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GI > Pharmacology of gastric secretion > Flashcards

Pharmacology of gastric secretion Flashcards

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?

A

Aspirin

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
Q

Examples of Histamine H2 receptors agonists?

A

Ranitidine
Cimetidine
Famotidine
Nizatidine

26
Q

Action of Histamine H2 receptors agonists?

A

Blocking H2 receptor eventually reduces HCL secretion, complete block of it produces rapid effect

27
Q

What are histamine H2 receptors indicated for?

A

Benign gastric acid ulceration

NSAIDs associated gastric ulceration

28
Q

What can cause peptic ulcers (bacteria)?

A

H. Pylori
Causes persistent inflammation that weakens mucosal barrier, eventually exposing sub-mucosa to attack from HCL and pepsin

29
Q

How to get rid of H. Pylori?

A

PPIs & antibiotics (clarithromycin & amoxicillan or metronidazole)

GI (15 decks)

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