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Neuro 2 > Vertigo Pharmacology > Flashcards

Vertigo Pharmacology Flashcards

1
Q

Drugs with the most prominent effects in producing vertigo impact what?

A

the structure and funciton of the vestibular apparatus (ex. hair cells of the inner ear)

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2
Q

What are the three major drug types that can lead to irreversible changes in the inner ear?

A

Aminoglycosides
Loop diuretics
Cytostatic drugs

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3
Q

What can improve aminoglycoside-induced inner ear toxicity (through not completely reverse it)?

A

N-acetylcysteine

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4
Q

Via what mechanism do aminoglycosides cause outer hair cell death?

A

either caspase-dependent or caspase-independent mechanisms

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5
Q

Via what mechanism does cisplatin cause outer hair cell death?

A

praimrily caspase-dependent

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6
Q

How do both aminoglycosides and cisplatin gain entry into outer hair cells?

A

mechano-transducer channels

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7
Q

What is the significance in the fact that aminoglycosides form complexes with iron when they gain entry into outer hair cells?

A

complex can react with electron donors (ex. arachidonic acid) to form ROS (ex. superoxide, hydroxyl radical, and hydrogen peroxide)

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8
Q

What do AG-iron complex induced ROS do in the outer hair cell?

A

activates JNK so that it can translocate to the nucleus and activate genes in the cell death pathway

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9
Q

Activation of genes in the cell death pathway leads to waht?

A

release of cytochrome C from the mitochondria (triggers apoptosis via caspases)

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10
Q

What happens to cisplatin after entering outer hair cells?

A

can be aquated to form the cisplatin- monohydrate complex (which is more reactive)

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11
Q

What is the role of cisplatin-monohydrate complex?

A

can activate NOX3 (resulting in ROS production)

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12
Q

Where to loop diuretics work in the inner ear?

A

stria vascularis

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13
Q

What channels do loop diuretics block in the inner ear?

A

Na+/K+/2Cl- co-transporter

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14
Q

What is the significance of blocking the Na+/K+/2Cl- co-transporter in the inner ear?

A

diuretics upset the fluid balance and this results in edema of stria vascularis and loss of function→ decrease in endocochlear potential.

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15
Q

What is different about loop diuretic ototoxicity compared to cisplatin and aminoglycoside induced toxicity?

A

it is dose-rate dependent (and only temporary, though worsened by comorbidities)

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16
Q

What part of the brain controls emesis? Where is it?

A

central emesis center in the lateral reticular formation of the mid-brainstem

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17
Q

What receptors are present in the CTZ?

A

high in 5-HT3, D2 and opiod receptors

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18
Q

What two structures is the central emesis center close to?

A

chemoreceptor trigger zone

solitary tract nucleus

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19
Q

What receptors are present in the STN?

A

Enkephalin, Histamine, Ach and 5-HT3

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20
Q

Where is the CTZ?

A

in the area postrema at the bottom of the fourth ventricle

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21
Q

List the Antihistamine/ Anticholinergics used to treat vertigo-induced emesis.

A

Meclizine HCl
Diphenhydramine
Promethazine HCl
Scopolamine

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22
Q

Which of the Antihistamine/ Anticholinergics has the longest half life?

A

scopolamine patches (72 hour)

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23
Q

MOA: M1 receptor blocker

A

Scopolamine

24
Q

MOA: Cerebellum H1 and M1 receptor blockers

A

Meclizine HCl
Diphenhydramine
Promethazine HCl

25
Q

Which Antihistamine/ Anticholinergic is a CYP2D6 substrate and inhibitor?

A

Diphenhydramine

Promethazine HCl

26
Q

Which Antihistamine/ Anticholinergic is a CYP2D6 substrate and should be used with caution with CYP inhibitors?

A

Meclizine HCl

27
Q

What are the major DDIs for antihistamine/anticholinergics?

A

caution with anti-muscarinics and sedatives

28
Q

Which group of people should NOT take Antihistamine/ Anticholinergics?

A

the elderly

29
Q

Which drug has a BBW: for use by injection → fatal respiratory depression in <2 yo?

A

Promethazine HCl

30
Q

What drug has xerostomia and ocular effects if you get it in your eye?

A

scopolamine (patch form worse)

31
Q

Which drug has WORSE drowsiness in WOMEN?

A

Meclizine HCl

32
Q

What drug is used to treat psychosomantic emesis?

A

Diazepam

33
Q

What are the serotonin antagonists used prophylacticly to treat emesis?

A

Dolasetron
Granisetron
Ondansetron
Palonsetron

34
Q

What is the MOA of the “setrons”?

A

Block 5-HT3 Receptors in the CTZ and STN

35
Q

How are the “setrons” usually given?

A

with corticosteroids for IV or PO prophylaxis of emesis

36
Q

Which “setron” needs to be dose adjusted in hepatic failure?

A

ondansetron

37
Q

What are the DDIs of concern with “setrons”?

A

CYP inhibitors or cardiac drugs

38
Q

TOXICITY: Chronic use→ blood marrow suppression/blood dyscrasias; risk of QT prolongation and torsade de pointes

A

Prochlorperazine

Chlorpromazine

39
Q

TOXICITY: Hypersensitivty reactions; QT prolongation; HA, constipation, diarrhea

A

Setrons

40
Q

Which “setrons” require EEG monitoring?

A

dolasetron and ondansetron

41
Q

List the D2 receptor antagonists.

A

Prochlorperazine

Chlorpromazine

42
Q

What is the major DDI with the D2 receptor antagonists?

A

antipsychotics (increase CNS adverse effects)

43
Q

What is the MOA of D2 receptor antagonists?

A

Block D2 receptors in CTZ and have anticholinergic and antihistaminic effects

44
Q

D2 receptor antagonists are useful in what type of vertigo?

A

motion sickness

45
Q

List the NK1/SP receptor antagonists used to treat emesis.

A

Aprepitant

Fosaprepitant

46
Q

What is the MOA of NK1/SP receptor antagonists?

A

Block receptors in the STN and GI

47
Q

Which of the NK1/SP receptor antagonists is a prodrug? How is it activated

A

Fosaprepitant is pro-drug activated by extra-hepatic metab.

48
Q

Do NK1/SP receptor antagonists have CYP interactions?

A

yes- CYP metabolized and inhibitor of CYP3A4

49
Q

List the cannabinoid receptor agonists.

A

Dronabinol

THC

50
Q

What is the MOA of cannabinoid receptor agonists?

A

GPCR coupled decrease in neuronal activity in medullary vomiting center and ST. Opposes 5-HT3 mediated stimulation from vagal afferents

51
Q

TOXICITY: Schedule III drug (produces high with elation and heightened awareness)

A

Dronabinol

THC

52
Q

In what patients should you avoid use of cannabinoid receptor agonists?

A

patients with h/o substance abuse

53
Q

How do cannabinoid receptor agonists stimulate appetite?

A

CB receptors in lateral hypothalamus

54
Q

What is commonly done for patients receiving highly emetogenic chemotherapy cocktails (ex. with cisplatin, carmustine, cyclophosphamide, etc)?

A

prophylactic drugs for emesis

55
Q

What are the main drugs used in prophylaxis of chemotherapy nausea/vomiting?

A

serotonin antagonist, an NK-1 antagonist, and a corticosteroid

56
Q

What drugs are just as effective as the normal anti-emesis cocktail for emesis prophylaxis but re ALWAYS used in combination?

A

corticosteroids (ex. methylprednisolone and dexamethasone)

57
Q

How do methylprednisolone and dexamethasone work to treat emesis?

A

antiemetic mechanism remains unclear, but possibly via steroid receptors in the STN or reduction in serotonin release

Neuro 2 (11 decks)

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