114 - Drugs Affecting the GIT Flashcards

1
Q

Things that can stimulate gastric acid secretion from antral cells

A

Gastrin (from distension of stomach)

ACh (acts on muscarinic receptors)

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2
Q

What releases gastrin?

A

G cells

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3
Q

Effect of gastrin on parietal cells

A

Activates H+/K+ ATPase through cAMP-mediated Ca2+ increase. Pumps H+ into stomach lumen.

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4
Q

Effect of muscarinic R agonists in the stomach

A

Stimulates H+ release

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5
Q

Drug that can block H+ release by parietal cells into stomach

A

Atropine (muscarinic R antagonist)

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6
Q

Helicobacter pylori

A

G-.
Attaches to gastric cells, releases urease which degrades urea to ammonium hydroxide, which forms an alkaline cloud around it (protects it from stomach acid).
Inflammation stimulates G cells to release gastrin, which increases acidity of the stomach

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7
Q

Common therapy for Helicobacter pylori

A

Omeprazole, clarithromucin and amoxycillin (triple therapy)

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8
Q

Composiiton of stomach mucus layer

A

Mucus with bicarbonate

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9
Q

Prostaglandins primarily synthesised within gastric mucus layer

A

PGE2, PHI2

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10
Q

Effect of PGE2 and PGI2 on stomach
1
2
3

A

1) Decrease acid secretion.
2) Increase blood flow through gastric blood vessels, which removes H+ from stomach.
3) Increase mucus secretion.

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11
Q

Things that can induce PUD (peptic ulcer disease)
1
2

A

1) NSAIDS (ibuprofen, naproxen, inhibitors of COXI)

2) H pylori

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12
Q

Old therapy for peptic ulcers

A

Smooth muscle relaxants

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13
Q

New therapies for peptic ulcers that stop acid production

A

1) Proton pump inhibitors

2) H2-receptor antagonists

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14
Q

Example of proton pump inhibitors

A

Omeprazole, Esomeprazole (very similar)

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15
Q

Proton pump inhibitor mechanism

A

Permanent inhibitor of proton pumps

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16
Q

Example of H2-receptor antagonist

A

Ranitidine

17
Q

Are H2R antagonists prescription drugs?

A

No

18
Q

How do ACh and gastrin cause H+ release?

A

Stimulate ECL cells to release histidine, which stimulates H2 receptors.
H2 receptor stimulation stimulates H+/K+ ATPase

19
Q

Antacids mechanism

A

Neutralise gastric acid.

20
Q

Problem with antacids

A

Side-effects, and can cause increased H+ release into stomach.

21
Q

Examples of antacids

A

Magnesium hydroxide, carbonate, oxide, trisilicate

22
Q

Side effect of the magnesium salt antacids

A

Laxative effect

23
Q

Problems with sodium bicarbonate as an antacid

A

Can lead to alkalosis.

Na+ can lead to/exacerbate hypertension.

24
Q

Example of a cytoprotective agent

A

Sucralfate (used to treat peptic ulcers)

25
Q

Examples of spasmolytics
1
2

A

1) Hyoscine butylbromide (muscarinic antagonist)

2) Mebeverine, peppermint oil (direct spasmolytics)

26
Q

Problems with muscarinic antagonists as spasmolytics

A

SLUD bloackade (salivation, lacrimation, urination, defecation)

27
Q

Why doesn’t hyoscine butylbromide cause systemic effects?

A

Not absorbed

28
Q

Peptic ulcer treatment that increases mucous secretion, blood flow and decreases gastric acid secretion.

A

Prostaglandin E analogues

29
Q

Misoprostol

A

Prostaglandin E analogue.

Used to treat peptic ulcers.

30
Q

Problems with misoprostol
1
2

A

1) Diarrhoea and spam

2) Can terminate pregnancy

31
Q

Chemoreceptor trigger zone

A

Group of neurons in the medulla that is outside the blood brain barrier.
Detects circulating agents, stimulates vomiting centre.

32
Q

Receptors involved in stimulation of chemoreceptor trigger zone

A

Dopamine D2 receptors, 5HT3 receptors.

33
Q

What do antiemetics for nausea affect?

A

Dopamine D2 receptors, 5HT3 receptors.

34
Q

Antiemetics used for motion sickness
1
2

A

1) Histamine H1 antagonists

2) Muscarinic receptor antagonists

35
Q

Receptors involved in direct stimulation of vomiting centre

A

H1 receptors

Muscarinic receptors

36
Q

Motion sickness muscarinic receptor antagonist

A

Hyoscine hydrobromide (can cross the blood brain barrier)