pharmacology of gastric secretion Flashcards

1
Q

what does mucus cells secrete

A

mucus and bicarbonate

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2
Q

what do parietal cells secrete

A

hydrochloric acid

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3
Q

what do eneterchromaffin cells secrete

A

histamine

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4
Q

what do chief cells secrete

A

pepsinogen

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5
Q

what do D cells secrete

A

somatostatin

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6
Q

what do G cells secrete

A

gastrin

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7
Q

explain HCl secretion from gastric parietal cells

A

??? bitch you tell me

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8
Q

explain histamine secretion

A
  • it is secreted in the gastric glands by enterochromaffin cells in response to stimulation by Acetylcholine
  • histamine binds to hydrogen receptors with subsequent activation of adenyly cyclase
  • the increase in cAMP increases the number of proton pumps, increasing gastric acid secretion from parietal cells
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9
Q

what release ACh

A

parasympathetic cholinergic neurones

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10
Q

what does ACh bind to

A

muscarinic ACh receptors
-on parietal cells with subsequent activation of PLC

> the increase in intracellular calcium evokes cell signalling pathways that increase the number of proton pumps, increasing gastric acid secretion from parietal cells

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11
Q

what is gastrin released by

A

G cells

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12
Q

what does gastrin bind to

A

CCK2 receptors on parietal cels with subsequent activation of PLC

> > increased intracellular calcium = more proton pumps = increased gastric acid secretion from parietal cells

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13
Q

what is somatostatin secreted by

A

D cells in the gastric gland

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14
Q

what does somatostatin bind to

A

SSTR receptors inhibiting adenylyl cyclase

> > the result =
a decrease in camp > decrease in gastric acid secretion

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15
Q

result of somatostatin binding to SSTR receptors on enterochromaffin cells

A

> reduced histamine release
reduced decreased gastric acid secretion
from parietal cells

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16
Q

effect of antacids

A

reduced the symptoms of excessive gastric acid secretion by buffering HCl

17
Q

examples of antacids

A

gaviscon
peptac

> use a sodium alginate ie NaHCO3 or CaCO3

18
Q

the action of NSAIDS on prostaglandins

A

> NSAIDS disrupt production of prostaglandins by inhibiting COX-1

-the reduced availability of prostaglandins results in histamine secretion from enterochromaffin cells > promoting HCl secretion from parietal cells

19
Q

what is misoprostol

A

> an analogue of prostaglandin E1

20
Q

when would you use misoprostol

A

> prophylaxis of NSIAD induced peptic ulcer

side effects include = abdominal pain and diarrhoea
**can also induce labour

21
Q

how do proton pumps work

A

they irreversibly inhibit H/K/ATPase pump > which reduces HCl secretion

22
Q

examples of PPIs

A

lansoprazole
omeprazole
pantoprazole

23
Q

when would PPIs be indicated

A

benign gastric acid ulceration and NSAID-associated gastric ulceration

> gastro-oesophageal reflux disease and Zollinger-Ellison syndrome

24
Q

side effects of PPIs

A

increased stomach pH

reduces defences against infection via the GI tract

25
Q

how do histamine H2 receptor antagonists work

A

block the H2 receptor which eventually reduces HCl secretion

26
Q

examples of histamine H2 receptor antagonists

A

ranitidine
cimetidine
famotidine
nizatidine

27
Q

when are histamine H2 receptors antagonists indicated

A

benign gastric acid ulceration and NSAID associated gastric ulceration

28
Q

how do treat an H. pylori infection ie peptic ulcer ?

A

PPIs + antibiotics (clarithromycin amoxicillin metronidazole)