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Therapeutics IV > Manage EPILEPSY > Flashcards

Manage EPILEPSY Flashcards

1
Q

Distinguish between seizure and epilepsy

A
  • Seizure: Transient signs and sx due to abnormal excessive or synchronous neuronal activity brain, caused by avoidable acute CNS insults
  • Epilepsy: brain disorder characterised by ENDURING PREDISPOSITION TO GENERATE EPILEPTIC SEIZURES

i. e. any of the following:
- ≥2 UNPROVOKED seizures occurring more than 24h apart, - generally having recurrence risk (60%) after first seizures over 10 yrs
- Dx epilepsy syndrome

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2
Q

Briefly describe the pathophysiology of epilepsy

A

Key concepts: Hyperexcitability and hypersynchronisation, leads to paroxysmal discharge in neurons within cortex

  • Hyperexcitability caused by excess K, Na, Ca, Cl OR insufficient inhibitory NT (GABA)
  • Hypersynchronisation: intrinsic organisation of local circuits at hippocampus, neocortex and thalamus cause synchronous nerve firing
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3
Q

List the factors that may be risk factors or triggers for seizures in susceptible individuals

A
  1. Genetic
  2. Structural (e.g. brain injury)
  3. Metabolic disorders (e.g. GLUT1 deficiency)
  4. Autoimmune
  5. Infectious (e.g. meningitis)

(MAGIS)

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4
Q

The difference between focal vs generalised onset in terms of CNS origin

A
  • Focal: begins in one hemisphere

- Generalised: both hemispheres

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5
Q

Describe clinical presentation for seizures classified as focal onset w/o dyscognitive features
(i.e. simple partial)

A
  1. Motor sx: CLONIC movements (arm shoulder face leg), speech arrest
  2. Sensory: numb/tingle, visual disturbances (flashing lights), raised epigastric sensation
  3. Autonomic: Sweat, salivate, pallor, increased BP/HR
  4. Psychic/somatosensory: flashbacks, hallucinations, affective sx (fear, depression anger)

(SPAM)

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6
Q

Describe clinical presentation for seizures classified as focal onset WITH dyscognitive features
(i.e. complex partial)

A
  1. Aura
  2. Impaired consciousness: Amnesia to event (patient not aware)
  3. Automatisms: e.g. lip smacking, chewing
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7
Q

Describe clinical presentation of Tonic-clonic seizure (GTC)

i.e. grand mal

A
  • Tonic phase: Stiffening of limbs
  • Clonic Phase: jerking of limbs and phase
  • May have aura
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8
Q

Describe clinical presentation of Clonic seizures

A

ASYMMETRICAL and IRREGULAR jerking, frequent in neonates, infants or young children

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9
Q

Describe clinical presentation of Tonic seizures

A

Sudden LOSS OF CONSCIOUSNESS and RIGID POSTURE of entire body for 10-20s

(A characteristic seizure type in Lennox-Gastaut Syndrome)

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10
Q

Describe clinical presentation of MYOCLONIC seizures

A

BRIEF RAPID CONTRACTIONS of muscles usually occurring on both sides of body, but may only involve one arm or one foot

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11
Q

Describe clinical presentation of absence seizures

A

Basic lapse in awareness that last a few seconds, often mistaken as persistent staring, usually in children

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12
Q

Distinguish between absence seizures and complex partial seizures. State the importance of differentiating between these two seizures

A 
Absence seizures:
1. NO aura
2. only last SECONDS (than minutes)
3. Begin very frequently, end abruptly
(3Hz spike waves)

Importance: Ensure correct medication Rx for correct type of seizure

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13
Q

Describe clinical presentation of atonic seizures

A

Class Drop attack

  • Sudden loss in muscle tone, collapse down to ground like rag doll
  • Immediate recovery
  • Frequent injuries due to falls
  • Associated with diffuse cerebral damage and learning disability
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14
Q

List the type of seizures with generalised onset

A
  1. Tonic-clonic
  2. Tonic
  3. Clonic
  4. Myoclonic
  5. Absence
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15
Q

List and describe some tools to help dx and manage seizures

A
  1. Scalp EEG
    - EEG normal ≠ no epilepsy (limitation)
    - Vice versa
  2. Video EEG
    - real time video of patient and eeg
  3. MRI with GD contrast to ID focal lesions
    - For adults with first seizure, or possible focal onset
  4. Biochemical/toxicology
    - Rule out electrolyte abnormalities
    - Serum prolactin: not used due to variability
    - Creatinine kinase: For GTC (raised due to contractions)
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16
Q

Based on ILAE 2017 classification of seizure types, how can seizures be classified?

A

Based on three key features

  1. Mode of onset: Focal vs Generalised
  2. For FOCAL: impaired consciousness/ no response to external stimuli properly
    - “with” or “without” “Dyscognitive features”
  3. Other features

Then further subdivided to motor and non-motor sx

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17
Q

Significance of ILAE 2017 seizure classification

A
  1. Fundamental characteristic by which to classify seizures

2. Tx and prognostic implications

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18
Q

Appropriate actions for seizure first aid

A
  1. Ease person on floor
  2. Turn person to one side (help breathing)
  3. Clear area around person (people, objects)
  4. Put soft object under head
  5. Remove eyewear
  6. Loosen clothing that may hinder breathing
  7. Time the seizure, 911 if >5min
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19
Q

INAPPROPRIATE actions for seizure first-aid

A
  1. Try to stop movements
  2. Put something in person mouth
  3. CPR
  4. Water or food
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20
Q

How does epilepsy affect someone’s life?

i.e. psychosocial issues

A
  1. Social stigma: marriage, starting fam
  2. Employment affected
    - Patient need more f/u
    - Higher medical costs by employer
  3. Cannot be driver at all (for SG)
  4. Burden to caregiver
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21
Q

List and describe the various non-pharmacological options for seizures. When will you use them?

A
  1. Ketogenic diet( low carb, high fats)
    - For patients cannot tolerate, or no response to AED tx
    - Usually children
    - Bad: Adhere long term difficult
  2. Surgery
    - Focal seizures ONLY: Remove part of brain causing seizures
  3. Vagus Nerve Stimulator (VNS)
    - For Intractable focal seizures only
    - Got implantable magnet to stimulate on demand (predict seizure episodes and prevent it)
  4. Responsive NT system (RNS)
    - Adjunct for partial-onset for patients
    - Invasive, under the scalp devise
    - Deliver pulses of stimulation when detect activity that may lead to seizure
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22
Q

Tx goals of seizures

A
  1. No epileptic seizure
  2. No AED-related SE
  3. QoL

(2/3 patients achieve seizure freedom)

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23
Q

Factors influencing AED Choice, and how do they influence the AED choice?

A
  1. Seizure type: Rapid or slow titration
  2. Other meds and morbidity:
    - DDI
    - Special population
    - Route of elimination
    - Some conditions cannot use some AED
  3. Patient lifestyle and preferences: Dosage form and frequency + Occupation
  4. National Institutional: Guidelines, availability and cost
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24
Q

List and Describe general principles of Pharmaco tx for AED

A
  1. Monotherapy preferred, SUBSTITUTE if non-response
  2. Start low titrate up slow, provided no SE
  3. If no response, review dx, AED of choice and adherence
  4. Consider combination, if tolerate 1st/2nd AED with sub-optimal response
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25
Q

Steps to determine tx for a patient

A
  1. Type of epilepsy: Focal or generalised onset?

2. New onset or refractory?

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26
Q

Describe some PK considerations when choosing AED?

A
  1. Protein binding (Hypoalbuminemia?)
  2. Route of elimination: ESRD patient?
  3. Interactions
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27
Q

2nd gen AEDs which have no effect on CYP

A
  1. Gabapentin (GBP)
  2. Levetiracetam (LEV)
  3. Pregabalin (PGB)
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28
Q

Major route of elimination for most 1st generation AEDs?

A

H

29
Q

Major route of elimination for most 2nd generation AEDs? What is an exception?

A

R

- Except; Lamotrigine (100%H)

30
Q

List the common 1st gen AED

A

CBZ, PHT, VPA, (PB)

  • CBZ = Carbamazapine
  • PHT = Phenytoin
  • VPA = Valproate
  • PB = Phenobarbital
31
Q

Amongst the first generation AED, which one is an exception, in that it is a potent enzyme INHIBITOR instead of inducer

A

VPA

32
Q

Significance of DDI in tx

A

Deinduction Interactions

- Adjust dose accordingly when enzymes are deinduced

33
Q

What are the issues with enzyme-inducing AEDs?

A
  1. DDI
  2. Reproductive consequences
  3. Bone health
  4. Vascular risk
34
Q

Caution when using PHT in NGT feeds

A

Reduced bioavailability and absorption

35
Q

Caution when using AED in ESRD or liver dysfunction patient. What 1st gen AED drugs to watch out for?

A

ESRD/H Dysfunc = Low albumin

  • PHT, VPA, CBZ is highly albumin bound
  • Low albumin = increase free drug = increase effect = High SE risk
36
Q

Caution when using PHT

A

Non-linear kinetics, hence concentration is NOT proportional to dose

37
Q

Characteristic of VPA PK that has important implication

A

Saturable protein-binding

  • Total [VPA] increase in non-linear with dose
  • Hence: interpreting [VPA] for hypoalbuminemia patients –> Does not correspond therapeutic efficacy
38
Q

Dosage form that is available in VPA and PHT but not in CBZ? What dosage forms is/are available in CBZ?

A

CBZ: unavailable in IV

- Available: Tabs IR/CR

39
Q

Characteristic of CBZ PK. What is the important implication

A

Autoinduction (of own metabolism)

  • No consistent half life
  • Lasts 2-3 weeks after initiation
  • Implication: start low titrate slow over first few weeks
40
Q

What are some ACUTE toxic effects of AEDs?

A

Toxic effects are DOSE DEPENDENT:

  1. CNS (e.g. dizzy, ataxia etc.)
  2. GI: NNV (CBZ, VPA)
  3. Psyc: Behaviour disturbance (LEV)
  4. Cognition: Decreased speech fluency (TPM)
  5. Allergy, within 1st few months of therapy
41
Q

In what situation do AED AEs have higher chance of occurring?

A

Combination Therapy

but may disappear as tolerance develops

42
Q

How to avoid or minimise the risk of SE for AEDs?

A
  1. Start low titrate slow
  2. Monotherapy if clinically feasible
  3. Adjust administration schedule
    - Largest dose HS
    - SR Tab
    - More frequent small doses
    - Reduce TDD if clinically safe
43
Q

HLA-B*1502 genotyping for Han Chinese and Asian ethnic groups should be done before initiating which AED(s), and why?

A

Prior to starting CBZ

  • Increased risk of CBZ-induced SJS/TEN
  • If positive, avoid CBZ and PHT
44
Q

Recommendation for Lamotrigine

A

Very slow titration (slower than other AEDs)

45
Q

Generally in terms of DDI, 1st gen AED has more or less than 2nd gen?

A

MORE

46
Q

Describe the indications for AED Therapeutic drug monitoring (TDM)

A
  1. Establish individual TI
  2. Assess reasons for lack of efficacy (e.g. fast metaboliser, compliance etc.)
  3. Assess Toxicity
  4. Assess loss of efficacy, which may cause breakthrough seizures
    - E.g. DDI, change in physiology, patho, changed formulation

(Summary: Find Efficacy and Tox SPECIFIC to patient)

47
Q

Information required when carrying out TDM

A
  1. AED dx
  2. Dose
  3. Sample: type and time taken
  4. Clinical condition: seizure control, baseline, comorbs
  5. Other labs and drugs
48
Q

How to manage preggo and lactating women who requires AED tx?

A

Refer to specialist

49
Q

Stuff to take note of for women of childbearing age?

A
  • Discuss fam planning
  • Some AED risk to fetus
  • OCs may have DDI, e.g. lower LTG causing breakthrough seizures
50
Q

General Definition of Status Epilepticus for Tonic-clonic

A

≥5 minutes seizure

51
Q

List the phases of therapy and the tx options of Status Epilepticus

A
  1. 5-20 mins: Initial therapy phase, Non-PO BZD (IV/IM)
  2. 20-40mins: Second phase: , IV VPA, LEV, fosPHT
  3. 40-60 min: Third therapy phase, repeat 2nd line OR anesthetic dose of anesthesia
52
Q

Can IV Midazolam be used for Status Epilepticus initial therapy phase? If not, what dosage form of Midazolam can be used?

A

NO, it is not as rapid acting as IM midazolam

53
Q

When does permanent damage occur in patient with status epilepticus?

A

≥30 mins of seizure, neuronal injuries

54
Q

Which AED must be used with caution in patients with depression or anxiety?

A

LEV

55
Q

What to avoid in women with child-bearing potential? What are the options for them

A
  • Avoid: PHT, VPA, TPM

- options: LEV/LTG

56
Q

Preferred AED option for elderly with focal onset epilepsy

A
  1. GBP

2. LTG

57
Q

General Tx options for generalised onset of epilepsy

A
  1. LTG
  2. TPM
  3. VPA
58
Q

The CHRONIC AE that PHT is associated with

A
  1. Gingival Hyeprplasia
  2. Hirsutism
  3. Neuro: Encephalopthy + Peripheral Neuropathy (AT HIGH DOSES)
  4. Osteomalacia
  5. Megaloblastic anemia
  6. Congenital Defects
59
Q

The CHRONIC AE that VPA is associated with

A
  1. Alopecia
  2. Weight Gain (reversible)
  3. Congenital defect: COGNITION

(recall that GI wise, VPA cause weight gain, but TPM and Felbamate coz anorexia and weight loss)

60
Q

The CHRONIC AE that CBZ is associated with

A
  1. Peripheral Neuropathy
  2. Osteomalacia
  3. Megaloblastic anemia

(“Subset” of PHT”)

61
Q

The CHRONIC AE that PB is associated with (although PB is no longer in market lol)

A
  1. Neuro: Encephalopathy + Peripheral Neuropathy
  2. Osteomalacia
  3. Megaloblastic Anemia
  4. Congenital Defects

(“Subset” of PHT”, nearly everything of CBZ but one extra Megaloblastic anemia)

62
Q

The CHRONIC AE that TPM is associated with

A
  1. Anorexia and Weight Loss (reversible)

2. Congenital Defects

63
Q

The CHRONIC AE associated with FElbamate

A

Anorexia and Weight Loss (reversible)

64
Q

The CHRONIC AE that is associated with MOST AEDs

A

Blood Dyscrasias

65
Q

PHT, CBZ and PB can cause this CHRONIC AE, which is RARE (<1%). It occurs predominantly in patients receiving PHT. What could this AE be?

A

Megaloblastic Anemia

66
Q

CHRONIC AE that is REVERSIBLE with drug discontinuation

A

GI AEs:

  • Weight gain (by VPA)
  • Weight Loss (by TPM and Felbamate)

(these are REVERSIBLE)

67
Q

Perhaps the most common AE that is observed in AEDs. Which drug is it associated with?

A

Gingival Hyperplasia, caused by chronic PHT therapy

68
Q

One LIFE-THREATENING AE (other than Megaloblastic anemia) that is associated with MOST AED

A

Suicidal Ideation

Therapeutics IV (9 decks)

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