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Drugs > FA Neuro Pharm > Flashcards

FA Neuro Pharm Flashcards

1
Q

Mu-opioid receptor partial agonist and kappa opioid receptor agonist; produces analgesia

A

Butophanol

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2
Q

Very weak opioid agonist; also inhibits serotonin and NE reuptake (used for chronic pain)

A

Tramadol

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3
Q

Facilitates GABAa action by increasing DURATION of Cl- channel opening, thus decreasing neuron firing (barbiturates increase duration). Contraindicated in porphyrias.

A

Barbituates

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4
Q

Facilitate GABAa action by increasing FREQUENCY of Cl- channel opening. Decrease REM sleep,

A

Benzos

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5
Q

Act via the BZ1 subtype of the GABA receptor. Effects reversed by flumazenil.

A

Nonbenzo hypnotics

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6
Q

Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons.

A

Local anesthetics

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7
Q

Prevents the release of Ca2+ from the SR of skeletal muscle

A

dantrolene

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8
Q

Selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepinephrine and 5-HT, thereby increasing the availability of dopamine

A

Selegiline

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9
Q

NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)

A

Memantine

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10
Q

AchE inhibitors

A

Donepezil, galantamine, rivastigmine

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11
Q

Inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release

A

Tetrabenzamine, reserpine

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12
Q

5-HT1B/1D agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction. Half-life < 2 hrs

A

Sumatriptan

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13
Q

Increases Na+ channel inactivation, zero-order kinetics

A

Phenytoin

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14
Q

Increases Na+ channel inactivation

A

Carbamazepine

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15
Q

Increases Na+ channel inactivation, increases GABA concentration by inhibiting GABA transaminase

A

Valproic acid

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16
Q

Primarily inhibits high-voltage-activated Ca2+ channels; designed as GABA analog

A

Gabapentin

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17
Q

Blocks thalamic T-type Ca2+ channels

A

Ethosuximide

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18
Q

Increases GABAa action

A

Phenobarbital

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19
Q

Blocks Na+ channels and increases GABA action

A

Topiramate

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20
Q

Blocks voltage-gated Na+ channels

A

Lamotrigine

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21
Q

Unknown; may modulate GABA and glutamate release

A

Levetiracetam

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22
Q

Increases GABA by inhibiting reuptake

A

Tiagabine

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23
Q

Increases GABA by irreversibly inhibiting GABA transaminase

A

Vigabatrin

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24
Q

Decreases aqueous humor synthesis via vasoconstriction

A

Epinephrine

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25
Q

Tox: Mydriasis; do NOT use in closed-angle glaucoma

A

Epinephrine

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26
Q

Alpha2 agonist that decreases aqueous humor synthesis

A

Brimonidine

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27
Q

Tox: Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic run, ocular pruritus

A

Brimonidine

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28
Q

5 classes of drugs that can be used for glaucoma

A
  1. alpha agonists
  2. beta blockers
  3. diuretics
  4. cholinomimetics (direct and indirect)
  5. prostaglandin
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29
Q

What beta blockers can be used for glaucoma?

A

Timolol, betaxolol, carteolol

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30
Q

What diuretic can be used for glaucoma?

A

Acetazolamide

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31
Q

What alpha agonists can be used for glaucoma?

A

Epinephrine, brimonidine

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32
Q

Decreases aqueous humor synthesis via inhibition of carbonic anhydrase

A

Acetazolamide

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33
Q

Two direct cholinomimetics that can be used for glaucoma

A

pilocarpine and carbachol

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34
Q

two indirect cholinomimetics that can be used for glaucoma

A

physostigmine and chothiophate

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35
Q

What drug do you use in a glaucomic emergency?

A

pilocarpine - very effective at opening meshwork into canal of Schlemm

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36
Q

What is the mechanisms of cholinomimetics in treatment of glaucoma?

A

Increased outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

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37
Q

What are the side effects of cholinomimetics in treatment of glaucoma?

A

miosis and cyclospasm (contraction of ciliary muscle)

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38
Q

What prostaglandin is useful in glaucoma treatment?

A

Latanoprost (PGF2alpha)

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39
Q

what is the mechanism of latanoprost?

A

increased outflow of aqueous humor

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40
Q

tox latanoprost

A

darkens color of iris

41
Q

agonist at mu receptors

A

morphine

42
Q

agonist at delta receptors

A

enkephalin

43
Q

agonist at kappa receptors

A

dynorphin

44
Q

what opioid is used for cough suppression?

A

dextromethorphan

45
Q

what opioid is used for diarrhea

A

loperamide, diphenoxylate

46
Q

opioid analgesic mechs

A

act as agonists at opioid receptors to (open K+ channels, close Ca2+ channels) –> decreased synaptic transmission Inhibit release of ACh, NE, 5-HT, glutamate, substance P

47
Q

opioid antidote

A

naloxone or naltrexone

48
Q

Butorphanol mech

A

mu opioid PARTIAL receptor agonist and kappa opioid receptor agonist; produces analgesia

49
Q

CU butorphanol

A

severe pain (migraine, labor); causes less respiratory depression that full opioid agonists

50
Q

Butorphanol Tox

A

can cause opioid withdrawal sx is pt is also taking full opioid agonist (competition for opioid receipts). OD not easily reversed w. naloxone

51
Q

Tramadol mech

A

very weak opioid agonst; also inhibits serotonin and NE reuptake (works on multiple NTs - “tram it all” in with tramadol).

52
Q

CU tramadol

A

chronic pain

53
Q

Tramadol tox

A

opioid tox, decreases seizure threshold, serotonin syndrome

54
Q

ethosuximide mech

A

blocks thalamic T-type Ca2+ channels

55
Q

Tox ethosuximide

A

EFGHIJ

Ethosuximide causes Fatigue, GI distress, Headache, Itching, stevens-Johnson

56
Q

barbiturate mech

A

facilitate GABA(A) action by increasing the DURATION of chloride channel opening, thus decreasing neuron firing (barbiDURATes increase DURATion). Contraindicated in porphyria

57
Q

barbiturate CU

A

sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)

58
Q

barbiturate tox

A

respiratory and CV depression (can be fatal!); CNS depression (exacerbated by EtOH); dependence; drug interaxns (INDUCES P450!).

59
Q

barbituate AD?

A

none! supprotive - assist respiration and maintain BP

60
Q

phenobarbital, pentobarbital, thiopental, secobarbital

A

barbiturates

61
Q

benzo mech

A

facilitate GABA(A) action by increasing FREQUENCY of chloride channel opening, decrease REM sleep

62
Q

highest addictive potential, shortest acting benzos

A

Triazolam
Oxazepam
Midazolam

63
Q

status epilepticus tx

A

lorazepam, diazepam

64
Q

benzo AD

A

flumazenil

65
Q

flumazenil mech

A

competitive antagonist at GABA benzo receptor

66
Q

Non benzo hypnotic examples

A

Zolpidem
Zaleplon
Eszopiclone

67
Q

Zolpidem mech

A

act via the BZ1 subtype of the GABA receptor

68
Q

MAC =

A

miminal alvelolar concentration required to prevent 50% of subjects from moving in response to noxious stimulus (e.g. skin incision)

69
Q

inhaled anesthetic with hepatotoxicity

A

halothane

70
Q

inhaled anesthetic with nephrotoxicity

A

methoxyflurane

71
Q

inhaled anesthetic that is proconvulsant

A

enflurane

72
Q

inhaled anesthetic that can cause expansion of trapped gas in a body gravity?

A

nitrous oxide

73
Q

the one inhaled anesthetic that doesn’t cause malignant hyperthermia

A

nitrous oxide

74
Q

what besides inhaled anesthetics can cause malignant hyperthermia

A

succinylcholine

75
Q

tx malignant hypertension

A

dantolene

76
Q

dantrolene mech

A

prevents the release of Ca2+ from SR of skeletal muscle

77
Q

what causes neuroleptic malignant syndrome?

A

antipsychotic drugs

78
Q

IV anesthetic barbiturate

A

thiopental

79
Q

IV anesthetic benzo

A

midazolam

80
Q

PCP analogs that act as dissociative anesthetics, Block NMDA receptors. CV stimulants. Cause disorientation, hallucination, and bad dreams. Increases cerebral BF

A

arylcyclohezylamines (ketamine)

81
Q

Used for sedation in ICU, rapid anesthesia induction, and short procedures. Less post operative nausea than thiopental. Potentiates GABA(A).

A

Propofol

82
Q

local anesthetic esters

A

procaine, cocaine, tetracaine

83
Q

local anesthetic amides

A

lidocaine, mepivacaine, bupivacaine,

84
Q

local anesthetic mechanism

A

blocks Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons. Teritiary amine local anesthetics penetrate membrane in uncharted form, then bind to ion channels in charged form.

85
Q

Strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction

A

succinylcholine (depolarizing nueromuscular blocking drug)

86
Q

reversal of non depolarizing neuromuscular blockade?

A

neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors)

87
Q

How to treat Parkinson dz?

A 
BALSA
Bromocriptine
Amantadine
Levodopa w/ carbidopa
Selegiline (and COMT inhibitors)
Antimuscarinics
88
Q

levodopa tox

A

arrythmias from increased peripheral formation of catecholamines. long term use can lead to dyskinesia following administration (“on off phenomenon”), akinesia between doses

89
Q

how to treat alzheimers?

A 
memantine (NMDA receptor antagonist)
AChE inhibitors (donepezil, galantamine, rivastigmine)
90
Q

memantine tox

A

dizziness, confusion, hallucinations

91
Q

AChE inhibitor tox

A

nausea, dizziness, insomnia

92
Q

NT changes in HD?

A

decreased GABA and ACh,

Increased dopamine

93
Q

HD tx

A

tetrabenazamine and reserpien;

haloperidol

94
Q

tetrabenazine and reserpine mech

A

inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release

95
Q

haloperidol mech

A

dopamine receptor antagonist

96
Q

sumatriptan mech

A

5HT1b/1D agonist. INhibts trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction. Half-life < 2 hours

97
Q

sumatriptan CU

A

acute migraine, cluster headache

98
Q

sumatriptan tox

A

coronary vasospasm (contraindicated in pts with CAD or Prinzmetal), mild tingling.

Drugs (21 decks)

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