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Pharm > GI Pharm > Flashcards

GI Pharm Flashcards

1
Q

What are the acid secreting cells within the stomach?

A

Parietal cells

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2
Q

What are the pepsin secreting cells within the stomach?

A

Chief cells

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3
Q

What are the two major “aggressive factors” that the stomach secretes?

A

Pepsinogen

HCl

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4
Q

What is the major “protective factor” that the stomach secretes?

A

bicarb

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5
Q

What are the transporters in parietal cells that secrete H+ ions?

A

H/K ATPase

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6
Q

What cells in the stomach secrete intrinsic factor? What is the role of intrinsic factor?

A

Parietal cells

Vitamin B12 absorption

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7
Q

What are the cells in the stomach that secrete mucus/bicarb?

A

Superficial epithelial cells

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8
Q

What are the cells in the stomach that secrete histamine?

A

ECL cells

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9
Q

What are the cells in the stomach that secrete gastrin?

A

G cells

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10
Q

What are the cells in the stomach that secrete ACh?

A

NErve cells

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11
Q

What is the role that ACh plays in the stomach?

A

Promotes mucus, bicarb, and HCl secretion

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12
Q

What are the cells in the stomach that serete somatostatin? What is the role of somatostatin?

A

D cells

Suppressses HCl secretion

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13
Q

What is the role of gastrin?

A

Increases HCl output from parietal cells

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14
Q

What is the effect of PGE2 in the stomach?

A

Decreases the output of H/K ATPases

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15
Q

What is the neuronal input to gatric acid secretion? Does this facilitate or impair secretion?

A

ACh

Facilitates

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16
Q

What is the paracrine input to gatric acid secretion? Does this facilitate or impair secretion?

A

Histamine

Facilitates

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17
Q

What is the endocrine input to gatric acid secretion? Does this facilitate or impair secretion?

A

Gastrin

Facilitates

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18
Q

What is the role of pepsinogen?

A

Protein digestion

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19
Q

What do enterochromaffin cells secrete?

A

Histamine

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20
Q

Besides their direct effect on parietal cells, how else do ACh and gastrin increase HCl secretion?

A

Induce histamine release

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21
Q

What are the two substances that increase protective factor secretion?

A

ACh

Prostaglandins

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22
Q

Do prostraglandin exert their effects on gastric cells via that endocrine, or paracrine pathway

A

Paracrine

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23
Q

What are the three major effects of prostagladins?

A
  1. Increase mucus/bicarb
  2. Suppress HCl
  3. Increase gastric blood flow
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24
Q

What are peptic ulcers?

A

Break i nthe protective mucosal lining of the lower esophagus, stomach, or duodenum

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25
Q

What are duodenal ulcers?

A

Ulcers of the duodenum

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26
Q

Which occur more frequently: peptic, duodenal, or gatric ulcers?

A

Duodenal

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27
Q

What are gastric ulcers?

A

Ulcers of the stomach

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28
Q

What is a cushing ulcer?

A

Stress ulcers associated with head trauma of brain surgery

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29
Q

What are ischemic ulcers?

A

Ulcers caused by hemorrhage, severe burns

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30
Q

What are the two most common causes of ulcers in the US?

A

NSAIDs

H. Pylori infx

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31
Q

True or false: rapid gastric empyting may cause ulcers?

A

True

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32
Q

ASA inhibits what enzyme?

33
Q

True or false: melena or BRBPR are symptoms of an ulcer

34
Q

The goal of antacids is to raise the pH of the stomach above what level?

35
Q

What are the two MOA of antacids?

A

neutralize acid

Stimulate prostaglandin secretion

36
Q

What is the duration of action for the simple antacids?

37
Q

What is the specific, adverse effect of using NaHCO3? (3)

A

metabolic alkalosis
Excessive NaCl absorption
Gas/bloating

38
Q

What is the specific adverse effect of using CaCO3?

A

acid rebound

gas/bloating

39
Q

What is the specific, adverse effect of using Mg(OH)2?

A

Osmotic diarrhea

Hypermagnesemia

40
Q

What is the specific, adverse effect of using Al(OH)2?

A

Constipation

41
Q

What is the major drawback of using simple antacids for treating ulcers?

A

Have to dose often

42
Q

What is the acid rebound effect of CaCO3?

A

Increase the output of acid when neutralized

43
Q

What disease increases the liklihood of having hypermagnesemia, hypercalcemia etc when taking simple antacids?

A

Renal insufficiency

44
Q

True or false: simple antacids are usually used in combination with other therapies

45
Q

True or false: simple antacids are equally efficacious as H2 receptor antagonists

46
Q

What is the GERD heal rate of simple antacids?

47
Q

What is the peptic ulcer rate heal rate of simple antacids?

48
Q

Milk of magnesia is what chemcial?

49
Q

Alka-seltzer is what chemial?

50
Q

Histamine receptors use what type of receptor (Na gates or G protein)?

A

G protein coupled

51
Q

Histamine inhibition of H2 receptors in competitive, or non-competitive?

A

Competitive

52
Q

What don’t H2 receptor antagonists decrease acid secretion by 100%?

A

Only affect the direct pathway; ACh and gastrin can still increase hitsmine secretion

53
Q

What are the H2 receptor antagonists suffix?

54
Q

What type of drug is cimetidine?

A

H2 receptor antagonist

55
Q

What type of drug is ranitidine?

A

H2 receptor antagonist

56
Q

What type of drug is nizatidine?

A

H2 receptor antagonist

57
Q

What type of drug is famotidine?

A

H2 receptor antagonist

58
Q

What is the most common effect of H2 receptor antagonists?

59
Q

What are the uncommon, but severe effects that H2 receptor antagonists cause?

A

CNS effects (hallucination, agitation etc)

Endocrine distruption

60
Q

How long do H2 receptors antagonists last?

61
Q

Which H2 receptor antagonist specifically has higher chances of adverse effects?

A

Cimetidine (tagemet)

62
Q

True or false: H2 receptor antagonists work directly in the stomach to antagonize H2 receptors?

A

False–have to absorb through the GI tract first. Too difficult to act in the stomach w/ mucus and all that

63
Q

What is the MOA of PPIs?

A

Inhibition of the K/H ATPase

64
Q

What activates PPIs?

65
Q

PPIs reversibly, or irreversibly bind the proton pumps?

A

Irreversibly

66
Q

What is the suffix that denotes a PPI?

67
Q

What type of drug is omeprazole?

68
Q

What type of drug is Lansoprazole?

69
Q

What type of drug is Rabeazole?

70
Q

What type of drug is Esomeprazole?

71
Q

What type of drug is Pantoprazole?

72
Q

What is the duration of action for PPIs?

A

24 hours, but 3-4 days to reach maximum effect

73
Q

What is the major concern with using PPIs?

A

B12 deficiency

74
Q

Why does it take 3-4 days for PPI to take maximal effect?

A

Vesicular network of stored proton pumps has to be depleted

75
Q

What is the GERD heal rate, and puptic ulcer heal rate of PPIs?

76
Q

What is the MOA of sucralfate?

A

Adheres to ulcer and creates a physical barrier

Stimulates mucus secretion

77
Q

What is the chemical in sucralfate?

A

sucrose + octasulfate + Al(OH)3

78
Q

What is the active ingredient in peptobismol?

A

Bismuth subsalicylate

79
Q

What is the MOA of bismuth (peptobismol)?

A

Adheres fo ulcer and creates a physical barrier

Stimulates mucus secretion

Pharm (73 decks)

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