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Year 1: Patho/Pharm > Seizures PHARM > Flashcards

Seizures PHARM Flashcards

1
Q

Neurotransmitters CNS
vs. PNS

A

CSN: 21 neurotransmitters
PNS: 3 neurotransmitters (E, NE, Ach)

  1. Monoamines
    - NE, E, DA, 5HT3
  2. Amino acids
    - glycine, glutamate, GABA, aspartame
  3. purines
    - adenosine, AMP, ATP
  4. opioid peptides
    - endorphins, enkephalins, dynorphins, etc.
  5. non-opioid peptides
    - oxytocin, somatostatin, substance P, ADH (etc.)
  6. other:
    - histamine, acetylcholine
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2
Q

Excitatory/Inhibitory Post Synaptic Potential
Pathophysiology

A

Dendrites

  • Ligand (NT) gated ion channels
  • NT binds Na/C ion channels
  • Excitatory post synaptic potential: influx Na+, influx Ca+ (more positive)
  • Inhibitory post synaptic potential: efflux K+ (more negative)

*Depolarization towards threshold -55mV = fire action potential

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3
Q

Resting Membrane Potential
Pathophysiology

A

-70mV
Na/K ATPase
3 Na+ out
2 K+ in

High concentration Na+ outside cell
High concentration K+ inside cell

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4
Q

Action Potential
Pathophysiology

A

Excitatory Post synaptic potentials
- depolarization through influx Na+ and Ca+ ligand gated ion channels
- moves towards -55mV (depolarization towards threshold)

Action potential fires
- Voltage gated sodium channels OPEN
- influx of sodium
- depolarization to +40mV
- voltage gated sodium channels CLOSED INACTIVE STATE (absolute refractory)

Hyperpolarization
- Voltage gated potassium channels OPEN (slower)
- efflux of K+
- hyper polarization (beyond -70mV) voltage gated sodium channels CLOSED (relative refractory period)
- voltage gated potassium channels CLOSE

Na/K ATPase
- restores resting membrane potential -70mV
- 3 Na+ out
- 2 K+ in

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5
Q

Excitatory vs. Inhibitory NT

A

Excitatory NT
- Glycine
- Glutamate

Inhibitory NT
- GABA
- NE
- HT
- cannabinoids
- opioids

*Dependent on the pre-synaptic receptor

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6
Q

Drugs that affect sodium influx
CLOSED INACTIVE voltage gated sodium channels

A

Drugs that keep voltage gated sodium channels in inactive state (CLOSED)

  • Phenytoin
  • Carbamazepine (Eslicarbazepine, Oxcarbazepine)
  • Lamotrigine
  • Lacosamide
  • Rufinamide
  • Topiramate
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7
Q

Drugs that affect Calcium influx

A

Ethosuximide

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8
Q

Drugs that affect GABA

A
  • Benzodiazepines (ex. diazepam)
  • Barbiturates (phenobarbitol, primidone)
  • Gabapentin
  • Valproic Acid
  • Vigabatrin
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9
Q

Drugs that affect glutamate receptors

A
  • topiramate
  • perampanel
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10
Q

Drugs with unknown mechanism of action for AED

A
  • levetiracetam
  • bivaracetam
  • pregabalin
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11
Q

Drugs for Absence seizures

A

ethosuximide (block calcium influx)

valproic acid (agonist GABA)

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12
Q

AED used for all seizure types

A

VPA
Valproic acid

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13
Q

Goal of AED therapy

A

Decrease seizure frequency, severity, duration

*not seizure free

Minimize SE and impact on ADLs

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14
Q

Pregnancy and AEDs

A

monotherapy
lowest dosage
avoid valproic acid at all costs
folic acid supplementation
Vitamin K supplementation
90% will have normal pregnancy

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15
Q

Pregnancy and Epilepsy

A

Increase risk of abortion, still birth, preterm labour

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16
Q

Phenytoin/Fosphenytoin
MOA

A

Targets hyperexcitable neurons in the seizure focus

Keeps voltage gated sodium channels closed and INACTIVATED

Cannot fire new action potential

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17
Q

Phenytoin / Fosphenytoin
SE

A

EYES: Nystagmus, blurred vision, diplopia

MSK: Ataxia

CNS: confusion, sedation

CARDIO: cardiovascular collapse with fast infusion

HEME: Bleeding risk (suppression Vitamin K coagulation factors), infection risk (bone marrow suppression)

ENDOCRINE: Hirsutism, gum hyperplasia and bleeding

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18
Q

Special considerations IV infusions
Phenytoin
Fosphenytoin

A
  1. Phenytoin (IV, PO)
    IV filter
    slow IV infusion to prevent cardiovascular collapse
  2. Fospheytoin (IV, IM)
    paraesthesia and pruritis of groin during IV infusion
    Pro-drug conversion, no filter needed
    decreased risk cardiovascular collapse
    can infuse faster
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19
Q

Phenytoin/Fosphenytoin
AE

A

HLA-1502
1. SJS, TENS, DRESS
Patient education: monitor for rash
*Asian Descent

  1. Teratogenic
    Patient education: condoms, oral contraceptives degraded
  2. Infection and bleeding risk
    Monitoring: CBC, INR
    Patient education: report bruising, signs of infection
  3. fractures
    - Phenytoin blocks vitamin D activation
    - results in hyperparathyroidism (secondary)
    - calcium is not absorbed from GI
    - bones are reabsorbed
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20
Q

Therapeutic Drug Monitoring
Phenytoin

A

Saturation Kinetics
- saturate hepatic enzyme quickly
- small change in dose, large change in drug level

Narrow therapeutic window
- small dose can cause 1. toxicity 2. therapeutic failure

Therapeutic drug monitoring
- plasma level
- trough level

*Drug interactions high

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21
Q

Administration considerations
Phenytoin/Fosphenytoin

A

Do not administer with food
1-2 hour hold

PRN
calcium
vitamin D

IV filter for phenytoin

Pharmacy to check drug interactions
saturation kinetics

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22
Q

Carbamazepine
MOA

A

Target: seizure focus (hyper excitable neurons) and surrounding neighbours

Keeps voltage gated sodium channels in INACTIVE and CLOSED state (prolongs absolute refractory period)

prevents firing of new action potential

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23
Q

Carbamazepine
SE

A

EYES: Nystagmus, blurred vision, diplopia
CNS: sedation
MSK: ataxia
- tolerance develops
- Patient education: start low, go slow, night admin

Bone marrow suppression: bleeding and infection risk

Teratogenic: NTD

SKIN: SJS, DRESS, TENS (HLA-1502)

OTHER:
Kidney failure
Increase ADH release: FVO, hyponatremia
Liver failure

24
Q

Carbamazepine
AE

A

Teratogenic: NTD
Patient education: folic acid, contraception condoms, oral

Kidney failure: FVO, hyponatremia, ADH hyper secretion
Patient education: weight gain, oliguria, S&S hyponatremia

Liver failure

Bone marrow suppression: Bleeding and infection (Fatal aplastic anemia D/C)

HLA1502: TENS, DRESS, SJS

25
Q

Patient Monitoring
Carbamazepine

A

CBC and diff
HLA-1502 status
LFTs
BUN, creatinine
serum sodium
serum ferritin
Weight
HCG

S&S liver failure: jaundice, anorexia, n/v
S&S kidney failure: weight gain, oliguria
S&S bleeding: bruising, pale, fatigue
S&S infection: fever, sore throat
S&S hyponatremia: fatigue, anorexia, loss muscular tone, depressed reflexes, orthostatic hypotension, etc.

26
Q

Carbamazepine
Indications

A

All seizures
*Exception - absence seizures

27
Q

Carbamazepine
Hepatic Metabolism

A

Induces its own metabolism
Induces metabolism of other AEDs
- phenytoin
- phenobarbital
- oral contraceptives

28
Q

Carbamazepine
Contraindications

A

Liver disease
Kidney disease
pregnancy
HLA1502
Blood disorders
Caution secondary Hyperparathyroidism
Heart failure
Hypertension

29
Q

Ethosuximide
MOA

A

Blocks calcium channels in pre-synaptic (Blocks EPSP) and post synaptic membrane (Blocks NT release)

Prevents transmission of excitatory impulse

30
Q

Ethosuximide
Indication

A

Absence seizures

31
Q

Ethosuximide
SE

A

EYES: Nystagmus, blurred vision, diplopia
CNS: sedation
Patient education: take at night, tolerance develops

GI: nausea, vomiting, weight loss
Patient education: take with food

SKIN: Rash

HEME: Bone marrow suppression, SLE

32
Q

Patient monitoring
Ethosuximide

A

Clinical response
- no drug monitoring
- absence seizures occur at high frequency

CBC and diff

Patient monitoring
S&S bleeding, infection, rash, weight loss

33
Q

Phenobarbital/Primidone
MOA

A

GABA agonist
increase activity of GABA
CNS depressant

*Phenobarbital is a metabolite of primidone

34
Q

Phenobarbital/Primidone
SE

A

CNS: sedation, dizziness, fatigue, learning impairment
Patient education: take at night, tolerance develops

PSYCH: depression/suicide adults, paradoxical agitation children/older people

HEME: porphyrin accumulation

RESP: respiratory depression

35
Q

Phenobarbital/Primidone
AE

A

Respiratory depression and death
Contraindicated: respiratory disorders, CNS depressants, liver/kidney disease (drug accumulation)

Addiction, depression, suicide
Contraindicated: psych history

Withdrawal

36
Q

Phenobarbital/Primidone
Contraindications

A

Respiratory disorders
liver and kidney disorders (drug accumulation)
history addiction, suicide, depression

37
Q

Patient Monitoring
Phenobarbital/Primidone

A

CBC and diff
LFT
BUN and Creatninine
Respiratory disorders
Medication: CNS depressants
Hx. addiction, mental health

38
Q

Primidone
MOA

A

Phenobarbital is a metabolite of primidone

GABA agonist
increase CNS depression

39
Q

Indication
Phenobarbital vs. Primidone

A

Phenobarbital
- All seizures exception absence

Primidone
- all seizures exception absence and status

40
Q

Valproic Acid
Indication

A

ALL SEIZURES
* absence included

Rx combination seizures

41
Q

Valproic Acid
MOA

A

Unknown
Thought to be a GABA agonist
Increase CNS depression

42
Q

Valproic Acid
SE/AE

A

CNS: *Minimal sedation
MSK: tremor

GI: N/V/anorexia/abdominal pain, weight gain
Patient education: administer with food

HEME: bone marrow suppression

Kidney: Ammonia accumulation

Hepatitis and liver failure

pancreatitis

Teratogenic

43
Q

Valproic Acid
AE

A

Teratogenic: 4x higher than other AEDs

Kidney: Ammonium accumulation and encephalopathy (N/V/anorexia, HA, ataxia, seizures, coma)

Liver: hepatitis and liver failure (anorexia, N/V, jaundice, dark urine, pale stools)

Pancreatitis: debilitating RUQ pain, radiation back, hypotensive shock, ARDs, DIC, GI hemorrhage, multiple organ failure

44
Q

Contraindications
Valproic acid

A
  1. Pregnancy
    - teratogenic 4x
  2. < 2 years of age and multiple AEDs
    - hepatitis and pancreatitis
    - death
  3. Liver disease, pancreatic disease
  4. blood dyscarias
45
Q

Patient monitoring
VPA

A

CBC and diff
LFTs
BUN and creatininine
serum lipase
HCG

46
Q

Patient education
VPA

A

S&S: bleeding, bruising, pallor, fatigue, infection (bone marrow suppression)

S&S: anorexia, nausea, vomiting, jaundice (liver failure)

S&S: RUQ pain, hypotensive shock, DIC, fever (pancreatitis)

pregnancy: oral contraceptive and condom

S&S encephalopathy ammonium: ataxia, N/V/HA, coma, seizures

47
Q

levetiracetam
MOA and indication

A

unknown MOA

All seizures exception absence

48
Q

Levetiracetam
safety profile

A

safest AED
doesn’t require hepatic metabolism
doesn’t interact with other AEDs

49
Q

Levetiracetam
SE

A

CNS: Sedation

Psych: aggression, agitation, anxiety, depression, psychosis

MSK: asthenia (lack of strength)

Kidney: query renal failure

50
Q

Seizure Threshold and Pregnancy

A

Pregnancy hormones (estrogen) lowers the seizure threshold

Increased plasma volume lowers the AED level

*predisposes people to seizures

51
Q

Seizure effect on fetus and mother

A

Increase risked of fetal and maternal death

Fetus
- decrease heart rate, perfusion
- increase risk of pre-term labour, stillborns, miscarriage

Mother
- increased risk of death

52
Q

AED Strategy during pregnancy

A

AEDs teratogenic
- phenytoin
- carbamazepine: NTD (folic acid supplementation)
- Valproic acid: absolute contraindication 4x risk

Monotherapy
lowest dose
Vitamin K and folic acid supplements

53
Q

AEDs that lower oral contraceptive levels (hepatic metabolism)

A
  • Phenytoin
  • carbamazepine
  • valproic acid
  • phenobarbital/ primidone
  • toperiamate
  • lamotrigine
54
Q

Ketogenic Diet
Therapeutic effect

A

Indication: Medication resistant epilepsy

Decrease seizure frequency, severity

Diet high in fat, protein, low in carbohydrate
Induce a state of ketosis
Ketone bodies produced
Increase the seizure threshold

55
Q

Ketogenic Diet
SE

A

Metabolic acidosis
- ketone bodies (keto acids)

Hypoglycemia
- SNS effects: diaphoresis, sweating, tachycardia
- CNS effects: lethargy, sedation, coma

Systemic:
- CAD, atheroscelerosis, dyslipidemia
- pancreatitis
- kidney stones (high protein)

56
Q

Weaning AED

A

six weeks to wean
wean 1 drug at a time

57
Q

Driving and Epilepsy

A
  • 6 to 12 months seizure free before can drive
  • 16 years of age mandatory reporting in Ontario (even if do not have licence)

Year 1: Patho/Pharm (39 decks)

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