Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

digestion and metabolism - Wk 3 > gastric pharmacology > Flashcards

gastric pharmacology Flashcards

1
Q

what are the 4 types of medications used in the treatment of gastric ulcers and gastroesophageal reflux disease

A
  1. chemical diffusion barriers
  2. histamine receptor antagonists
  3. H+, K+ ATPase antagonists (proton pump inhibitors)
  4. promotility drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is an example of a chemical diffusion barrier drug

A

sucralfate (sucramal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does sucralfate dissociate into

A

sucrose octasulfate and aluminum hydroxide in acid of the sotmach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does sucrose octasulfate do

A

polymerizes forming a paste that binds to damaged gastric epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the mechanism of action of sucralfate

A

forms a physical barrier against stomach acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is an example of a histamine receptor antagonist

A

famotidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what happens when histamine is released from ECL cells

A

stimulates H2 receptors on the parietal cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is an H2 receptor

histamine receptor

A

located on parietal cells and regulates histamine-mediated gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is famotidine (pepcid)

A
  • 3rd generation H2-selective antagonist
  • has poor bioavailability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are examples of H+, K+ ATPase antagonists

A

omeprazole, pantoprazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does H+, K+ ATPase (proton pump) secrete

A

H+ into lumen of the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is omeprazole (prilosec) supplied as

A

enteric-coated capsule/tablet to survive the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

where is omeprazole (prilosec) absorbed

A

in alkaline pH of duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how does omeprazole (prilosec) inactivate the pump

A

protonated form of the drug “covalently” and “irreversibly” binds to and inactivates the pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why is it ok that omeprazole has a short half life

A

efficacy last longer than predicted from the plasma drug concentration (activoty despite no plasma conc)

b/c its irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is pantoprazole

A
  • compound is a weak base like omeprazole
  • supplied as a delayed-release tablet and delayed-release granules to survive the stomach

also covalent inhibitor

17
Q

what are examples of promotility drugs

A
  • cisapride
  • metoclopramide
  • erythromycin
  • nizatidine
18
Q

what does a promotility/prokinetic drug do

A
  • helps control acid reflux by strengthening the lower esophageal sphincter
  • decreases stomach emptying time allowing less time for reflux to occur
  • stimulates smooth muscle contraction of stomach to speed emptying allowing less time for reflux to occur
19
Q

what is cisapride (propulsid)

A
  • 5HT4 receptor agonist that directly stimulates gastric motility
  • increases the release of ACh at nerve endings in the myenteric plexus controlling gut motility in the ENS
20
Q

what is metaclopromide (reglan)

A
  • D2 antagonist activity
  • results in increased LES and stomach tone
  • results in increased nerve terminal ACh release and therefore increased ACh-mediated gastric motility
21
Q

what do erythromycin and azithromycin do

A
  • antibiotics are weak agonists for motilin receptor (GPCR) (serendipity)
  • motilin binding to the motilin receptor on enteric neurons stimulates gastric motility
22
Q

what do ranitidine and nizatidine do

A
  • H2 antagonists that inhibit histamine-mediated gastric acid secretion
  • weak inhibitors of the enzyme acetylcholinesterase
  • blockade of acetylcholinesterase (ACh’ase) results in increased ACh at synapses increasing gastric motility
23
Q

where is emesis coordinated

A

in the “emetic center” in the lateral reticular formation in the medulla oblongata

24
Q

what are the 4 control centers of emesis

A
  1. chemotrigger zone (CRTZ)
  2. vestibular system (ear)
  3. peripheral sensory/irritant receptors (stomach, intestine)
  4. higher CNS centers
25
Q

what are the 4 types of drugs that control emesis

A
  1. alpha-2 adrenergic antagonists
  2. dopamine antagonists
  3. 5-HT3 serotonin antagonists
  4. neurokinin-1 antagonists
26
Q

what is an example of an alpha-2 adrenergic antagonists drug

A

chlorpromazine

27
Q

what is chlorpromazine and what does it do

A
  • alpha-2 adrenergic antagonism
  • blocks vomiting reflex at emetic center and CRTZ
28
Q

what is an example of a dopamine antagonist drug

A

metaclopramide

29
Q

what is metoclopramide

A

anti-emetic action due to blockade of D2 dopamine receptors in the CRTZ

30
Q

what is an example of a 5-HT3 serotonin antagonist drug

A

ondansteron

31
Q

what is ondansteron

A

anti-emetic action dur to blockade of 5-HT3 serotonin receptors in the CRTZ and in the GI tract

does not relieve nausea

32
Q

what is an example of a neurokinin-1 antagonists

A

maropitant

33
Q

what happens when NK-1 receptor by substance-P in the CRTZ gets activated

A

induces vomiting

34
Q

what does maropitant (cerenia) do

A
  • blocks NK-1 receptor activation in CRTZ reduces vomiting
  • blocks NK-1 receptors in the emetic center

digestion and metabolism - Wk 3 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions