stomach patho Flashcards
gastritis
inflammation of gastric mucosa resulting from exposure to acid and other agents, can be a acute or chronic
acute gastritis
could be asymptomatic up to epigastric pain, N/V, ulceration, hemorrhage, hematemesis
stomach is usually shielded from acid by mucin (secretes bicarb to neutralize) and blood supply that buffers and removes caustic agents
injury can cause this problem and you will see presence of neutrophils in endothelial layer
common causes of chemical gastritis
NSAIDs (inhibit prostaglandins), uremia and infection by h pylori (inhibit bicarb), chemical exposure (direct injury)
stress gastritis
patients with severe trauma, burns, critical illness probe to developing stress ulcers
local ischemia d/t systemic hypotension, reduced blood flow, SNS vasoconstriction causes increased acid production
for ICU patients, prevent with PPIs
H pylori gastritis
spiral shaped bacillus detectable in gastric mucosal biopsies from many patients with duodenal ulcer and chronic gastritis
- bacteria invade the gastric mucosa and can persist for life
- associated with increased risk of gastric carcinoma
bacterial enzymes and other toxic products directly damage endothelial cells, increased production of gastric acid, production of protease that degrade normally protective glycoproteins in the mucous layer, exposing epithelial cells to harsh gastric contents
stimulation of acute and chronic inflammation and cytokine release
diagnosis of h pylori
symptoms will be like gastritis
diagnosis will be with biopsy to ID h pylori via stain/culture breath test (looking for ammonia) stool test (presence of h pylori)
peptic ulcer disease
benign ulcer composed of granulation tissue and necrotic cell debris and inflammatory cells resting on fibrous scar
results from excess gastric acid and impaired mucosal defense
more frequent in duodenum and stomach and seen in middle to older age adults
gastritis treatments
antacid (relief of dyspepsia), H 2 receptor antagonists (inhibits gastric acid secretion), PPIs (covalently bind/inhibit HK pump), prostaglandin analogues (enhance bicarb secretion, stimulate mucosal blood flow, decrease mucosal cell turnover)
polyp
inflammatory abnormal tissue when cells grow and divide more they should or do not die when they should
adenoma
abnormal tissue that may serve as precursor for cancer
most common malignancy of stomach
can spread to involve duodenum, pancreas, retroperitoneum
neuroendocrine tumors
grows from neuroendocrine cells (found throughout body)
carcinoid - often grow slowly
most 75% found in GI tract (small intestine) - 25% found in lungs
foregut (stomach, duodenum, esophagus) tumors rarely spread
midgut (small intestine) are aggressive
hindgut (appendix, colon) benign
Zollinger Ellison Syndrome
gastrinoma - gastrin secreting tumor which increases HCL via gastrin and histamine stimulation
leads to peptic ulcer disease, erosive esophagitis, and diarrhea
multiple endocrine neoplasi type 1 - hereditary, neoplasia of parathyroid glands, pancreatic islet cell tumors, pituitary gland tumors
anesthetic considerations of zollinger ellison
GERD, large gastric fluid volume, IV volume depletion, hypokalemia, maintain PPI, assess for liver metastases
carcinoid syndrome
tumors secrete vasoactive and other hormone like stubstances
when tumor is intestinal, vasoactive mediators are metabolized in liver - symptoms then reflect metastatic disease
two factor release
- direct physical
- beta adrenergic
carcinoid syndrome symptoms = flush, sweat, bronchospasm, abd pain, diarrhea, cardiac valve abnormalities
carcinoid heart disease
seen in up to 60% of patient with carcinoid syndrome
triad = cardiac involvement, flushing, diarrhea
right sided failure from valvular and myocardial plaque formation, left side protected by lung metabolism of serotonin
50% of carcinoid death results from heart failure