Brainscape's Knowledge GenomeTM

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


See full index

ZCP301 > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

What are some causes of epilepsy?

A

Traumatic brain injury, stroke, infection, Brain tumour.

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

What are some classification of seizures?

A

Focal onset seizures - focal aware seizure, focal impaired-awareness seizure
Generalised onset seizures - tonic-clonic seizures, generalised absence seizure, myoclonic seizure, atonic seizure
Status epilepticus - a series of seizures

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

Define tonic, clonic, atonic and absence

A

Tonic - tonic muscle contractions -limb extension and arching of the back
Clonic - presents as limb jerking
Atonic - sudden lose in muscle tone
Absence - brief lapses in consciousness without loss of posture

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

What is the basic MOA of anti-seizure drugs?

A

Prolongation of the inactivated state of voltage-gated Na+ channels, positive modulation of K channels, inhibition of Ca2+ channels
Enhancement of GABA neurotransmission
Modulation of synaptic release process
Diminishing synaptic excitation mediation by inotropic glutamate receptors

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

What is the MOA of phenytoin?

A

Membrane stabilizing effect: use-dependent blockade of Na+ channel, preferred binding to inactivated state, decrease neuronal excitability, decrease repetitive action potentials
Decrease glutamate release and Ca influx

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

What is the action of sodium channels of phenytoin?

A

Binds to this channel in the inactivated state, causes the channel to stabilise in this state.
Sodium channels cycle rapidly through to the inactivated state thus this block accumulates. This leads to use-dependant blocking action. It also has a voltage dependence to its blocking action.

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

What are some phenytoin pharmacokinetics?

A

A- well absorbed orally
D- 90-95% bound to albumin
M- metabolised by CYP3A4, CYP2C9 (Inducer)
E- inactive metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a special consideration of phenytoin?

A

It has a narrow therapeutic index so therapeutic drug monitoring is needed.

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

What are some adverse effects of phenytoin?

A

Nystagmus, dizziness, cognitive impairment
Hirsutism, folate deficiency, peripheral neuropathy

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

What are some drug interactions of phenytoin?

A

Lamotrigine (metobolism may be induced), Antiretrovirals (PIs)
Lithium, oral contraceptives (no protection), warfarin

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

What is the MOA of carbamazepine?

A

Use dependent blockade of Na channels, decreases high frequency repetitive neuronal firing
Decreases Ca entry, could interact with K ion channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are adverse effects of carbamazepine?

A

Diplopia, dizziness, nausea, rash, hyponatremia

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

What happens to the auto-induction of carbamazepine?

A

Starts within 3-5 days of treatment, complete after 21-28 days of continous therapy. Thus we start low (100mg-200mg) BD, increase weekly by 100-200mg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are significant drug interactions of carbamazepine?

A

MAOIs, Lithium, rifampicin, antiretrovirals

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

What is the MOA of sodium valproate?

A

Inhibits breakdown of GABA by inhibiting transporter, promote synthesis of GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the pharmacokinetics of SV?

A

D- Vd confined to extracellular water, highly teratogenic
M- enzyme inhibitor

17
Q

What are some sodium valproate adverse effects?

A

Dose dependent: GIT distress, tremor and ataxia.
Idiosyncratic: hepatotoxicity, weight gain
Chronic: PCOS-like snydrome.

18
Q

What are some DI of sodium valproate?

A

Carbapenems, warfarin, aspirin, dipyridamole (may prolong bleeding time), zidovudine (increased)

19
Q

What is the indication and MOA of ethosuximide?

A

DOC for absence seizures.
MOA: Inhibits of low-threshold Ca currents presynaptically.

20
Q

What are pharmacokientics of ethosuximide?

A

Good, complete oral absorption, low plasma protein binding. Half-life is 40 hours.

21
Q

What are adverse effects of ethosuximide?

A

Dose dependent: GIT distress, ataxia, sedation
Idiosyncratic: Rash, blood dyscrasias.
Chronic: Headache, Behavioural changes

22
Q

What are some DIs of ethosuximide?

A

Valproate: etho levels increases, valproate levels may be reduced. CNS depressants: enhance sedative effects.
Antiretrovirals: nevirapine and efavirenz reduce ethos levels.

23
Q

What are some indications of gabapentin and its MOA?

A

Used as monotherapy or as add-on treatment of focal seizures (not for absence seizures) only for over 12 years of age. Off label for neuropathic pain.

Its a GABA-analogue, appears to alter synaptic release of GABA BUT does not act directly on GABA receptors.

24
Q

What are some pharmacokinetic properties of gabapentin?

A

No food effects, dose-dependent bioavailability. No CYP involvement, excreted unchanged in the urine, dosage adjustments in renal impairment. Drug interaction with antacids.

25
Q

What are some adverse effects of gabapentin?

A

Dose dependent: ataxia, dizziness, nystagmus, headache, somnolence.
Idiosyncratic: pedal oedema
Chronic: weight gain, behavioural changes in children.

26
Q

What is the MOA of pregabalin?

A

GABA analogue.
Presynaptic - decrease glutamate release and NA, substance P and calcitonin gene-related peptide.

27
Q

What is the indication and MOA of vigabatrin?

A

Add-on therapy for focal seizures where all other aporopriate treatment combinations have failed. Worses absence/myoclonic seizures.

Analogue of GABA. Irreverisible inhibitor of GABA-T

28
Q

What are some adverse effects of vigabatrin?

A

Dose dependent: Permanent vision loss, fatigue, tremor, blurred vision

Idiosyncratic: anaemia, peripheral neuropathy

Chronic: weight gain, permanent vision loss, neuropsychiatric complications.

29
Q

What are some indications of lamotrigine?

A

Focal seizures and primary generealised seizures. Generalised tonic-clonic seizures. Adjunctive therapy for Lennox-Gastaut syndrome. Bipolar affective disorders.

30
Q

What is the MOA of lamotrigine?

A

Causes a voltage and use-dependent block of sodium channels (suppresses sustained rapid neuronal firing)
Blocks voltage gated Ca channels to decrease glutamate release into synapse.

31
Q

What are some pharmacokinetic properties of lamotrigine?

A

No food effects, 50% protein bound, weak auto-inducer, prolonged half-life in renal impairment.

32
Q

What are some adverse effects of lamotrigine?

A

Dose dependent: dizziness, headache, ataxia, insomnia, diplopia.
Idiosyncratic: Haematological disturbances, maculopapular rash - slow dose titration.

ZCP301 (15 decks)

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