45b - Vertigo Therapy Flashcards

1
Q

Which drugs produce notable irreversible ototoxicity?

A

aminoglycoside antibiotics and cisplatin, also possibly loop diuretics

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2
Q

What drugs can cause ototoxicity?

A

aminoglycosides, erythromycin, minocycline, fluoroquinolones, NSAIDs/salicylates, loop iduretics, cytostatic drugs and antimalarials

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3
Q

How do aminoglycosides cause ototoxicty?

A

drug entry into the outer hair cell results in cell death by either caspase-dependent OR independent mechanisms.
1 AG entry into outer hair cell through mechnoelectrical channels
2 formation of AG-iron complex creacts with arachidonic cid to form ROS
3 ROS can activate JNK
4 JNK translocates to nucleus to activate cell death

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4
Q

How does cisplatin cause hair cell death?

A

through caspase dependent mechanisms.

  1. CP enters outer hair cell
  2. CP forms mnohydrate complex MHC, MHC activates NOX-3, resulitng in ROS
  3. ROS activates JNK which translocates to nucleus
  4. nuclesu activates genes in cell death pathway to translocate to mitochondria
  5. mitochondria releases cty c and triggers Capsase apoptosis
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5
Q

How do loop diuretics cause ototoxicity?

A

by their natural mechanism of inhibiting Na/K/2Cl co-transporter, which is important in the ears as well as kidneys. Act through the stria medullaris to cause edema and loss of function that is dose-dependent.

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6
Q

What are treatments for vertigo?

A

M1 or H1 antagonists OR diazepam for psychosomatic induced vertigo

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7
Q

BBW for promethazine?

A

BBW for use by injection. Sedation and fatal respiratory depression

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8
Q

What are ADE of scopalamine?

A

xerostomia, drowsiness, oular effects after touching patch.

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9
Q

What is longest acting anti-vertigo drug?

A

scopalamine transdermal patch

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10
Q

What is MOA of meclinzine?

A

H1 and M1 antagonist

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11
Q

What is MOA of promethazine?

A

H1 and M1 antagonist

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12
Q

What is MOA diphenhydramine?

A

H1 and M1 antagonist

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13
Q

Which anti-vertigo drug should NOT be used with a cyp2D6 inhibitor?

A

meclizine because it is predominantly hepatic CYP2D6 metabolized.

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14
Q

Which antiemetic needs dose adjustmant in hepatic dysfunction?

A

ondansetron

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15
Q

ADE of D2 receptor antagonists?

A

chronic use leads to bone marrow suppression and blood dyscrasias,
risk of proonged QT and torsade de pointes
Don’t give with antipsychotics

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16
Q

Where do NK1 antagonists act?

A

in the substantia nigra

17
Q

What is primary interaction concern with N1 antagonists?

A

they are CYP3A4 inhibitors.

18
Q

What is mechanism of cannabinoid agonists?

A

G-protein coupled decrease in neuronal activity in medullary vomiting center and solitary tract nucleus.

19
Q

ADE of cannabinoid receptor agonists?

A

causes high. Caution in pts with history of stustance abuse. Most ommon effect is elation and heightened awareness

20
Q

What is treatment of choice for emesis from antineoplastics?

A

serotonin receptor antagonist + a corticosteroid and possibly an NK-1 antagonist.

21
Q

What is mechanism of corticosteroids as anti-emetics?

A

act on steroid receptors in STN to possibly reduce release of serotonin.