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Pharm module 5 > epilepsy / parkinsons / migraines > Flashcards

epilepsy / parkinsons / migraines Flashcards

1
Q

What are the common symptoms with parkinsons

A

tremor of rest
bradykinesia
tendency to stoop
mortality

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2
Q

What is the cause of parkinsons

A

degeneration of neurons in the substantial nigra

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3
Q

Which dopamine receptor is excitatory

A

D1

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4
Q

Which dopamine receptor is inhibitory

A

D2

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5
Q

What does a decrease in neurons cause

A

a decrease in cortical stimulation

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6
Q

What is the direct pathway in the brain dominated by

A

D1 receptors

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7
Q

What is a dopamine precursor

A

L-Dopa

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8
Q

What does levodopa do

A

crosses the BBB
actively taken up into neurons
converted into dopamine

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9
Q

Which enzyme converts L-dopa in dopamine

A

DA decarboxylase

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10
Q

What are the adverse affects of levodopa

A

Dyskinesia
hallucinations/confusion

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11
Q

Why can L-dopa cause hallucinations or confusion

A

when dopamine levels in the brain are disrupted in any way, it can cause forms of psychosis

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12
Q

If someone on L-dopa has symptoms of psychosis, how would you treat them

A

with antipsychotics (do so cautiously)

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13
Q

What is always given with L-dopa and why

A

carbidopa

allows L-dopa to fully cross the BBB without being converted to DA too early

Reduces peripheral side effects

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14
Q

What is the MOA of carbidopa

A

peripheral inhibitor of L-aa decarboxylase

Prevents conversion to DA in periphery

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15
Q

What is entacapone

A

Levodopa adjunct therapy

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16
Q

What is the MOA of entacapone

A

inhibits COMT

prevents degradation of levodopa

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17
Q

What is COMT

A

secondary pathway to metabolize levodopa, DA, and NE

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18
Q

What are the adverse effects of entacapone

A

dyskinesia
nausea
diarrhea

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19
Q

When is entacapone used for parkinsons treatment

A

When the disease progresses and the L-dopa/Carbidopa combo is no longer sufficient

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20
Q

When does L-dopa work the best in parkinsons treatment

A

The earlier in the disease you treat the better

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21
Q

What happens when someone is on L-dopa for a long time

A

motor fluctuation from receptor adaptation
-on/off effect

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22
Q

What is an example of an MAO B inhibitor

A

selegiline

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23
Q

What is the MOA for selegiline

A

Prevents metabolism of DA, NE, and serotonin

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24
Q

What is 5-HT

A

seretonin

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25
Q

What is the benefit of using Selegiline

A

Reduces the dose of levodopa needed

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26
Q

What drug is interchangeable with Selegiline

A

Rasagiline

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27
Q

What are the adverse effects of selegiline

A

Amphetamine - like side effects
Seretonin syndrome
sweating
arrhythmia
diarrhea

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28
Q

What is selegiline metabolized by and what is the product

A

Metabolized in the liver by CYP450

turns partially into amphetamine

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29
Q

What is a dopamine receptor agonist that is used in parkinsons treatment

A

Bromocriptine
Ropinorole

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30
Q

What is the MOA for Bromocriptine

A

Delay the need for L-Dopa or in advanced parkinsons

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31
Q

What is the adverse effect of bromocriptine

A

cardiac valve fibrosis

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32
Q

How is Ropinorole different from bromocriptine

A

Rompinirole is less selective

Rompinirole is also useful for restless leg syndrome

Ropinirole has less adverse effects

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33
Q

What are alternatives to Ropinirole

A

Pramipexole

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34
Q

How is Ropinirole metabolized

A

CYP450

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35
Q

What are adverse effects for ropinirole

A

Increased risky behavior

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36
Q

What is the MOA for Trihexyphenidyl

A

mACh receptor antagonist will allow for DA to work in the striatum

Helps reduce dyskinetic movement and spastic contraction

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37
Q

What are the adverse effects on Trihexyphenidyl

A

Anticholinergic effect (sedation/confusion/constipation/urinary retention)

Pharmakinetics: gets excreted unchanged

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38
Q

How is Trihexyphenidyl often administered

A

In combination with DA agonists

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39
Q

What is Benzotropine

A

A non-DA parkinsons treatment

Helps with excess amounts of dopamine

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40
Q

What can excessive dopamine cause

A

rigidity

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41
Q

What is amantadine

A

Antiviral

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42
Q

What is the MOA of Amantadine

A

Increases DA release and blocked the NMDA glutamate receptors

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43
Q

What are the adverse effects of amantadine

A

confusion
psychosis

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44
Q

Where is the neuronal loss in Huntingtons disease

A

Caudate/putamen
Striatum
Loss of GABA function

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45
Q

What is treatment for Huntingtons based on

A

The most pronounced symptoms

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46
Q

What is the mainstay therapy for Huntingtons

A

Neuroleptic D2 blockers

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47
Q

What is an example of a neuroleptic D2 blocker

A

Haloperidol

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48
Q

What is a drug that can be given for the treatment of chorea

A

deutetrabenazine

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49
Q

What is the MOA of deutetrabenazine

A

Inhibits neurotransmitter storage

which reduces uncontrolled hyperkinetic movements

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50
Q

How is duetetrabenazine metabolized

A

CYP450

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51
Q

What is the primary damage done to the brain with Alzheimers

A

Cholinergic damage
-loss of enzymes for ACh synthesis
-loss of cholinergic neurons in basal forebrain

52
Q

What are acetylcholinesterase inhibitors that are used for Alzheimers

A

Donezepil
Rivastigmine

53
Q

What are the adverse affects of Donezepil

A

N/V
Diarrhea
Sleep disturbances (vivd dreams)

54
Q

What is an NMDA receptor agonist that is used for Alzheimers treatment

55
Q

How is Memantine usually given

A

With dozenepil b/c it works on different receptors
OR
If a patient cannot take dozenepil

56
Q

What is the MOA for memantine

A

Thought to reduce excitotoxicity by blocking the activation for NMDA receptors

57
Q

What are common side effects to Memantine

A

Dizziness
headache
constipation
confusion

58
Q

What is a simple partial seizure

A

Hyperactive neurons exhibiting abnormal electrical activity in a single locus in the brain

No LOC and usually will exhibit abnormal activity of a single limb or muscle group controlled by that area

59
Q

What is a partial complex seizure

A

Exhibit complex sensory hallucination and mental distortion

Will generally start locally and then progress

60
Q

What are the different types of generalized seizures

A

Tonic-clonic
Absence
Myoclonic
Infantile spasm
Status epilepticus

61
Q

What is a tonic-clonic seizure

A

LOC followed by convulsions

62
Q

What is an absence seizure

A

Brief, abrupt, self limiting LOC
-may start or have rapid eye blinking lasting 3-5 second

63
Q

Why is a myoclonic seizure

A

short episodes of muscle contractions that may reoccur within several minutes

64
Q

What is status epilepticus

A

two or more seizures that occur without recovery of full consciousness between them

65
Q

What are the 3 mechanisms that ASM can work

A

Blocking Na+ or Ca2+ gated channels

enhancing GABA impulses

Interfering with glutamate transmission

66
Q

What is the MOA of blocking Na+ gated channels

A

Prevents sodium from entering the cell which will cause the depolarization for muscle contraction

67
Q

What is the MOA for the calcium channel blockade

A

Prevent the release of internal calcium stores into the cell

68
Q

What is the MOA for GABA enhancers

A

The drug will irreversible bind to and inhibit GABA transaminase which breaks down GABA

Keeping GABA within the cell keeps it hyper-polarized (more negative) so a muscle contraction cannot occur

69
Q

What are the GABA inhibitory drugs

A

Benzodiazepines
-diazepam
-Lorazepam

70
Q

How are diazepam and lorazepam different

A

Lorazepam has a shorter half life but remains in the brain longer

Diazepam can be used rectally

71
Q

What is the MOA of Cabamazepine

A

Blocks Na+ channels
-effective for partial seizures
*DO NOT PERSCRIBE FOR ABSENCE SEIZURE->CAN INCREASE SEIZURES

72
Q

What is an adverse effect of carbamazepine

A

Induces CYP enzymes, make sure other drugs aren’t metabolized by these enzymes

73
Q

What is the MOA for ethosuximide

A

Blocks Ca2+

Reduces propagation of abnormal electrical activity in the brain

74
Q

What is ethosuximide used for

A

treating generalized absence seizures

75
Q

What is gabapentin used for

A

Adjunct therapy for partial seizures and postherpetic neuralgia

Tolerated well in the elderly

76
Q

What are the side effects of gabapentin

A

Sedating effects
renal dose adjustment

77
Q

How does gabapentin relate to GABA

A

It is an analog but does not act on GABA in any way

78
Q

What is the MOA for Lamotrigine

A

Blocks Na+ channels and Ca2+ channels

79
Q

What is lamotrigine used for

A

Partial seizures, generalized seizures, typical absence seizures, and Lennox gastaut syndrome

Bi-polar disorder

80
Q

What are the adverse effect of lamatrogine

A

Rapid titration has been known to lead to SJS

81
Q

What can you combine Lamatrogine with and why

A

Valproate->reduces drug degradation when given together
*must reduce dosage with combination

82
Q

What is the DOC with seizure disorders

A

Levetiracetam (Keppra)

83
Q

When is Levetriacetam used

A

adjunct therapy for partial onset seizures, myoclonic seizures, primary generalized. tonic-clonic seizures

84
Q

What are the dose effects of Levetiracetam

A

Dizziness
sleep disturbance
headache
weakness

85
Q

What type of drug is Oxcarbazepine

A

A pro-drug
*reduces to MHD which has anticonvulsant activity

86
Q

What is the MOA for Oxcarbazepine

A

Blocks Na+ and Ca2+ Chanels

87
Q

What seizures is Oxcarbazepine used for

A

Adults and children with partial onset seizures

88
Q

What are the adverse effects of Oxcarbazepine

A

N/V
Headache
Visual disturbances

89
Q

What is the MOA for Phenobarbital

A

Enhances inhibitory effects of GABA mediated neurons

90
Q

When should phenobarbital be used

A

Status epilepticus treatment
alcohol withdrawal

91
Q

What has to happen with phenobarbital is used

A

Taper drug off when discontinued

Monitor phenobarbital levels in the body

92
Q

What is the MOA for phenytoin and Fosphenytoin

A

blocks Na+ channels by selectively binding in the channels inactive state and slowing its recovery

93
Q

When are phenytoin and Fosphenytoin used

A

Partial seizures
status
generalized tonic-clonic

94
Q

What are phenytoin and Fosphenytoin bound to

95
Q

What are the adverse effects of Phenytoin and Fosphenytoin

A

Small increases in daily dose can cause large increases in serum concentration

Nystagmus and ataxia

Induces CYP metabolism

96
Q

What is the difference between phenytoin and fosphenytoin

A

Phenytoin can NOT be given IM/IV
Phenytoin can cause purple hand syndrome

97
Q

What is a major side effect of phenytoin

A

Gingival hyperplasia
peripheral neuropathies
osteoporosis

98
Q

What happens when Fosphenytoin is administered

A

Rapidly get converted to phenytoin in the blood, reaching high levels in minutes

99
Q

What is the MOA of pregabalin

A

Binds to a subunit of Ca2+ channels that inhibit release of excitatory neurotransmitters

100
Q

When is pregabalin used

A

Partial onset seizures
neuralgia
neuropathic pain
fibromyalgia
postherpetic pain

101
Q

What are the adverse effects of pregabalin

A

Drowsiness (fogginess)
Blurred vision
weight gain
LE peripheral edema

102
Q

What is the MOA of Topiramate

A

Blocks Na+ channels

Increases Cl- channel opening by binding with GABA

Ca2+ current is reduced

Carbonic anyhrase inhibitor that may act on NMDA

103
Q

What is Topiramate used for

A

migraines
partial and primarily generalized epilepsy

104
Q

What are the adverse effects of topiramate

A

Somnolence
weight loss
paresthesia
Kindly stones
Glaucoma
oligohydrosis=hyperthermia

105
Q

What would be a positive effect of co-administering topiramate

A

Reduction of ethinyl estradiol

106
Q

What happens when you give a patient divalproex

A

It will be converted into valproate when it reaches the GI tract
*developed to improve GI tolerance of valproate

107
Q

What is the MOA of Valproate

A

Na+ blocker
GABA transaminase blocker
Activation of T-type calcium channels
*inhibits CYP enzymes

108
Q

What are valproate / divalproex used for

A

partial and primary generalized epilepsies

109
Q

How does valproate travel in the body

A

bound to albumin

110
Q

What are the adverse effects of valproate

A

Hepatic toxicity
teratogenicity

111
Q

What is Zonisamide

A

Sulfonamide derivative

112
Q

What is the MOA for Zonisamide

A

Blocks Na+ and Ca2+
limited amount of carbonic anhydrase activity

113
Q

When can zonisamide be used

A

Patients with partial seizures

114
Q

What are the adverse effects of zonisamide

A

Kidney stones
oligohydrosis
typical CNS side effects

115
Q

What drugs should be avoided in pregnant women with epilepsy

A

valproate/Divalproex
Barbituates

116
Q

What is the first like treatment for migraines

117
Q

What drugs can be used to abort migraines

A

5-HT 1D receptor agonists
-triptans
-dihydreoergotamine

118
Q

What is the MOA of 5-HT 1D receptor agonists

A

Leads to either vasoconstriction of inhibition of the release of proinflammatory neuropeptides on the trigeminal nerve

119
Q

What is a therapy used to prevent migraines and when is it indicated

A

Propanolol

When 2+ attacks occur in a month

120
Q

How is sumatriptan given and why

A

SQ usually for a 20 minute onset vs. the 1-2 hours if taken orally

121
Q

How long does sumatriptan last

A

2 hour half life

122
Q

How many doses is typically required to abort the headache with sumatriptan

123
Q

What type of headache is sumatriptan typically used for

A

cluster headaches

124
Q

What is the adverse effects of sumatriptan

A

High BP
Cardiac events
* avoid in those with CAD
Pain/pressure in chest/neck/throat/jaw

125
Q

How is ergotamine administered

A

IV with similar efficacy to sumatriptan

126
Q

What is the MOA for ergotamine

A

Constricts intracranial extracerebral blood vessels and inhibits trigeminal neurotransmission

Pharm module 5 (1 decks)

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