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Flashcards in CNS Drugs Deck (56)
1

Name the barbiturates

phenobarbital, pnetobarbital, thiopental, secobarbital

2

Mechanism of barbiturates

facilitate GABAa action by increasing duration of Cl- channel opening, thus decrease neuron firing (increases duration)

3

Contraindication of barbiturates

in porphyria

4

Use of barbiturates

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

5

Toxicity of barbiturates

respiratory and cardiovascular depression
CNS depression (EtOH exacerbated)
INDUCES cytochrome p450

6

Overdose tx of barbiturates

supportive (assist respiration and maintain BP)

7

Name the benzodiazepines

diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, clordiazepoxide, alprazolam

8

Mechanism of benzodiazepines

facilitate GABAa action by increasing frequency of Cl- channel opening
decreases REM sleep

9

Name the benzos with short-half lives and NO active metabolites

Alprazolam, triazolam, oxazepam, midazolam --> higher addictive potential

10

Use of benzodiazepines

anxiety, spasticity, status epilepticus, detoxification (especially alcohol withdrawal and DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia)

11

Which benzos used for status epilepticus?

lorazepam and diazepam

12

Toxicity of benzodiazepines

dependence, additive CNS depression effects with alcohol
less risk of respiratory depression and coma than with barbiturates

13

Overdose tx for benzos

with flumazenil (competitive antagonist at GABA benzodiazepine receptor)

14

Name the non-benzo hypnotics

zlopidem, zaleplon, esZopiclone

15

Mechanism of the non-benzo hypnotics

act via the BZ1 subtype of the GABA receptor
effects reversed by flumazenil

16

Use of non-benzo hypnotics

insomnia

17

Toxicity of non-benzo hypnotics

ataxia, headaches, confusion
short duration because of rapid metabolism by liver enzymes
only cause modest day-after psychomotor depression and few amnestic effects
decreased dependence risk than benzos

18

Name the dopamine agonists

ergot - bromocriptine
non-ergot (preferred) - pramipexole, ropinirole

19

Parkinson disease NT levels

loss of dopaminergic neurons and excess cholinergic activity

20

Name drug that increases dopamine availability

Amantadine

21

Mechanism of amantadine

increase dopamine release and decrease dopamine reuptake

22

Uses for amantadine

PARKINSON

antiviral against influenza A and rubella

23

Toxicity of amantadine

ataxia
livedo reticularis (skin rash, purple and lace like)

24

How do drugs increase L-DOPA availability pre-BBB?

agents prevent peripheral (Pre-BBB) L-dopa degradation (because dopamine cannot cross BBB) --> increased L-DOPA entering the CNS

central L-DOPA available for conversion to dopamine

25

Name the drugs that increase L-DOPA availability entering brain

Levodopa (L-DOPA)/carbidopa
Entacapone, tolcapone

26

Mechanism of carbidopa

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

also reduces side effects of peripheral L-dopa conversion to dopamine (nausea, vomiting)

27

Mechanism of entacapone and tolcapone

prevent peripheral L-dopa degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT

28

How do drugs prevent dopamine breakdown?

agents act centrally (post-BBB) to block breakdown of dopamine --> increased available dopamine

29

Drugs that prevent dopamine breakdown in CNS

selegiline and tolcapone

30

Mechanism of selegiline

blocks conversion of dopamine to DOPAC by selectively inhibiting MAO-B in brain

31

Mechanism of tolcapone

blocks conversion of dopamine to 3-MT by inhibiting central COMT

32

Drugs that curb excess cholinergic activity

benztropine

33

Mechanism of benztropine

antimuscarinic
improves tremor and rigidity but has little effect on bradykinesia

34

Mechanism of Levodopa/Carbidopa combo

increase level of DA in brain
carbidopa inhibits peripheral conversion of L-dopa to DA via inhibition of dopa decarboxylase

35

Can dopamine cross BBB?

NO

36

Can L-DOPA cross BBB?

YES

37

Use of levodopa/carbidopa

parkinson disease

38

toxicity of levodopa/carbidopa

arrhythmias from increased peripheral formation of catecholamines
long term can lead to dyskinesia following administration, akinesia between doses = "on/off" phenomenon

39

Mechanism of selegiline

selectively inhibits MAO-B, which preferentially metabolizes dopamine over NE and 5-HT, thereby increasing the availability of dopamine in CNS

40

Use of selegiline

adjunctive agents to L-dopa in treatment of Parkinsons

41

Toxicity of selegiline

may enhance adverse effects of L-dopa

42

Mechanism of memantine

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

43

Toxicity of memantine

dizziness, confusion, hallucinations

44

Use of memantine

Alzheimer's disease

45

Mechanism of donepezil, galantamine, rivastigmine, tacrine

AChE inhibitors

46

Use of donepezil, galantamine, rivastigmine, tacrine

Alzheimer's disease

47

Toxicity of donepezil, galantamine, rivastigmine, tacrine

nausea, dizziness, insomnia

48

Drugs used for Alzheimers

memantine (NMDA antagonist)
donepezil, galantamine, rivastigmine, tacrine (AChE Inhibitors)

49

NTs altered in Alzheimers

decreased ACh

50

NTs altered in Huntington's

decreased GABA, ACh; increased dopamine

51

Treatments for Huntington's

tetrabenazine and reserpine
haloperidol

52

Mechanism of tetrabenazine and reserpine

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

53

Mechanism of haloperidol

D2 receptor antagonist

54

Mechanism of sumatriptan (and "-triptans"

5-HT1b/1d agonists
inhibit trigeminal nerve activation
prevent vasoactive peptide release and induce vasoconstriction

55

Use of sumatriptan

acute migraine, cluster headache attacks

56

Toxicity of sumatriptan

coronary vasocpasm (contraindicated in patients with CAD or prinzmetal angina)
mild paresthesia