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GI Week 6 > Decontamination Agents and Antiemetics > Flashcards

Decontamination Agents and Antiemetics Flashcards

1
Q

What are the 4 important locations when you think about receptors involved in vomiting?

A
  1. peripheral for sensory input: inner ear, pharynx and stomach/small itnestine
  2. Chemoreceptor trigger zone (CTX)
  3. Vomiting center
  4. higher centers
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2
Q

Where is the chemoreceptove trigger zone?

A

in the area postrema on the floor of the 4th ventricle

OUTSIDE THE BBB

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3
Q

The CTX is the region primarily responsible for detection of what type of emetics?

A

blood-borne emetics

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4
Q

Where is the vomiting center located?

A

in the medulla

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5
Q

WHat is the vomiting center responsible for?

A

the initiation and coordination of the complex motor patterns needed for vomiting

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6
Q

The higher centers are necessary for vomiting associated with what?

A

memory, fear, dread and anticipation

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7
Q

What receptor is commonly involved at the peripheral receptors, chemoreceptive trigger zone and vomiting center?

A

5HT3 is located at all of them

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8
Q

What are some other receptors involved in the periphery?

A

D2 receptors

muscularinic H1 receptors, NK1 receptors, opiod receptors

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9
Q

Where does the inner ear send info to in this pathway?

A

cerebellum and then to vomiting center

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10
Q

Where do the pharynx and stomach.small intestine send info to in this pathway?

A

solitary tract nucleus, and then to vomiting center

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11
Q

What receptors are involved in the CTX besides 5HT3?

A

D2, opioid, M1 and H1

syringes help men on drugs

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12
Q

What receptors besides 5HT3 are involved in the vmoiting center?

A

D2 and M

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13
Q

What receptor is associated with the higher centers?

A

NK1 and cannabinoid

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14
Q

What are the three major types of stimuli that activate the vomiting center?

A
  1. mechanical and/or painflu stimuli
  2. blood borne emetics
  3. higher center stimuli - anticipation
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15
Q

What are mechanical stimuli that will trigger the inner ear?

A

motion, aminoglycoside antibiotics

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16
Q

How will local GI irritation trigger 5HT3 receptors in the solitary tract nucleus and CTZ?

A

by triggering vagal and sympathetic afferents from the stomahc and small intestine

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17
Q

What sets of afferents will be triggered in the pharynx

A

the gag reflex, so glossopharyngeal and trigeminal

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18
Q

What are the two GI deconominants we know?

A
  1. activated charcoal

2. Polyethylene glycol-eectrolyte solution

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19
Q

Which one works better in the upper GI? lower GI?

A

activated charcoal in the upper GI and polyethylene glycol in the lower GI

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20
Q

How does activated charcoal work?

A

absorbs many drugs and poisons due to its large surface area

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21
Q

How much activated charcoal should ou give?

A

give in a ratio of at least 10:1 (charcoal:toxin) by weight

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22
Q

What will activated charcoal NOT bind?

A

iron, lithium, potassium

alcohol and cyanide very poorly

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23
Q

In what poisoning cases will activated charcoal NOT be useful

A

corosive mineral acids or alkalis

24
Q

How does polyethylene glycol work as a decontaminant?

A

it’s a cathartic, so hastens removal of toxins and reduces absorption

whole bowel irrigation can enhance this decontamination following iron tablets, enteric coated medicines, illicit drug-filled packets and foriegn bodies

25
Q

Wat emetic agent was previously used as a decontaminant OTC, but is now controversial?

A

IPECAC

26
Q

How does IPECAC work?

A
  1. it has a direct local irritant effect that triggers emesis
  2. indirectly activates the CTZ
27
Q

Why does IPECAC only really work if you give it within an hour after ingestion?

A

emesis won’t occur if the stomach is empty, so if the poison is already in the small bowel, you won’t puke and then the IPECAC is stuck in the stomach and you cause damage

28
Q

Why is IPECAC particularly dangerous is the suspected poison is corrosive, a petroleum distillate or a rapidly-acting convulsant?

A

If they get aspirated into the lungs, you get a bad pneumonitis

29
Q

What is likely the key mechanism for most antiemetics (particularly older ones)?

A

sedation

30
Q

Are antiemetics more effective at preventing vomiting or stopping emesis once its’started?

A

prevention

31
Q

What are the 7 groups of antiemetics?

A
  1. 5HT3 antagonists
  2. antimuscarinics
  3. NK1 antagonists
  4. Antihistamines (H!)
  5. dopamine D2 antagonists
  6. Cannabinoids
  7. Corticosteroids
32
Q

What group is the most effective anti-emetic?

A

serotonin antagonists - the setrons

33
Q

What are the 5 serotonin 5HT3 receptor antagonists we know?

A

Dolasetron
Granistetron
Ondansteron
Palonosetron

34
Q

What is the mechanism of action for the 5HT3 antagonists?

A

they block peripheral 5HT3 receptors on the primary afferent receptors of the GI tract

also block receptors in the CTZ and vomiting centers

this redundancy is what makes them so effective

35
Q

What is the most important therapeutic use for the 5HT3 antagonists?

A

prevent nause aand vomiting in chemotherapy - particularly the acute phase

gives 30 minutes prior ot antineoplastic to circumvent the development of anticipatory nausea

36
Q

what other forms of nausea will the 5HT3 antagonists work for?

A

post op and post-radiation

37
Q

Why don’t the 5HT3 antagonists work for motion sickness?

A

motion sickness is by th einner ear pathway and doesn’t use the vagal pathway

38
Q

What are the potential side effects for the 5HT3 antagonists?

A

they’re generally well tolerated

also safe with a long track record of use

Most SEs are transient - constipation, dizziness and mild HA

small elongation of QT, but not clinically relevant

39
Q

What is the most effective treatment for motion sickness?

A

scopalomine

40
Q

What is the mechanism of action for scopalomine?

A

it’s an antimuscarinic and antidopaminergic antagonist in the cerebellum (widely distributed in CNS)

41
Q

How is scopalomine administered for motion sickness?

A

a transdermal patch to avoid the antimuscarinic side effects

42
Q

What are the two neurokinin receptor 1 antagonists?

A

Aprepitant
Fosaprepitant

actually the same drug - Aprepitant is oral and Fosaprepitant is IV

43
Q

How do the NK1 antagonists work?

A

they block the binding of substance P to the NK1 receptor

44
Q

Where are the NK1 receptors located in aprticular?

A

the higher order dcenters

45
Q

What are the therapeutic uses for the NK1 receptors like aprepitant and fosaprepitant?

A

chemo-induced N/V (particularly anticipation-nausea)

46
Q

What are the NK1 receptor antagonists usually given in combo with?

A

5HT3 and dextramethasone

47
Q

What are the side effects of the NK1 receptor antagonists?

A

well tolerated - maybe fatigue, dyspnea and idarrhea

they’re metabolized by cyp 3A4 enzymes, so you can get drug interactions if given with chemo agents also metabolized by this pathway — raises a concern for increased bone marrow suppression

48
Q

What are the three antihistamine (H1) blockers used as anti-emetics?

A

dimenhydrinate, diphenhydramine, meclizine

49
Q

What’s the primary mechanism for the H1 blockers in this situation?

A

probably sedation - H1 may not be the actual target though; probably muscarinics (this is why the first gens work better than the more selective second gens)

50
Q

Wat are the side effects of the H1 blockers?

A

anti-muscarinic effects: confusion, dry mouth, urinary retention, etc.

drug interactions with antibiotics

DON”T USE IN PREGNANCY

51
Q

What are the 5 dopamine (D@) receptor antagonists used as anti=emetics?

A 
Droperidol
metoclopramide
prochlorperazine
promethazine
thiethylperazine
52
Q

How do the D2 receptor antagonists work as anti-emetics?

A
  1. they inhibit D2 and muscarinic receptors in the CTZ
  2. may reset GI motility
  3. maybe sedating
53
Q

What are the two cannabinoids used for antiemetics?

A

dronabinol

nabilone

54
Q

How do the cannabinoids work?

A

they act on the central cannabinoid receptors

probably sedation too

but there are better agents available at this time

55
Q

What are the side effects of the cannabinoics?

A

weed…

euphoria, sedation, hallucinations, dry mouth, increase appetite

56
Q

What two corticosteroids are used for antiemetic agents?

A

dexamethasone

methylprednisolone

57
Q

What is the mechanism of action for the corticosteroids in antiemetic sense?

A

we don’t know

GI Week 6 (14 decks)

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