Oto Pharm Flashcards

1
Q

Irreversible ototoxic drugs

A

Aminoglycosides, cisplatin, and maybe loop diuretics (furosemide)

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2
Q

MOA of ototox seen in aminoglycosides

A

Entry into outer hair cell through mechanoelectrical transucer channels -> formation of AG-Fe complex to form ROS -> Activation of JNK -> nucleus for increase in cell death pathway -> to mitochondria -> increase cytochrome c -> increase capsases and cases-independent apoptosis

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3
Q

MOA of cisplatin ototox

A

entry into outer hair cell -> formation of monohydrate complex -> activate NOX -> increase ROS -> activate JNK -> … -> apop via CAPSASE DEPENDENT MECH ONLY

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4
Q

MOA of ototox seen with furosemide (loop diuretics)

A

Block Na/K/2Cl channels also in ear= disruption of fluid balance with edema and loss of fx

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5
Q

T/F: Dose dependent ototox with aminoglycosides and loop diuretics

A

True

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6
Q

Which drugs are considered inappropriate for use in geriatric pts

A

Antihistaminergics aka Diphenhydramine, meclizine, and promethazine

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7
Q

Vertigo tx with longest duration

A

Scopalamine

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8
Q

Which antihistaminergic has a BBW for use by injection

A

Promethazine

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9
Q

AntiCHOLINERGIC used in vertigo that blocks M1 and stimulation of VIII

A

Scopalamine

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10
Q

Antihistamines utilized in vertigo affect which receptors

A

H1 and M1 (block)

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11
Q

Major receptors found in chemoreceptor trigger zone (CTZ).

A

Serotonin (5-HT), dopamine (D2), and opiods

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12
Q

Major receptors found in solitary nucleus tract (STN)

A

Enkephalin, histamine, Ach, and Serotonin (5-HT3)

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13
Q

3 phases of vomiting

A

Pre-ejection, retching, and ejection

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14
Q

Location of the central emesis center

A

Lateral reticular formation

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15
Q

How does CTZ monitor blood and CSF for toxic substances to trigger nausea and vomiting sensations through central emesis center?

A

Lack of BBB

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16
Q

Central emesis center receives information from what areas?

A

Gut (vagus n), CTZ, Cerebral cortex (anticipatory vomiting), and vestibular apparatus (motion sick)

17
Q

Efferents from central emesis go where?

A

Nuclei in charge of salivation, respiration and vasomotor activity

18
Q

Ex of serotonin antagonists

A

OndanSETRON, graniSETRON, dolaSETRON

19
Q

ADE of Setrons

A

Hypersensitivity rxn, QT prolongation, interactions with CYP inhibitors

20
Q

What drug increases the 5HT-3 blockage of setrons?

A

Dexamethasone

21
Q

Most effective class of anti-emetics

A

Setrons (serotonin blockers)

22
Q

T/F: D2 antagonists are for use in Chemo-induced NV

23
Q

D2 receptor antagonism works at which part of the NV cascade

A

Chemoreceptor trigger zone

24
Q

ADE with chronic use of Clor-azine

A

Bone marrow suppression and blood dyscrasias and QT prolongations

25
What drug class are you worried about mixing with chlor-azines
Antipsychotics
26
Two D2 receptor antagonists
ProCHLORperAZINE and CHLORpromAZINE
27
MOA of AREPITANT and fosapREPITANT
Substance P/neurokinin-1 recep antagonist (work in solitary tract)
28
T/F: REPITANTS do not interact with CYP
F (CYP 3A4)
29
Two cannabinoid recep agonists
Dronabinol and THC
30
MOA of Dronabinol and THC
Opposes 5-HT3 mediated stimulation of vagus and appetite stimulation
31
ADE of Dronabinol and THC (if its really an ADE)
Getting highhhhhhhhh and the munchies
32
In terms of an antiemesis effect, where do corticosteroids work
Steroid receptors in STN
33
Drug used in anticipatory vomiting (CNS effect) and vertigo
Diazepam
34
Cisplatin, mechlorethamine, streptozotocin, cyclophosphamide, carmustine and dacarbazine have what in common?
All high likelihood of emesis when used as chemotherapy