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Pharmacology > Gut motility and emesis > Flashcards

Gut motility and emesis Flashcards

1
Q

List the three types of purgatives.

A

Laxatives, faecal, stimulant purgatives

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2
Q

What are bulk laxatives?

A

Poorly digested compounds (methylcellulose, psyllium) of plant origin.

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3
Q

What is the mechanism of action of bulk laxatives?

A

Polysaccharide polymers are not broken down by normal digestive processes. Form bulky hydrated mass in GI lumen, promoting peristalsis.

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4
Q

What are the side effects of bulk laxatives?

A

Affect pharmacokinetics of drugs, bloating

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5
Q

What are osmotic laxatives?

A

Poorly absorbed solutes, e.g. salts or sugars

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6
Q

What is the mechanism of action of osmotic laxatives?

A

Increase osmotic pressure in the lumen, driving water into the lumen.
Sugars broken down by bacteria in GIT creating acidic metabolites that attract water.

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7
Q

What are side effects of osmotic laxatives?

A 
Abdominal cramps (not significant for PEG)
Systemic effects of salts
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8
Q

What are faecal softeners?

A

Surfactant, reduce surface tension of water, promoting softer faeces.
Weak

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9
Q

When are faecal softeners used?

A

When straining should be avoided.

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10
Q

What is the effect of stimulant laxatives?

A

Increase electrolyte and water secretion by mucosa, increase peristalsis (via enteric nerves)
Bowel can become lazy with use.

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11
Q

Which drugs treat constipation without purgation?

A

D2 receptor antagonists

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12
Q

What is the effect of D2 receptor antagonists?

A

Stimulates cholinergic smooth muscle activation, increases lower oesophageal sphincter pressure, enhancing gastric emptying.
May also block D2 receptors in CTZ.

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13
Q

Which agents are antidiarrhoeal?

A

Opioid derivatives, e.g. loperamide

Muscarinic receptor antagonists

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14
Q

What is the mechanism of action of loperamide as an antidiarrhoeal agent?

A

Selective for GIT
Decreases activity of the myenteric plexus
Decreases tone of longitudinal muscle (peristalsis) and increased tone of circular muscle (segmentation)

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15
Q

When is rescue treatment no effective for vomiting?

A

Post-operative

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16
Q

Which two brain structures are important in vomiting?

A

CTZ: in medulla, lacks BBB, dopamine and tryptamine (5HT) input

Vomiting centre: not a discrete area, inputs from CTZ, GIT, CVS, limbic system, labyrinths via vestibular nuclei, mechano/chemo receptors in GIT (5HT, ACh, histamine, DA, neurokinins)

17
Q

Which antiemetics are best for motion sickness and are prophylactic as well as relieving?

A

Antimuscarinics

18
Q

What is the mechanism of action of antihistamines in emesis?

A

H1 receptor antagonists (CTZ, block vestibular communication), some anticholinergic activity.

19
Q

When are H1 receptor antagonists useful for emesis?

A

Motional sickness, morning sickness, not chemotherapy-induced.

20
Q

What are the side effects of H1 receptor antagonists?

A

Anti-muscarinic

21
Q

Where do D2 receptor antagonists act?

A

CTZ and gastric emptying through 5-HT4 agonism.

22
Q

What is the mechanism of action of setrons in emesis?

A

5HT3 receptor antagonists with central and peripheral action.

23
Q

When are setrons used for emesis?

A

CINV, PONV, acts at CTZ (GIT and NTS)

24
Q

What are the side effects of setrons?

A

Constipation due to GIT

25
Q

Which drug is commonly used as an adjuct to antiemetic therapy?

A

Glucocorticosteroids, potentiate effects of antiemetics, reduce GIT inflammation reducing stimuli to CTZ.

26
Q

List the drugs used for antiemesis.

A 
Antimuscarinins
H1R antagonists
D2R antagonists
5HT3R antagonists
Glucocorticosteroids
BZNs
NK1 receptor antagonists
Pyridoxine (vitB6)
Ginger
Cannabinoids
27
Q

Where are NK1 receptors abundant?

A

GIT, CTZ, CNS

28
Q

When are NK1 receptor antagonists useful for emesis?

A

Chemotherapy, motion sickness, alcohol.

Pharmacology (14 decks)

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