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CNS Drugs Flashcards

1
Q

Name the barbiturates

A

phenobarbital, pnetobarbital, thiopental, secobarbital

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2
Q

Mechanism of barbiturates

A

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

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3
Q

Contraindication of barbiturates

A

in porphyria

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4
Q

Use of barbiturates

A

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

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5
Q

Toxicity of barbiturates

A

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

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6
Q

Overdose tx of barbiturates

A

supportive (assist respiration and maintain BP)

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7
Q

Name the benzodiazepines

A

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

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8
Q

Mechanism of benzodiazepines

A

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

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9
Q

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

A

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

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10
Q

Use of benzodiazepines

A

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

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11
Q

Which benzos used for status epilepticus?

A

lorazepam and diazepam

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12
Q

Toxicity of benzodiazepines

A

dependence, additive CNS depression effects with alcohol

less risk of respiratory depression and coma than with barbiturates

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13
Q

Overdose tx for benzos

A

with flumazenil (competitive antagonist at GABA benzodiazepine receptor)

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14
Q

Name the non-benzo hypnotics

A

zlopidem, zaleplon, esZopiclone

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15
Q

Mechanism of the non-benzo hypnotics

A

act via the BZ1 subtype of the GABA receptor

effects reversed by flumazenil

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16
Q

Use of non-benzo hypnotics

A

insomnia

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17
Q

Toxicity of non-benzo hypnotics

A

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

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18
Q

Name the dopamine agonists

A

ergot - bromocriptine

non-ergot (preferred) - pramipexole, ropinirole

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19
Q

Parkinson disease NT levels

A

loss of dopaminergic neurons and excess cholinergic activity

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20
Q

Name drug that increases dopamine availability

A

Amantadine

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21
Q

Mechanism of amantadine

A

increase dopamine release and decrease dopamine reuptake

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22
Q

Uses for amantadine

A

PARKINSON

antiviral against influenza A and rubella

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23
Q

Toxicity of amantadine

A 
ataxia
livedo reticularis (skin rash, purple and lace like)
24
Q

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

A

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 ```

STEP 1 (26 decks)

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