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BMS150 Post-MT2 > GI Pharmacology - Acid Suppressors and Anti-Nausea Agents > Flashcards

GI Pharmacology - Acid Suppressors and Anti-Nausea Agents Flashcards

1
Q

Gastrin receptor?

A
  • CKK-receptor
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2
Q

Acetylcholine receptor?

A
  • M3-receptor (muscarinic)
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3
Q

Histamine receptor?

A
  • H2- receptor
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4
Q

Prostaglandin receptor?

A
  • PGE-receptor
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5
Q

Stimulatory G-protein signalling?

A

Gastrin, Ach, Histamine

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6
Q

Inhibitory G-protein signalling?

A

Prostaglandin

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7
Q

H2-Blocker mechanism of action?

A

Competitive block of H2-R on parietal cells

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8
Q

Common H2-Blockers? (3)

A
  • Cimetidine
  • Ranitidine
  • Famotidine
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9
Q

Therapeutic uses of H2-Blockers? (3)

A
  • Ulcers
  • Management of Zollinger-Ellison syndrome (?)
  • GERD
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10
Q

What type of infection are H2-blockers often associated with?

A

H. pylori

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11
Q

Mechanism of action of anticholinergics?

A

Block M3-receptors on parietal cells

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12
Q

What NT normally acts on M3 receptors? Which nerve releases this NT at the level of the viscera?

A

Acetylcholine - Vagus nerve

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13
Q

Therapeutic uses of anticholinergics?

A

Ulcers

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14
Q

PPI mechanism of action?

A

H+, K+-ATPase inhibition

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15
Q

Specific PPI medications?

A
  • Omeprazole
  • Esomeprazole
  • Pantoprazole
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16
Q

Therapeutic uses of PPIs?

A
  • Ulcers
  • GERD
  • Management of Zollinger-Ellison syndrome
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17
Q

Which do you think would be more effective to manage Zollinger-Ellison syndrome, H2-blockers or PPI’s? Why?

A

Better with PPI, as inhibits HCl from all stimulatory routes (gastrin, ACH, histamine) and not just via H2 receptors

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18
Q

What are prostaglandins considered?

A

Eicosanoids

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19
Q

What are the two structural categories of lipids?

A
  • Triglycerides and phospholipids
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20
Q

What specific lipids are most eicosanoids derived from?

A

Arachodonic acid

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21
Q

Mechanism of action of PGE1 analogues? (2)

A
  1. Decreased proton pump activity
  2. Increased bicarbonate and mucous secretion
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22
Q

PGE1 medication analogue?

A

Misoprostal

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23
Q

Therapeutic use of PGE1 analogues?

A

Most common = prevention of NSAID-induced ulcer/GI bleed

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24
Q

What is the connection between NSAIDs and PGs including the enzymes involved?

A

NSAIDs block COX, which blocks production of PG’s

25
Q

Why is Misoprostol contraindicated in pregnancy?

A

Causes uterine contractions

26
Q

Agents that decrease motility?

A
  • Diphenoxylate-atropine (Lomotil)
  • Loperamide (Imodium)
27
Q

Agents that increase motility?

A
  • Laxatives
  • Metoclopramide (Maxeran, Reglan)
  • Domperidone (Motilium)
28
Q

Diphenoxylate-atropine mechanism of action - DIPHENOXYLATE?

A
  • Opioid receptor agonist
  • Inhibits ACH release in enteric system at low doses
29
Q

What does Ach usually do for gut motility?

A

Increases gut motility

30
Q

Diphenoxylate-atropine
mechanism of action - ATROPINE?

A

M-blocker = Synergistic effects with diphenoxylate to decrease Ach effects on the gut

31
Q

What are the side effects of anticholinergics? What does this cause?

A

Dry mouth - low abuse potential

32
Q

Anticholinergic side effects occur before _______ effects are felt?

A

Euphoric opioid

33
Q

Drug similar to diphenoxylate-atropine, but without the atropine?

A

Loperamide

34
Q

Why does Loperamide lack CNS effects - therefore having an extremely low abuse potential?

A

Does not cross BBB

35
Q

Laxative mechanisms? (4)

A
  • Bulking agents
  • Osmotic laxatives
  • Chemical stimulants
  • Stool softeners
36
Q

Examples of Bulking laxatives?

A

Bran, psyllium

37
Q

Non-absorbed agents that create bulkier stools and draw water into stools?

A

Bulking laxatives

38
Q

Examples of Osmotic laxatives?

A

Mg sulfate, Mg hydroxide, lactulose

39
Q

Osmotic laxatives are not well-absorbed from the intestinal tract, what does this cause?

A

Increase in osmotic pressure leading to retention of water in intestine, lumen extension, and increased bowel action

40
Q

What can low dose of Mg hydroxide do?

A

Can neutralize stomach acid

41
Q

What is lactulose?

A

Disaccharide that is not broken down well in the SI
=> Reaches colon, broken down by bacteria to produce lactic acid

42
Q

Will lactulose increase or decrease excretion of ammonia? Why?

A

Increase => charged so less likely to be reabsorbed and therefore more likely to be excreted

43
Q

Examples of chemical stimulant laxatives?

A

Emodin (active ingredient in senna, aloe, cascara)

44
Q

What is the mechanism of action of chemical stimulants?

A

Irritate the gut to induce peristalsis and increase mucous production

45
Q

Examples of stool softeners?

A

Mineral oil, sodium docusate

46
Q

What do stool softeners use?

A

Water or oil to soften stool

47
Q

What does mineral oil do?

A

Lubricates stools for easier passage

48
Q

What does sodium docusate do?

A

Detergent that allows water to penetrate stools = prevents hard, dry stools and allows for easier passage

49
Q

Metoclopramide mechanism of action for increased motility?

A

Block of peripheral D-receptors (dopamine is inhibitory to GIT)

50
Q

What does blocking dopamine result in?

A

Allows Ach effects to predominate:
- Increased peristalsis
- Increased tone of LES

51
Q

Metoclopramide mechanism of action for anti-nausea/vomiting?

A

Antiemetic action comes from block of D2-receptors in medulla (trigger zone from vomiting)

52
Q

Therapeutic uses of Metaclopramide for nausea and vomiting?

A
  • GERD
  • Diabetic gastric stasis
  • Nausea and vomiting with chemo
53
Q

What happens when you take the peripheral effects of Metoclopramide too far?

A

Diarrhea

54
Q

Blocking dopamine causes increased prolactin, which can cause?

A

Hyperprolactinemia

55
Q

What is similar to metoclopramide, but less likely to cross BBB or into breast milk?

A

Domperidome

56
Q

How can domperidone stimulate milk production in lactating mothers?

A

Increased prolactin

57
Q

How do anticholinergics have anti-nausea effects?

A

Block cholinergic transmissions between vestibular and vomiting centers in the CNS

58
Q

Specific anticholinergic anti-nausea agents?

A
  • Scopolamine (M-receptor)
  • Promethazine (M-blocker and H1-blocker)

BMS150 Post-MT2 (17 decks)

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