Epilepsy Flashcards

1
Q

What are the common symptoms of abnormal electrical activity in epilepsy?

A

Loss of consciousness, abnormal movements, atypical behavior, and distorted perception.

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2
Q

What percentage of individuals are affected by epilepsy by the age of 80?

A

Approximately 3%.

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3
Q

What is the rank of epilepsy among neurological disorders?

A

It is the 3rd most common after cardiovascular and Alzheimer diseases.

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4
Q

What percentage of epilepsy cases can be completely controlled?

A

70-80%.

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5
Q

What percentage of epilepsy cases require more than one drug?

A

10-15%.

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6
Q

What percentage of epilepsy patients may not achieve complete seizure control?

A

10%.

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7
Q

What is the cause of epilepsy in most cases?

A

In most cases, epilepsy has no identifiable cause.

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8
Q

How can epilepsy be classified?

A

Idiopathic (unknown etiology) and symptomatic (secondary to an identifiable condition).

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9
Q

What are some conditions that can cause symptomatic epilepsy?

A

Alterations in blood gases, pH, electrolytes, blood glucose level, sleep deprivation, alcohol intake, and stress.

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10
Q

What is idiopathic epilepsy also known as?

A

Cryptogenic (primary) epilepsy.

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11
Q

What is a key characteristic of idiopathic epilepsy?

A

No specific anatomic cause for the seizure is evident.

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12
Q

What is the common cause of idiopathic epilepsy?

A

Inherited abnormality in the central nervous system.

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13
Q

What type of epilepsy constitutes most cases?

A

Idiopathic epilepsy.

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14
Q

What are some causes of symptomatic epilepsy?

A

Illicit drug use, tumor, head injury, hypoglycemia, meningeal infection, and rapid withdrawal of alcohol.

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15
Q

Why is the appropriate classification of seizures important?

A

Because it leads to appropriate treatment.

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16
Q

What characterizes a simple partial seizure?

A

Consciousness is preserved.

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17
Q

What characterizes a complex partial seizure?

A

Loss of consciousness and possible memory impairment.

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18
Q

What characterizes generalized seizures?

A

They involve both hemispheres of the brain and usually result in loss of consciousness.

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19
Q

What part of the brain is affected by partial seizures?

A

Only a portion of the brain, typically one lobe of one hemisphere.

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20
Q

What do the symptoms of partial seizures depend on?

A

The site of neuronal discharge and the extent to which the electrical activity spreads to other neurons.

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21
Q

Is consciousness preserved during partial seizures?

A

Yes, consciousness is usually preserved.

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22
Q

Where are the hyperactive neurons confined in a simple partial seizure?

A

To a single locus in the brain.

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23
Q

Does the patient lose consciousness during a simple partial seizure?

A

No, the patient does not lose consciousness.

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24
Q

What type of abnormal activity occurs in a simple partial seizure?

A

Abnormal activity of a single limb or muscle group.

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25
Q

What sensory symptoms are associated with simple partial seizures?

A

Sensory distortions.

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26
Q

What are the sensory and mental symptoms of complex partial seizures?

A

Complex sensory hallucinations and mental distortion.

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27
Q

What types of motor dysfunction can occur during complex partial seizures?

A

Chewing movements, diarrhea, and/or urination.

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28
Q

Is consciousness preserved or altered during complex partial seizures?

A

Consciousness is altered.

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29
Q

What characterizes generalized seizures?

A

They may begin locally and progress to both hemispheres of the brain, resulting in immediate loss of consciousness.

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30
Q

What are the phases of a tonic-clonic seizure?

A

Loss of consciousness followed by tonic (continuous contraction) and clonic (rapid contraction and relaxation) phases.

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31
Q

What are the characteristics of absence seizures?

A

Brief, abrupt, self-limiting loss of consciousness, onset at 3-5 years, with rapid eye-blinking lasting 3-5 seconds.

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32
Q

What characterizes myoclonic seizures?

A

Short episodes of muscle contractions that may recur for several minutes. These seizures usually occur after waking up, and manifest as brief jerks of the limbs.

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33
Q

What age groups are at risk of being affected by myoclonic seizures?

A

Can occur at any age but usually begins around puberty or early adulthood.

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34
Q

Who is most commonly affected by febrile seizures?

A

Young children.

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35
Q

What triggers febrile seizures?

A

Illness accompanied by high fever, resulting in generalized tonic-clonic convulsions of short duration.

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36
Q

What defines status epilepticus?

A

Two or more seizures occur without full recovery of consciousness between them, requiring emergency treatment.

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37
Q

What are the mechanisms of action for antiepileptic drugs?

A

Blocking voltage-gated channels (Na+ or Ca2+), enhancing inhibitory GABAergic impulses, and interfering with excitatory glutamate transmission.

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38
Q

What factors influence the choice of antiepileptic drug?

A

Classification of the seizures, patient-specific variables, and characteristics of the drug.

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39
Q

What is the initial treatment strategy for newly diagnosed epilepsy patients?

A

Monotherapy with a single agent until seizures are controlled or toxicity occurs.

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40
Q

What are the benefits of monotherapy in epilepsy treatment?

A

Better adherence and fewer side effects.

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41
Q

What are some 1st generation antiepileptic drugs?

A

Phenobarbital, phenytoin, carbamazepine, ethosuximide, divalproex, and valproic acid.

Proud People Can End Dangerous Violence

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42
Q

What are some 2nd generation antiepileptic drugs?

A

Gabapentin, lamotrigine, levetiracetam, oxcarbazepine, topiramate, and zonisamide.

Great Lions Leap Over Tall Zebras

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43
Q

What is the mechanism of action for benzodiazepines in epilepsy?

A

They bind to GABA inhibitory receptors and reduce the firing rate of neurons.

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44
Q

For which types of seizures are diazepam and lorazepam used?

A

Myoclonic, partial, and generalized tonic-clonic seizures.

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45
Q

Why is diazepam available for rectal administration?

A

To avoid prolonged generalized tonic-clonic seizures.

46
Q

What is the first-line treatment for status epilepticus according to FDA guidelines?

A

Benzodiazepines, specifically diazepam and lorazepam.

47
Q

What is the mechanism of action for carbamazepine?

A

It blocks sodium channels, inhibiting repetitive action potentials and preventing their spread.

48
Q

For which conditions is carbamazepine effective?

A

Partial seizures, generalized tonic-clonic seizures, trigeminal neuralgia, and bipolar disorder.

49
Q

Why should carbamazepine not be prescribed for patients with absence seizures?

A

Because it may cause an increase in seizures, due to the activation of GABA receptors in ventrobasal complex (which aggregates absence seizures).

50
Q

What are some side effects of carbamazepine?

A

Diplopia, blurred vision, and hyponatremia.

Can’t see straight, can’t see shit, can’t keep the fucking salt.

51
Q

What is a significant metabolic effect of carbamazepine?

A

It induces its own metabolism and increases the metabolism of other drugs through CYP450 and UGT enzyme induction.

52
Q

What is the active metabolite of carbamazepine?

A

Epoxide metabolite –> Causes blood dyscrasias.

53
Q

What is oxcarbazepine and how is it activated?

A

It is a prodrug reduced to the monohydroxy (MHD) metabolite, which is responsible for its anticonvulsant activity.

54
Q

What is the mechanism of action for oxcarbazepine?

A

It blocks sodium channels, preventing the spread of abnormal discharge.

55
Q

For which type of seizures is oxcarbazepine effective?

A

Partial onset seizures.

56
Q

How does oxcarbazepine compare to carbamazepine in terms of drug interactions?

A

It is a less potent inducer of CYP3A4 and UGT, resulting in lower drug-drug interactions.

57
Q

What are some side effects of oxcarbazepine?

A

Nausea, vomiting, headache, and visual disturbances.

Feel like I am gonna puke, fuck, I am vomiting, shit, my head’s fucked up and I can’t see shit.

58
Q

What is the mechanism of action for phenytoin and fosphenytoin?

A

They block voltage-gated sodium channels by binding to the inactive state and slowing recovery. At high concentrations, phenytoin can also block calcium channels and interfere with monoaminergic neurotransmitters.

59
Q

For which conditions is phenytoin effective?

A

Partial seizures, generalized tonic-clonic seizures, status epilepticus, and trigeminal neuralgia.

60
Q

Why should phenytoin not be used in absence seizures?

A

Because it can exacerbate absence epilepsy.

61
Q

What are some side effects of phenytoin?

A

CNS depression causing nystagmus and ataxia, gingival hyperplasia, peripheral neuropathies, osteoporosis, and risk of megaloblastic anemia.

Mnemonic: “Phenytoin: Can’t See Straight, Can’t Walk, Gums Gone Wild, Numb as Hell, Bones Like Glass, Blood’s a Mess”

Can’t See Straight - Nystagmus (eye movement disorder)
Can’t Walk - Ataxia (lack of muscle coordination)
Gums Gone Wild - Gingival hyperplasia (overgrown gums)
Numb as Hell - Peripheral neuropathies (nerve damage)
Bones Like Glass - Osteoporosis (weak bones)
Blood’s a Mess - Risk of megaloblastic anemia (impaired blood cell production)

62
Q

What is fosphenytoin and how is it activated?

A

Fosphenytoin is a prodrug rapidly converted to phenytoin in the blood.

63
Q

What metabolic characteristics does phenytoin have?

A

It induces drug-metabolizing enzymes, has saturable metabolism at low serum concentrations, and small dose increases can lead to large plasma concentration increases, causing toxicity.

64
Q

What is gabapentin and how does it function?

A

It is an analog of GABA but does not bind to GABA receptors or activate them; its mechanism is unknown.

65
Q

For which conditions is gabapentin used as an adjunct therapy?

A

Partial seizures and postherpetic neuralgia (nerve pain due to damage caused by the varicella zoster virus).

66
Q

What is a notable pharmacokinetic property of gabapentin?

A

It has nonlinear pharmacokinetics due to uptake by a saturable transporter in the gut.

67
Q

How is gabapentin excreted, and what is its significance regarding drug interactions?

A

It is excreted unchanged through the kidneys and does not bind to plasma proteins, resulting in low drug-drug interaction.

68
Q

Why is gabapentin considered a good choice for older patients?

A

It is well-tolerated due to its mild side effects.

69
Q

What is the mechanism of action for tiagabine?

A

It blocks GABA uptake into presynaptic neurons, allowing more GABA to be available for receptor binding and enhancing inhibitory activity.

70
Q

For which type of epilepsy is tiagabine effective?

A

Partial onset epilepsy.

71
Q

Is tiagabine approved for use in absence seizures?

A

No, it is not used for absence seizures.

72
Q

What is the mechanism of action for lamotrigine?

A

It blocks sodium channels and high voltage-dependent calcium channels.

73
Q

For which types of seizures is lamotrigine effective?

A

Partial seizures, generalized seizures, and typical absence seizures.

74
Q

What is another condition for which lamotrigine is used?

A

Bipolar disorder.

75
Q

How is lamotrigine’s half-life affected by other drugs?

A

Reduced by enzyme-inducing drugs (carbamazepine) and increased by enzyme-inhibitor drugs (valproate).

76
Q

What is a potential side effect of rapid titration of lamotrigine?

A

It can cause a rash, potentially progressing to a serious, life-threatening reaction.

77
Q

Why is lamotrigine well tolerated by the elderly?

A

Due to its minor side effects.

78
Q

For which types of seizures is levetiracetam effective?

A

Partial onset seizures, myoclonic seizures, and primary generalized tonic-clonic seizures in adults and children.

79
Q

What is the proposed mechanism of action for levetiracetam?

A

It is unknown, but most probably acts on synaptic vesicle protein SV2A.

80
Q

How does levetiracetam interact with metabolic systems?

A

It does not interact with CYP or UGT metabolism systems, resulting in low drug-drug interactions.

81
Q

What is the mechanism of action for phenobarbital?

A

Enhancing the inhibitory effects of GABA-mediated neurons.

82
Q

For what condition is phenobarbital primarily used?

A

Treatment of status epilepticus.

83
Q

Why is phenobarbital considered for chronic therapy only in refractory patients?

A

Due to its high side effects, including sedation, enzyme induction, and osteoporosis.

84
Q

Which antiepileptic drugs are associated with decreased bone cell proliferation and decreased Vitamin D levels?

A

Phenytoin, carbamazepine, and phenobarbital.

85
Q

What is the spectrum of action for felbamate?

A

Broad spectrum of anticonvulsant action.

86
Q

What are the proposed mechanisms of action for felbamate?

A

Blocking voltage-dependent sodium channels, competing with the glycine binding site on the NMDA glutamate receptor, blocking calcium channels, and potentiating the action of GABA.

87
Q

Why does felbamate have high drug-drug interactions?

A

It inhibits drugs metabolized by CYP2C19 and ß-oxidation and induces drugs metabolized by CYP3A4.

88
Q

Why is felbamate used only in refractory epilepsies?

A

Due to the risk of aplastic anemia and heart failure.

89
Q

What is divalproex sodium and why is it used?

A

It is a combination of sodium valproate and valproic acid converted to valproate in the gastrointestinal tract to improve GIT tolerance of valproic acid.

90
Q

What are the mechanisms of action for valproic acid and divalproex?

A

Sodium channel blockade, blockade of GABA transaminase, and blockade action at T-type calcium channels.

91
Q

For which types of epilepsies are valproic acid and divalproex effective?

A

Partial and primary generalized epilepsies.

92
Q

How do valproic acid and divalproex interact with metabolic systems?

A

They inhibit the metabolism of CYP2C9, UGT, and epoxide hydrolase systems, resulting in high drug-drug interactions.

93
Q

What are some rare and serious side effects of valproic acid and divalproex?

A

Hepatic toxicity and teratogenic effects causing neural tube defects, contraindicating use in pregnancy.

94
Q

What are the mechanisms of action for topiramate?

A

Blocks voltage-dependent sodium channels, increases chloride channel opening by binding to the GABA receptor, inhibits high-voltage calcium currents, acts as a carbonic anhydrase inhibitor, and may act at NMDA sites.

95
Q

For which conditions is topiramate used?

A

Partial and primary generalized epilepsy, migraine, and absence seizures.

96
Q

How does topiramate interact with metabolic systems?

A

It inhibits CYP2C19 and is sensitive to induction by phenytoin and carbamazepine. It also reduces ethinyl estradiol levels, requiring additional birth control methods for women.

97
Q

What are some adverse effects of topiramate?

A

Somnolence, weight loss, paresthesias, renal stones, glaucoma, and oligohidrosis leading to hyperthermia.

Mnemonic: “Topiramate: Sleepy as Hell, Skinny as F*ck, Tingling Toes, Pissing Rocks, Eyes Gone Bad, Sweating Like Crazy”

Sleepy as Hell - Somnolence
Skinny as F*ck - Weight loss
Tingling Toes - Paresthesias (tingling sensation)
Pissing Rocks - Renal stones (kidney stones)
Eyes Gone Bad - Glaucoma
Sweating Like Crazy - Oligohidrosis (reduced sweating leading to hyperthermia)

98
Q

What is the mechanism of action for zonisamide?

A

Blockade of both voltage-gated sodium channels and T-type calcium currents with limited carbonic anhydrase activity.

99
Q

For which type of epilepsy is zonisamide used?

A

Partial epilepsy.

100
Q

What are some side effects of zonisamide?

A

CNS toxicity, kidney stones, increased temperature, and oligohidrosis.

Mnemonic: “Zonisamide: Brain’s F*cked, Pissing Rocks, Hot as Hell, Dry as a Desert”

Brain’s F*cked - CNS toxicity
Pissing Rocks - Kidney stones
Hot as Hell - Increased temperature
Dry as a Desert - Oligohidrosis (reduced sweating)

101
Q

What is the mechanism of action for ethosuximide?

A

It inhibits T-type calcium channels, reducing the propagation of abnormal electrical activity in the brain.

102
Q

For which type of seizures is ethosuximide the first-line treatment?

A

Primary generalized absence seizures.

103
Q

Why is the use of ethosuximide limited?

A

Because of its very narrow spectrum of activity.

104
Q

What does vagal nerve stimulation require?

A

A surgical implant of a small pulse generator with a battery and a lead wire for stimulus.

105
Q

How does vagal nerve stimulation help seizure patients?

A

It prevents abnormal electrical activity in seizure patients through electrical vagus stimulation.

106
Q

When do patients activate the vagal nerve stimulator?

A

When they anticipate a seizure.

107
Q

For which type of seizures is vagal nerve stimulation effective?

A

Partial onset seizures.

108
Q

What benefit does vagal nerve stimulation provide besides seizure control?

A

It enables the reduction of drug therapy and is used for refractory patients.

109
Q

What is recommended for women with epilepsy before conception?

A

High doses of folic acid.

110
Q

Which medications should be avoided during pregnancy for women with epilepsy?

A

Divalproex and barbiturates.

111
Q

What should be done with seizure medication during pregnancy once seizures are controlled?

A

The maintenance medication should be reduced to the lowest dose that provides control.