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General Boards > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Biochemical findings in EPI: B12, folate, TLI, and PLI?

A

B12: Normal or low (worse prognosis if low)
Folate: Normal or elevated
TLI: Low
PLI: Normal or low

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2
Q

Biochemical findings in pancreatitis: B12, folate, TLI, and PLI?

A

B12: Normal
Folate: Normal
TLI: Normal or elevated
PLI: Elevated

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3
Q

Biochemical findings in antibiotic responsive diarrhea: B12, folate, TLI, and PLI?

A

B12: Low or normal
Folate: Normal or elevated
TLI: Normal
PLI: Normal

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4
Q

Biochemical findings in IBD: B12, folate, TLI, and PLI?

A

B12: Low (if distal S.I. malabsorption)
Folate: Low (if proximal S.I. malabsorption)
TLI: Normal
PLI: Normal

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5
Q

Treatment of Boxer granulomatous colitis?

A

Enrofloxacin

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6
Q

Ion exchanged for bicarbonate in intestines?

A

Chloride

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7
Q

Stimulus for acid secretion in stomach?

A

Acetylcholine (from PSNS), gastrin, histamine

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8
Q

Enzyme responsible for trypsinogen activation?

A

Enterokinase

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9
Q

Hormone stimulating appetite?

A

Ghrelin

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10
Q

Major inhibitor of trypsin in acute pancreatitis?

A

Trypsin inhibitor

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11
Q

Function of Enterochromaffin-like cells?

A

Secrete histamine to stimulate acid production (stimulated by gastrin)

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12
Q

How are proteins metabolized in the G.I.?

A

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

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13
Q

Where is gastrin produced and what is its function?

A

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

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14
Q

What is responsible for the conversion of pepsinogen to pepsin?

A

HCl

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15
Q

How does the peptide pump work in the G.I.?

A

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

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16
Q

What is the indication for misoprostol and how does it work?

A

PGE2 analog, enhances mucosal defense mechanisms and healing in response to acid-related injuries; use for G.I. ulceration secondary to NSAID’s

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17
Q

How does bradykinin effect the blood flow and secretory capacity of the G.I. system?

A

Causes vasodilation (Increased G.I. bloodflow) and increased secretions

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18
Q

Diagram the flow of bile

A

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

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19
Q

Where is lecithin found and what is it’s function?

A

Constituent of bile, combines with bile salts and cholesterol to form micelles, keeps cholesterol in solution in the bile

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20
Q

Cisapride MOA?

A

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.

21
Q

PLE test?

A

Panhypoprteinemia with normal UPC and bile acids; Alpha-1 protease inhibitor is also useful for confirmation of PLE

22
Q

How do NSAID’s cause G.I. ulceration?

A

Through inhibition of “friendly prostaglandins” such as PGE2, which serve gastroprotective functions in the G.I.

23
Q

Explain carbohydrate metabolism in the small intestine

A

Pancreatic alpha amylase breaks starch down into maltose, other glucose polymers. Enterocytes on brush border contain lactase, sucrase, maltase, and alpha-dextrinase into monosaccharides

24
Q

What is the protein responsible for iron transport in the small intestine?

A

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.

25
Q

Where is cholecystokinin made and what is its function?

A

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

26
Q

Main prosaglandin responsible for mucous secretion in stomach?

A

PGE2

27
Q

Where is secretin made and what is its function?

A

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

28
Q

Where is motilin made and what is its function?

A

Produced in the M cells of the duodenum, stimulates gastric and intestinal motility; released cyclically

29
Q

Function of the chief cells?

A

Secrete pepsinogen

30
Q

Function of the parietal cells?

A

Secrete HCl and intrinsic factor

31
Q

Function of intrinsic factor?

A

Essential for absorption of B12 (cobalamin) in the distal S.I. (ileum)

32
Q

MOA of erythromycin as a pro-motility agent?

A

At sub-antimicrobial dosages, mimics the effects of motilin and 5-HT3, ehances gastric motility and colonic motility (in dogs, not cats)

33
Q

What is the mechanism of action of metoclopramide?

A

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

34
Q

What is the mechanism of action of domperidone?

A

Antagonist of D2 (dopaminergic) receptors in the CRTZ (similar mechanism to metoclopramide)

35
Q

What is the mechanism of action of ranitidine (and similar drugs)?

A

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)

36
Q

What is the most common cause of EPI in dogs vs. cats?

A

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)
37
Q

Where does gastrin-releasing peptide (GRP, aka bombesin) come from and what is its action?

A

Source:
The nerves that innervate the G cells (thus it is a neurocrine hormone)

Action:
Stimulates gastrin release

38
Q

Where does vasoactive intestinal peptide (VIP) come from and what is its action?

A

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)

39
Q

Where does gastric inhibitory polypeptide (GIP, also known as glucose-dependent insulinotropic peptide) come from, what stimulates its release, and what is its action?

A

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)

40
Q

Where does somatostatin come from, what stimulates its release, and what is its action?

A

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

41
Q

Where does glucagon-like peptide-1 (GLP-1) come from, what stimulates its release, and what is its action?

A

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)

42
Q

Where does leptin come from, what stimulates its release, and what is its action?

A

Source:
Adipose cells, enterocytes

Stimulus:
Increased adipose tissue

Action:

1) Decrease appetite
2) Regulate fat intake
3) Decrease insulin secretion
4) Increase inflammation

43
Q

Where does peptide YY come from, what stimulates its release, and what is its action?

A

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”)

44
Q

Where does serotonin come from in the GIT, what stimulates its release, and what is its action?

A

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

45
Q

What 2 nervous system plexi are in the GI?

A

Myenteric and submucosal

46
Q

What is the main component of chylomicrons?

A

Triglycerides (TG)

47
Q

Absorption of conjugated bile acids in the G.I.T?

A

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

48
Q

Where are folate and cobalamin absorbed in the intestines?

A

Folate is absorbed in the proximal G.I. and cobalamin is absorbed in the distal G.I. (ileum)

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