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

25
what is hyoscine
muscarinic receptor antagonists
26
what is the mechanism of action of 5HT3 receptor antagonists
selective, competitive, act at CTZ and visceral afferents
27
what example of a drug is a 5HT3 receptor antagonist
ondansetron
28
what is ondansetron
5HT3 receptor antagonist
29
when do they like to use 5HT3 receptor antagonist
chemotherapy-induced emesis
30
how do chemo agents cause emesis
they release 5HT from enterochromaffin cells & directly stimulate CTZ and visceral nerves
31
is ondansetron good for motion sickness
no not effective
32
what is a bad thing about ondansetron
it can cause long QT syndrome
33
what is the mechanism of D2 receptor antagonists
selective, competitive, antagonist in the CTZ
34
what are 2 examples of D2 receptor antagonists
metoclopramide and domperidone
35
what is metoclopramide
D2 receptor antagonists
36
what is domperidone
D2 receptor antagonists
37
what is the difference with domperidone and metoclopramide
metoclopramide crosses BBB, domperidone doesnt
38
how does metoclopramide compare to ondansetron
its not as good for chemitherapy vomiting
39
what are 2 uses for metoclopramide
chemo-induced vomiting and increasing GI motility
40
what is a bad thing about metoclopramide
it crosses BBB so it can cause movement disorders
41
does metoclopramide cross the BBB
yes
42
does domperidone cross the BBB
no
43
does domperidone increase gut motility
yes
44
does metoclopramide increase gut motility
yes
45
what are 4 other anti emetics (besides D2 5HT3 and musc antagonists)
antipsychotic phenothiazines, cannabinoids, glucocorticoids, NK1 receptor antagonists
46
what do we use antipsychotic phenothiazines for
treatment of more severe nausea and vomiting associated with cancer, radiation therapy, cytotoxic drugs, opioids, anesthetics, etc
47
what is the mechanism of action of antipsychotic phenothiazines
D2 receptor antagonists: act in CTZ, but can also block histamine and muscarinic receptors
48
why dont we use antipsychotic phenothiazines a lot
because of unwanted effects
49
what is the mechanism of cannabiniods in anti-emesis
act in CTZ
50
what is the mechanism of glucocorticoids in anti-emesis
unknown
51
when are glucocorticoids used for nausea
with chemo
52
what is the mechanism of NK1 receptor antagonists in anti-emesis
action at CTZ and vomiting center
53
when do you use NK1 receptor antagonists
with chemo induced vomiting, combo with glucocorticoids