Neuro drugs 2

Question 1

other inhaled anesthetic other than the -anes?

Answer 1

Nitrous oxide (N2O)

Question 2

inhaled anesthetic mechanism?

Answer 2

unknown

Question 3

Effects of inhaled anesthetics

Answer 3

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

Question 4

methoxyflurane AE

Answer 4

nephrotoxic

Question 5

nitrous oxide AE

Answer 5

expansion of trapped gas in a body cavity

Question 6

what else can cause malignant hyperthermia?

Answer 6

succinylcholine

Question 7

malignant hyperthermia genetics and inheritance

Answer 7

1) autosomal dominant with variable penetrance

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

Question 8

Dantrolene mechanism

Answer 8

Ryanodine receptor antagonist

Question 9

IV anesthetics

Answer 9

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

Question 10

thiopental profile

Answer 10

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.

Question 11

thiopental uses

Answer 11

Induction of anesthesia and short surgical procedures.

Question 12

Midazolam use

Answer 12

endoscopy; used adjectively with gaseous anesthetics and narcotics.

Question 13

midazolam AE’s

Answer 13

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

Question 14

ketamine mechanism

Answer 14

PCP analog, thus blocks NMDA receptors. Cardiovascular stimulant.

Question 15

ketamine effects

Answer 15

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

Question 16

propofol uses

Answer 16

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

Question 17

nice thing about propofol

Answer 17

less postop nausea than thiopental

Question 18

opioid IV anesthetics and use

Answer 18

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

Question 19

NMDA receptor structure

Answer 19

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

Question 20

esters vs. amides nomenclature

Answer 20

Amides have 2 I’s. Esters have 1.

Question 21

use of neuromuscular blocking drugs?

Answer 21

muscle paralysis in surgery or mechanical ventilation.

Question 22

depolarizing neuromuscular blocking drug?

Answer 22

succinylcholine

Question 23

succinylcholine MOA

Answer 23

Strong ACh receptor agonist; produces sustained depolarization.

Question 24

succinylcholine complicatoins

Answer 24

1) hypercalcemia
2) hyperkalemia
3) malignant hyperthermia

Question 25

Reversal of depolarizing blockade: Phase I

Answer 25

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

Question 26

Reversal of depolarizing blockade: Phase II

Answer 26

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

Question 27

non depolarizing NMJ drugs

Answer 27

``` Tubocurarine Atracurium Mivacurium Pancuronium Vecuronium Rocuronium ```

Question 28

non depolarizing NMJ drug MOA

Answer 28

competitive ACh antagonists

Question 29

How do you reverse blockade with non depolarizing drugs?

Answer 29

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

Question 30

baclofen MOA

Answer 30

GABA B agonist

Question 31

ergot dopamine agonists

Answer 31

bromocriptine

Question 32

non-ergot dopamine agonists

Answer 32

pramipexole, ropinirole

Question 33

which dopamine agonists are preferred for PD?

Answer 33

non-ergot (pramipexole, ropinirole)

Question 34

Amantadine MOA for PD

Answer 34

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

Question 35

amantadine toxicity

Answer 35

1) Ataxia | 2) livedo reticularis

Question 36

carbidopa MOA

Answer 36

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

Question 37

Other benefit of carbidopa

Answer 37

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

Question 38

entacapone, tolcapone MOA

Answer 38

inhibit COMT

Question 39

COMT action

Answer 39

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

Question 40

selegiline MOA

Answer 40

inhibits MAO-B

Question 41

MAO-B action

Answer 41

converts dopamine to DOPAC

Question 42

Why is benztropine used?

Answer 42

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

Question 43

Difference between L-dopa and dopamine

Answer 43

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

Question 44

AE's of levodopa/carbidopa

Answer 44

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

Question 45

other drug like selegiline?

Answer 45

rasagiline

Question 46

selegiline/rasagiline AE

Answer 46

May enhance adverse effects of L-dopa.

Question 47

Memantine use

Answer 47

AD

Question 48

memantine MOA

Answer 48

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

Question 49

memantine AE's

Answer 49

Dizziness + confusion + hallucinations

Question 50

other AChE inhibitor used for AD?

Answer 50

tacrine

Question 51

AChE inhibitor (donepezil AE's)..

Answer 51

1) nausea 2) dizziness 3) insomnia

Question 52

HD drugs?

Answer 52

1) tetrabenazine 2) reserpine 3) haloperidol

Question 53

haloperidol MOA

Answer 53

D*2 receptor antagonist

Question 54

tetrabenazine/reserpine MOA

Answer 54

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

Question 55

Riluzole MOA

Answer 55

decreases glutamate excitotoxicity via an unclear mechanism.

Question 56

Efficacy of riluzole?

Answer 56

not great, only modestly increases survival.

Question 57

What serotonin receptor do triptans target?

Answer 57

5-HT*1B/1D

Question 58

Triptan effects?

Answer 58

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

Question 59

triptan AE's

Answer 59

1) coronary vasospasm | 2) mild paresthesia

Question 60

triptans AE's

Answer 60

1) CAD | 2) prinzmetal angina