Concepts of GI Disease Flashcards
What are the three main fxns of the stomach?
- adjustable food reservoir
- mix food
- gradual emptying
The stomach’s ability to increase in volume during a meal without an associated increase in intragastric pressure.
accomodation
Vagal mediated decrease in LES pressure and fundic cx to allow a food bolus to move into the stomach without an increase in intragastric pressure.
Receptive relaxation
What is the general mL/kg the stomach can hold?
What is the clinically relevant concentration?
80 ml/kg
45-60 ml/kg
What is the alkaline tide?
The increase in blood bicarb post-prandial d/t to the production of H+ by the parietal and concurrent release of CO2 to produce bicarb. The majority of bicarb is released into the mucous layer of the stomach but some moves into the blood.
With inflammatory and neoplastic diseases in the stomach, how do they affect receptive relaxation?
The stomach becomes less compliant→ intragastric pressure increases→stretch receptors activated→causes pain, nausea & vomiting
What are the components of gastric acid secretions?
hydrogen ions, sodium, potassium, chloride and water, pepsinogen, lipase and varying quantities of mucus
Name three phases of gastric acid secretion?
- cephalic
- gastric
- intestinal
Is gastric acid secreted continuously in dogs & cats?
What feedback mechanisms inhibit acid secretion?
no
Gastric secretion is inhibited by acid (low pH) bathing the antral mucosa. Secretion is also inhibited by acid, fat and hyperosmolar solutions bathing the duodenal mucosa.
What do the different gastric cells secrete?
secretion:
chief cells- pepsinogen
parietal- H ions
G cells- gastrin
endocrine- enterchromatin cells- histamine
Describe the different hormones produced by gastric cells that act on the parietal cell to alter H+ secretion?
How does uremia disrupt the gastric mucosal barrier?
bacteria breakdown urea into NH3 which is cytolytic
What is the mechanism by which gastric barrier disruption causes gastritis?
barrier disrupted→ H+ leaks back into mucosa→H+ accumulated and exhausts the intracellular buffers→cell pH decreases→cell damage & death→damaged mast cells release histamine→disrupt mucosal blood vessels→ ischemia, hypoxia, vascular stasis, leakage of plasma proteins & blood into lumen
What are the 6 components of the gastric mucosal barrier?
1) surface mucus
2) bicarbonate secreted by gastric epithelial cells
3) the epithelial cell membranes themselves which possess a relative impermeability to ions
4) gastric mucosal blood flow
5) prostaglandins and cytoprotection
6) the basal membrane
What are the two components of the gastric motor unit?
- proximal receptacle (fundus)
- distal pump (antrum)
What is the difference between emptying of liquids and food from the antrum into the duodenum?
liquids→ only depends on duodenal pressure
food→depends on antral cx, duodenal pressure & pyloric pressure
A patient comes in with signs of vomiting and you are not sure if it is delayed gastric emptying. It has been 8 hours since the dog ate its meal and then it vomits.
not considered delayed gastric emptying because >12hr post meal
Why do NSAIDs cause ulcers?
disrupt PG production which is important for maintaining blood flow to the GI tract
How are digestible vs. non-digestible solids emptied from the stomach?
digestible: via antral cx (cx phase)
non-digestible: via migrating motility complex (interdigestion phase)
What factors affect the rate of gastric emptying into the SI?
What ultimately determines gastric emptying?
[H+], osmolality, fatty acids, and tryptophan (the physical & chemical composition of the meal)
calorie content of the meal
What parts of the brain affect the emetic center?
Describe the various stimuli of the emetic center?
What are the three phases of the vomiting reflex?
nausea
retching
vomiting
Which part of the intestine absorbs the most water?
Which part of the intestine is the most efficient at absorption?
SI (ileum and duodenum)
Large colon
What modifications to the SI allow for increased absorption?
On the villi, where is the location of absorption? Secretion?
Cell division?
villus tip
villus crypts for secretion & cell division
What are the different mechanisms of diarrhea?
osmotic (EPI & dysbiosis; excess osmotically active molecule secreted in the lumen)
secretory (excess secretion overwhelms absorptive capability; Enterotoxigenic E. coli→HLT→increase cAMP→increase secretion )
exudative (increase tissue permeability; leakage of tissue fluid, serum proteins, blood; IBD, parasites, bacteria)
disordered motility
mixed
How does fat malabsorption result in secretory diarrhea?
hydroxylation of FA by bacteria→causes increased secretion
Mechanisms of exudative diarrhea.
increased mucosal permeability
lymphangiectasia (lacteal dilate and swell→rupture→leak protein into GI)
decreased oncotic pressure (hypoalbuminemia; edema in wall→prevent absorption)
increased hydrostatic pressure (R-side CHF; portal hypertension)
What three characteristics of the fecal matter is changed with diarrhea?
volume
fluidity
frequency
What is the lifespan of an enterocyte?
If there is damage to the villi, how long does it normally take to regenerate the enterocytes at the villus tip?
3-5 days
2-3 days
Why is a low fat diet recommended in patients with diarrheal disease?
fats not absorbed can be hydroxylated via bacteria→leads to excess secretion of water→diarrhea
What is the colonic absorptive reserve capacity?
the ability of the colon to increase the amount of water absorbed from intestinal contents (esp. when SI disease results in increase water delivery to LI)
If the colon is inflammaed, it cannot distend to accomodate the fluid volumes→diarrhea
What are the four mechanisms of diarrhea?
1) osmotic retention of water within the intestinal lumen
2) secretion of solute (and accompanying water) into the intestinal lumen
3) exudation of blood and tissue fluid due to increased mucosal permeability
4) disordered contact time between chyme and the absorptive surface due to disordered motility.
How does intestinal dysbiosis result in secretory diarrhea?
bacteria breakdown nutrients in the lumen→osmotically active products
At what level of hypoalbuminemia will fluid absorption in the SI stop?
<4.5 g/dL
What types of infections/diseases will result in hemorrhagic diarrhea?
C. perfringens colitis
severe hookworm infections
salmonellosis
parvovirus
hemorrhagic gastroenteritis
(need a 10,000x increase in permeability for blood to leak)
What are the two major motor abnormalities associated with diarrhea via disordered motility?
- suppressed phasic migrating motor complex
- stimulation of giant migrating motor complex (ultrarapid transit ofr food/secretions from SI to LI)
