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Pharmacology > CNS drugs - EX 4 > Flashcards

CNS drugs - EX 4 Flashcards

1
Q

What are the CNS neurotransmitters?

A

Acetylcholine, Glutamate, Dopamine, and GABA

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2
Q

What is acetylcholine used for?

A

memory and learning

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3
Q

What is dopamine used for?

A

“Joy” and motor control

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4
Q

What is glutamate used for?

A

memory

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5
Q

what is GABA used for?

A

memory and movement

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6
Q

What is parkinson’s disease?

A

too little dopamine and too much acetylcholine

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7
Q

What two types of medications treat parkinsons

A

Dopaminergic agnes (more commonly used) and anticholinergic agents

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8
Q

How do dopaminergic agent work to treat parkinsons

A

directly or indirectly activate dopamine receptors

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9
Q

how do anticholinergic agents works to treat parkinsons

A

blocks receptors for acetylcholine

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10
Q

what is Levodopa?

A

Dopamine replacement

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11
Q

what is the MOA of Levodopa

A

increases the amount of available dopamine

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12
Q

what does it mean that Levodopa is a prodrug

A

converted into active form after crossing BBB (inactive until reaching brain)
only 2% reaches the brain

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13
Q

Important considerations for Levodopa

A

food delays absorption, esp meals high in protein
short T1/2 of 1-2 hrs
“loss of effect” common

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14
Q

adverse effects of Levodopa

A

N/V
Dyskinesis (involuntary mvt)
Cardiovascular
Psychosis
Harmless darkening of sweat and urine

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15
Q

what are the drug interactions of Levodopa? (bad vs. good)

A

bad: meds that block dopamine receptors
- not given with first class antipsychotics
good: anticholinergics block acetylcholine
-

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16
Q

Education considerations for levodopa

A
  • take without food
    -requires multiple doses in a day
  • darkens sweat and urine
  • report loss of effect
  • rise slowly
  • report any new tremors, palpitations, hallucinations/paranoia
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17
Q

what is Carbidopa/Levodopa

A

Sinemet

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18
Q

Carbidopa/Levodopa works how?

A

as a crossing guard
prevent decarboxylase actions

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19
Q

Carbidopa/Levodopa allows what?

A

to give a lower dose of levodopa

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20
Q

Carbidopa/Levodopa is only available how?

A

in a combo pill

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21
Q

What is Entacapone/levodopa/carbidopa

A

stalevo

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22
Q

how does Entacapone/levodopa/carbidopa work

A

like a RR crossing arm
inhibits COMT enzyme from breaking down levodopa

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23
Q

COMT stands for

A

catechol-o-methyltransferase

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24
Q

Entacapone/levodopa/carbidopa action:

A

extends half life of levodopa

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25
Q

Entacapone/levodopa/carbidopa only available in what form?

A

combo pill

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26
Q

Pramipexole is what

A

dopamine receptor agonist

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27
Q

what is the MOA of Pramipexole

A

directly activates dopamine receptors in the brain

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28
Q

when is Pramipexole of used?

A

in first line
alone in early stages
used with levodopa/carbidopa in advanced stages

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29
Q

what are the adverse side effects of Pramipexole?

A
  • produced by receptor activation
    Pramipexole alone: nausea, dizziness, weakness, sleep changes
    Pramipexole + levodopa/carbidopa O-hypotension, dyskinesias, hallucinataions
    • sleep attacks *
  • impulse control disorders/ compulsive behaviors
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30
Q

education considerations for Pramipexole

A
  • OK to take w/meals
  • rise slowly
  • report sleep attacks
  • report any impulse control concerns
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31
Q

For alzheimer’s what do pts. have low levels of

A

acetylcholine

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32
Q

what are the two major drug classes to treat alzheimers

A

cholinesterase inhibitors
NMDA antagonists

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33
Q

Donepezil is what

A

cholinesterase inhibitor

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34
Q

MOA of Donepezil

A

prevents breakdown of acetylcholine

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35
Q

benefits of Donepezil

A

improved QOL, memory, reasoning

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36
Q

does Donepezil delay alzheimer’s disease progression?

A

no

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37
Q

considerations for Donepezil

A

highly protein bound = long half life

increase in acetylcholine causes cholinergic effects

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38
Q

cholinergic side effects (Donepezil effects)

A

SLUDGE
Salivation
Lacrimation
Urination
Defecation
Gastric upset
Emesis

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39
Q

what is rivastigmine

A

cholinesterase inhibitor

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40
Q

what is the MOA of rivastigmine

A

prevents breakdown of acetylcholine

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41
Q

benefits of rivastigmine

A

improved QOL, memory, reasoning

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42
Q

does rivastigmine delay disease progression?

A

no

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43
Q

considerations of rivastigmine

A

available as a transdermal patch

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44
Q

adverse side effects of rivastigmine

A

increase acetylcholine causes cholinergic effects (SLUDGE) and CV effects (bradycardia –> fainting, falls)

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45
Q

what is memantine

A

NMDA antagonist

46
Q

what is the memantine MOA

A

blocks NMDA receptors and prevents excessive calcium accumulation in the neurons

47
Q

benefits of memantine

A

slow decline, may improve symptoms

48
Q

does memantine modify the underlying disease process

A

no

49
Q

what are the adverse effects of memantine

A

minimal
potential effect: donepezil and memantine

50
Q

what is Multiple Sclerosis?

A

chronic, progressive, inflammatory, autoimmune disorders affecting the myelin sheath of neurons on the spinal cord

51
Q

what type of MS are we focusing on?

A

relapsing-remitting

52
Q

immunomodulator considerations

A
  • not just for MS
  • indicated for all pts. w/relapsing-remitting subtype
  • very expensive
53
Q

what is interferon beta

A

immunomodulator

54
Q

how does interferon beta work

A

slows inflammation of CNS myelin

55
Q

how is interferon beta administered

A

parenterally (SQ or IM); dosing interval varies

56
Q

what are the adverse effects of interferon beta

A

common - flu like symptoms
hepatotoxicity
bone marrow suppression
injection site problems
headache

57
Q

when pts have a headache as a side effect of interferon beta is it okay to take tylenol or ibuprofen?

A

yes

58
Q

immunosuppressants considerations

A
  • less preferred (stronger immunosuppression and more toxic)
  • used in pts who don’t respond to immunomodulators
  • effective against all subtypes of MS
59
Q

what is mitoxantrone?

A

immunosuppressant

60
Q

how does mitoxantrone work

A

suppresses productions of immune cells

61
Q

how is mitoxantrone administered?

A

IV infusion every 3 months

62
Q

adverse effects of mitoxantrone

A

hepatotoxicity - monitor LFTs
Bone marrow suppression - infections precautions
Cardiotoxicity - looks like HF
Toxic to frequently dividing cells - teratanogenic

63
Q

how do you treat the MS symptom fatigue?

A

stimulants, SSRIS

64
Q

how do you treat the MS symptom muscle spasticity

A

CNS muscle relaxants

65
Q

how do you treat the MS symptom neuropathic pain

A

antiepileptics, antidepressants

66
Q

how do you treat the MS symptom bladder dysfunction

A

anticholinergic or alpha adrenergic blocker drugs

67
Q

how do you treat the MS symptom constipation

A

bulk laxatives, stool softeners

68
Q

how do you treat the MS symptom sexual dysfunction

A

lubricant for women, sildenafil (viagra) for men

69
Q

what is the treatment for acute MS flares?

A

high dose IV steroids for 3-5 days

70
Q

what does a high dose of steroids for 3-5 days to treat an MS flare cause

A

reduces acute inflammation

71
Q

What is the first way Antiepileptic drugs (AEDs) work

A

suppression of sodium influx in cell membranes = decreases ability of neurons to fire at high frequency

72
Q

what is the second way Antiepileptic drugs (AEDs) work

A

suppression of calcium influx in axon terminals = blocks channels to suppress transmission

73
Q

what is the third way Antiepileptic drugs (AEDs) work

A

antagonism of glutamate - NT

74
Q

what is the fourth way Antiepileptic drugs (AEDs) work

A

potentiation of GABA - NT

75
Q

what is the goal of using AEDs

A

decrease focal epileptic activity and prevent spread to other areas of the brain

76
Q

AED consideration

A

adherence is important to meet therapeutic response

77
Q

traditional AED consideration

A

less expensive
teratogenic
more interactions
more adverse effects

78
Q

new AED considerations

A

more expensive
safer in pregnancy
less interactions
less adverse effects

79
Q

Traditional AED examples and MOA

A

Phenytoin - sodium channel suppression
Phenobarbital - potentiates GABA
Valproic acid - sodium channel suppression and GAB potentiation

80
Q

Newer AED example and MOA

A

Oxcarbazepine - sodium channel suppression

81
Q

Phenytoin considerations

A

NTI drug - therapeutic levels 1-20 mcg/Ml
first line med and most widely used
long T1/2 life

82
Q

How is Phenytoin metabolized?

A

liver is easily overwhelmed by this drug = toxic levels
half life is dose dependent (8-60 hrs)
CYp enzyme inducer

83
Q

adverse effects of phenytoin

A

CNS effects
- headache, drowsiness, irritability,
- levels >20 mcg/mL: Nystagmus, sedation, ataxia, diplopia, cog impairments
Gingival hyperplasia
Rash
Teratogenic
lots of drug interax

84
Q

Valproic acid used for

A

all major seizure types and bipolar disorder and migraines

85
Q

Valproic acid adverse effects

A

GI effect common, rare hepatotoxicity, SERIOUS teratogen

86
Q

Phenobarbital consideration

A

sedation
many adverse side effects

87
Q

oxcarbazepine adverse effects

A

CNS
Rare- hyponatremia
serious skin rxns
teratogenic
lots of drug interax

88
Q

what is a spasm

A

involuntary contraction of a muscle or a muscle group

89
Q

what is spasticity

A

prolonged muscle tightness or contraction

90
Q

what are the s/sx of a spasm

A

pain and reduced funtion

91
Q

what are causes of spasms

A

epilepsy, hypocalcemia, chronic pain syndrome, localized muscle injury

92
Q

what are s/sx of spasticity

A

increased muscle tone, spasms, deacred fine motor control/dexterity,

93
Q

what causes spasticity

A

multiple sclerosis, cerebral palsy, stroke, traumatic spinal cord lesions

94
Q

What drugs treats spasms

A

cyclobenzaprine

95
Q

what class is cyclobenzaprine

A

centrally acting muscle relaxers

96
Q

what drugs treat spasticity?

A

baclofen, dantrolene, diazepam

97
Q

what is the class of baclofen?

A

centrally acting muscle relaxer

98
Q

what class is dantrolene

A

direct acting muscle relaxer

99
Q

what class is diazepam

A

benzodiazepine

100
Q

what are some treatments for muscle spasms

A

medications : acetaminophen, ibuprofen, cyclobenzaprine
physical therapy: stretching, flexibility exercises, TENS
local hear: heating pad, whirlpool, or warm baths

101
Q

therapeutic uses of cyclobenzaprine?

A

relief of pain from acute muscle spasm, to increase ROM
not effective to treat spasticity

102
Q

status epilepticus

A

extended period of continuous seizure
medical emergency
goal is to intervene in the first 5 minutes

103
Q

treatment of status epilepticus?

A

secure airway, give IV benzodiazepine, followed by antiepileptics

104
Q

adverse effects of cyclobenzaprine?

A

CNS effects (drowsiness, dizziness, sedation)
Anticholinergic effects (dry mouth, blurry vision, urinary retention, constipation - can’t pee cant see cant spit cant poop-

105
Q

cyclobenzaprine interacts with?

A

alcohol and other CNS depressants (increased drowsiness)
antidepressants (risk for serotonin syndromes)
- tolerance and dependence can develop

106
Q

Baclofen acts within?

A

within the spinal cords to suppress hyperactive reflexes

107
Q

main adverse side effect of baclofen and diazepam (valium)

A

sedation

108
Q

Dantrolene acts directly on?

A

skeletal muscle

109
Q

Dantrole PO dosing used for?

A

spasticity

110
Q

Dantrolene IV dosing used for?

A

malignant hyperthermia

Pharmacology (8 decks)

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