Pearls of GIT?

IMPORTANT POINTS
GI hormones: gastrin, CCK, GIP
-release, stimuli, action Gastrin
-stomach G cells (antrum) of parietal cells
-stimuli: protein, stomach distension, Ach
-action: stomach acid and motility
CCK
-SI parietal cells
-stimuli: FAs, peptides
-action: protein ezymes, gall bladder contractions
GIP
-SI parietal cells
-stimuli: acid
-action: inhibits stomach acid, boosts insulin
Smooth muscle contractile patterns: tonic, peristalsis, segmentation tonic: sust
ained smooth muscle contraction in sphincters
peristalsis: rapid waves of contraction pushes food to distal end
segmentation: back and forth mixing movement, slows food
Things that promote gastric emptying: -gastric distention
-fluidity of chymes
stimuli: gastrin, vagus nerve
Inhibition of gastric emptying: ENTEROGASTRONES from the SI:
secretin: bicarbonate
CCK: pancreatic enzymes, bile
GIP: decr stomach acid, insulin
Four conditions that influence absorption: permeability: water vs lipid soluble,
large vs small, water itself
surface area: villi, micro villi
enterocyte replacement: produced in crypts, migrate up villi
luminal conditions: optimal pH for enzymes
Enzymes in carb digestion: maltase
sucrase
lactase
isomaltase
Enzymes in protein digestion:
stimuli, release, action Pepsin:
-simuli: gastrin, vagus
-stomach chief cels
-action: bd polypeptides
Pancreatic enzymes:
-enteropeptidase in brush border convert trypsin
-trypsin converts itself and chymotrypsin, elastase
Aminopeptidases:
-brush border and intracellular
-cleave single amino acids for di/tripeptides
Water soluble vs fat-soluble vitamins Water soluble:
-Vitamins B, C, folate
-require intrinsic factor from SI parietal cells
Fat-Soluble:
-Vitamins A, D, E, K
-diffuse passively
Gastric acid secretagogues:
(stimulate gastric acid production in the stomach) Acetylcholine
-vagus nerve
-action: gastrin, histamine release
Histamine
-Ach, gastrin stimuli
-from ECL cells (enterochromaffin-like)
-action: bind to H2 receptors on stomach parietal cells, cause H release

Gastrin
-Ach stimuli, gastric distention, protein
-action: histamine release, stomach motility
Mechanisms for mucosal protection Tight junctions: acid cannot penetrate
Mucus: secreted by surface and neck cells
Bicaronate: neutralizes acid
Prostaglandins:
-decreases acid secretion
-cytoprotective
-fluid secretions
Secretions of duct and acinar cells of the pancreas duct:
-exocrine (nerve) secretions
-bicarbonate
acinar:
-CCK: stimuli by FAs, peptides,
-an enterogastrone
-secrete pancreatic enzymes
GERD gastroesophageal reflux disease
-heartburn
-caused by poor tone of LES
Dumping Syndrome -caused by rapid movement of high-osmolarity chyme out of the s
tomach
-causes fluid secretion, low BP, and diarrhea
Pancreatitis -inflammation of the pancreas
-block pancreatic enzyme secretion, causing maldigestion and malabsorption
Celiac's disease -gluten allergy
-causes decrease in surface area of the upper small intestine by destruction of
enterocytes/villi
Chron's disease -caused by inflammation of the lower small intestine (ileum)
-can be caused by malabsorption of bile salts after fat digestion, which enter t
he colon and cause colonic irritation, fluid secretion, and diarrhea
Pernicious Anemia -caused by lack of intrinsic factor secreted from stomach pari
etal cels, resulting in malabsorption of vitamin B12
-results in impaired RBC formation, and nerve health
Peptic Ulcers -H.pylori bacteria can survive the acidic environment of the stoma
ch, by producing urease enzymes that create ammonia (basic), protective shell ar
ound it
-causes inflammation in the stomach, creating ulcers
Cystic Fibrosis -defect CFTR, preventing Cl transport into the lumen
-less fluid secretion, and more mucus
-blocks pancreatic enzymes secretion, resulting in maldigestion..
Credit Fcps Physiology