stomach Flashcards
parietal cells in stomach secrete
intrinsic factor
gastric acid
chief cells in stomach secrete
pepsinogen
activated by gastric acid to pepsin
G cells in stomach secrete
gastrin
mucosal cell cells in stomach secrete
HCO3
gastrin-secreting tumor (gastrinoma) usually in pancreas → ↑ gastric acid → recurrent duodenal ulcers
Zollinger-Ellison syndrome
pancreatic gastrinoma (seen in Zollinger-Ellison syndrome) is associated with
MEN type I
complications of chronic gastritis due to autoimmune destruction of parietal cells (called pernicious anemia)
no IF → vitamin B12 deficiency:
megaloblastic anemia
peripheral neuropathy
dementia
drugs that are potent stimulators of gastrin release from G cells of stomach → ↑gastrin → ↑H+ →GERD → ulceration
phenylalanine
tryptophan
hypercalcemia
sites of HCO3 secretion to neutralize acid in GI tract
mucosal cells - stomach, duodenum (S cells), salivary glands, pancreatic duct
Brunner glands - duodenum
treatment of ZE syndrome
PPI +/- octreotide (if tumor has octreotide R)
↑ gastric acid production or ↓ HCO3/mucosal lining →
breakdown of mucosal lining → inflammation of stomach
acute gastritis
causes of acute gastritis
NSAIDs and aspirin (inhibit COX - inhibit PG - ↑H, ↓PG)
alcohol
burns (curling ulcer)
brain injury (cushing ulcer)
type of ulcer associated with burn injury
curling ulcer (like curling iron) stress of burn →↓ mucosal lining production →ulcer → acute gastritis
type of ulcer associated with brain injury
cushing ulcer
causes of chronic gastritis
H. pylori (spiral shaped, in gastric glands)
autoimmune destruction of gastric parietal cells
H pylori in gastric glands
neutrophils + lymphocytes invading gastric glands
chronic gastritis
complication of chronic gastritis due to H.pylori
↑ risk of:
MALT lymphoma (due to chronic lymphocyte infiltration)
gastric cancer
stomach biopsy shows neutrophils above BM, loss of surface epithelium, fibrin-containing purulent exudate
acute gastritis
stomach biopsy reveals lymphoid aggregates in lamina propria, columnar absorptive cells, atrophy of glandular structures
chronic gastritis
diffuse thickening of gastric folds, elevated serum gastrin levels, biopsy reveals glandular hyperplasia without foveolar hyperplasia
ZE syndrome (gastrin secreting tumor of pancreas)
causes of gastric ulcers
H pylori - 70% (↓ mucosal protection)
NSAIDs (gastritis → ulceration)
gastric acid erodes through mucosa into submucosa
if in stomach: peptic ulcer
in duodenum: duodenal ulcer
upper abdominal and epigastric pain AFTER eating (↑ H production after eating) weight loss (avoid eating)
gastric ulcer
complication of gastric ulcers (due to H. pylori or NSAIDs)
↑ risk gastric cancer (take biopsy around ulcer to ensure no cancer)
upper abdominal and epigastric pain RELIEVED by eating (HCO3 production in duodenum after eating) pain returns several hours after eating weight gain (eating makes it better) biopsy: clean, smooth borders with H.pylori in ulcer, hypertrophy of Brunner glands in duodenum (submucosal)
duodenal ulcer
causes of duodenal ulcers
H. pylori (↓ mucosal protection) - 95%
ZE syndrome - rare - (secrete gastrin - ↑ gastric acid)
complications of gastric + duodenal ulcers
ulcerate into vessel → hemorrhage
perforation (esp duodenal ulcers) → peritonitis
treat actively bleeding peptic ulcer
somatostatin (octreotide) ↓ splanchnic blood flow
most common cause of gastric + duodenal ulcers
H pylori
treatment for irradicating H pylori
triple therapy:
PPI + clarithromycin + amoxicillin (if pen allergy: metronidazole)
quad therapy (if resistance to clarithromycin):
PPI + bismuth + metronidazole + tetracycline
treatment for neutralizing gastric acid to protect stomach + ↓ gastric acid secretion (prevent gastric ulcers, also adjuncts for H. pylori infection)
neutralize stomach acid: antacid ↓ gastric acid secretion: H2 blockers, PPIs less commonly used: bismuth + sucralfate misoprostol
precursor to gastric adenocarcinoma
hypertrophy of mucus producing cells → rugae look like gyri of brain
atrophy of parietal cells → ↓ gastric acid production
enteric protein loss → hyopalbuminemia → edema
Menetrier disease
most common type of cancer in GI tract
adenocarcinoma except esophagus (can have esophageal squamous cell carcinoma in smokers too)
risk factors for gastric adenocarcinoma
H pylori infection chronic gastritis nitrosamines (cured, smoked) men >50 yo japanese people in Japan
weight loss +
mass in L supraclavicular node (Virchow node)
metastasis of GI cancer (usually gastric adenomcarcinoma)
metastasis of gastric adenomcarcinoma
L supraclavicular node (Virchow node) periumbilical node (sister mary joseph nodule) mets to bilateral ovaries (Krukenberg tumor)
> 40 yo with new acanthosis nigricans (velvety darkening of skin, near neck)
diabetes
50% have visceral malignancies: stomach cancer
signet ring cells: mucous in cytoplasm pushes nucleus to periphery
1) gastric adenocarcinoma
may be from ovary biopsy (krukenberg tumor - gastric cancer with mets)
mucous in cytoplasm pushes nucleus to periphery
2) lobular carcinoma in situ (LCIS) or invasive lobular carcinoma
pylorus hypertrophied → narrowed gastric outlet → ↓ stomach emptying
nonbillious projectile vomit
presents 2-6 wks of age
palpable olive structure in epigastric region
most common in firstborn males, most common congenital surgery in 1st mo of life
congenital pyloric stenosis
diarrhea can cause
hypokalemia
prolonged vomitting (days-wks) can cause
vomit HCl from stomach →
hypochloremia
metabolic alkalosis (low serum H+ concentration) → correct alkalosis in serum at K/H exchanger: cells release H+ from cells to serum, K+ from serum to cell → hypokalemia (vs acidosis: H+ out → hyperkalemia)
treatment of Zollinger-Ellison syndrome
high dose PPI
sporadic: surgery to resect
metastatic: somatostatin analog (octreotide), IFN, chemo, radiothearpy
