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GI - Week 1 > Peptic ulcers & H. pylori > Flashcards

Peptic ulcers & H. pylori Flashcards

1
Q

a disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation

A

Peptic ulcer

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2
Q

These three compounds are GPCRs associated with stimulation of gastric acid production

A

Histamine
Acetylcholine
Gastrin

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3
Q

These 2 compounds are GPCRs that inhibit gastric acid production

A

Somatostatin
Prostaglandins

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4
Q

Prostaglandins and somatostatin inhibit this pathway, which is usually activated by the stimulation of the histamine H2 receptors

A

Adenylate cyclase

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5
Q

Prostaglandins and somatostatin inhibit the adenylate cyclase pathway, which is usually activated by the stimulation of these receptors

A

Histamine H2

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6
Q

The primary mechanism by which the gastric mucosa is protected from the acidic luminal environment is the production of this by the surface mucous cells

A

Mucus-bicarbonate gel layer

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7
Q

During the formation of ulcers, the gastric mucosal barrier is broken, and these two compounds begin to erode the mucosa

A

HCl and Pepsin

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8
Q

This stimulates the release of histamine from cells in the submucosa

A

Acid

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9
Q

What forms a bleeding ulcer?

A

Acid and pepsin gain access to vasculature at the basolateral side of the damaged region

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10
Q

The MOA of these drugs are simple neutralization of gastric acid
Cytoprotective action on gastric mucosa mediated by endogenous prostaglandin release

A

Antacids

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11
Q

Antacids have cytoprotective action on gastric mucosa mediated by endogenous release of this

A

Prostaglandin

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12
Q

Formulations of these drugs for peptic ulcer disease are metal-based salts, such as aluminum, calcium, magnesium, sodium

A

Antacids

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13
Q

This type of drug for peptic ulcer disease interacts with drugs that chelate metals, and drugs dependent on acid for dissolution, absorption, and excretion

A

Antacids

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14
Q

Combination of these drugs with calcium antacids can lead to hypercalcemia

A

Thiazide diuretics

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15
Q

Thiazide diuretics combined with this type of drug for peptic ulcer disease, can lead to hypercalcemia

A

Calcium antacids

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16
Q

Thiazide Diuretics combined with calcium antacids can lead to this

A

Hypercalcemia

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17
Q

Antacid formulations with magnesium salts particularly have this adverse reaction

A

Diarrhea

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18
Q

Antacid formulations with calcium and aluminum particularly have this adverse reaction

A

Constipation

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19
Q

Patients with renal insufficiency may experience a prolonged hypercalcemia from continuous use of this type of drug for peptic ulcers

A

Calcium-based antacids

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20
Q

Patients with renal insufficiency may experience prolongation of this adverse reaction from continuous use of calcium-based antacids

A

Hypercalcemia

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21
Q

Patients with this condition may experience a prolonged hypercalcemia from continuous use of calcium-based antacids

A

Renal insufficiency

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22
Q

This type of drug for peptic ulcers remove potentiation, resulting in attenuation of acetylcholine and gastrin too
However, they do not abolish the effects of acetylcholine and gastrin

A

H2 receptor antagonists

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23
Q

Do H2 receptor antagonists remove potentiation, resulting in attenuation of acetylcholine and gastrin?

A

Yes

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24
Q

Do H2 receptor antagonists abolish the effects of acetylcholine and gastrin?

A

No

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25
Q

Cimetidine is this type of drug

A

H2 receptor antagonists

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26
Q

Ranitidine is this type of drug

A

H2 receptor antagonists

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27
Q

Famotidine is this type of drug

A

H2 receptor antagonists

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28
Q

Are H2 receptor antagonists effective in NSAID-induced ulcers?

A

No

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29
Q

This type of drug for peptic ulcers is limited by tolerance, and only therapeutically beneficial for 2-3 weeks

A

H2 receptor antagonists

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30
Q

This H2 receptor antagonist has more relative adverse reactions and drug interactions than others, on a “per use” basis

A

Cimetidine

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31
Q

These two H2 receptor antagonists are being removed due to the presence of N-nitrosodimethylamine (NMDA)

A

Ranitidine and Nizatidine

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32
Q

Ranitidine and Nizatidine are H2 receptor antagonists being removed due to the presence of this compound

A

N-nitrosodimethylamine (NMDA)

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33
Q

This is the primary elimination process for H2 receptor antagonists

A

Renal excretion
(Biotransformation by cytochrome P450 is secondary)

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34
Q

Confusion and hallucinations occur especially in elderly with this type of drug for peptic ulcers
Other toxicities include seizures, QT prolongation, cardiac conditions, bone marrow depression

A

H2 receptor antagonists

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35
Q

These are the preferred drugs for the treatment of acid hypersecretion disorders

A

Proton pump inhibitors (PPIs)

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36
Q

Proton pump inhibitors (PPIs) irreversibly block this, which is located on the apical side of the parietal cell

A

H+/K+ - ATPase (the proton pump)

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37
Q

This type of drug for peptic ulcers blocks both basal as well as stimulated gastric acid secretion carried out by histamine, acetylcholine, and gastrin

A

Proton pump inhibitors (PPIs)

38
Q

Omeprazole is this type of drug

A

Proton pump inhibitors (PPIs)

39
Q

Are Proton pump inhibitors (PPIs) effective in preventing NSAID-related ulcers?

40
Q

This type of drug for peptic ulcers is considered superior to H2 receptor antagonists in the treatment of moderate to severe GERD

A

Proton pump inhibitors (PPIs)

41
Q

Proton pump inhibitors (PPIs) are extensively metabolized by this

A

Cytochrome p450 (in liver)

42
Q

The half life of Proton pump inhibitors (PPIs) is less than this

A

8 hours
(but the duration of proton pump inhibition is significantly longer)

43
Q

This type of drug for peptic ulcers is provided in enteric-coated granules to protect from acid

A

Proton pump inhibitors (PPIs)

44
Q

This type of drug for peptic ulcers delays elimination of drugs metabolized by mixed function oxidases
(warfarin, diazepam, phenytoin)

A

Proton pump inhibitors (PPIs)

45
Q

This type of drug for peptic ulcers has increased risk of fractures of hip, wrist, and spine
Possibly related to disruption of calcium and magnesium absorption

A

Proton pump inhibitors (PPIs)

46
Q

This type of drug for peptic ulcers has possible increased risk of C. diff colitis

A

Proton pump inhibitors (PPIs)

47
Q

Omeprazole reduces the efficacy of the anti-clotting agent clopidogrel (Plavix) since both are extensively metabolized by this

A

Cytochrome p450 2C19

48
Q

This PPI reduces the efficacy of the anti-clotting agent clopidogrel (Plavix) since both are extensively metabolized by the cytochrome p450 2c19

A

Omeprazole

49
Q

Omeprazole reduces the efficacy of this anti-clotting agent since both are extensively metabolized by the cytochrome p450 2c19

A

Clopidogrel (Plavix)

50
Q

Hypomagnesia can be an adverse effect of this type of drug for peptic ulcers, and can be severe

A

Proton pump inhibitors (PPIs)

51
Q

This type of drug for peptic ulcers has been linked to an increased risk of hospital-acquired pneumonia

A

Proton pump inhibitors (PPIs)

52
Q

This drug for peptic ulcers is a stable analog of prostaglandin E1

A

Misoprostol

53
Q

Misoprostol is a stable analog of this

A

Prostaglandin E1

54
Q

This drug for peptic ulcers has potent antisecretory and cytoprotective effects

A

Misoprostol

55
Q

This drug for ulcers is able to directly inhibit gastric acid secretion by parietal cells, through inhibition of the adenylate cyclase pathway

A

Misoprostol

56
Q

Misoprostol is able to directly inhibit gastric acid secretion by parietal cells through inhibition of this pathway

A

Adenylate cyclase

57
Q

Misoprostol is cytoprotective, as it increases the secretion of these two compounds

A

Mucus, Bicarbonate

58
Q

This drug opposes many of the ulcerogenic actions of NSAIDs, which reduces prostaglandin production

A

Misoprostol

59
Q

Is Misoprostol or H2 receptor antagonists better for preventing NSAID-caused ulcers?

A

Misoprostol

60
Q

Excessive GI toxicity limits use of this drug for peptic ulcers

A

Misoprostol
(PPIs are better tolerated in this indication)

61
Q

This drug for peptic ulcers can cause uterine contractions, and can induce complete or incomplete abortion during the first trimester

A

Misoprostol

62
Q

Is Misoprostol safe in pregnancy?

A

NO
Can cause uterine contractions, and induces complete or incomplete abortion during the first trimester

63
Q

This drug for peptic ulcers leads to increased intestinal mucosal secretion, increased motility, decreased transit time and reduced absorption

A

Misoprostol

64
Q

This drug for peptic ulcers is a basic aluminum salt of sucrose octasulfate
In acid, it forms a viscous, sticky gel that adheres to epithelial cells and very strongly to ulcer craters
Bind and sequester pepsin and bile salts
Stimulates local growth factors
Antibacterial (but not against H. pylori)

A

Sucralfate

65
Q

What is the main MOA of Sucralfate in ulcers?

A

In acid, it forms a viscous, sticky gel that adheres to epithelial cells and ulcer craters

66
Q

Does Sucralfate have antibacterial action?

A

Yes - but not against H. pylori

67
Q

This drug for peptic ulcers has no significant absorption from the GI tract, and continues the healing process, even in smokers

A

Sucralfate

68
Q

Does Sucralfate have significant absorption from the GI tract?

69
Q

Does Sucralfate continue the healing process, even in patients who smoke?

70
Q

Sucralfate contains this metal

A

Aluminum
(use with caution in renal impaired patients)

71
Q

This drug for peptic ulcers interferes the absorption of a variety of agents, including tetracycline, phenytoin, quinidine, theophylline, digoxin, fluoroquinolones

A

Sucralfate

72
Q

Is Helicobacter pylori gram positive or negative?

73
Q

What is the shape of Helicobacter pylori?

A

Curved rod

74
Q

Does Helicobacter pylori have a flagella?

A

Yes
Has a polar flagella, enabling them to move

75
Q

Is Helicobacter pylori urease positive?

76
Q

Is Helicobacter pylori catalase positive?

77
Q

Is Helicobacter pylori oxidase positive?

78
Q

Helicobacter pylori is a frequently asymptomatic inhabitant of this organ

79
Q

This is the route of transmission for Helicobacter pylori

A

Fecal-oral

80
Q

This is the most important virulence factor for Helicobacter pylori
Neutralizes gastric acid
Causes gastric mucosal injury (by ammonia)

81
Q

Does Helicobacter pylori colonize the intestinal epithelium?

82
Q

Helicobacter pylori appears as bluish flecks on this stain

A

Warthin-Starry

83
Q

This laboratory test for diagnosis of Helicobacter pylori only shows eposure

A

Blood antibody test

84
Q

This is the most useful diagnostic tool for Helicobacter pylori, which is very sensitive and specific

A

Stool antigen (using ELISA)

85
Q

Is culture useful for diagnosing Helicobacter pylori?

86
Q

This is the first line treatment for Helicobacter pylori

A

Optimized bismuth quadruple therapy
1. PPI
2. Bismuth
3. Tetracycline
4. Metronidazole

87
Q

Quadruple therapy for Helicobacter pylori includes these 4 drugs

A

PPI
Bismuth
Tetracycline
Metronidazole

88
Q

This drug is a potassium competitive acid blocker (PCAB)

A

Vonoprazan

89
Q

Vonoprazan is a competitive acid blocker of this ion

90
Q

These three drugs comprise Pylera

A

Bismuth
Tetracycline
Metronidazole

GI - Week 1 (11 decks)

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