GI Flashcards
G cells of stomach
produce gastrin, a hormone that facilitates productions of HCl
parietal cells
produce HCl to help break down food
produce intrinsic factor (IF) to protect mucosa
chief cells
secrete pepsin–digests protein
epithelial cells
secrete bicarbonate-rich solution to coat and protect mucosa
Crypts of Lieberkuhn
intestinal glands that secrete about 2L of fluid/day into lumen of intestine
goblet cells and Brunner glands
secrete large amts of mucus to protect small intestine from damage of acidic gastric juices
gastritis
temporary inflammation of the stomach lining only
generally lasts 2-10 days
causes: irritating substances (ETOH), drugs (NSAIDs), infectious agents (H. pylori)
chronic gastritis
progressive disorder with chronic inflammation of the stomach (weeks to years)
complications: PUD, bleeding ulcers, anemia, gastric CA
etiologies: autoimmune→ attacks parietal cells
H. Pylori
Helicobacter pylori
gram negative spiral bacteria
thrives in acidic env.
transmitted person to person via saliva, fecal matter, or vomit; contaminated food or water
acute or chronic gastritis
clinical manifestations
asymptomatic anorexia N/V postprandial discomfort intestinal gas hematemesis tarry stools anemia
acute gastroenteritis
inflammation of stomach AND small intestines etiology: viral, bacterial, parasitic 1-3 days, up to 10 days clinical manifestations: watery diarrhea (may be bloody if bacterial) abdominal pain N/V fever, malaise complications: FVD
Peptic Ulcer Disease (PUD)
Ulcerative disorder of the upper GI tract
esophageal
stomach→ gastric ulcers
duodenum→ peptic ulcers
develop when GI tract exposed to acid AND H. pylori
PUD
etiology
H. pylori injury-causing substances excess secretion of acid smoking family history stress--increased acid secretion with stress; doesn't cause but can worsen once developed
PUD
risk factors
Age higher doses of NSAIDs Hx of PUD use of corticosteroids and anticoagulants serious systemic disorders H. pylori infection
PUD
pathogenesis
mucosa is damaged
histamine is secreted → ↑acid and pepsin secretion causing further tissue damage; vasodilation → edema
if blood vessels destroyed → bleeding
duodenal ulcer
type and age
most common
any age, early adulthood
gastric/peptic ulcer
age/reason
peak age 50-70
increased used of NSAIDs, corticosteroids, anticoagulants and serious systemic illnesses at this age
PUD
clinical manifestations
Asymptomatic N/V, anorexia weight loss bleeding burning pain → middle of abdomen that's usually worse when stomach is empty
gastric → 1-2 hours after eating
duodenal → 2-4 hours after eating
PUD complications
HOP
Hemorrhage
Obstruction → creates scar tissue/strictures
Perforation & Peritonitis
appendicitis
complications: gangrene, abscess formation, peritonitis
pain in RLQ
Rebound pain
sudden pain relief may indicate rupture
peritonitis
complications
inflammation
fluid shifts → third spacing leading to hypovolemic shock and sepsis
decreased peristalsis
paralytic ileus and intestinal obstruction
peritonitis
causes
perforated ulcer ruptured gallbladder pancreatitis ruptured spleen ruptured bladder ruptured appendix
peritonitis
clinical manifestations
Rigid, board-like abdomen usually sudden and severe tenderness N/V fever ↑ WBC ↑ HR ↓ BP
irritable bowel syndrome
chronic condition characterized by alterations in bowel pattern due to changes in intestinal motility
S/S vary by individual
abd distension, fullness, flatus, bloating
intermittent abd pain exacerbated by stress, relieved by defecation
bowel urgency
intolerance to certain foods
non-bloody stool that may contain mucous