Concepts of GI Disease Flashcards
3 major stomach functions
filling
mixing
emptying
gastric filling
- acts as a reservoir for food and liquid
- two components
- receptive relaxation
- accommodation
accommodation
stomach adjusts size to increase volume without increasing intragastric pressure
its mediated by vagal inhibitory fibers
receptive relaxation
when bolus of food enters stomach and vagal inhibitory fibers decease the lower esophageal sphincter pressure and fundic contractions
gastric filling dysfunction
-
inflammatory and neoplastic disease
- failure to relax
- increase in postprandial intragastric pressure causes pain, nausea and vomiting
gastric mixing
-
mix food with gastric secretions
- begins intragastric digestion
- fundus and body are the receptacle for food
- antrum is distal “pump”
gastric emptying
- stomach empties only when intragastric pressure exceeds duodenal pressure and pyloric resistance
- influenced by the physical and chemical composition of a meal and by food type, pH and osmolarity
dysfunction of gastric emptying
-
gastric and small intestinal diseases
- most delay emptying and cause vomiting
- gastric outlet obstruction results in gastric distention and stasis
How much time after eating will the stomach empty in a dog?
12-14 hours
the final determinant is the caloric content of the meal
gastric mucosal barrier
- protects stomach from autodigestion
-
anatomic and chemical defense mechanisms
- surface mucus
- bicarb
- epithelial cells
- mucosal blood flow
- prostaglandins
- basal membrane
- gastric juice is not secreted continuously
for each hydrogen ion secreted:
a molecule of CO2 is made
the CO2 combines with water to make bicarb and goes into interstitial fluid where its taken up by mucosal capillaries
What cells secrete acid?
parietal cells
gastric barrier dysfunction
- damage allows H+ to leak back into the mucosa
- it saturates the buffers and cell pH decreases causing injury and cell death
- result is local ischemia, hypoxia, vascular stasis, leakage of plasma proteins and blood into the lumen, mucosal erosions or ulcers
- common in dogs but less so in cats
vomiting
- a spontaneous forceful ejection of gastric contents through the mouth
- occurs when vomiting center receives sufficient stimulation to reach threshold and initiate the reflex
vomiting reflex
- three phases
- nausea
- retching
- vomiting
- well developed in dogs and cats
- mediated through the emetic center in the medulla
How can the emetic center be activated?
- directly and indirectly from higher centers, cerebellum, viscera, extra visceral sources (HW, tonsils), drugs or toxins
what are some drugs or toxins that can cause vomiting?
apomorphine
uremic toxins
hepatotoxins
endotoxins
cardiac glycosides
the emetic center can be directly stimulated by:
the cerebral cortex, chemoreceptor trigger zone, oculovestibular system (cats only) or the GI tract
where is the chemoreceptor trigger zone located and how is it stimulated?
-
outside the BBB so it can sample chemicals in the blood without it getting to the brain
- usually responsible for repeat vomiting
- directly stimulated by emetic toxins and the oculovestibular system of dogs only
diarrhea
increased fecal water content which results in change of frequency, fluidity and volume of bowel movements
How much of the fluid in the intestines comes from the diet and how much from endogenous secretions of the GI tract?
20% from the diet
80% from endogenous secretions
What are the potential causes of fluid exchange disruption?
increased secretion or decreased absorption
where is the most water absorbed in GI tract?
50% in the upper small intestines
90% of what is presented to the colon (more efficient)
How do cereal based diets affect fecal water volume?
increased fiber, more water absorbed
doubles volume of fecal water output
which diseases are associated with more fluid loss (proximal or distal tract disease)?
proximal small intestine
what determines the efficiency of absorption of the GI tract and what can disrupt this?
tightness of intercellular junctions (tighter in distal SI and colon)
disrupted by inflammation
why are most acute diarrheal disease self-limiting?
rapid cell turnover rate in villus, bad cells get replaced quickly
if cause is eliminated and crypts aren’t severely damaged, function is restored in 2-3 days
what are the 3 main areas of the villus?
crypt: secretory cells, undifferentiated cells that migrate to tip
maturation zone
tip: absorptive cells, slough off after 3-5 days
what are the four pathophysiologic mechanisms of diarrhea?
osmotic
secretory
exudative
disordered motility
what are the characteristics and causes of osmotic diarrhea
- excess of poorly absorbable osmotically active solutes
- occurs when nutrients are maldigested or malabsorbed
- seen with pancreatic/enteric disease (EPI), laxatives, other disorders, SIBO/dysbiosis
what are the characteristics and causes of secretory diarrhea?
- stimulation of excess secretion overwhelms absorption (usually SI)
- caused by E. coli heat labile toxin (LT) and fat malabsorption (hydroxyl fatty acids)
what are the characteristics and causes of exudative diarrhea?
- increased mucosal permeability causes leakage of fluid, electrolytes, and proteins (also ulcers leaking blood and mucus)
- IBD, parasite or bacteria infections, lymphangiectasia, hypoalbuminemia, increased hydrostatic pressure (R sided CHF or portal hypertension)
- diseases associated with this mechanism cause PLE
what are the characteristics and causes of disorder motility diarrhea?
- inflammation suppresses phasic contractions and stimulates giant migrating motor complexes
- makes fluid move faster than it can be absorbed
most cases of diarrhea are what kind?
mixed
