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GI > PHARM: PUD and GI Disorders > Flashcards

PHARM: PUD and GI Disorders Flashcards

1
Q

What is the role of surface epithelial cells in the stomach?

A

protection: make mucous and bicarbonate

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2
Q

What is the role of parietal cells in the stomach?

A

secrete HCl to bring the pH of hte stomach to below 1 (needed to convert pepsinogen to pepsin)

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3
Q

What are the most powerful stimulators of the neurotransmitters that stimulate parietal cells?

A

Vagus Nerve
Food
Protein

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4
Q

The vagus nerve releases _____ to stimulate _____ to make _____ which stimulates the parietal cells to release HCl.

A

The vagus nerve releases ACETYLCHOLINE to stimulate G CELLS to make GASTRIN which stimulates the parietal cells to release HCl

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5
Q

Other than G Cells, which cells are stimulated by the vagus nerve?

A

ECL cells (release histamine to also regulate HCl secretion by parietal cells)

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6
Q

What type of parietal cell receptors do gastrin and Ach act on?

A

Gq receptors

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7
Q

What type of parietal cell receptors does Histamine act on?

A

Gs receptors

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8
Q

What type of parietal cell receptors do somatostatins and prostaglandins act on?

A

Gi receptors

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9
Q

What do both Gq and Gs receptors cause?

A

drive the H+/K+ ATPase and send H+ out into lumen

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10
Q

What condition is cause by normal or reduced gastric acid output with altered mucosal resistance (or low bicarbonate) leading to damage?

A

Gastric ulcers

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11
Q

What condition is caused by high gastric acid output (especially at night) with inadequate duodenal bicarbonate secretion and insufficient acid neutralization?

A

Duodenal ulcers

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12
Q

What condition is caused by insufficient constriction of the esophageal sphincter, resulting in exposure of esophagus to gastric acids?

A

GERD

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13
Q

List the 3 drugs that work to increase protective mechanisms of the stomach.

A

Bismuth Subsalicylate
Sucralfate
Misoprostol

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14
Q

What is Bismuth Subsalicylate?

A

Pepto Bismol

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15
Q

MOA: stimulates mucus and HCO3- production (at super-therapeutic doses)

A

Misoprostol

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16
Q

MOA: enhances secretion of mucus and HCO3-, weakly inhibits pepsin activity, chelates with proteins at the base of the ulcer crater and forms protective barrier against acid and pepsin, and inhibits H. Pylori

A

Bismuth Subsalicylate

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17
Q

MOA: forms sticky, viscous gel that adheres to gastric epithelial cells protecting them from acid and pepsin

A

Sucralfate

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18
Q

Which cytoprotective agent requires an acidic pH to act?

A

Sucralfate

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19
Q

Which cytoprotective agent is an analog of PGE1?

A

Misoprostol

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20
Q

Which cytoprotective agent is used in PPI induced pneumonia and PUD?

A

sucralfate

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21
Q

Which cytoprotective agent is rarely used, and only really used in patients who must use NSAIDs?

A

Misoprostol

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22
Q

Which cytoprotective agent gives intolerable diarrhea in 40% of patients?

A

Misoprostol

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23
Q

Which macrolide is used to eradicate H. Pylori?

A

Clarithromycin

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24
Q

Which beta-lactam is used to eradicate H. pylori?

A

Amoxicillin

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25
Q

Which antibiotic is used to eradicate H. pylori in patients with allergies to penicillin?

A

tetracycline

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26
Q

Which antibiotic has high likelihood of resistance so is ALWAYS used in combinations?

A

metronidazole

27
Q

What type of bugs does metronidazole selectively kill?

A

obligate anaerobes

28
Q

What is the name of the Nitrofuran antibacterial and antiprotozoal used to kill H. pylori?

A

furazolidine

29
Q

What is tritec? Why is it not commonly used anymore?

A

Ranitidine, Bismuth and Clarithromycin

H2 blockers are not as effective as PPIs in triple therapy

30
Q

What is Helidac?

A

Pepto-Bismol, metronidazole, tetracycline

31
Q

What is the quadruple regimen used in quadruple therapy for H. pylori eradication?

A

omeprazole, Pepto-Bismol, clarithromycin, metrondiazole

32
Q

When do patients with GERD regurgitate food?

A

night (when stomach is full)

33
Q

What are the 2 things that must occur to lead to a reflux episode?

A
  • GI contents must be ready to reflux

* Anti-reflux mechanism at LES is compromised

34
Q

True or false: Peptic Ulcer Disease is typically NOT caused by NSAIDs or hyperacidity/stress

A

TRUE

35
Q

What is implicated as the underlying cause of 92% of duodenal ulcers and 70% of gastric ulcers?

A

H. pylori infection

36
Q

How do you diagnose H. pylori infection?

A

blood antibody or urea breath tests.

37
Q

MOA: neutralize gastric acid in the stomach (NaHCO3 + HCl → NaCl + CO2 +H2O)

A

Antacids

38
Q

MOA: Bind to and block H2 receptor stimulation by histamine (competitive antagonists)

A

H2 blockers

39
Q

MOA: delivered to parietal cells to diffuse into the secretory canaliculi where it gets trapped by the proton pump due to acidic pH (and becomes protonated) and irreversibly inhibits the H+ ion pump

A

PPIs

40
Q

Why are antacids not used as sole therapy for things like PUD?

A

CANNOT prevent transformation of pepsinogen to pepsin (would need pH >4)

41
Q

When do H2 blockers work best?

A

inhibit mostly basal and nocturnal gastric secretion (volume and H+ concentration)

42
Q

Can pepsin be formed with H2 blocker therapy?

A

YES, only slight change in pH occurs

43
Q

What are the indications for H2 blockers?

A
  • Rarely used for PUD
  • Used for mild symptoms of GERD
  • Prevent stress-related upper GI bleeds in seriously ill patients (rarely)
44
Q

What is unique about PPIs pharmacokinetics?

A

Have enteric coating that releases drug into intestine (absorbed into blood where it can return and SPECIFICALLY inhibit parietal cells)

45
Q

List the 2 types of non-systemic antacids.

A

Aluminum Hydroxides

Magnesium Hydroxides

46
Q

List the types of systemic antacids.

A

Calcium or Sodium Bicarbonate

47
Q

List the antiflatulant used to decrease gas tension.

A

Simethicon

48
Q

What is the most potent H2 antagonist.

A

Famotidine

49
Q

What is the least potent H2 antagonist.

A

Cimetidine

50
Q

What is the PPI with the least CYP450 metabolism?

A

Rabeprazole

51
Q

What antacid gives constipation?

A

aluminum hydroxides

52
Q

What antacid gives diarrhea?

A

Magnesium hydroxides

53
Q

What antacids can lead to acid reflux and fluid retention?

A

calicum or sodium bicarbonate

54
Q

What must you be mindful of when taking antacids?

A

do NOT take these within 1-2 hours of other drugs (significantly alters absorption)

55
Q

Which antacid class is for SHORT TERM USE ONLY?

A

systemic (calcium or sodium bicarbonate)

56
Q

When should you take antacids?

A

1hr and 3hr after a meal and at bedtime

57
Q

List some examples of behavioral therapies for GERD.

A
  • Decrease gastric contents (decrease meal size, no food after 7pm)
  • Weight reduction (stops abdomen from pushing on stomach)
  • Head of bed elevation (food not pushed up against esophagus in supine position)
  • Avoid agents that decrease LES tone: fat, coffee, peppermint
58
Q

What is the role of prokinetics in GERD treatment?

A

increase gastric motility (improve LES tone and competence to enhance esophageal clearance and improve gastric emptying)

59
Q

List the prokinetics.

A

Metoclopramide
Domperidone
Cisapride (not in US unless special permission)

60
Q

MOA: Dopaminergic neuron secretes dopamine to inhibit firing of post-synaptic motor neurons and prevent Ach release from causing constriction of SM in LES

A

Metoclopramide and Domperidone

61
Q

MOA: NANC targeted by 5-HT4 (positive regulator, releases Ach on post-synaptic motor neuron to cause contraction of SM in LES)

A

Cisapride

62
Q

What is the major difference between Metoclopramide/Domperidone MOA and Cisapride MOA?

A

Metoclopramide/Domperidone constrict LES and increase gastric emptying while Cisapride only works to contract LES

63
Q

What is the major adverse effect seen with Metoclopramide?

A

tardive dyskinesia (only give drug 1-2 weeks at a time, because if you get this, it is IRREVERSIBLE)

GI (21 decks)

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