Vertigo, Hearing Loss & N/V Flashcards

1
Q

emesis location

A

CEC in lateral reticular formation of midbrain, adjacent to CTZ, area postrema and solitary tract nucleus

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2
Q

receptor types in CTZ

A

5HT-3, D2, opioids

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3
Q

receptor types in STN

A

encephalin, H, ACh, 5-HT3

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4
Q

antihistaminergics & antichoinergics

A

meclizine, diphenhydramine, promethazine, scopolamine

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5
Q

which drugs block H1 and M1

A

meclizine, diphenhydramine, promethazine

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6
Q

which drug blocks M1 only

A

scopolamine

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7
Q

AE of meclizine & diphenhydramine

A

drowsiness, dizziness, asthenia, weakness & confusion

∙ Meclizine has ↑in women

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8
Q

AE of promethazine

A

drowsiness/sedation, fatal respiratory depression < 2 y/o. BBW if by INJECTION

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9
Q

AE of scopolamine

A

xerostomia, drowsiness, ocular effects after touching patch & rubbing eye

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10
Q

metabolism of the Anti-H and anti-M

A

heaptic (meclizine is CYP2D6 dominant)

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11
Q

clinical utility for anti-H and anti-M

A

short term treatment of vertigo

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12
Q

benzodiazepine used for anticipatory n/v

A

diazepam

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13
Q

moa of diazepam

A

change in receptor activity & shift dose curve for GABA binding to left, ↑potency but NOT efficacy

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14
Q

corticosteroids for n/v

A

dexamethasone, methylprednisone

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15
Q

MOA of corticosteroids

A

unknown effect, presumably via steroid receptors in STN

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16
Q

D2 antagonists for n/v

A

prochlorperazine, chlorpromazine

17
Q

d2 antagonists MOA

A

d2 receptor antagonism in CTZ, also posses anti-H and anti-M activities

18
Q

AE of d2 antagonists

A

chronic use at risk for BM suppression, risk for QT prolongation and torsade de pointes, co-admin with antipsychotics may ↑CNS effects

19
Q

metabolism of D2 antagonists

A

extensive hepatic

20
Q

clinical utility for D2 antagonists

A

“general purpose” n/v

21
Q

5HT3 antagonists

A

dolasetron, granisetron, ondansetron

22
Q

moa of 5HT3 antagonists

A

Antagonize 5-HT¬3 receptors in CTZ & solitary tract nucleus (STN)

23
Q

AE of 5HT3 antagonists

A

hypersensitivity reactions, QT prolongation, headache, constipation & diarrhea (MC)

24
Q

metabolism of 5HT3 antagonists

A

M: hepatic – CYP interactions

∙ dose adjust ONLY for ondansetron

25
Q

clinical utility for 5HT3 antagonists

A

Use for idiopathic n/v and post-operative n/v prophylaxis; often with corticosteroid

26
Q

substance P/NK1 antagonists

A

aprepitant, fosaprepitant

27
Q

MOA of aprepitant

A

Central action (solitary tract) essential, some contribution from peripheral effects

28
Q

AE of aprepitant

A

headache, constipation & diarrhea

29
Q

DDI of aprepitant

A

numerous, CYP

30
Q

Metabolism of aprepitant

A

xtensive hepatic (CYP) metabolism & 3A4 inhibitor

31
Q

ototoxics

A

aminoglycosides, cisplatin, loop diuretics

32
Q

MOA of toxicity of aminoglycosides

A

cell death of hair cells via caspase dependent & independent mechanism (JNK pathway releases cyt C)

33
Q

reversible agent for aminoglycoside toxicity

A

if reversible, give N-acetylcysteine

34
Q

moa of toxicity of cytotoxics

A

irreversible, enter outer hair cells and result in cell death via caspase-dependent mechanism only

35
Q

moa of toxicity of loop diuretics

A

fluid imbalance in production and maintenance of endolymph, usually temporary