Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

NEUROLOGY: SEIZURE, PARKINSON, PAIN Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

three types of generalized seizures

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

absence seizure

A

impaired consciousness

features: staring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

atonic

A

impaired consciousness

loss of muscle tone ( drop attacks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

myoclonic

A

no impairment consciousness

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

1st and 2nd line for absence seizure,

A

1: ethosuximide
2: Lamotrigine
valproic acid/divalproex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

1st and 2nd line for myoclonic and atonic?

A

1: VPA
2: brivaracetam clobazam

lamotrigine
stiripentol​[d]
topiramate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

first line for focal (partial)

A

carbamazepine

lamotrigine

levetiracetam

oxcarbazepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

most common AED to be associate with skin rashes?

A

lamotrigine, CBZ, phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which AED that is non enzyme inducing

A

brivaracetam

clobazam

ethosuximide

gabapentin

lacosamide

lamotrigine

levetiracetam

valproic acid

vigabatrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which AED that is non enzyme inducing

A

brivaracetam

clobazam

ethosuximide

gabapentin

lacosamide

lamotrigine

levetiracetam

valproic acid

vigabatrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Valproic acid MOA and AE

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

main advantage of VPA and disadvantage

A

broad spectrum
no hepatic enzyme induction

disadvantage: teratogenic, avoid in women of childbearing potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Gabapentin AE

A

CNS, tremors, vision changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Main disadvantages of Vigabatrin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

which drug is ONLY indicated for absence seizure

A

ethosuximide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

MOA of phenytoin and ae

A

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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

main disadvantage of phenytoin

A

main disadvantage:
Long-term cosmetic adverse effects ( acne, skin thickening)

Dosing complicated by saturation kinetics (nonlinear pharmacokinetics).

drug inducing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MOA of CBZ? AE?

A

blocks voltage gated Na+ cHANNELS

CNS, GI, RASH, anemia, exfoliative dermatitis, hypoantremia, hepatic toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

disadvantage of CBZ?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Ethosuximide MOA and AE?

A

inhibits t-type calcium channels

AE: CNS and GI upset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the advantages and disadvantages of levetiracetam

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

main disadvantage of lacosamide

A

PR interval prolongation; caution in patients with cardiac conduction abnormalities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what s the evidence for perampanel? main AE / disadvantages?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the main limitation in using topiramate

A

cognitive effects limits its use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

when should we complete BMD?

A

after 5 year of AED use and before starting AED in postmenopausal women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

when to stop AED

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

will patient required AED after first seizure

A

Many patients will not require AED treatment after a single seizure

35
Q

what is the role of AED in provoke seizure

A

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
Q

time frame to monitor for reduce or elimination of seizure

A

1-4 weeks

37
Q

parkinson’disease is defined as

A

movement disorder caused by loss of dopamine

(symptoms do not occur until loss of 70-80% of dopaminergic production in the substania nigra

38
Q

4 cardinal clinical symptoms of parkinson

A

resting tremor
bradykinesia
rigidity
postural instability

39
Q

list drug that can cause drug induced parkinsonism

A

antipsychotic: phenothiazine, butyrophenones, risperidone
antiemetics: metoclopramide, prochlorperazine
reserpine
valproic acid, lithium: tremor
antidepressants: TCA, SSRI

40
Q

is non pharmacotherapy only adequate to properly manage PD?

A

no, need pharmacotherapy

41
Q

pharmacological options for mild/eldery PD and moderate/severe PD?

A

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
Q

difference between selegiline and rasagiline

A

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
Q

benefit of MAO-B inhibitor

A

used for early stage PD ( mild)

rasagiline is more potent and can be used for wearing off symptoms ( advance disease)

44
Q

AE of MAO-B inhibitor

A

headache, insomnia, nausea, orthostatic hypotension

selegiline specific: sympathomimetic effects ( due to interactions involving tyramine): HTN, tachycardia, jitteriness

45
Q

MOA of anticholinergics, what is the benefit of anticholinergics in PD?

A

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
Q

AE of anticholinergic?

A

confusion, memory impairment, hallucinations, dry mouth, blurred vision, urinary retention, constipation and somnolence.

47
Q

precautions for anticholinergics and contraindication

A

avoid due in elderly patient due to S/E

contraindicated in glaucoma, BPH, patient with dementia ( due to cognitive impairment)

48
Q

benefit of amantadine and AE?

A

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
Q

which agents are ergot agents and which is non ergot

A

ergot: bromocriptine and pergolide

non-ergot: pramipexole, ropinorole, rotigotine

50
Q

what is the difference between ergot agents

A

pergolide is 13x more potent than bromocriptine

51
Q

differences b/w non-ergot agents

A

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
Q

what is the disadvantage of non-ergot

A

although it has favourable S/E profile, non ergot can caused compulsive behaviour ( gambling or shopping)
*

53
Q

what is benefit/ role of dopamine agonist?

A
  • 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
Q

AE of dopamine agonist?

A

Nausea, diarrhea, somnolence, daytime drowsiness, orthostatic hypotension, hallucination, confusion

55
Q

unique AE of bromocriptine?

A

pulmonary fibrosis

56
Q

why does levodopa need too be in combination with decarboxylase inhibitor ( carbidopa, benserazide?

A

to cross BBB

57
Q

advantages and disadvantages of levodopa/carbo

A

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
Q

AE of levodopa

A

N/V/D, orthostatic hypotension, cardiac arrhythmias, restlessness

59
Q

administration requirement for levodopa

A

separate from meals ( decrease bioavailability

60
Q

drugs that are COMT inhibitors

A

entacapone

61
Q

what is the role of COMT-I

A

use with L-DOPA to extends duration of therapy to manage “wearing off”

extends L-Dopa effect ( 1-2.5 hrs)

62
Q

important counselling points for entacapone

A

discoloured your urine ( brownish orange)

63
Q

L-DOPA is given how often

A

TID

64
Q

adverse effects of COMT-I

A

dopamine effects ( dyskinesia, psychoses, diarrhea, abdominal pain)

65
Q

managing delayed “on” response

A

chew or crush tablets and drink full glass of water
use regular tablet formulation ( NOT SR)
reduce protein intake with levodopa administration

66
Q

managing “wearing off”

A

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
Q

management of “freezing”

A

non-pharm: physiotherapy

medication changes are not helpful

68
Q

management of “off period” dystonia

A

bedtime administration of controlled-release
baclofen use
selective chemical denervation with injections of botulinum toxin

69
Q

administering l-dopa with entacapone

A

decreased L-DOPA by 15-30%

70
Q

antipsychotic that can be used for psychosis in patient is parkinson

A

quetiapine, clozapine

71
Q

managing vomiting/nausea in PD

A

use domperidone

avoid metoclopramide

72
Q

managing depression in PD

A

avoid SSRI, SNRI, bupropion if on MAO-B

73
Q

motor complications in patient taking levodopa will occur in — years

A

5 years

74
Q

which dopamine agonist are available in patch

A

Rotigotine

75
Q

role of apomorphine?

A

dopamine agonist that has fast onset of action, used in “wearing off”
significant GI upset ( need 3 days pretreatment with domperidone)

76
Q

treatment for REM behaviour disorder in PD

A

clonazepam and melatonin

77
Q

does dopamine therapy need to be taper

A

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
Q

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?

A

1) lorazepam 4mg IV

2) Phenobarbital 1,500 mg IV administered 50-75 mg/min.

79
Q

What is the usual maintenance dose of gabapentin?:

A

900-3600 mg/day divided Q6-8H

80
Q

what the serum drug concentration for valproic acid

A

50-100 mcg/ml

81
Q

indication for lacosamide

A

Adjunctive therapy in the management of partial-onset seizures in adult patients with epilepsy who are not satisfactorily controlled with conventional therapy.

82
Q

which drug can cause side effects of hyper sexual behaviour and pathologic gambling

A

) 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
Q

which drug can used side effects of hyper sexual behaviour and pathologic gambling

A

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
Q

What is the typical starting dose of Levodopa / Carbidopa combination?

A

50/12.5 mg BID

84
Q

what dose of amantadine

A

100mg BID

85
Q

Amantadine side effects

A

Live do reticularis

86
Q

Which anticonvulsant can cause menstrual cycle abnormalities in female patient

A

Valproate

Pharmacy CPS Flashcards (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions