1/32
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai | Chat |
|---|
No analytics yet
Send a link to your students to track their progress
layers of the GI tract
serosa- outer most layer
muscularis
submucosa
mucosa
serosa
connective tissue layer
peritoneum
muscularis
circular muscle layer
longitudinal muscle layer
mucosa
mucous epithelium
lamina propria
muscularis mucoseae
digestive process
1) cephalic phase
2) gastric phase
3) intestinal phase
cephalic phase
secretion of acetylcholine (PSNS), gastrin, & histamine
gastric phase
parietal cells- secrete HCl; Acetylcholine, histamine, and gastrin binds and triggers proton pump (increase H+ ion)
Goblet cells- secrete mucus, release digestive enzymes, and absorb nutrients
Chief cells- secrete pepsinogen → pepsin
Gastric mucosal cells - secrete prostaglandin E2 (PEG2); PEG2 stimulates gastric mucus production and bicarb secretion, decrease effects of HCl
G cells (gastrin cells located in the pylorus) -stimulate secretions from parietal and chief cells
Intestinal phase
small intestine first, then large
3 parts of stomach
fundus, body, antrum
typical questions of GI assessment
swallowing, indigestion, weight loss, appetite, nausea/vomiting, pain, elimination, family history
substances affecting upper GI
alcohol, smoking, nasaids
diagnostic tests
upper and lower GI endoscopy
videocapsule endoscopy
laparoscopy(scope) and laparotomy(open)
upper GI series (barium study)
H.Pylori antibody (blood)
constipation
defined as infrequent or difficult defecation
diarrhea
increased frequency of bowel movements
increased volume, fluidity, weight of the feces
major mechanisms:
osmotic diarrhea
secretory diarrhea
motility diarrhea
osomotic diarrhea
malabsorption syndromes (lactose intolerance); laxatives
mild
secretory diarrhea
infections (toxins), medications (chemo)
severe
motility diarrhea
irritable bowel
two issues that occur with reflux
relaxation of the les (inadequate closure)
Gastroparesis- delayed emptying from the stomach to duodenum
contributing factors of GERD
laying flat or bending over, alcohol, chocolate, coffee, fatty meals, obesity, pregnancy, some medications, nicotine, hiatal hernia
Hiatal Hernia
part of the stomach pushes up through the opening in the diaphragm and protruding into the thoracic cavity
allows stomach acid to reflux back into esophagus
many are undiagnosed, asymptomatic, and discovered incidentally
lifestyle changes for GERD and Hiatal Hernia
weight loss, small meals, coffee limitation, smoking cessation, refrain from lying down after eating, sleeping with the head of bed elevated
avoiding certain foods
Obstruction
any condition that prevents the flow of chyme through the intestinal lumen
can be partial or complete
can be SBO or LBO
Ileus
failure of normal intestinal motility (in the absence of an obstructing lesion)
Ileostomy
the ileum of the small intestine is surgically brought out to the exterior abdominal wall through an incision in the anterior abdominal wall
colostomy
the colon is imilarly brought out to the anterior abdomen
acute gastritis
inflammatory disorder of the gastric mucosa
diagnosis is confirmed with endoscopy and a biopsy of the affected tissue
chronic gastritis or nonerosive gastritis
presence of the H. pylori is most common cause
causes atrophy of the stomach lining
precursor for stomach cancer
Peptic Ulcer disease (PUD)
inflammatory erosion in the stomach or duodenal lining
ulceration occurs 4x more often in the duodenum than stomach
endoscopy and tissue biopsy
pathophysiology of PUD
hyper secretion of HCl
ineffective GI mucus production
poor cellular repair
Irritable bowl syndrome (IBS)
recurrent abdominal pain and discomfort associated with altered bowel habits
diarrhea or constipation, or both
IBS Risk factors
female, under 40, family history, stress, a person may have food triggers
esophageal cancer
risk factors: male, gerd & barrett’s esophagus, chronic alcohol consumption, particularly whiskey , tobacco use, genetic markers
pathophysiology: chronic irritation of the epithelial cells cause cellular injury and leads to metaplastic changes, metaplastic becomes dysplasia, proliferation of cancer cells
symptoms: dysphagia, change in eating patterns, weight loss, dyspepsia, sore throat/hoarseness, cough
colorectal cancer
half of all colon cancers occurs in the rectosigmoid area
risk factors: genetic factors are highest risk, polyps, red meat, obesity, sedentary life, insulin resistance, tobacco, alcohol