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X Pharmacological Treatment Of Disease > GI Motility / Nausea and Vomiting > Flashcards

GI Motility / Nausea and Vomiting Flashcards

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1
Q

what drugs are there to control GI motility and vomiting?

A
  • motility stimulants
  • antispasmodics
  • laxatives
  • antidiarrhoeals
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2
Q

where is the myenteric plexus and what is it?

A

major nerve supply to GI tract to control motility

between circular and submucosal muscles

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3
Q

where is the submucosal plexus and what is it?

A

nerves derived from the myenteric plexus

controls the movement of the mucosa

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4
Q

what is the mesentry and what is it used for?

A

holds the gut together

used as a pharmacological base

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5
Q

what is a perfusion pump used for

A

used to inject drugs, e.g. vasoconstriction drugs

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6
Q

describe the autonomic control of the GI tract

A

parasympathetic = excitatory - releases ACh at ganglia
nicotonic

sympathetic = inhibitory - releases NA at the ganglia which affects ACh

ACh released on the smooth muscle

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7
Q

what are motility stimulants and what are they used to treat?

A

increase GI motility without a laxative effect

treats:

  • GORD
  • Gastroparesis
  • Gastric stasis
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8
Q

what is an example of a muscarinic agonist?

A

bethanechol

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9
Q

what is bethanechol used to treat?

A
  • post-op gastric distension
  • post-op ileus
  • post-op atony
  • can’t use ACh- not selective enough
  • resistant to AChE
  • to expel gas from the intestine prior to x-ray examination and to reduce transit time of barium
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10
Q

how does bethanechol work?

A

cholinergic- stimulate ACh receptors directly

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11
Q

how else can ACh be increased, apart from stimulating the release of ACh?

A

anticholinesterases to prevent ACh from being broken down

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12
Q

what is dopamine?

A

inhibitory
decrease oesophageal sphincter
decrease intragastric pressure

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13
Q

what are examples of dopamine antagonists?

A

metaclopramide and domperidone

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14
Q

what do dopamine antagonists do?

A

stimulate gastric motility and gastric empyting

block D2 receptors -decrease the inhibition of DA and ACh release
stimulates 5-HT receptors

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15
Q

what is the mechanism of action of dopamine normally?

A

dopamine normally inhibits ACh release at ganglia via D2 receptors

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16
Q

what is the mechanism of action of dopamine agonists?

A

block D2 receptors to reduce how much ACh release is inhibited

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17
Q

what are the features of serotonin?

A

important role in normal motor and secretory function of the GI tract

most is produced by enterochromaffin cells in the mucosa

serotonin released in response to chemical and mechanical stimulation = stimulation of peristalsis

found in neurones of myenteric plexus

stimulates smooth muscle, ganglion cells and sensory nerve endings

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18
Q

what is the synthesis and metabolism of serotonin?

A

tryptophan (from diet) -> 5-hydroxytryptophan VIA TRYPTOPHAN HYDROXYLASE

5-hydroxytryptophan -> 5-HT VIA NON-SPECIFIC DECARBOXYLASE

5-HT -> 5-HIAA VIA MAO

-> excretion

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19
Q

what is an example of a 5-HT4 receptor agonist?

A

tegaserod - partial agonist at 5-HT4 recepotrs

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20
Q

what is tegaserod used for?

A

initially for constipation in IBS

now for gastroparesis

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21
Q

how does tegaserod work?

A

promote peristaltic activity by acting on presynaptic 5-HT to enhance release of ACh

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22
Q

what is an alternative drug to tegaserod?

A

prucalopride

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23
Q

what is an example of a motilin agonist?

A

erythromycin

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24
Q

what does erythromycin do?

Study These Flashcards
A

stimulate motilin receptors on GI smooth muscle

promote peristalsis

tolerance quickly develops

25
what is the migrating motor complex?
``` every 80-90-100 mins 3 phases 1) quiet period 2) irregular contraction 3) peristaltic rush - starting in stomach. increased gastric pancreatic and biliary secretion ```
26
what are antispasmodics? drug type example?
muscarinic antagonists
27
what are the features of muscarinic antagonists and what are they used to treat?
reduce GI motility tract IBS (reduce spasm) non-ulcer dyspepsia diverticular disease
28
what is an example of a muscarinic antagonist?
dicyclomine - direct effect on smooth muscle
29
what is constipation caused by?
poor diet low fluid intake improper bowel movements ``` loss of rhythm surgery pregnancy diabetes hypothyroidism kidney dialysis constipating drugs laxative abuse ageing-reduces bowel movement lack of abdominal muscle movements ```
30
what do osmotic laxatives do in the lumen?
increase intestinal fluid secretion
31
what do stimulant laxatives do?
stimulate enteric NS
32
what do bulk laxatives do?
swells and distends colon
33
what is an example of a bulk laxative?
methylcellulose, bran
34
what are the features of bulk laxatives?
increase volume of faecal material distends smooth muscle of GIT - promoting refelx peristalsis act within days
35
what is an example of an osmotic laxative?
lactulose, magnesium hydroxide/sulphate
36
what are the features of osmotic laxatives?
poorly absorbed increase osmotic pressure of intestinal contents draws water into the lumen of the GIT increased faecal volume distends smooth muscle - promoting reflex peristalsis
37
what is an example of a faecal softener laxative?
docusate sodium
38
what are the features of faecal softener laxatives?
detergent action reduces surface tension of luminal contents softens faeces weak laxative stimulant action
39
what is an example of a stimulant laxative?
(6-12 hours) senna bisacodyl sodium picosulphate
40
what are the features of stimulant laxatives?
senna - contains anthracene derivatives which have a direct stimulant effect on the myenteric plexus bisacodyl - usually suppository - stimulates rectal muscosa sodium picosulphate - similar to bisacodyl but given orally prior to intestinal surgery
41
what are the causes of diarrhoea?
``` change in diet lactose intolerance stress/emotional disturbance toxins drugs infection that irritates/damages GI mucosa ```
42
what are the 3 approches to anti-diarrhoeal?
correct fluid and electrolyte balance antimicrobial agents anti motility agents and adsorbents
43
what opiod anti-motilities are there?
morphine, codeine etc.
44
what do opiod anti-motilitiesdo?
inhibit GI activity by stimulating u-opiod receptors increase segmentation receptors but reduce peristalsis forward movement is slowed and absorption of water is increased = increased viscocity of GI contents
45
what is loperamide?
anti-motility synthetic opiod cant cross BBB - low abuse potential
46
what are the two main centres involved in nausea and vomiting?
- chemoreceptor trigger zone (CTZ) | - vomiting centre in the medulla
47
what stimulates CTZ?
drugs, toxins, vestibular centre
48
what stimulates the vomiting centre?
CTZ
49
what neuronal pathways act on the vomiting centre?
higher cortical centres chemoreceptor trigger zones stomach small intestine labyrinths
50
what happens when the vomiting centre is stimulated?
contraction of diaphragm, anterior abdominal muscles and stomach closure of the glottis abdominal wall moves upwards vomiting occurs
51
what neurotransmitters are involved in the vomiting reflex?
acetylcholine dopamine histamine serotonin
52
what are the drug targets for vomiting?
M1- decrease vestibular centre and impact of CTZ on vomiting centre H1- decrease vestibular centre and impact of CTZ on vomiting centre D2- decrease CTZ impact on vomiting centre 5-HT3- decrease CTZ impact on vomiting centre
53
what is an example of antihistamines?
cinnarizine,
54
what is an example of muscarinic receptor antagnonist?
hyocine
55
what is an example of 5HT3 receptor antagonist?
graniestron
56
what is an example of dopamine antagonist?
metaclopramide,
57
what is an example of cannabinoids?
nabilone | CB1 GIT
58
what is an example of NK1 receptor antagonists?
aprepritant
59
what is an example of glucocorticoids?
dexamethasone

X Pharmacological Treatment Of Disease (9 decks)

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