Brainscape's Knowledge GenomeTM

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


See full index

54 CNS > Seizure & Epilepsy > Flashcards

Seizure & Epilepsy Flashcards

1
Q

How is epilepsy defined?

A

Any one of:
- at least 2 unprovoked seizures >24h apart
- 1 unprovoked and probability of further seizures after 2 unprovoked seizures, occurring in the next 10 years
- diagnosis of epilepsy syndrome

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

What are acute symptomatic seizures?

A

Seizures that result from some immediately recognisable stimulus or cause (eg. about a week after acute brain injury)

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

What are remote seizures?

A

Seizures that occur longer than 1 week following a disorder (known to increase risk of developing epilepsy)

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

What re unprovoked seizures?

A

Seizures occurring in absence of a potentially responsible clinical condition OR beyond interval estimated (~1 week) for occurence of symptomatic

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

Metabolic causes of acute symptomatic seizures

A

Hyponatremia
Hypoglycemia
Hypocalcemia
Hypomagnesemia

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

Toxic/drug causes of acute symptomatic seizures

A

Illicit drugs (cocaine, amphetamines)
Drugs (tricyclic antidepressants, carbapenems, baclofen)
ETOH
Benzodiazepine withdrawal

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

Structural causes of acute symptomatic seizures

A

Stroke
Traumatic brain injury

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

Infection/inflammation causing acute symptomatic seizures

A

CNS infection
Febrile illness

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

Non-epileptic seizures

A

Not related to abnormal epileptiform discharges

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

What is the general pathophysiology for epilepsies?

A

Neuronal hyperexcitability and hypersynchronisation

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

What can result in neuronal hyperexcitability?

A
  • Voltage- or ligand-gated channels
  • Abnormalities in intra & extracellular substances
  • Excessive excitatory neurotransmitters
  • Insufficient inhibitory neurotransmitters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which parts of the brain is associated with neuronal synchronisation?

A

Hippocampus, neocortex and thalamus

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

Focal onset

A

Seizure begins only in one hemisphere

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

Generalised onset

A

Seizure begins in both hemispheres

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

Secondary generalised

A

Seizure begins in one hemisphere, then spread to other

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

What do clinical characteristic of a seizure depend on?

A
  • Site of focus
  • Degree of irritability of the area surround the focus
  • Intensity of impulse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Phases of a seizure (in order)

A
  1. Prodromal
  2. Early ictal (“aura”)
  3. Ictal
  4. Postictal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Motor symptoms of focal onset (simple partial)

A
  • Clonic movements (twitching/jerking) of arm, shoulder, face, leg
  • Speech arrest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Desired outcomes of epilepsy treatment

A
  1. Absence of epileptic seizures
  2. Absence of ASM-related side effects
  3. Attainment of quality of life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are some 1st generation ASMs?

A
  • Carbamazepine
  • Phenobarbitone/Phenobarbital
  • Phenytoin
  • Sodium Valproate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some 2nd generation ASMs?

A
  • Lamotrigine
  • Levetiracetam
  • Topiramate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

1st line AEDs for generalised tonic-clonic

A
  • Carbamazepine
  • Sodium Valproate
  • Lamotrigine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

1st line AEDs for tonic/atonic

A

Sodium Valproate

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

1st line AEDs for absence

A

Lamotrigine
Sodium Valproate

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

1st line AEDs for focal

A
  • Carbamazepine
  • Sodium Valproate
  • Lamotrigine
  • Levetiracetam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are some problems with 1st generation ASMs?

A
  • Poor water solubility
  • Extensive protein binding
  • Extensive oxidative metabolism
  • Multiple DDIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the potential advantages of newer ASMs?

A
  • Improved water solubility → predictable F
  • Negligible protein binding → no need to worry about hypoalbuminemia
  • Less reliance on CYP metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Potent enzyme inducers in 1st generation ASMs

A

Carbamazepine: CYP (1A2, 2C, 3A4), UGTs
Phenytoin: CYP (2C, 3A), UGTs
Phenobarbital: CYP (1A, 2A6,2B,3A), UGTs

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

Potent enzyme inhibitors in 1st generation ASMs

A

Valproate: CYP2C9, UGTs

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

MOA of Carbamazepine

A

Blockade of voltage gated sodium channels → reduces repetitive firing of sodium dependent action potentials in depolarised neurons

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

Starting dose of Carbamazepine

A

Epilepsy: 100-200mg QD or BD
Mania: 100-400mg in 2-4 divided dose
Trigeminal neuralgia: 200-400mg QD

32
Q

Indications of Carbamazepine

A
  1. Epilepsy (NOT for absence!)
  2. Acute mania
  3. Trigeminal neuralgia (1st line)
33
Q

Carbamazepine - renal

A

No renal adjustment required
DO NOT use for moderate-severe impairment

34
Q

Carbamazepine - elderly

A

Beer’s list: Use with caution (likely due to neurological SEs)

35
Q

Carbamazepine - hepatic

A

No hepatic adjustment required
Consider dose reduction
Hepatotoxicity is a concern

36
Q

Carbamazepine - trigeminal

A

Elderly: 100mg BD

37
Q

Carbamazepine - common SEs

A

GI effects - N/V/C/D, loss of appetite, stomach upset
Hyponatremia - muscle cramps, weakness, mental status change
Neurological - drowsy, lightheaded, headache, blurry or double vision

38
Q

Carbamazepine - rare & serious SEs

A

SJS/TEN - monitor closely in first 3 months
Liver failure
Blood dycrasias

39
Q

ASMs & pregnancy principles

A

Early planning with physicians
- Evaluate concomitant medines + choose ASM with least risk
- Gradually switch to one with lower risk before pregnancy
- Or monitor and adjust accordingly

40
Q

Carbamazepine - pregnancy

A

Teratogenic (major congenital malformations)
If used,
- Folic acid supplementation
- Vit K during last period of pregnancy
- TDM
- Switch to levetiracetam, lamotrigine if possible

41
Q

Carbamazepine - breastfeeding

A

Encouraged to continue, unless AEs in infants observed.

42
Q

Carbamazepine - protein binding

A

75% protein bound; albuminuria increases free drug concentration

43
Q

Carbamazepine - significant pK

A

Undergoes autoinduction (induces own metabolism):
Stabilises in around 3 weeks
Increase CL, decrease t1/2
→ start low dose, titrate up, more frequent dosing

44
Q

Carbamazepine - Initiation

A

Pharmacogenomic testing (HLA-B*1502)
- To identify risk of SJS/TEN
- Asian patients
- If positive, avoid CBZ & phenytoin
- If negative, continue to monitor patients (at risk of developing SCAR (DRESS))

45
Q

Carbamazepine - DDI (1)

A

Macrolides (e.g. clarithromycin)
- CYP3A4 inhibitor
Reduce dose of CBZ

46
Q

Carbamazepine - DDI (2)

A

OC (e.g. ethinyl estradiol)
- CBZ induces CYP3A4-mediated metabolism of OC
Consider CBZ alternatives, or use back up contraceptive during co-administration and at least 28 days after discontinuing CBZ

47
Q

How does Carbamazepine induce hyponatremia

A

Increases ADH which cause increase expression of aquaporin 2 channels in renal tubules

48
Q

Carbamazepine & hyponatremia

A

Serum Na <136mmol/L
Acute onset <48h, associated with neurological complications

49
Q

Management of hyponatremia when taking Carbamazepine

A

Symptomatic: stop CBZ and switch to levetiracetam)
Asymptomatic: fluid restriction
Chronic, asymtomatic: fluid restrict + oral salt tablets or loop diuretic

Monitor: serum electrolytes

50
Q

Carbamazepine - formulation

A

High oral F → oral formulation
Poor solubility → does not have parenteral

51
Q

Carbamazepine - monitoring

A

Baseline:
- FBC, BUN, liver&kidney function, serum Na, ophthalmic test
Follow up:
- Drug concentrations, FBC, liver&kidney function

52
Q

MOA of Phenytoin

A

Blockade of voltage-gated sodium channels → reduces repetitive firing of sodium-dependent action potentials in depolarised neurons

53
Q

Indications of phenytoin

A

All types of seizures except absence seizure

54
Q

Phenytoin - bioavailability

A

Complete but slow absorption
Reduced at higher dose
Reduced by interactions with enteral feeds
- space apart by 2h

55
Q

Phenytoin - protein binding

A

Highly protein bound
- Low albumin = more free phenytoin

56
Q

Phenytoin - pK

A

Zero-order kinetics (increase in dose =/= increase in concentration)

57
Q

Phenytoin - pregnancy

A

Teratogenic

58
Q

Phenytoin - monitoring

A

Labs measure total phenytoin level
Corrected equation:
Cobserved/[x(albumin/10)+0.1]
x = 0.275 when CrCl≥10
x = 0.2 when CrCl<10

59
Q

What drug class is phenobarbital?

A

Barbiturate

60
Q

MOA of phenobarbital

A

Enhance GABA binding (GABA causes Cl- ion channels to open) → greater entry of Cl- → hyperpolarises neurons
At different binding site from benzodiazepines

61
Q

Which group of patient is phenobarbital mainly used for?

A

Neonates/paediatric (IV LD followed by PO/IV MD)

62
Q

Phenobarbital - disadvantages

A
  • Tendency to develop tolerance and dependance
  • Severe withdrawal symptoms
63
Q

Valproate - dosage forms

A

Oral (tablet, syrup)
Injection (solution, powder)

64
Q

Valproate - dose

A

(Starting)
Epilepsy
Absence: 15mg/kg/day (1-4 divided dose)
Complex partial: 10-15mg/kg/day (1-4 divided dose)
GTC: 250mg/day

65
Q

Valproate - common SEs

A

Dizziness - get up slowly from sitting/lying
Drowsy
Diarrhoea - drink more water
N/V, stomach cramp
Hirsutism
Weight gain
Slight tremors of hands and fingers when you first start

66
Q

MOA of valproate

A

Blockade of voltage-gated sodium and calcium channels
Inhibits GABA transaminase → increase GABA

67
Q

Valproate - pregnancy

A

Teratogenic
Major congenital malformations, decreased IQ, neurodevelopmental disorders

68
Q

Valproate - breastfeeding

A

Encouraged

69
Q

Valproate - renal

A

No dose adjustment necessary but closely monitor clinical response, tolerability, free valproic acid concentration

70
Q

Valproate - liver

A

Mild to moderate: not recommended
Severe: Contraindicated

71
Q

Valproate - elderly

A

Lower initial and maintenance dose
Monitor closely for AEs

72
Q

Valproate - paediatric

A

Weight-based dosing

73
Q

Valproate - DDIs (1)

A

CNS depressants
- Strongly bound to plasma proteins, may displace other drugs

74
Q

Valproate - DDIs (2)

A

Carbapenems
- May decrease serum concentration of valproate

75
Q

Valproate - DDIs (3)

A

Lamotrigine
- May enhance AE & increase serum concentration of lamotrigine
- Lamotrigine dose reduction required; increase monitoring for lamotrigine toxicity (rash, hematologic toxicities)

76
Q

Valproate - Drug-disease interaction

A

Hepatotoxicity induced by sodium valproate
Avoid concomitant use of salicylates

54 CNS (13 decks)

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