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

GI Motility / Nausea and Vomiting Flashcards

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?

A

stimulate motilin receptors on GI smooth muscle

promote peristalsis

tolerance quickly develops

25
Q

what is the migrating motor complex?

A 
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
Q

what are antispasmodics? drug type example?

A

muscarinic antagonists

27
Q

what are the features of muscarinic antagonists and what are they used to treat?

A

reduce GI motility tract

IBS (reduce spasm)
non-ulcer dyspepsia
diverticular disease

28
Q

what is an example of a muscarinic antagonist?

A

dicyclomine - direct effect on smooth muscle

29
Q

what is constipation caused by?

A

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
Q

what do osmotic laxatives do in the lumen?

A

increase intestinal fluid secretion

31
Q

what do stimulant laxatives do?

A

stimulate enteric NS

32
Q

what do bulk laxatives do?

A

swells and distends colon

33
Q

what is an example of a bulk laxative?

A

methylcellulose, bran

34
Q

what are the features of bulk laxatives?

A

increase volume of faecal material
distends smooth muscle of GIT - promoting refelx peristalsis
act within days

35
Q

what is an example of an osmotic laxative?

A

lactulose, magnesium hydroxide/sulphate

36
Q

what are the features of osmotic laxatives?

A

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
Q

what is an example of a faecal softener laxative?

A

docusate sodium

38
Q

what are the features of faecal softener laxatives?

A

detergent action reduces surface tension of luminal contents
softens faeces
weak laxative stimulant action

39
Q

what is an example of a stimulant laxative?

A

(6-12 hours)

senna
bisacodyl
sodium picosulphate

40
Q

what are the features of stimulant laxatives?

A

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
Q

what are the causes of diarrhoea?

A 
change in diet
lactose intolerance
stress/emotional disturbance
toxins
drugs
infection that irritates/damages GI mucosa
42
Q

what are the 3 approches to anti-diarrhoeal?

A

correct fluid and electrolyte balance

antimicrobial agents

anti motility agents and adsorbents

43
Q

what opiod anti-motilities are there?

A

morphine, codeine etc.

44
Q

what do opiod anti-motilitiesdo?

A

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
Q

what is loperamide?

A

anti-motility

synthetic opiod

cant cross BBB - low abuse potential

46
Q

what are the two main centres involved in nausea and vomiting?

A
  • chemoreceptor trigger zone (CTZ)

- vomiting centre in the medulla

47
Q

what stimulates CTZ?

A

drugs, toxins, vestibular centre

48
Q

what stimulates the vomiting centre?

A

CTZ

49
Q

what neuronal pathways act on the vomiting centre?

A

higher cortical centres
chemoreceptor trigger zones
stomach small intestine
labyrinths

50
Q

what happens when the vomiting centre is stimulated?

A

contraction of diaphragm, anterior abdominal muscles and stomach

closure of the glottis

abdominal wall moves upwards

vomiting occurs

51
Q

what neurotransmitters are involved in the vomiting reflex?

A

acetylcholine
dopamine
histamine
serotonin

52
Q

what are the drug targets for vomiting?

A

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
Q

what is an example of antihistamines?

A

cinnarizine,

54
Q

what is an example of muscarinic receptor antagnonist?

A

hyocine

55
Q

what is an example of 5HT3 receptor antagonist?

A

graniestron

56
Q

what is an example of dopamine antagonist?

A

metaclopramide,

57
Q

what is an example of cannabinoids?

A

nabilone

CB1 GIT

58
Q

what is an example of NK1 receptor antagonists?

A

aprepritant

59
Q

what is an example of glucocorticoids?

A

dexamethasone

X Pharmacological Treatment Of Disease (9 decks)

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