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Pharmacy CPS Flashcards > NEUROLOGY: SEIZURE, PARKINSON, PAIN > Flashcards

NEUROLOGY: SEIZURE, PARKINSON, PAIN Flashcards

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1
Q

defined epilepsy and status epilepticus

A

epilepsy: 2 or more unprovoked seizure occurring >24 hours apart or 1 unprovoked with high probability of reoccurrence >60%
epilepticus: seizure lasting >5 mins or seizures occurring close together where patient doesn’t recover in between episodes

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2
Q

focal seizures

A

partial (affects one side of the brain)
simple: no impairment of awareness
complex : impairment of awareness, lasting longer (1-2 mins)

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3
Q

three types of generalized seizures

A

absence ( petit mal)
generalized tonic clonic ( grand mal)
atonic
myoclonic

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4
Q

absence seizure

A

impaired consciousness

features: staring

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5
Q

generalized tonic clonic grand mal

A 
impaired consciousness 
rigid muscle (tonic) followed by jerking of muscles ( clonic), jerking muscle possible tongue biting, incontinence
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6
Q

atonic

A

impaired consciousness

loss of muscle tone ( drop attacks)

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7
Q

myoclonic

A

no impairment consciousness

brief bilateral “shock-like” jerks or jerking of ground of muscles

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8
Q

1st and 2nd line for generalized tonic clonic seizure

A 
first line: carbamazepine, lamotrigine, 
levetiracetam, oxcarbazepine
valproic acid/divalproex
2nd: clobazam, perampanel​, 
phenytoin, 
topiramate
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9
Q

1st and 2nd line for absence seizure,

A

1: ethosuximide
2: Lamotrigine
valproic acid/divalproex

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10
Q

1st and 2nd line for myoclonic and atonic?

A

1: VPA
2: brivaracetam clobazam

lamotrigine
stiripentol​[d]
topiramate

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11
Q

first line for focal (partial)

A

carbamazepine

lamotrigine

levetiracetam

oxcarbazepine

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12
Q

most common AE of AED?

A

CNS and GI effects (dose dependent)

idiosyncratic: skin rash ( occur within 6 weeks of therapy)
chronic: low bone density and fractures

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13
Q

most common AED to be associate with skin rashes?

A

lamotrigine, CBZ, phenytoin

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14
Q

which AED is enzyme inducing

A

carbamazepine

eslicarbazepine

oxcarbazepine

perampanel (8 mg daily or higher)

phenobarbital

phenytoin

primidone

rufinamide

topiramate (200 mg daily or higher)

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15
Q

which AED that is non enzyme inducing

A

brivaracetam

clobazam

ethosuximide

gabapentin

lacosamide

lamotrigine

levetiracetam

valproic acid

vigabatrin

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15
Q

which AED that is non enzyme inducing

A

brivaracetam

clobazam

ethosuximide

gabapentin

lacosamide

lamotrigine

levetiracetam

valproic acid

vigabatrin

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16
Q

what drug interaction is significant with lamotrigine

A

lamotrigine + COC
lamotrigine levels can be expected to drop by at least 50% after a COC is started.
consider doubling the dose of lamotrigine

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17
Q

MOA of barbiturates

and AE

A

phenobarbital and primidone
potentiates GABA effects on GABA receptor, increasing Cl- channel activity
AE: behaviour and cognitive problems, mood changes, sedation, depression

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18
Q

which BZD is used as AED?

what are its main disadvantages?

A

clobazam

, Tolerance (initial good response followed by loss of seizure control).

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19
Q

Valproic acid MOA and AE

A

increased GABA activity, Na+ and K+ channels
AE:
CNS ( drowsiness), tremor, WEIGHT GAIN, menstrual cycle abnormalities

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20
Q

main advantage of VPA and disadvantage

A

broad spectrum
no hepatic enzyme induction

disadvantage: teratogenic, avoid in women of childbearing potential

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21
Q

Gabapentin AE

A

CNS, tremors, vision changes

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22
Q

Main disadvantages of Vigabatrin

A

Reports of visual field defects have severely limited use of this drug.

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23
Q

which drug is ONLY indicated for absence seizure

A

ethosuximide

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24
MOA of phenytoin and ae
GABA, inhibits NA + CI- channels AE: sedation, rash, hyperplasia gingival, body hair Long-term cosmetic adverse effects ( acne, skin thickening) Dosing complicated by saturation kinetics (nonlinear pharmacokinetics).
25
main disadvantage of phenytoin
main disadvantage: Long-term cosmetic adverse effects ( acne, skin thickening) Dosing complicated by saturation kinetics (nonlinear pharmacokinetics). drug inducing
26
MOA of CBZ? AE?
blocks voltage gated Na+ cHANNELS CNS, GI, RASH, anemia, exfoliative dermatitis, hypoantremia, hepatic toxicity
26
disadvantage of CBZ?
worsen absence seizures, exacerbate/ produce myoclonus oxcarbazepine: higher risk of hypoantremia compared to CBZ and eslicarbazepine ( lowest risk of hypoantremia both oxcarbazepine and eslicarbazepine have minimal enzyme induction **hepatoxicity, avoid use in patient with active liver disease, elderly**
27
Ethosuximide MOA and AE?
inhibits t-type calcium channels | AE: CNS and GI upset
28
what are the advantages and disadvantages of levetiracetam
ad: BID dosing, broad spectrum, no drug interactions, rapid titration dis: Psychiatric side effects, irritability, depression. avoid if abuse potential or history of mental illness , may increase or decrease breast milk
29
main disadvantage of lacosamide
PR interval prolongation; caution in patients with cardiac conduction abnormalities.
30
what s the evidence for perampanel? main AE / disadvantages?
strong evidence to support efficacy for drug-resistant primary generalized tonic-clonic seizure AE: CNS. serious psychiatric effects in patients with or without history of psychiatric conditions avoid use with alcohol
31
what is the main limitation in using topiramate
cognitive effects limits its use
32
when should we complete BMD?
after 5 year of AED use and before starting AED in postmenopausal women
33
when to stop AED
``` AED are typically lifelong but favour successful discontinuation are: seizure free for 2-4 years complete seizure control within 1 year onset of seizure between 2-35 normal neurological exam normal ECG ```
34
will patient required AED after first seizure
Many patients will not require AED treatment after a single seizure
35
what is the role of AED in provoke seizure
there is no role for AEDs in patients with acute symptomatic (provoked) seizures, such as those provoked by metabolic derangements (e.g., hypoglycemia, hyponatremia) or withdrawal from drugs or alcohol.
36
time frame to monitor for reduce or elimination of seizure
1-4 weeks
37
parkinson'disease is defined as
movement disorder caused by loss of dopamine | (symptoms do not occur until loss of 70-80% of dopaminergic production in the substania nigra
38
4 cardinal clinical symptoms of parkinson
resting tremor bradykinesia rigidity postural instability
39
list drug that can cause drug induced parkinsonism
antipsychotic: phenothiazine, butyrophenones, risperidone antiemetics: metoclopramide, prochlorperazine reserpine valproic acid, lithium: tremor antidepressants: TCA, SSRI
40
is non pharmacotherapy only adequate to properly manage PD?
no, need pharmacotherapy
41
pharmacological options for mild/eldery PD and moderate/severe PD?
mild: MAO-B inhibitor ( rasagiline, selegiline) dopamine precursor+ DOPA decarboxylase inhibitor dopamine agonist: NOT ERGOT-derived as first line moderate/ severe PD: combination therapy with above classes COMT inhibitor: may be added in advance PD amantadine: may not be effective in early PD, use in later stages
42
difference between selegiline and rasagiline
selegiline: amphetamine metabolite non-selective MAO-B inhibitor ( tyramine drug interaction) available as orally disintegrating tablet ( increasing bioavailability) rasagiline: longer duration of action ( once daily dosing) selective MAO-B inhibitor
43
benefit of MAO-B inhibitor
used for early stage PD ( mild) | rasagiline is more potent and can be used for wearing off symptoms ( advance disease)
44
AE of MAO-B inhibitor
headache, insomnia, nausea, orthostatic hypotension | selegiline specific: sympathomimetic effects ( due to interactions involving tyramine): HTN, tachycardia, jitteriness
45
MOA of anticholinergics, what is the benefit of anticholinergics in PD?
Benztropine, trihexyphendiyl, procyclidine, ethoproprazine counteracts increased cholinergic activity ( decreasing dopamine) which contributes to tremor benefits against resting tremor but no effects on bradykinesia, improves dystonic symptoms
46
AE of anticholinergic?
confusion, memory impairment, hallucinations, dry mouth, blurred vision, urinary retention, constipation and somnolence.
47
precautions for anticholinergics and contraindication
avoid due in elderly patient due to S/E | contraindicated in glaucoma, BPH, patient with dementia ( due to cognitive impairment)
48
benefit of amantadine and AE?
useful in later stages to reduce choleric movement ( L-Dopa induced dyskinesia) AE: hallucinations, confusion, nightmares, insomnia, leg edema, nausea, dry mouth, lived reticularis ( diffuse mottling skin)
49
which agents are ergot agents and which is non ergot
ergot: bromocriptine and pergolide | non-ergot: pramipexole, ropinorole, rotigotine
50
what is the difference between ergot agents
pergolide is 13x more potent than bromocriptine
51
differences b/w non-ergot agents
pramipexole: interacts with drugs that are secreted by cationic transport system ( cimetidine, ranitidine, verapamil and diltiazem)- up to 20% decreased clearance ropinorole: interacts with drugs that inhibit/ induce CYP1A2
52
what is the disadvantage of non-ergot
although it has favourable S/E profile, non ergot can caused compulsive behaviour ( gambling or shopping) *
53
what is benefit/ role of dopamine agonist?
- useful in wearing off symptoms - younger patient who do not want to start on levodopa - less motor complication long term compared to levodopa - patient who cannot tolerate high doses of levo-dopa
54
AE of dopamine agonist?
Nausea, diarrhea, somnolence, daytime drowsiness, orthostatic hypotension, hallucination, confusion
55
unique AE of bromocriptine?
pulmonary fibrosis
56
why does levodopa need too be in combination with decarboxylase inhibitor ( carbidopa, benserazide?
to cross BBB
57
advantages and disadvantages of levodopa/carbo
advantages: everyone will need, use it in older adults due to greater AE with other agents and older patient may not live long enough to experience motor complications disadvantages: earlier onset of dyskinesia (peak dose effects ) wearing off delayed response may be seen with SR formulations
58
AE of levodopa
N/V/D, orthostatic hypotension, cardiac arrhythmias, restlessness
59
administration requirement for levodopa
separate from meals ( decrease bioavailability
60
drugs that are COMT inhibitors
entacapone
61
what is the role of COMT-I
use with L-DOPA to extends duration of therapy to manage "wearing off" extends L-Dopa effect ( 1-2.5 hrs)
62
important counselling points for entacapone
discoloured your urine ( brownish orange)
63
L-DOPA is given how often
TID
64
adverse effects of COMT-I
dopamine effects ( dyskinesia, psychoses, diarrhea, abdominal pain)
65
managing delayed "on" response
chew or crush tablets and drink full glass of water use regular tablet formulation ( NOT SR) reduce protein intake with levodopa administration
66
managing "wearing off"
increased levo dosing or dosing frequency add dopamine agonist ( pramipexole or ropinirole) add rasagiline administer levo CR or dopamine agonist HS add entacapone SQ short acting apomorphine ( rapid onset of action)
67
management of "freezing"
non-pharm: physiotherapy | medication changes are not helpful
68
management of "off period" dystonia
bedtime administration of controlled-release baclofen use selective chemical denervation with injections of botulinum toxin
69
administering l-dopa with entacapone
decreased L-DOPA by 15-30%
70
antipsychotic that can be used for psychosis in patient is parkinson
quetiapine, clozapine
71
managing vomiting/nausea in PD
use domperidone | avoid metoclopramide
72
managing depression in PD
avoid SSRI, SNRI, bupropion if on MAO-B
73
motor complications in patient taking levodopa will occur in --- years
5 years
74
which dopamine agonist are available in patch
Rotigotine
75
role of apomorphine?
dopamine agonist that has fast onset of action, used in "wearing off" significant GI upset ( need 3 days pretreatment with domperidone)
76
treatment for REM behaviour disorder in PD
clonazepam and melatonin
77
does dopamine therapy need to be taper
yes, Parkinsonism-hyperpyrexia syndrome (similar to neuroleptic malignant syndrome) is a potentially fatal complication of PD treatment usually associated with abrupt reduction or discontinuation of dopaminergic drugs
78
1) how should you treat status epilepticus 2) you are the emergency room pharmacist at the local hospital. After 10-15 minutes of administration of diazepam IV, you suggest the following drug for status epilepticus?
1) lorazepam 4mg IV | 2) Phenobarbital 1,500 mg IV administered 50-75 mg/min.
79
What is the usual maintenance dose of gabapentin?:
900-3600 mg/day divided Q6-8H
80
what the serum drug concentration for valproic acid
50-100 mcg/ml
81
indication for lacosamide
Adjunctive therapy in the management of partial-onset seizures in adult patients with epilepsy who are not satisfactorily controlled with conventional therapy.
82
which drug can cause side effects of hyper sexual behaviour and pathologic gambling
) Dopamine agonists such as pramipexole, and drugs that convert to dopamine such as levodopa can cause impulse control disorders such as hypersexual behaviour and pathologic gambling in about 15% of patients.
82
which drug can used side effects of hyper sexual behaviour and pathologic gambling
Correct answer: b) Dopamine agonists such as pramipexole, and drugs that conver to dopamine such as levodopa can cause impulse control disorders such as hypersexual behaviour and pathologic gambling in about 15% of patients.
83
What is the typical starting dose of Levodopa / Carbidopa combination?
50/12.5 mg BID
84
what dose of amantadine
100mg BID
85
Amantadine side effects
Live do reticularis
86
Which anticonvulsant can cause menstrual cycle abnormalities in female patient
Valproate

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