Concepts of GI Disease

Question 1

What are the three main fxns of the stomach?

Answer 1

1. adjustable food reservoir
2. mix food
3. gradual emptying

Question 2

The stomach’s ability to increase in volume during a meal without an associated increase in intragastric pressure.

Answer 2

accomodation

Question 3

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.

Answer 3

Receptive relaxation

Question 4

What is the general mL/kg the stomach can hold?

What is the clinically relevant concentration?

Answer 4

80 ml/kg

45-60 ml/kg

Question 5

What is the alkaline tide?

Answer 5

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.

Question 6

With inflammatory and neoplastic diseases in the stomach, how do they affect receptive relaxation?

Answer 6

The stomach becomes less compliant→ intragastric pressure increases→stretch receptors activated→causes pain, nausea & vomiting

Question 7

What are the components of gastric acid secretions?

Answer 7

hydrogen ions, sodium, potassium, chloride and water, pepsinogen, lipase and varying quantities of mucus

Question 8

Name three phases of gastric acid secretion?

Answer 8

1. cephalic
2. gastric
3. intestinal

Question 9

Is gastric acid secreted continuously in dogs & cats?

What feedback mechanisms inhibit acid secretion?

Answer 9

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.

Question 10

What do the different gastric cells secrete?

Answer 10

secretion:
chief cells- pepsinogen
parietal- H ions
G cells- gastrin
endocrine- enterchromatin cells- histamine

Question 11

Describe the different hormones produced by gastric cells that act on the parietal cell to alter H+ secretion?

Answer 11

Question 12

How does uremia disrupt the gastric mucosal barrier?

Answer 12

bacteria breakdown urea into NH3 which is cytolytic

Question 13

What is the mechanism by which gastric barrier disruption causes gastritis?

Answer 13

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

Question 14

What are the 6 components of the gastric mucosal barrier?

Answer 14

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

Question 15

What are the two components of the gastric motor unit?

Answer 15

1. proximal receptacle (fundus)
2. distal pump (antrum)

Question 16

What is the difference between emptying of liquids and food from the antrum into the duodenum?

Answer 16

liquids→ only depends on duodenal pressure

food→depends on antral cx, duodenal pressure & pyloric pressure

Question 17

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.

Answer 17

not considered delayed gastric emptying because >12hr post meal

Question 18

Why do NSAIDs cause ulcers?

Answer 18

disrupt PG production which is important for maintaining blood flow to the GI tract

Question 19

How are digestible vs. non-digestible solids emptied from the stomach?

Answer 19

digestible: via antral cx (cx phase)

non-digestible: via migrating motility complex (interdigestion phase)

Question 20

What factors affect the rate of gastric emptying into the SI?

What ultimately determines gastric emptying?

Answer 20

[H+], osmolality, fatty acids, and tryptophan (the physical & chemical composition of the meal)

calorie content of the meal

Question 21

What parts of the brain affect the emetic center?

Answer 21

Question 22

Describe the various stimuli of the emetic center?

Answer 22

Question 23

What are the three phases of the vomiting reflex?

Answer 23

nausea

retching

vomiting

Question 24

Which part of the intestine absorbs the most water?

Which part of the intestine is the most efficient at absorption?

Answer 24

SI (ileum and duodenum)

Large colon

Question 25

What modifications to the SI allow for increased absorption?

Answer 25

Question 26

On the villi, where is the location of absorption? Secretion? Cell division?

Answer 26

villus tip villus crypts for secretion & cell division

Question 27

What are the different mechanisms of diarrhea?

Answer 27

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

Question 28

How does fat malabsorption result in secretory diarrhea?

Answer 28

hydroxylation of FA by bacteria→causes increased secretion

Question 29

Mechanisms of exudative diarrhea.

Answer 29

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)

Question 30

What three characteristics of the fecal matter is changed with diarrhea?

Answer 30

volume fluidity frequency

Question 31

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?

Answer 31

3-5 days 2-3 days

Question 32

Why is a low fat diet recommended in patients with diarrheal disease?

Answer 32

fats not absorbed can be hydroxylated via bacteria→leads to excess secretion of water→diarrhea

Question 33

What is the colonic absorptive reserve capacity?

Answer 33

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

Question 34

What are the four mechanisms of diarrhea?

Answer 34

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.

Question 35

How does intestinal dysbiosis result in secretory diarrhea?

Answer 35

bacteria breakdown nutrients in the lumen→osmotically active products

Question 36

At what level of hypoalbuminemia will fluid absorption in the SI stop?

Answer 36

\<4.5 g/dL

Question 37

What types of infections/diseases will result in hemorrhagic diarrhea?

Answer 37

C. perfringens colitis severe hookworm infections salmonellosis parvovirus hemorrhagic gastroenteritis (need a 10,000x increase in permeability for blood to leak)

Question 38

What are the two major motor abnormalities associated with diarrhea via disordered motility?

Answer 38

1. suppressed phasic migrating motor complex 2. stimulation of giant migrating motor complex (ultrarapid transit ofr food/secretions from SI to LI)