Week 10 (drugs of abuse and CNS) Flashcards

1
Q

Differences between Pramipexole, Ropinrole, and Rotigotine

A

Pramipexole is used w/ mild PD, or w/ levodopa in severe PD
Side effects are more common with Ropinrole, but less common when combined with L-dopa
Mechanism of action for Rotigotine is not known, probably in the substantia nigra (not D2 and D3 receptor binding like the other ones)

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2
Q

Another name for Non ergot alkaloids

A

dopamine agonists

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3
Q

Contraindications for non ergot alkaloids

A

if N/V occurs can’t give with seratonin antagonists like zofran (orthostatic hypotension) or dopamine receptor antagonists (opposite effects)

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4
Q

AE of apomorphine

A

Injection site rxns (no PO dosing) hallucinations,
drowsiness,
dyskinesia,
N/V.
4% serious CV events

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5
Q

Difference between Selegiline and Rasagline

A

Metabolites of Selegiline are amphetamine and methamphetamine, so they can cause CNS excitation and insomnia
Rasagiline may increase risk for malignant hyperthermia, assess skin

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6
Q

What is amantadine used for?

A

helps manage dyskinesias with L-dopa
rapid response that decreases within 3-6 mo

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7
Q

What is the benefit of entacapone with L-dopa

A

It helps L-dopa reach the brain so it can work, also causing less peripheral side effects d/t conversion to dopamine

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8
Q

How do dopamine agonists work and what are they used for

A

Dopamine agonists (ergot alkaloids and non ergot alkaloids) work by direct agonism of dopamine receptors in striatum. They are used for PD

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9
Q

When giving any medications that suppress immune responses, what are points of patient education? (hint: re: illness, infection, vaccines)

A

Before starting treatment, patients should become up to date on vaccines, since once the immune system is suppressed, it will be hard for the immune system to create new antibodies, and person will need increased immunity because they have less of an ability to fight infections
Once treatments are started the person is considered immunocompromised, so they should avoid sick people and encourage loved ones to get vaccinated to prevent giving them illnesses
Avoid concurrent administration of multiple immunosuppressants
These meds can also be very expensive, and are sometimes not covered by insurance

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10
Q

What is benzotropine used for

A

PD, as a second line drug for tremor
it is less effective than L-dopa or dopamine agonists but is better tolerated

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11
Q

AE of benzotropine

A

CNS (sedation, confusion, hallucinations)
peripheral: anticholonergic effects

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12
Q

What is Mitoxantrone used for and how does it work?

A

mitoxantrone is used as a immunosuppressant to slow the progression of MS, it works by inhibiting DNA repair and synthesis (decreased immune cell proliferation/activation, decreased myelin destruction)

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13
Q

List the three MAJOR adverse effects of mitoxantrone.

A

Myelosuppression (neutropenia, anemia, thrombocytopenia)
Irreversible cardiotoxicity, can occur years after drug has been stopped
Fetal injury (even in low doses, r/o pregnancy before each dose)

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14
Q

Knowing that Na+ channel receptors have 3 states (open, inactivated, and closed) how do these types of antiseizure drugs prevent neuronal transmission on some neurons, but not all neurons?

A

Slows progression from inactive to closed, so action potential only in hyperactive neurons are suppressed

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15
Q

Discuss PK variances of antiseizure medications

A

Phenobarbital – CYP450 inducer
carbamazepine – CYP 450 inducer, is metabolized by CYP450
Oxycarbemazepine – Induces CYP450, can increase metabolism of oral contraceptives
Lamotrigine – estrogen lowers drug levels
topiramate w/ phenytoin – lowered drug levels of both
tiagabine – metabolized by CYP 450

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16
Q

What is ethosuximide used for?

A

Absence seizures

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17
Q

AE of Oxcarbazepine

A

CNS depression
Hyponatremia
Hypothyroidism
Skin rxns and hypersensitivity

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18
Q

nursing considerations for oxcarbazepine

A

avoid alc and other hypo Na+ drugs

19
Q

contraindications for valproate

A

CNS depression and bad drug toxicity when combined with other anti-seizure meds
pregnancy

20
Q

AE of bupropion

A

dry mouth, insomnia, HA, rare seizure risk,

21
Q

Contraindications of bupropion

A

contraindicated with MAOI use, avoid in those with seizures

22
Q

How does memantine work?

A

regulates glutamate at NMDA receptors causing more normal Ca2+ influx (in neuron that still work)

23
Q

What are Beta-a drugs (endogenous inteferon B) used for? What do they do?

A

these immunomodulators are used in MS to modify immune responses (including B and T cells)

24
Q

cautions with interferon beta

A

antibody stimulation against the drug itself can occur, rxns can range from mild to anaphylaxis
They also require special handling, esp for pregnant RNs

25
Q

What is dalfampridine used for and how does it work?

A

dalfampridine is used for gait issues in MS (improves walking speed). It is a k+ channel blocker, but the mechanism is a little unclear

26
Q

Mechanism of action of lamotrigine

A

Na+ channel inactivation (mostly) and Ca2+ channel blocker

27
Q

Unusual AE of lamotrigine

A

more SI

28
Q

Mechanism of action of pregabalin

A

binds Ca2+ presynaptically, inhibits glutamate, NE, and substance P

29
Q

Unusual AE of pregabalin

A

hypersensitivity rxns
Euphoria (thus a controlled substance)
decreased fertility

30
Q

Unusual AE of levetiracetam

A

maybe renal injurry

31
Q

Mechanism of action of topiramate

A

GABA potentiation,
Na+ and Ca2+ block,
glutamate receptor block

32
Q

Mechanism of action of tiagabine

A

decreased GABA reuptake

33
Q

Unusual PK of tiagabine

A

metabolized by CYP450

34
Q

Unusual AE of topiramate

A

metabolic acidosis is a risk,
higher SI maybe

35
Q

Unusual PK of topiramate

A

w/ phenytoin, altered drug lvls of both

36
Q

AE of baclofen

A

(minimal)
CNS depression. OD –> coma, resp depression
GI = N/V, constipation, urinary retention
w/d symptoms occur (hallucinations, paranoia, seizures)

37
Q

CI of baclofen

A

other CNS depressants (avoid EtOH)
urinary retention (BPH, anticholinergics)
Psych conditions (may be exacerbated)

38
Q

AE of dantrolene

A

reduction in strength/weakness
hepatic toxicity (1:1000)
drowsiness
diarrhea

39
Q

CI of dantrolene

A

caution w/ calcium channel blockers (bc of both decreased influx and efflux of Ca2+, could case HF

40
Q

AE of cyclobenzaprine

A

CNS depression (subsides w/ use)
similar structure to TCAs –> anticholinergic effects, cardiac rhythm changes

41
Q

AE of naltrexone

A

Nausea
HA
dizziness
sedation

42
Q

AE of varenicline

A

Nausea (decreases w/ time)
HA
sleep disturbances
constipation
dry mouth
flatulence
altered sense of taste

43
Q

Mechanism, effects and PK of Marijuana

A

mechanism: activation of cannabinoid receptors
Effects: pleasure, memory, thinking, concentration, appetite, sensory and time perception
PK: CYP450 inhibitor

44
Q

Approved uses of marijuana

A

supression of emisis (esp in CA chemo)
appetite stimulation in AIDS
Tx of sz in Lennox-Gastuat and Davet syndrome
Relief of neuropathic pain in MS (not approved in the US yet)