114 - Drugs Affecting the GIT Flashcards

(36 cards)

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

17
Q

Are H2R antagonists prescription drugs?

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
Examples of spasmolytics 1 2
1) Hyoscine butylbromide (muscarinic antagonist) | 2) Mebeverine, peppermint oil (direct spasmolytics)
26
Problems with muscarinic antagonists as spasmolytics
SLUD bloackade (salivation, lacrimation, urination, defecation)
27
Why doesn't hyoscine butylbromide cause systemic effects?
Not absorbed
28
Peptic ulcer treatment that increases mucous secretion, blood flow and decreases gastric acid secretion.
Prostaglandin E analogues
29
Misoprostol
Prostaglandin E analogue. | Used to treat peptic ulcers.
30
Problems with misoprostol 1 2
1) Diarrhoea and spam | 2) Can terminate pregnancy
31
Chemoreceptor trigger zone
Group of neurons in the medulla that is outside the blood brain barrier. Detects circulating agents, stimulates vomiting centre.
32
Receptors involved in stimulation of chemoreceptor trigger zone
Dopamine D2 receptors, 5HT3 receptors.
33
What do antiemetics for nausea affect?
Dopamine D2 receptors, 5HT3 receptors.
34
Antiemetics used for motion sickness 1 2
1) Histamine H1 antagonists | 2) Muscarinic receptor antagonists
35
Receptors involved in direct stimulation of vomiting centre
H1 receptors | Muscarinic receptors
36
Motion sickness muscarinic receptor antagonist
Hyoscine hydrobromide (can cross the blood brain barrier)