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STEP > Neuro drugs 2 > Flashcards

Neuro drugs 2 Flashcards

1
Q

other inhaled anesthetic other than the -anes?

A

Nitrous oxide (N2O)

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2
Q

inhaled anesthetic mechanism?

A

unknown

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3
Q

Effects of inhaled anesthetics

A

1) myocardial depression
2) respiratory depression
3) nausea/emesis
4) increased cerebral blood flow (due to decreased cerebral metabolic demand)

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4
Q

methoxyflurane AE

A

nephrotoxic

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5
Q

nitrous oxide AE

A

expansion of trapped gas in a body cavity

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6
Q

what else can cause malignant hyperthermia?

A

succinylcholine

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7
Q

malignant hyperthermia genetics and inheritance

A

1) autosomal dominant with variable penetrance

2) mutations in voltage-sensitive ryanoidine receptor causing increased calcium release.

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8
Q

Dantrolene mechanism

A

Ryanodine receptor antagonist

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9
Q

IV anesthetics

A 
The Mighty King Proposes Foolishly to Oprah
Barbiturates (thiopental)
Benzos (Midazolam)
Arylcyclohexylamines (Ketamine)
Propofol
Opioids
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10
Q

thiopental profile

A

1) High potency, high lipid solubility, rapid entry of brain
2) Effect terminated by rapid redistribution into tissue and fat.
3) decreased cerebral blood flow.

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11
Q

thiopental uses

A

Induction of anesthesia and short surgical procedures.

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12
Q

Midazolam use

A

endoscopy; used adjectively with gaseous anesthetics and narcotics.

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13
Q

midazolam AE’s

A

1) severe postoperative respiratory depression.
2) drops BP
3) anterograde amnesia

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14
Q

ketamine mechanism

A

PCP analog, thus blocks NMDA receptors. Cardiovascular stimulant.

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15
Q

ketamine effects

A

1) disorientation
2) hallucination
3) bad dreams
4) increased cerebral blood flow.

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16
Q

propofol uses

A

1) sedation in ICU
2) rapid anesthesia induction
3) short procedures

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17
Q

nice thing about propofol

A

less postop nausea than thiopental

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18
Q

opioid IV anesthetics and use

A

morphine, fentanyl used with other CNS depressants during general anesthesia.

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19
Q

NMDA receptor structure

A

Glutamate receptor and ion channel protein. Glutamate and glycine bind.
- magnesium ion.

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20
Q

esters vs. amides nomenclature

A

Amides have 2 I’s. Esters have 1.

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21
Q

use of neuromuscular blocking drugs?

A

muscle paralysis in surgery or mechanical ventilation.

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22
Q

depolarizing neuromuscular blocking drug?

A

succinylcholine

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23
Q

succinylcholine MOA

A

Strong ACh receptor agonist; produces sustained depolarization.

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24
Q

succinylcholine complicatoins

A

1) hypercalcemia
2) hyperkalemia
3) malignant hyperthermia

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25
Q

Reversal of depolarizing blockade: Phase I

A

Phase I = prolonged depolarization.

No antidote. Block potentiated by cholinesterase inhibitors.

26
Q

Reversal of depolarizing blockade: Phase II

A

Phase iI = Repolarized but blocked; ACh receptors available but desensitized)—may be reversed with cholinesterase inhibitors.

27
Q

non depolarizing NMJ drugs

A 
Tubocurarine
Atracurium
Mivacurium
Pancuronium
Vecuronium
Rocuronium
28
Q

non depolarizing NMJ drug MOA

A

competitive ACh antagonists

29
Q

How do you reverse blockade with non depolarizing drugs?

A 
Neostigmine + atropine (need to give atropine to prevent muscarinic effects such as bradycardia) 
OR
edrophonium
Or
other cholinesterase inhibitors
30
Q

baclofen MOA

A

GABA B agonist

31
Q

ergot dopamine agonists

A

bromocriptine

32
Q

non-ergot dopamine agonists

A

pramipexole, ropinirole

33
Q

which dopamine agonists are preferred for PD?

A

non-ergot (pramipexole, ropinirole)

34
Q

Amantadine MOA for PD

A

increases dopamine availability (increases dopamine release and decreases dopamine reuptake)

35
Q

amantadine toxicity

A

1) Ataxia

2) livedo reticularis

36
Q

carbidopa MOA

A

blocks peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase.

37
Q

Other benefit of carbidopa

A

Reduces side effects of peripheral L-dopa conversion into dopamine (nausea, vomiting)

38
Q

entacapone, tolcapone MOA

A

inhibit COMT

39
Q

COMT action

A

degrades peripheral L-dopa to 3-O-methyldopa (3-OMD)

40
Q

selegiline MOA

A

inhibits MAO-B

41
Q

MAO-B action

A

converts dopamine to DOPAC

42
Q

Why is benztropine used?

A

curbs excess cholinergic activity, thus improving tremor and rigidity. *no effect on bradykinesia.

43
Q

Difference between L-dopa and dopamine

A

L-dopa can cross BBB and is converted by dopa decarboxylase to dopamine.

44
Q

AE’s of levodopa/carbidopa

A
  • Arrhythmias from increased peripheral formation of catecholamines.
  • long-term use can lead to dyskinesia following administration (“on-off” phenomenon).
  • akinesia between doses.
45
Q

other drug like selegiline?

A

rasagiline

46
Q

selegiline/rasagiline AE

A

May enhance adverse effects of L-dopa.

47
Q

Memantine use

A

AD

48
Q

memantine MOA

A

1) NMDA receptor antagonist

2) helps prevent excitotoxicity (mediated by Ca2+)

49
Q

memantine AE’s

A

Dizziness + confusion + hallucinations

50
Q

other AChE inhibitor used for AD?

A

tacrine

51
Q

AChE inhibitor (donepezil AE’s)..

A

1) nausea
2) dizziness
3) insomnia

52
Q

HD drugs?

A

1) tetrabenazine
2) reserpine
3) haloperidol

53
Q

haloperidol MOA

A

D*2 receptor antagonist

54
Q

tetrabenazine/reserpine MOA

A

Inhibit VMAT, leading to decreased dopamine vesicle packaging and release.

55
Q

Riluzole MOA

A

decreases glutamate excitotoxicity via an unclear mechanism.

56
Q

Efficacy of riluzole?

A

not great, only modestly increases survival.

57
Q

What serotonin receptor do triptans target?

A

5-HT*1B/1D

58
Q

Triptan effects?

A

1) inhibit trigeminal nerve activation
2) prevent vasoactive peptide release
3) induce vasoconstriction

59
Q

triptan AE’s

A

1) coronary vasospasm

2) mild paresthesia

60
Q

triptans AE’s

A

1) CAD

2) prinzmetal angina

STEP (85 decks)

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