Pharmacology of gastric secretion Flashcards

(29 cards)

1
Q

What do mucus cells secrete?

A

Mucous and bicarbonate

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2
Q

What do parietal cells secret?

A

HCL

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3
Q

What do enterochramaffin-like cells secrete?

A

Histamine

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4
Q

What do G cells secret?

A

Gastrin

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5
Q

What do D cells secret?

A

Somatostatin

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6
Q

Action of histamine?

A
  • Secreted by enterochromaffin-like cells in gastric glands in response to stimulation by Ach
  • Histamine binds to H2 receptors with subsequent activation of adenylyl cyclase
  • Increase in cAMP increases number of proton pumps increasing gastric acid secretion from parietal cells
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7
Q

What is histamine secreted by? And why?

A

Enterochromaffin-like cells in gastric glands in response to stimulation by ACh

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8
Q

What does histamine bind to?

A

H2 receptors with subsequent activation of adenylyl cyclase- this increases no. of proton pumps, increasing gastric acid secretion from parietal cells

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9
Q

What is ACh released by?

A

Parasympathetic cholinergic neurons

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10
Q

What does ACh bind to?

A

Muscarinic M3 ACh receptors on parietal cells with subsequent activation of PLC (phopsholipase?)- The increase in extracellular Ca2+ evokes cell signalling pathways that increase the no. 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 cells with subsequent activation if PLC
-Increase in extracellular Ca+ increases the no. of proton pumps, increasing gastric acid secretion from parietal cells

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13
Q

What secretes somatostatin?

A

Secreted by D cells in gastric glands

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14
Q

What does somatostatin bind to?

A

SST2 receptors inhibiting adenylyl cyclase, decrease in cAMP results in decreased gastric acid secretion from parietal cells

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15
Q

What is the result of somatostatin binding to SST2R receptors or enterochromaffin-like cells?

A

Reduced histamine release and decreased gastric acid secretion from parietal cells

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16
Q

What is the action of NSAIDs?

A

Disrupts the production of prostaglandins by inhibiting COX-1

17
Q

What effect does NSAIDS action have?

A

Reduced availability of prostaglandins results in histamine secretion from enter-chromaffin like cells= promoting HCL secretion from parietal cells

18
Q

Example of an NSAIDs?

19
Q

Diverse affects of NSAIDs and what can help them?

A

Peptic ulcers
Misoprostol (analogue of prostaglandin E1)
Side effects= abdominal pain and diarrhoea, also induces labour

20
Q

Side effects of misoprostol?

A

Abdominal pain and diarrhoea
Induces labour
-Helps peptic ulcers

21
Q

Examples of Proton pump inhibitors?(PPIs)

A

Lanzoprazole
Omeprazole
Pantoprazole

22
Q

What do PPIs do?

A

Irreversibly inhibit H+/K+ ATPase- reduces HCL secretion

23
Q

What are PPIs indicated for?

A

Benign gastric peptic ulceration and NSAID- associated gastric ulceration
Gastro-oesphageal reflux
Zollinger-Ellison syndrome

24
Q

Side effects of PPI?

A

Inreased stomach pH reduces defences against GI tract infections

25
Examples of Histamine H2 receptors agonists?
Ranitidine Cimetidine Famotidine Nizatidine
26
Action of Histamine H2 receptors agonists?
Blocking H2 receptor eventually reduces HCL secretion, complete block of it produces rapid effect
27
What are histamine H2 receptors indicated for?
Benign gastric acid ulceration | NSAIDs associated gastric ulceration
28
What can cause peptic ulcers (bacteria)?
H. Pylori Causes persistent inflammation that weakens mucosal barrier, eventually exposing sub-mucosa to attack from HCL and pepsin
29
How to get rid of H. Pylori?
PPIs & antibiotics (clarithromycin & amoxicillan or metronidazole)