasia
majority - h. pylori infection
autoimmune - pernicious anemia - < 10%
also with drugs, alcoholi, toxins
giemsa and steiner silver stain
h. pylori
CagA
toxin of h. pyloric - may be involved in ulcer or cancer development
chronic inflammation of antrum
almost always h. pylori
increased acid production
entire stomach chronic inflammation
alcohol, smoking, etc.
h. pylori virulence
1 flagella
2 urease
3 adhesins
4 toxins - CagA
duodenal ulcers
increased risk with h pylori chronic gastritis
active chronic gastritis
PMNs
-hallmark of ongoing h. pylori infection
swallow urea with carbon-14 tag - do breath test
if positive - h. pylori
-takes up C-14 and CO2 given off has this tagged carbon
mucosal atrophy in chronic gastritis
marker for increased cancer risk
tx h pylori
PPIs and antibiotics
h pylori diagnosis
detection of organism in biopsy
often in antrum
autoimmune gastritis
spares antrum
- includes hypergastrinemia - achlorydia
- defective gastric acid secretion
aka atrophic
autoimmune gastritis path
Abs to parietal cells and IF - detected in serum and gastric secretions
CD4 T cells against parietal cell components** - H/K ATPase
chief cells also get destroyed
pernicious anemia
with autoimmune gastritis if severe
oxyntic mucosa
acid producing
autoimmune gastritis histo
glandular atrophy and inflammatory infiltrates
destroys acid producing mucosa in body nd fundus
may see intestinal metaplasia
autoimmune gastritis
60yo female
often with other autoimmune disease - hashimotos, DM, addison, graves, etc.
atrophic glossitis
smooth beefy tongue
-with B12 deficiency
reactive gastropathy
chemical injury
NSAID use
bile reflux
trauma
eosinophilic gastritis
allergy, parasites, h. pylori
lymphocytic gastritic
celiac
granulomatous gastritis
crohn, mycobacteria, fungi, CMV, h. pylori
trichobezoar
hair ball in stomach
peptic ulcer
chronic solitary lesions in part of GI tract exposed to lots of acid
usually with chronic gastritis - association with h. pylori and NSAID use
ulcer
by definition through the muscularis mucosa
erosion
limited to mucosa
PUD clinical
duodenal, male, h. pylori related
also esophagus with GERD or meckel diverticulum with gastric mucosa
pretty common
zollinger ellison syndrome
uncontrolled release of gastrin by tumor
get lots of acid - can cause ulcers
hypercalcemia
stimulate gastrin production and increased acid secretion
classic peptic ulcer
sharply punched out defect
heaped up margins - in cancer
pneumoperitoneum
air within abdominal cavity
tx of PUD
antibiotics - h pylori
PPI
surgery if severe bleeding/perforation
melena
black tarry stools
stool in contact with acid - in upper GI bleeds
hematochezia
bright red blood in stool
-lower GI bleed
coffee grounds
slow bleeding/oozing
red blood/clots
active ongoing bleeding
bile stained
no bleeding above treitz ligament
clear
competent pylorus - but bleeding could still be occuring
confirmation of bleeding location
upper GI endoscopy
- EGD
- diagnostic and therapeutic
- inject epi or electro coag techniques
can biopsy with EGD - determine h. pylori infection
