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OS9.2 - Neuro > Pharm > Flashcards

Pharm Flashcards

1
Q

MOA of Benzodiazepines

end in -lam or -pam

A
  • binds the BZD receptor site on the alpha subunit of the GABA receptor
  • there are 3 receptor subgroups: BZ1, 2, 3; BZDs act at all 3 and each results in a different depressive effect:
    BZ 1 - sedation, amnesia
    BZ 2 - anxiolysis
    BZ 3 - myorelaxation, anticonvulsant
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2
Q

MOA of Zolpidem [Ambien], Zaleplon, and Eszopiclone

A

Benzodiazepine receptor agonists; only bind the BZ-1 receptor subgroup

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3
Q

MOA of Ramelteon

A

Melatonin receptor agonist; MT is a GPCR and stimulation induces sleep

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4
Q

MOA of Doxepin, Mitazapine, Trazodone

A
  • Antidepressants (doxepin is a TCA)
  • sedation is a side effect when used for depression but for insomnia it achieves clinical utility
  • caution with SI and psychosis
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5
Q

Suvorexant

A
  • Dual orexin receptor antagonist
  • orexin mediates transition between sleep and wake
  • CI’d in narcolepsy
  • beware SI
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6
Q

Major drug classes commonly used to treat insomnia

A 
On-label for insomnia:
- Benzodiazepines
- BZD receptor agonists
Most are used off-label:
- melatonin agonist
- Antidepressants
- TCA
- 1st gen antihistamines (diphenhydramine and doxylamine)
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7
Q

MOA of barbiturates

A

binds/stimulates GABA receptor in the middle of the transmembrane portion

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8
Q

Which is allowed in pregnancy: BZDs or BzRAs?

A

BzRAs - these are Category C

BZDs are Cat X

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9
Q

Flumazenil

A

BZD and BzRA antagonist; given IV, can be antidote for OD but may cause withdrawal symptoms and/or seizures

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10
Q

Sedative MOA of antihistamines

A
  • cross BBB, act on histamine receptors in tuberomammillary nucleus; removing histaminergic tone reduces wakeful state
  • don’t use in elderly
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11
Q

Treatment of tension HA

A

NSAIDs

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12
Q

Treatment of cluster HA

A
  • triptans, or

- ergots plus “burst-and-taper” steroids

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13
Q

Prophylaxis of migraine

A 
Involves 1/more different drug classes: antiepileptic, antidepressants, beta-blockers.
1st line drugs:
- amitriptyline
- divalproex or valproic acid
- propanolol or timolol
- topiramate
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14
Q

Acute treatment of migraine

A
  • aimed at mitigating action of “inflammatory” mediators, which are NTs/NPs released that cause a sterile inflammatory response
  • tx includes NSAIDs, ergots, triptans
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15
Q

MOA of triptans

A

serotonin agonists:
- produce selective vasoconstriction via 5-HT1 B receptors,
and
- presynaptic inhibition of the trigeminovascular inflammatory response via 5-HT1 D/F receptors

Nasal spray for fast onset: sumatriptan and zolmitriptan.
More effective than ergots.

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16
Q

MOA of NSAIDs for treating migraine

A

COX inhibition, decreased synthesis of inflammatory mediators

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17
Q

MOA of ergots

A
  • sm muscle contractions, like muscular arteries –> vasoconstriction
  • too much (as in mold in middle ages) would constriction distal arteries and lead to a painful gangrenous death
  • less effective than triptans; DON’T take within 24hrs of triptans because they both do vasoconstriction
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18
Q

What to do for a pregnant woman with migraines?

A

Acetaminophen in 1st trimester.
If persists - opioids.
DON’T USE ERGOTS (also avoid during lactation).

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19
Q

MOA of Amitriptyline

A

decreases reuptake of NE and 5HT; strong anticholinergic action
*off-label for migraine

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20
Q

MOA of Divalproex or Valproic acid

A

Na channel blocker; increases GABA activity

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21
Q

MOA of Topiramate

A

blocks Na and Glutamate; increases GABA activity

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22
Q

MOA of Propranolol and Timolol

A

decreases arterial dilation, decreases NE-induced lipolysis

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23
Q

Only FDA approved drug for migraine prophylaxis in kids

A

propranolol

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24
Q

Why are brain tumors hard to treat?

A
  • BBB
  • astrocytes help protect tumor cells
  • traditional resistance mechanisms
  • brain tumors overexpress P-gp
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25
Q

Carmustine (BCNU): MOA

A
  • DNA alkylator PLUS its breakdown product carbamylate proteins which inhibits DNA repair (“carmustine carbamylates”)
  • indicated for astro, medulloblastoma, brain mets, and malignant glioma
  • parenteral; wafer for high grade gliomas
  • lipophylic, non-ionized
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26
Q

Lamustine (CCNU): MOA

A
  • DNA alkylator
  • only indicated for malignant glioma
  • oral
  • lipophylic, non-ionized
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27
Q

Temozolamide: MOA

A
  • oral pro-drug that is non-enzymatically activated to DNA methylating agent
  • MGMT can undo the methylation, tumor cells can upregulate MGMT
  • causes myelosuppression, N/V; teratogen
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28
Q

Local delivery techniques for chemo to brain tumors

A
  • carmustine wafer

- convection enhanced delivery (infusion catheter)

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29
Q

Chemo-fog: what is it and how is it produced

A
  • chemo-related cognitive impairment: verbal/visual memory, attention, concentration, motor skills, multitasking
  • may be 2/2 direct neurotoxic effects of the chemo, or mediated via cytokines (TNF ab is protective in animal models)
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30
Q

What treatments are there for brain tumors?

A
  • steroids (edema)
  • anticonvulsants (seizures)
  • surgery, WBRT, radiosurgery; alone or in combination
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31
Q

Bacterial Meningitis treatment for a patient 1mo-50yo

A

Vancomycin + cefotaxime or ceftriaxone + ampicillin if listeria suspected

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32
Q

MOA, AEs of cephalosporins

A

MOA: inhibits cell wall synthesis (transpeptidation)
AEs: GI upset, diarrhea, vomiting, injection site pain/phlebitis, rash

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33
Q

MOA, AEs of vancomycin

A

MOA: inhibits cell was synthesis (transpeptidation and transglycosylation)
AEs: nephro-/oto-toxicity

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34
Q

Aspergillosis

A

Voriconazole IV

Alt: Lipid AmpB

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35
Q

Blastomycosis, mild

A

Itraconazole PO

Alt: Fluconazole

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36
Q

Blastomycosis, severe

A

Amp B IV then Itraconazole PO

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37
Q

Candidiasis

A

Fluconazole PO

Alt: Azole, or AmpB, or fungin agent

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38
Q

Coccidiodiomycosis

A

Fluconazole IV/PO or Itraconazole PO

Alt: AmpB

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39
Q

Cryptococcus

A

AmpB IV plus Flucytosine PO, then Fluconazole PO

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40
Q

Histoplasmosis

A

AmpB IV plus Itraconazole PO

Alt: Fluconazole

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41
Q

Mucormycosis

A

AmpB

Alt: Posaconazole

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42
Q

Sporotrichosis

A

AmpB IV and/or Itraconazole PO

Alt: Itraconazole PO

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43
Q

What antifungals penetrate CSF?

A

Fluconazole, Voriconazole, and Flucytosine

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44
Q

Flucytosine - MOA, indication, AE

A
  • converted to 5-FU by fungus, block thymidylate synthase, disrupts DNA synthesis
  • cryptococcus
  • not used alone b/c resistance develops rapidly
  • AEs: bone marrow toxicity, derangement of liver enzymes (sometimes)
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45
Q

Nitrous oxide

A

Enhances inhibition:

  1. potentiates 2-pore K channels
  2. also potentiates GABAa, inwardly rectifying K channels, and glycine
  3. inhibits NMDA, nAChR, 5HT, and KAR
    - maintains CO2 reflex drive to breathe (no effect on protective reflexes)
    - questionable damages; animal teratogen, spont. abortions?, neuronal damage in babies?; unclear
    - second gas effect means this plus another inhaled agent is additive
    - analgesic effects
    - must administer O2 upon awakening 2/2 diffusional hypoxia
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46
Q

Halothane

A
  • highest blood:gas partition coefficient, so it takes the longest time and most volume to build up in the blood
  • highest % metabolized (hepatically), so it takes the longest to leave the body
  • highest lipophilicity, so it gets bound by blood very well
  • lowest MAC
  • can cause halothane hepatitis
  • rarely used anymore
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47
Q

Enflurane

A
  • effects on muscle relaxation

- pro-epileptic

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48
Q

Isoflurane

A
  1. potentiates GABAa, 2-pore K channels, glycine, serotonin, and kainate
  2. inhibits inwardly rectifying K channels and AMPAR’s
    - effects on muscle relaxation
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49
Q

Desflurane

A
  1. potentiates GABAa
  2. sorta potentiates muscarinic ACh
  3. inhibits voltage-gated K channels and KARs
    * much lower BGPC than halothane therefore go air–>blood–>brain (and back) much faster
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50
Q

Sevoflurane

A
  1. potentiates GABAa and glycine

* much lower BGPC than halothane therefore go air–>blood–>brain (and back) much faster

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51
Q

Meyer-Overton hypothesis

A

states that anesthetic activity is directly linked to lipid solubility - the more soluble, the greater anesthetic activity
(not entirely true)

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52
Q

Inhalational anesthetic agents basically have what 2 MOAs?

A
  1. enhance inhibitory signaling (GABA, glycine)

2. inhibit excitatory signaling (glutamate, ACh, NMDARs, AMPARs)

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53
Q

Guedel stages of anesthesia

A
  1. analgesia
  2. delerium: inc. BP, mydriasis, inc. muscle tone; likely removing inhibitory paths
  3. Plane 1: BP normal, miosis, muscle tone trending down
  4. Plane 2: dec. BP, dec. muscle tone
  5. Plane 3: HOTN, mydriasis again
  6. Plane 4: HOTN, mydriasis
  7. medullary paralysis/death
    * with depth of unconsciousness comes depression of both CV (BP, HR, CO) and pulm (RR, TV) systems
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54
Q

Different anesthesia concentrations are required to produce

A
  • action on different neuronal pathways (dose-dependent)

- degree of absorption (higher concentration)

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55
Q

Blood-gas partition coefficient

A
  • there’s a difference in concentration of a gas in going from gas (air) to liquid (blood)
  • partial pressure/tension will be maintained but absolute mass/volume of the anesthetic agent will change
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56
Q

MAC

A
  • minimum alveolar concentration (volume %): measure of potency
  • NO is highest, Halothane is lowest
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57
Q

Agents used for anesthesia induction

A
  • thiopental, propofol, etomidate

- enhance GABA/glycine, inhibit excitation

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58
Q

Propofol

A
  • enhances GABA and glycine
  • inhibit NMDARs (not as much as ketamine; blocks Glut binding) and nACh/mACh/AMPA
  • anti-emetic; propofol infusion syndrome (met acidosis, rhabdomyolysis, arrhythmia, CF, RF)
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59
Q

Ketamine

A
  • potentiates GABA and 5-HT
  • inhibits NMDARs (physically occlude the channel) and mACHRs
  • the only IV anesthetic that increases (instead of depresses) CBF O2 and ICP; is also cardiostimulatory
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60
Q

Benzodiazepines for anesthesia

A
  • diazepam, lorazepam, and midazolam
  • they potentiate GABAa by binding and altering the conformation, which increases potency of whatever GABA is present
  • have the longest onset of action and half-lives
  • very hard to OD (compared to barbs) since they have a ceiling of CNS depression (exception is in combo with alcohol/other drugs)
  • no analgesia; anticonvulsant/amnesic
  • antidote: flumazenil
61
Q

Opioids for anesthesia

A
  • morphine, meperidine, fentanyl (20min drug), remifentanil (ultra short-acting)
  • controversial because they can cause bradycardia (vagus or direct on SA/AV nodes) and HOTN/HTN; also dose-dependent respiratory depression
62
Q

4 goals of balanced anesthesia

A
  1. relax muscles
  2. relieve anxiety
  3. prevent secretions
  4. induce unconsciousness
63
Q

Etomidate

A
  • used for anesthesia induction
64
Q

Barbiturates for anesthesia

A
  • thiopental
  • they potentiate GABAa by binding within the channel (on the left in the picture) and prolonging GABA binding, which increases efficacy
  • quintessential CYP inducers – can exacerbate porphyria
65
Q

Neurolept-Analgesia

A

the use of a drug combination that produces pain relief and provides a state of indifference

66
Q

Malignant hyperthermia

A
  • MOA: IC Ca release from SR which stimulates metabolism and generates heat; muscle rigidity and tachycardia/tachypnea
    Culprits:
  • Succinylcholine (NM blocker)
  • all volatile anesthetic agents (desflurane, isoflurane)

Treatment: Dantrolene (returns Ca to SR), hyperventilate with O2, cool core temp, correct hyperK and acidosis

67
Q

MOA of Local anesthetics

A
  • block neuronal V-gated Na channels from the INSIDE
  • must be lipophilic to pass into membrane
  • differential blockade of nerve fibers in a bundle
68
Q

Nerve type order of sensitivity to local anesthetic application

A

small > large; non-myelin > myelinated

  1. B fibers
  2. C fibers (SNS and dorsal root) and Adelta fibers
  3. Agamma fibers
  4. Abeta fibers
  5. Aalpha fibers
69
Q

What conditions do local anesthetics prefer?

A
  1. When the nerve is firing: the agent can only reach the internal binding site when the channel is open or when it’s inactivated
  2. Basic: most are weak bases (pKa~8), so more of the agent will be non-ionized in an environment with pH>8; within the nerve the pH is 7, so the agent is recharged which also happens to be better for binding; if the pH is lower (like in area of inflammation) it’d be a weaker, less durable nerve block because not as much gets into the cell
70
Q

How is the LA structure represented in the name?

A
  • if word leading up to “-caine” contains an i, it’s an amide (which also contains an i)
  • if it does not contain an i, it’s an ester
    *Exception: articaine contains both
    Amide vs. ester is the linker btw the amine and aromatic appendage comprising the local anesthetic
71
Q

Phentolamine

A
  • alpha adrenergic blocker

- applied following local anesthetic to reverse VC and increase blood flow to the region, hasten removal of anesthetic

72
Q

Local Anesthetics with these duration of action:

  • short-acting
  • intermediate-acting
  • long-acting
A 
- short-acting (least potent):
   procaine
   chloroprocaine
- intermediate-acting: PALM
   prilocaine, articaine, 
   lidocaine, mepivacaine
- long-acting (more potent): BRT
   bupivacaine
   ropivacaine
   tetracaine
73
Q

Acquired methemoglobinemia

A
  • excess accumulation of ferric form of Hgb that can’t release O2
  • associated with prilocaine, and to a lesser extent benzocaine
  • will see blue skin, HA, SOB, lack of energy
  • treat with ascorbic acid or methylene blue
74
Q

Topical local anesthetics

A
  • benzocaine
  • dyclonine
  • dibucaine (ONLY skin)
  • pramoxine (ONLY skin)
75
Q

EMLA and LET

A 
EMLA = "eutectic mixture of local anesthetics"; lidocaine + prilocaine used before cannulation or skin graft harvesting
LET = lidocaine-epi-tetracaine; liquid application for stitches that provides both analgesia and VC
Lidocaine-oxymetazoline = used for reducing vessels, used by otolaryngologists
76
Q

What’s the typical pre-operative drug sequence, and what’s the role of each drug?

A
  1. Psych prep - relieve anxiety (BZD*, phenothiazines, antihistamines 1st gen), sedation, amnesia, +/- analgesia (NSAID/opiate)
  2. Reduce ANS - dry secretions, dec. gastric volume, inc. gastric pH; all to prevent aspiration
  3. Prophylaxis - against allergic rxn
    Then off to surgery.
    *which BZD chosen depends on desired duration of action.
77
Q

H1 vs. H2 antagonist CNS effects

A

H1 - Diphenhydramine; Promethazine; Hydroxyxine
- sedative, cholinergic antagonism (drying secretions), anti-emetic

H2 - Cimetidine; Ranitidine

  • only cimetidine has some sedative effect
  • no other CNS effects
78
Q

Drugs (and MOA) for anti-emesis

A
  • they inhibit the chemo trigger zone (operates with ACh, 5HT, DA, Hist, SP, opioids), or suppress emetic signals from GI tract (via vagus n.)
  1. Ondansetron - 5HT3 receptor antagonist
  2. Scopolamine - muscarinic antagonist
  3. Metoclopramide - D2 receptor antagonist
79
Q

Roles of drugs employed in rapid sequence intubation

A
  1. oxygenation
  2. avoid inc. ICP: lidocaine, fentanyl, vecuronium
  3. sedative + short-acting NMB (usually succinylcholine)
80
Q

Post-op drugs used in respiratory and CV support

A

Dopamine, Phenylephrine, Nitroprusside, Trimethaphan

81
Q

What are the pharmacologic reasons for delayed awakening from anesthesia?

A
  • MCC is residual anesthetics and ancillary drugs

- reversal aimed at most likely agent: usually narcotic or BZD

82
Q

Gastrokinetic agent

A
  • Metoclopramide to accelerate gastric emptying (compromised by antagonism from anti-ACh and narcotics)
  • can also use water to stimulate the gastric stretch receptors
83
Q

Atropine, Scopolamine, and Glycopyrrolate

A

These are anticholinergics that block muscarinic stimulation arising from Anti-AChE’s; used to mitigate reflex bradycardia, block vagal activity, and dry secretions:

  • glycopyrrolate has the most anti-sialogogue effect
  • atropine has the strongest vagolytic effect
  • scopolamine has the strongest sedative effect
  • atropine and scopolamine can cause delirium and cognitive decline
84
Q

Drugs used for sedation

A

BZDs and 1st gen H1 antagonists:

  • diazepam, lorazepam
  • promethazine, hydroxyzine, diphenhydramine
85
Q

Drugs used for amnesia

A
  • BZDs (also used for sedation and anxiety)
86
Q

Drugs used for anxiolysis

A
  • BZDs (also used for sedation and amnesia)
  • phenothiazines (anti-DA/ACh/Hist effects)
  • 1st gen antihistamines
87
Q

Anaphylactic reaction - precipitating drugs?

A

epinephrine, aminophylline, hydrocortisone, methylprednisolone, barbiturates, etomidate, local anesthetics, NMBs, and narcotics

88
Q

What are the symptoms of an anaphylactic reaction, and what to do about it? (prevention and treatment)

A
  • Sx: respiratory depression and bronchospasm, CV issues, and cutaneous urticaria/flushing/edema
  • Prevention: H1/H2 receptor blockers (won’t prevent histamine release)
  • Acute Tx: stop drug/anesthesia, give O2, give epi, expand intravascular volume for CV support
89
Q

Potential errors of Drug Administration

A
  • wrong drug, wrong dose, wrong solution
  • incompatible combination
  • wrong site
  • wrong rate of administration
90
Q

Muscarinic antagonists for ocular administration: Mnemonic

A 
ACH anTagonistS
A = atropine
C = cyclopentolate
H = homotropine
T = tropicamide
S = scopolamine
*These drugs produce cycloplegia and mydriasis; used to treat inflammation and for eye exam; CI'd in glaucoma/sulfa allergy
91
Q

Sympathomimetics for ocular administration (suffixes)

A
  • Ephrine: dipivefrin and phenylephrine
  • onidine: Apraclonidine, brimonidine
  • zoline: Naphazoline, Tetrahydrozoline

–> stimulate the alpha-2 receptors in the ciliary body to reduce aqueous production; stimulate a1s in vessels to vasoconstriction and reduce diffusion

92
Q

Muscarinic agonists for ocular administration: Mnemonic

A 
CAP:
Carbachol
ACh
Pilocarpine
--> constrict pupil, open TM for outflow
93
Q

Timolol

A

Beta-adrenergic antagonist; blocks the production of aqueous humor by ciliary body

94
Q

Levobunolol

A

Beta-adrenergic antagonist; blocks the production of aqueous humor by ciliary body

95
Q

Metipranolol

A

Beta-adrenergic antagonist; blocks the production of aqueous humor by ciliary body

96
Q

Carteolol

A

Beta-adrenergic antagonist; blocks the production of aqueous humor by ciliary body

97
Q

Carbachol

A

Muscarinic agonist; constricts the pupil to open the TM for aqueous outflow

98
Q

Pilocarpine

A

Muscarinic agonist; constricts the pupil to open the TM for aqueous outflow

99
Q

Dipivefrin

A

Sympathomimetic; stimulates alpha 2 in ciliary body to reduce aqueous production, vasoconstricts (a1) vessels to ciliary body to reduce diffusion

100
Q

Phenylephrine

A

Sympathomimetic; stimulates alpha 2 in ciliary body to reduce aqueous production, vasoconstricts (a1) to reduce diffusion

101
Q

Apraclonidine

A

Sympathomimetic; stimulates alpha 2 in ciliary body to reduce aqueous production
*This is pretty selective for a2

102
Q

Brimonidine

A

Sympathomimetic; stimulates alpha 2 in ciliary body to reduce aqueous production, vasoconstricts (a1) to reduce diffusion

103
Q

Naphazoline

A

Sympathomimetic; stimulates alpha 2 in ciliary body to reduce aqueous production, vasoconstricts (a1) to reduce diffusion

104
Q

Tetrahydrozoline

A

Sympathomimetic; stimulates alpha 2 in ciliary body to reduce aqueous production, vasoconstricts (a1) to reduce diffusion

105
Q

Aflibercept

A

decoy receptor for VEGF in the tx of macular degeneration

106
Q

Pegaptanib

A

VEGF antagonist; tx for macular degeneration

107
Q

Ranibizumab

A

mab for VEGF for macular degeneration

108
Q

Bevacizumab

A

mab for VEGF for macular degeneration

109
Q

Verteporfin

A
  • IV agent that (when activated by laser) generates free radicals which cause vessel damage and occlusion of choroidal neovascularization
  • tx for macular degeneration
  • AEs: temp photosensitization
110
Q

Where are SNS receptors in the eye?

A
  • -> a1: dilator smooth (aka iris radial) muscle, oriented radially, contracts to cause mydriasis
  • -> a1: lacrimal gland secretions
  • -> a2: SNS autoreceptor in ciliary epithelium; stimulation is sympatholytic
  • -> B2: stimulate ciliary epithelium to produce aq. humor
  • -> B2: ciliary muscle relaxation
111
Q

Where are PSNS receptors in the eye?

A
  • -> M3: pupillary sphincter smooth muscle, oriented circularly, contracts to cause miosis
  • -> M2/3: stimulate lacrimal secretions
  • -> M3: ciliary muscle accommodation
112
Q

Ciliary body

A

2 functions:

  1. secretes aqueous humor by epithelial bilayer (stimulated by B2, inhibited by a2 SNS)
  2. change shape of the lens by ciliary muscle (accom. by M3 PSNS; relaxation by B2 SNS)
113
Q

How do eyedrops cause systemic toxicity?

A
  • absorbed via conjunctiva, sclera in the eye
  • absorbed via ocular blood vessels
  • after draining from the eye to the nasopharynx they can be absorbed through mucosa, or drip down to GI tract
114
Q

What drug classes produce miosis/loss of accommodation?

Produce mydriasis?

A
  • miosis: PSNS mimics and opioids*
  • mydriasis: SNS mimics
  • opioids remove the inhibition of EW nucleus and allow it to dominate tone
115
Q

How to treat open and closed angle glaucoma?

A

Open: decrease aq. humor production; inc. outflow; use PGs, sympathomimetics, or miotics

Closed: surgical iridectomy; short-term meds to dec. IOP prior to surgery

116
Q

What drugs are used to treat glaucoma?

A

1st line: PG(F2) analogs (thought to facilitate outflow; can cause iris hyperpigmentation and hypotrichosis)
Then:
- beta-blockers (recall B2 stimulate aq humor prod)
- carbonic anhydrase inhibitors: -zolamides
- sympathomimetics: stimulation of a2 auto-receptors inhibits SNS action, a1 stimulation vasoconstricts

117
Q

Carbonic anhydrase inhibitors

A

“-zolamide”

  • reduce bicarb secretion and fluid transport, thereby dec. IOP
  • taste disturbance
  • sulfa drug - allergies
118
Q

Macular degeneration treatment

A
  • they all have to interrupt VEGF-mediated vascular growth
  • injected into vitreous humor
  • beware of arterial thromboembolic events (ATEs)
119
Q

Carbamazepine

A
  • inhibits Na channels (from intracellular side)
  • AEs: CNS sx like dizziness, drowsy, ataxia, blurred vision; routine monitoring for agranulocytosis or aplastic anemia; rare derm effects (rash/DRESS; SJS/TEN in asians)
  • teratogen
120
Q

Ethosuximide

A
  • inhibits T-type Ca channels to reduce pacemaker currents
121
Q

Gabapentin

A
  • acts presynaptically to enhance GABA release

- inhibits Ca channel subunit

122
Q

Lamotrigine

A
  • inhibits Na channels (from intracellular side)
  • serious rash - SJS/TEN
  • teratogen
123
Q

Phenytoin

A
  • inhibits Na channels (from intracellular side)
  • zero-order kinetics, so half-life varies with dose
  • gingival hyperplasia (>15%)
  • hypertrichosis, hirsutism, SJS/TEN are rare
  • CNS effect MC are nystagmus, HA, ataxia, incoordination
  • teratogen
124
Q

Valproate

A
  • inhibits Na channels (from intracellular side)
  • inhibit Ca channels to reduce pacemaker currents
  • enhances GABA activity (pre-synaptically? vs. in the cleft?)
  • CNS effects, thrombocytopenia, rare derm effects (SJS/TEN/DRESS)
  • worst teratogen
125
Q

Clonazepam

A

GABA agonist (BZD)

126
Q

Felbamate

A
  • enhances GABA
  • dec. NMDA activity
  • **Aplastic anemia, myelosuppression, hepatic disease
127
Q

Pregabalin

A
  • inhibits Ca channels
128
Q

Topiramate

A
  • inhibits Na channels (from intracellular side)
  • decreases Glut activity
  • inc. GABA; inc. K current
  • weak CA inh, so monitor serum bicarb and beware of kidney stones
129
Q

Zonisamide

A
  • inhibits Na channels (from intracellular side)
  • inhibits T-type Ca channels
  • accumulates in RBCs
  • weak CA inh, so monitor serum bicarb and beware of kidney stones
130
Q

Lacosamide

A
  • inhibits Na channels (from intracellular side)
131
Q

Oxcarbazepine

A
  • inhibits Na channels (from intracellular side)

- possibly inc. K current and inhibits Ca channels

132
Q

ADME of AEDs

A
  • most are PO, may be slow-release
  • limited protein binding - except phenytoin and valproate
  • hepatic metabolism - exception: Gabapentin (no metabolism)
  • may interact with CYPs: esp. Carbamazepine and Phenytoin, so dose adjustment is needed over time (monitor serum with Carb, Ethosux, Gabapentin, Pheny, Valp)
  • urinary elimination
  • long half-lives
133
Q

First line drugs for primary generalized tonic-clonic seizures

A

Valproate
Lamotrigine
Keppra

134
Q

First line drugs for Absence seizures

A

Ethosuximide

Valproate

135
Q

First line drugs for atypical Absence, Myoclonic, Atonic seizures

A

Valproate
Lamotrigine
Keppra

136
Q

First line drugs for Status Epilepticus

A 
BZDs (IV lorazepam, IM midazolam, PR diazepam) - can rapidly terminate SE, but the have short half life so must be followed by IV AED:
Valproate
Phenytoin
Keppra
Phenobarbital
137
Q

Ototoxic drugs

A

Aminoglycosides - usually permanent
Cisplatin - irreversible
Loop diuretics - can be irreversible

138
Q

What is the etiology of drug-induced vertigo?

A
  • direct: affect hair cells

- indirect: changes BP (pre-syncope dizziness)

139
Q

What is the mechanism of ototoxicity for those drugs acting through caspase-dependent mechanisms?

A
  • AG enters outer hair cell, forms AG-Fe complex, makes ROS which activate JNK
  • Cisplatin enters outer hair cell and forms monohydrate complex, activates NOX3, ROS which activate JNK

JNK transcribes genes which trigger cytC release; apoptosis

140
Q

What is the mechanism of ototoxicity for loop diuretics?

A
  • inhibit Na/K/2Cl transporter

- upsets endolymph which results in edema and loss of function

141
Q

MOA of short-term tx of vertigo

A
  • act primarily on the H1 and M1 receptors; block them
  • meclizine hydrochloride
  • diphenhydramine
  • scopolamine (TD patch) - lasts 72hr
  • promethazine - BBW for injection
  • diazepam - for nausea from higher cortical centers (fear, emotion, anticipation, etc)
142
Q

Drugs to treat emesis

A
  1. Setrons: Serotonin antagonists; act in CTZ and NTS
  2. -axines: D2R antagonists
  3. -prepitants: SP/NK1 receptor antagonists
  4. Cannabinoid agonist
143
Q

Prochlorperazine

A
  • D2R at CTZ for anti-emesis
  • also have anti-hist/ACh activities
  • all-purpose, but NOT for CINV
144
Q

Chlorpromazine

A
  • D2R at CTZ for anti-emesis
  • also have anti-hist/ACh activities
  • all-purpose, but NOT for CINV
145
Q

MOA of Aprepitant and Fosaprepitant

A
  • substance P (SP) and neurokinin-1 (NK1) receptor antagonists
  • action at Nucleus Tractus Solitarius
  • fosaprepitant is a pro-drug
  • CYP3A4
146
Q

Dronabinol

A
  • agonist at the cannabinoid receptor
  • GPCR dec. activity in medullary vomiting center and NTS; opposes 5HT mediated vagal stimulation
  • stimulates appetite in lateral hypothalamus
147
Q

Prophylaxis of chemo-induced N/V (CINV)

A

MC: 5HT antagonist + NK1 antagonist + corticosteroid

148
Q

CYP activators among the anti-emesis drugs?

A

3A4: SP/NK1 antagonist
2D6: H1/M1 blockers
CYPs (in general): 5HT

OS9.2 - Neuro (10 decks)

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