GI Pathophysio Flashcards
vitamin a deficiency
night blindness
bitot spos (squamous cell prolif)
corneal perforation
How to diagnose diverticulitis
clinical if mild
CT scan or ultrasound

epithelium of the stomach
simple layer of columnar epithelial cells
secrete mucus and bicarb
pits provide glands access to the lumen
symptoms of pancreatic exocrine insufficeincy
bulky foul smelling stool
oily residue in toilet water
irritant laxatives
castor oil, senna
cause irritation of the enteric mucosa/nerves –> water secretion –> softer stool and increased peristalsis due to increased volume
may cause abdominal pain, flatulents
bile acid deficiency
when bile salt pool is very low, get maldigestion of fat and fat soluble vitamins
from liver disease (low production) or ileal resection (low recycling)

trituration
first, peristalsis down through stomach
terminal antral contraction closes pyloris
allows mixing of foodstuff into small particles until 1-2 mm
3-4 hours

NSAIDs and ulcer formation
decrease mucin and HCO3 so HCl can touch the cell
injury to cell - HCl can get closer!

vitamin D
fat solumble
storage form = 25OH, active form 1, 25 OH
found naturally in very few foods (fortified and sun)
calcium-phosphorus homeostasis (break down bone if not enough)
bone metabolism
IBS
Rome criteria -
absence of detectable structural or biochemical abnormaility
abdominal pain
altered bowel habits (alternating between diarrhea and constimation)
abdominal pain is most universal!
IBS-C
IBS with constipation
how do you diagnose celiac disease?
high antibody levels to: TTG IgA, DPG (deaminated peptide)
abnormal small bowel biopsies
response to gluten free diet
consequences of bacterial overgrowth
unconjugate bile acids
use vit b12

treatment of pancreatic exocrine insufficiency
pancreatic enzyme supplements wiht food
viberzi
binds to opioid receptors in GI tract controling motility and hypersensitivity
types of glands in the cardia
branched and tortuous
mucus
endocrine
pancreatic exocrine insufficiency
maldigestion of fat, protein, carbs
limited amylase, lipase, proteases
from CF, chronic pancreatitis, pancreatic resection
need to lose >90%
pre-epithelial defense in the esophagus
lacks a definable surface mucus layer!
has saliva which contains mucins
surface squamous cells can not secrete bicarb! rel unprotected
esohageal peristalisis in smooth muscle
inhibition followed by excitation
gradient of increasing inhibition (latency gradient)

beri beri
B1 deficiency
dry - peripheral neruopathy
wet - CHF
vitamin d deficiency
bone demineralization
hypocalcemia, hypophosphatemia
B12 absorption
dietary intake (meat, dairy)
pepsin in the stomach cleaves protein from B12
secretion of IF by gastric parietal cells
bound to R protein
unbound - binds to IF in the intestine
in the ileum - special R and complex absorbed into blood

diverticular bleeding pathophysiology
eccentric intimal thickening and medial thinning
segmental weakening
rupture where vessels run over the dome of a diverticulum
usually abrupt and painless - 75% stops on own

erythromycin
primarily prokinetic
motilin receptor agonist
The main function of motilin is to increase the migrating myoelectric complex component of gastrointestinal motility and stimulate the production of pepsin. Motilin is also called “housekeeper of the gut” because it improves peristalsis in the small intestine and clears out the gut to prepare for the next meal.[7] A high level of motilin secreted between meals into the blood stimulates the contraction of the fundus and antrum and accelerates gastric emptying. It then contracts the gallbladder and increases the squeeze pressure of the lower esophageal sphincter. Other functions of motilin include increasing the release of pancreatic polypeptide and somatostatin[11]
































