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PMCOL 344 > GI - emesis > Flashcards

GI - emesis Flashcards

1
Q

what is emesis

A

forceful evacuation of gastric contents through mouth

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2
Q

what are 3 reasons for vomiting

A

physiological response to: irritating substances in gut/blood, excessive vestibular stimulation (motion sickness), physiological stimuli (fear, odours)

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3
Q

what is nausea

A

feeling of impending vomiting

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4
Q

are all anti emetics anti nauseant

A

no, most arent

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5
Q

is nausea or vomiting harder to control pharmacologically

A

nausea

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6
Q

what are emetic drugs / what do they do + why do we use them

A

induce vomiting to prevent absorption of ingested toxic substances

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7
Q

what is ipecac

A

emetic drug

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8
Q

why is vomiting bad in lots of treatments

A

it reduces effectiveness by causing dehydration of nutrient depletion

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9
Q

where is vomiting regulated

A

centrally by medulla

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10
Q

what is the chemoreceptor trigger zone

A

BBB near the CTZ is relatively permeable, allowing circulating emetogenic mediators to act, communicates to vomiting center

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11
Q

what kind of inputs does the chemoreceptor trigger zone receive / where from

A

vestibular nuclei and directly from GI tract

and of course the circulating substances in blood by the zone too

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12
Q

where is the chemoreceptor trigger zone located

A

in the area postrema

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13
Q

what is the difference between chemoreceptor trigger zone and area postrema

A

The CTZ is located within the area postrema

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14
Q

what is the vomiting center (what happens here) (where are impulses received from)

A

impulses from CTZ, GI tract and higher cortical centers, coordinate physical act of vomiting

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15
Q

what is the vestibular nuclei

A

imputs from inner ear, it is responsible for dizziness and nausea

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16
Q

what are the 3 main components in the vomiting reflex

A

chemoreceptor trigger zone, vomiting center, vestibular nuclei

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17
Q

what are the roles of higher cortical centers in vomiting

A

reaction to pain, repulsive sights, smells, emotional factors

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18
Q

what is the role of vagal afferents in vomiting

A

convey signals from gut to brainstem

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19
Q

what is the main site for sensing emetic stimuli

A

chemoreceptor trigger zone

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20
Q

what do enterochromaffin cells have to do with the vomiting reflex

A

they sense toxic chemicals or toxins in the gut

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21
Q

what is the mechanism of muscarinic receptor antagonists as anti emetics

A

selective, competitive antagonists at the vomiting center & vestibular nuclei

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22
Q

when do you use muscarinic receptor antagonists

A

prophylactically for motion sickness and post op emesis

23
Q

what are the side effects of muscarinic receptor antagonists

A

dry mouth, blurred vision, sedation, constipation

24
Q

what is an example of a muscarinic receptor antagonists

A

hyoscine

25
Q

what is hyoscine

A

muscarinic receptor antagonists

26
Q

what is the mechanism of action of 5HT3 receptor antagonists

A

selective, competitive, act at CTZ and visceral afferents

27
Q

what example of a drug is a 5HT3 receptor antagonist

A

ondansetron

28
Q

what is ondansetron

A

5HT3 receptor antagonist

29
Q

when do they like to use 5HT3 receptor antagonist

A

chemotherapy-induced emesis

30
Q

how do chemo agents cause emesis

A

they release 5HT from enterochromaffin cells & directly stimulate CTZ and visceral nerves

31
Q

is ondansetron good for motion sickness

A

no not effective

32
Q

what is a bad thing about ondansetron

A

it can cause long QT syndrome

33
Q

what is the mechanism of D2 receptor antagonists

A

selective, competitive, antagonist in the CTZ

34
Q

what are 2 examples of D2 receptor antagonists

A

metoclopramide and domperidone

35
Q

what is metoclopramide

A

D2 receptor antagonists

36
Q

what is domperidone

A

D2 receptor antagonists

37
Q

what is the difference with domperidone and metoclopramide

A

metoclopramide crosses BBB, domperidone doesnt

38
Q

how does metoclopramide compare to ondansetron

A

its not as good for chemitherapy vomiting

39
Q

what are 2 uses for metoclopramide

A

chemo-induced vomiting and increasing GI motility

40
Q

what is a bad thing about metoclopramide

A

it crosses BBB so it can cause movement disorders

41
Q

does metoclopramide cross the BBB

A

yes

42
Q

does domperidone cross the BBB

A

no

43
Q

does domperidone increase gut motility

A

yes

44
Q

does metoclopramide increase gut motility

A

yes

45
Q

what are 4 other anti emetics (besides D2 5HT3 and musc antagonists)

A

antipsychotic phenothiazines, cannabinoids, glucocorticoids, NK1 receptor antagonists

46
Q

what do we use antipsychotic phenothiazines for

A

treatment of more severe nausea and vomiting associated with cancer, radiation therapy, cytotoxic drugs, opioids, anesthetics, etc

47
Q

what is the mechanism of action of antipsychotic phenothiazines

A

D2 receptor antagonists: act in CTZ, but can also block histamine and muscarinic receptors

48
Q

why dont we use antipsychotic phenothiazines a lot

A

because of unwanted effects

49
Q

what is the mechanism of cannabiniods in anti-emesis

A

act in CTZ

50
Q

what is the mechanism of glucocorticoids in anti-emesis

A

unknown

51
Q

when are glucocorticoids used for nausea

A

with chemo

52
Q

what is the mechanism of NK1 receptor antagonists in anti-emesis

A

action at CTZ and vomiting center

53
Q

when do you use NK1 receptor antagonists

A

with chemo induced vomiting, combo with glucocorticoids

PMCOL 344 (27 decks)

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