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

A

False

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
Q

What drug class are you worried about mixing with chlor-azines

A

Antipsychotics

26
Q

Two D2 receptor antagonists

A

ProCHLORperAZINE and CHLORpromAZINE

27
Q

MOA of AREPITANT and fosapREPITANT

A

Substance P/neurokinin-1 recep antagonist (work in solitary tract)

28
Q

T/F: REPITANTS do not interact with CYP

A

F (CYP 3A4)

29
Q

Two cannabinoid recep agonists

A

Dronabinol and THC

30
Q

MOA of Dronabinol and THC

A

Opposes 5-HT3 mediated stimulation of vagus and appetite stimulation

31
Q

ADE of Dronabinol and THC (if its really an ADE)

A

Getting highhhhhhhhh and the munchies

32
Q

In terms of an antiemesis effect, where do corticosteroids work

A

Steroid receptors in STN

33
Q

Drug used in anticipatory vomiting (CNS effect) and vertigo

A

Diazepam

34
Q

Cisplatin, mechlorethamine, streptozotocin, cyclophosphamide, carmustine and dacarbazine have what in common?

A

All high likelihood of emesis when used as chemotherapy