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Flashcards in Neuro drugs 2 Deck (60):
1

other inhaled anesthetic other than the -anes?

Nitrous oxide (N2O)

2

inhaled anesthetic mechanism?

unknown

3

Effects of inhaled anesthetics

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

4

methoxyflurane AE

nephrotoxic

5

nitrous oxide AE

expansion of trapped gas in a body cavity

6

what else can cause malignant hyperthermia?

succinylcholine

7

malignant hyperthermia genetics and inheritance

1) autosomal dominant with variable penetrance
2) mutations in voltage-sensitive ryanoidine receptor causing increased calcium release.

8

Dantrolene mechanism

Ryanodine receptor antagonist

9

IV anesthetics

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

10

thiopental profile

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.

11

thiopental uses

Induction of anesthesia and short surgical procedures.

12

Midazolam use

endoscopy; used adjectively with gaseous anesthetics and narcotics.

13

midazolam AE's

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

14

ketamine mechanism

PCP analog, thus blocks NMDA receptors. Cardiovascular stimulant.

15

ketamine effects

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

16

propofol uses

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

17

nice thing about propofol

less postop nausea than thiopental

18

opioid IV anesthetics and use

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

19

NMDA receptor structure

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

20

esters vs. amides nomenclature

Amides have 2 I's. Esters have 1.

21

use of neuromuscular blocking drugs?

muscle paralysis in surgery or mechanical ventilation.

22

depolarizing neuromuscular blocking drug?

succinylcholine

23

succinylcholine MOA

Strong ACh receptor agonist; produces sustained depolarization.

24

succinylcholine complicatoins

1) hypercalcemia
2) hyperkalemia
3) malignant hyperthermia

25

Reversal of depolarizing blockade: Phase I

Phase I = prolonged depolarization.
No antidote. Block potentiated by cholinesterase inhibitors.

26

Reversal of depolarizing blockade: Phase II

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

27

non depolarizing NMJ drugs

Tubocurarine
Atracurium
Mivacurium
Pancuronium
Vecuronium
Rocuronium

28

non depolarizing NMJ drug MOA

competitive ACh antagonists

29

How do you reverse blockade with non depolarizing drugs?

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

30

baclofen MOA

GABA B agonist

31

ergot dopamine agonists

bromocriptine

32

non-ergot dopamine agonists

pramipexole, ropinirole

33

which dopamine agonists are preferred for PD?

non-ergot (pramipexole, ropinirole)

34

Amantadine MOA for PD

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

35

amantadine toxicity

1) Ataxia
2) livedo reticularis

36

carbidopa MOA

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

37

Other benefit of carbidopa

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

38

entacapone, tolcapone MOA

inhibit COMT

39

COMT action

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

40

selegiline MOA

inhibits MAO-B

41

MAO-B action

converts dopamine to DOPAC

42

Why is benztropine used?

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

43

Difference between L-dopa and dopamine

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

44

AE's of levodopa/carbidopa

- Arrhythmias from increased peripheral formation of catecholamines.
- long-term use can lead to dyskinesia following administration ("on-off" phenomenon).
- akinesia between doses.

45

other drug like selegiline?

rasagiline

46

selegiline/rasagiline AE

May enhance adverse effects of L-dopa.

47

Memantine use

AD

48

memantine MOA

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

49

memantine AE's

Dizziness + confusion + hallucinations

50

other AChE inhibitor used for AD?

tacrine

51

AChE inhibitor (donepezil AE's)..

1) nausea
2) dizziness
3) insomnia

52

HD drugs?

1) tetrabenazine
2) reserpine
3) haloperidol

53

haloperidol MOA

D*2 receptor antagonist

54

tetrabenazine/reserpine MOA

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

55

Riluzole MOA

decreases glutamate excitotoxicity via an unclear mechanism.

56

Efficacy of riluzole?

not great, only modestly increases survival.

57

What serotonin receptor do triptans target?

5-HT*1B/1D

58

Triptan effects?

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

59

triptan AE's

1) coronary vasospasm
2) mild paresthesia

60

triptans AE's

1) CAD
2) prinzmetal angina