Gastrointestinal Flashcards
Biochemical findings in EPI: B12, folate, TLI, and PLI?
B12: Normal or low (worse prognosis if low)
Folate: Normal or elevated
TLI: Low
PLI: Normal or low
Biochemical findings in pancreatitis: B12, folate, TLI, and PLI?
B12: Normal
Folate: Normal
TLI: Normal or elevated
PLI: Elevated
Biochemical findings in antibiotic responsive diarrhea: B12, folate, TLI, and PLI?
B12: Low or normal
Folate: Normal or elevated
TLI: Normal
PLI: Normal
Biochemical findings in IBD: B12, folate, TLI, and PLI?
B12: Low (if distal S.I. malabsorption)
Folate: Low (if proximal S.I. malabsorption)
TLI: Normal
PLI: Normal
Treatment of Boxer granulomatous colitis?
Enrofloxacin
Ion exchanged for bicarbonate in intestines?
Chloride
Stimulus for acid secretion in stomach?
Acetylcholine (from PSNS), gastrin, histamine
Enzyme responsible for trypsinogen activation?
Enterokinase
Hormone stimulating appetite?
Ghrelin
Major inhibitor of trypsin in acute pancreatitis?
Trypsin inhibitor
Function of Enterochromaffin-like cells?
Secrete histamine to stimulate acid production (stimulated by gastrin)
How are proteins metabolized in the G.I.?
Starts with pepsin in the stomach (10-20%), pancreatic enzymes (trypsin, chymotrypsin, carboxypolypetidase, elastase) split proteins into polypeptides in S.I., carboxypolypeptidase cleaves caroboxyl ends, enterocytes use peptidase enzymes (aminopolypeptidase, dipeptidase) to cleave into tripeptides, dipeptides, and AA’s, further broken down into single AA’s in cytosol of enterocytes
Where is gastrin produced and what is its function?
Secreted by G cells in antrum of stomach, induces histamine release from ECF cells, induces parietal cells directly to secrete acid. Also has functions to increase gastric motility and mucosal hypertrophy
What is responsible for the conversion of pepsinogen to pepsin?
HCl
How does the peptide pump work in the G.I.?
Sodium is actively transported out of the epithelial cells through basolateral membrane. Low intracellular Na pull sodium in through transport protein, which co-transports sodium into the cell (secondary active transport) along with carbohydrate/peptide/AA specific for that transport protein
What is the indication for misoprostol and how does it work?
PGE2 analog, enhances mucosal defense mechanisms and healing in response to acid-related injuries; use for G.I. ulceration secondary to NSAID’s
How does bradykinin effect the blood flow and secretory capacity of the G.I. system?
Causes vasodilation (Increased G.I. bloodflow) and increased secretions
Diagram the flow of bile
Released from the hepatocytes into the bile cananliculi, into terminal bile ducts, hepatic duct, common bile duct. Either empties into the duodenum or is diverted through the cystic duct into the gall bladder
Where is lecithin found and what is it’s function?
Constituent of bile, combines with bile salts and cholesterol to form micelles, keeps cholesterol in solution in the bile
Cisapride MOA?
5-HT4-receptor agonist, enhances release of acetylcholine at the myenteric plexus; increases distal esophageal motility (not dogs due to striated mm), stomach, S.I., and L.I.
PLE test?
Panhypoprteinemia with normal UPC and bile acids; Alpha-1 protease inhibitor is also useful for confirmation of PLE
How do NSAID’s cause G.I. ulceration?
Through inhibition of “friendly prostaglandins” such as PGE2, which serve gastroprotective functions in the G.I.
Explain carbohydrate metabolism in the small intestine
Pancreatic alpha amylase breaks starch down into maltose, other glucose polymers. Enterocytes on brush border contain lactase, sucrase, maltase, and alpha-dextrinase into monosaccharides
What is the protein responsible for iron transport in the small intestine?
Apotransferrin (when unbound to iron) is secreted in bile, binds to iron products in diet (transferrin when bound to iron), pinocytosis into the epithelial cells of S.I.
Where is cholecystokinin made and what is its function?
Produced in I cells of duodenal mucosal cells, causes increase in pancreatic digestive enzyme production/release and stimulates release of bile from gall bladder. Also suppresses hunger (increases satiety) and inhibits gastric emptying
Main prosaglandin responsible for mucous secretion in stomach?
PGE2
Where is secretin made and what is its function?
Produced in S cells in duodenum, released in response to gastric juice entering the duodenum, promotes secretion of HCO3 from the pancreas. Also decreases acid production in the stomach and induces pepsin secretion
Where is motilin made and what is its function?
Produced in the M cells of the duodenum, stimulates gastric and intestinal motility; released cyclically
Function of the chief cells?
Secrete pepsinogen
Function of the parietal cells?
Secrete HCl and intrinsic factor
Function of intrinsic factor?
Essential for absorption of B12 (cobalamin) in the distal S.I. (ileum)
MOA of erythromycin as a pro-motility agent?
At sub-antimicrobial dosages, mimics the effects of motilin and 5-HT3, ehances gastric motility and colonic motility (in dogs, not cats)
What is the mechanism of action of metoclopramide?
Antagonist of D2 (dopaminergic) receptors in the CRTZ and agonist of 5HT (serotonergic) receptors
Increases pressure in the lower esophageal sphincter and accelerates gastric emptying; inhibits vomiting via its effects on the CRTZ
What is the mechanism of action of domperidone?
Antagonist of D2 (dopaminergic) receptors in the CRTZ (similar mechanism to metoclopramide)
What is the mechanism of action of ranitidine (and similar drugs)?
Antagonist of H2 (histaminergic) receptors
Inhibits gastric acid secretion and stimulates GI motility by decreasing acetylcholinesterase activity (thus increasing ACh available to bind to smooth muscle muscarinic cholinergic receptors)
What is the most common cause of EPI in dogs vs. cats?
Dogs:
Pancreatic acinar atrophy - due to an autoimmune atrophic lymphocytic pancreatitis; common in GSDs, rough collies
Cats: Chronic pancreatitis (both exocrine and endocrine parts affected)
Where does gastrin-releasing peptide (GRP, aka bombesin) come from and what is its action?
Source:
The nerves that innervate the G cells (thus it is a neurocrine hormone)
Action:
Stimulates gastrin release
Where does vasoactive intestinal peptide (VIP) come from and what is its action?
Source:
Neurons in the mucosa and smooth muscle of the GIT (thus it is a neurocrine hormone)
Action:
1) Relaxation of GI smooth muscle (specifically the lower esophageal sphincter)
2) Stimulates pancreatic HCO3- secretion
3) Inhibits gastric acid secretion (inhibits parietal cells)
Where does gastric inhibitory polypeptide (GIP, also known as glucose-dependent insulinotropic peptide) come from, what stimulates its release, and what is its action?
Source:
K cells of the duodenum
Stimulus:
Fatty acids, amino acids, and to a lesser extent carbohydrates in the SI
Action:
1) Stimulates insulin secretion (thus it is an incretin)
2) Inhibits gastric acid secretion (inhibits parietal cells)
Where does somatostatin come from, what stimulates its release, and what is its action?
Source:
D cells in the stomach, as well as other cells throughout the GIT
Stimulus:
Low pH in the SI
Action:
1) Inhibits release of all true GI hormones (gastrin, CCK, secretin, GIP)
2) Inhibits insulin and glucagon secretion
3) Inhibits pituitary secretion of GH
Where does glucagon-like peptide-1 (GLP-1) come from, what stimulates its release, and what is its action?
Source:
L cells of the ileum and colon
Stimulus:
Low pH in the SI
Action:
1) Stimulates insulin secretion (thus it is an incretin)
2) Inhibits gastric emptying
3) Inhibits gastric acid secretion (inhibits parietal cells)
Where does leptin come from, what stimulates its release, and what is its action?
Source:
Adipose cells, enterocytes
Stimulus:
Increased adipose tissue
Action:
1) Decrease appetite
2) Regulate fat intake
3) Decrease insulin secretion
4) Increase inflammation
Where does peptide YY come from, what stimulates its release, and what is its action?
Source:
Ileum, colon
Stimulus: Fatty acids (post-prandial)
Action:
1) Decrease gastric motility
2) Inhibit CCK and secretin
3) Proliferation of gut mucosa
4) Slow gastric emptying (the “ileal brake”)
Where does serotonin come from in the GIT, what stimulates its release, and what is its action?
Source:
ECL cells throughout the GIT
Stimulus:
Mechanical stimulation of mucosal cells (food moving through)
Action:
1) Stimulation of smooth muscle contraction in the intestine
2) Intestinal electrolyte secretion
What 2 nervous system plexi are in the GI?
Myenteric and submucosal
What is the main component of chylomicrons?
Triglycerides (TG)
Absorption of conjugated bile acids in the G.I.T?
Approximately 90% of conjugated BAs are actively reabsorbed in the ileum through the apical sodium‐dependent bile acid transporter (ASBT) and returned to the liver via the portal system
The ileum is considered the main site of BA uptake in many mammalian species
Where are folate and cobalamin absorbed in the intestines?
Folate is absorbed in the proximal G.I. and cobalamin is absorbed in the distal G.I. (ileum)
