Pharm Ii: Aed's

Front 1

This drug is effective against all seizure types except absence (petit mal).

Back 1

Phenobarbital

Front 2

These drugs are useful in status elepticus

Back 2

Phenobarbital, Phenytoin, Benzodiazepines (old AED's)

Front 3

This is the mechanism of phenobarbital

Back 3

GABA receptor agonist, opening Cl- channels to hyperpolarize neurons.

Front 4

Administration of phenobarbital

Back 4

IV and oral

Front 5

Metabolism of phenobarbital

Back 5

Hepatic

Front 6

Clearance of phenobarbital

Back 6

Renal

Front 7

Half life of phenobarbital

Back 7

Long. 100 hours

Front 8

Without loading, it takes this many half-lives for any drug to reach steady-state blood levels

Back 8

Five half lives

Front 9

This drug tends to increase phenobarbital levels

Back 9

Valproate (Divalproex)

Front 10

This drug is a CYP-450 inducer that therefore decreases the levels and effectiveness of most other drugs

Back 10

Phenobarbital

Front 11

Hyperactivity in children and sedation in adults is a toxicity of this drug

Back 11

Phenobarbital

Front 12

This drug must be withdrawn slowly (over weeks) or status ellepticus may result

Back 12

Phenobarbital

Front 13

These are the side effects of phenobarbital

Back 13

Allergic rash, joint and CT problems

Front 14

This drug is effective against all seizure types except absence (petit mal), but is better for partial and secondarily generalized seizures

Back 14

Phenytoin

Front 15

Mechanism of Phenytoin

Back 15

Blocks Na+ channels

Front 16

This drug blocks seizures spread from epileptic foci to normal neurons, with relatively little effect on seizure Tz

Back 16

Phenytoin

Front 17

This drug has variable oral absorption that is worse in children

Back 17

Phenytoin

Front 18

This drug has zero-order kinetics at high concentration because of enzyme saturation, which can lead to sudden toxicity

Back 18

Phenytoin

Front 19

Half-life of Phenytoin

Back 19

6-24 hrs (at low doses)

Front 20

Clearance of phenytoin

Back 20

Urine and bile

Front 21

This drug is mostly protein bound in the blood, and binding may be lowered in uremia, hypoalbuminemia and co-administration of Valproate (Divalproex)

Back 21

Phenytoin

Front 22

Unbound levels of this drug should be monitored to avoid OD and toxicity

Back 22

Phenytoin

Front 23

This drug induces the metabolism of most drugs, making them less effective

Back 23

Phenytoin

Front 24

This drug increases vitamin K turnover; therefore it should be supplemented in pregnant women

Back 24

Phenytoin

Front 25

This drug is a folate antagonist

Back 25

Phenytoin

Front 26

Phenytoin toxicity can result from administration of these drugs

Back 26

INH disulfiram, cimetidine

Front 27

These are the side effects of phenytoin

Back 27

Gingival hyperplasia, osteomalacia, cerebellar ataxia, allergic rash

Front 28

This drug is effective against absence seizures only

Back 28

Ethosuxide

Front 29

Mechanism of ethosuxide

Back 29

T-type Ca++ channel blocker

Front 30

Administration of ethosuxide

Back 30

Oral only. No IV formulation available

Front 31

Half-life of ethosuxide

Back 31

24-48 hrs (med).

Front 32

Metabolism of ethosuxide

Back 32

Hepatic, metabolized to inactive glucoronide

Front 33

Clearance of ethosuxide

Back 33

Some is excreted unchanged in urine

Front 34

This drug is a mild enzyme inducer, so other drug levels may fall off

Back 34

Ethosuxide

Front 35

These are the side effects of ethosuxide

Back 35

Sedation, GI upset, behavior changes in children, allergic reaction

Front 36

These are the uses of benzodiazepines

Back 36

Sedatives, hypnotics, anxiolytics, acute anti-epileptic

Front 37

This drug is effective against all seizure types, but resistence develops quickly

Back 37

Benzodiazepines

Front 38

This class of drugs is the treatment of choice for initial treatment of status epilepticus

Back 38

Benzodiazepines

Front 39

This class of drugs is used to treat EtOH withdrawal and delirium tremens

Back 39

Benzodiazepines

Front 40

Mechanism of benzodiazepines

Back 40

Noncompetitive GABA-A receptor agonist; different binding site than phenobarbital

Front 41

Administration of benzodiazepines

Back 41

Good oral absorption, and can be given IV

Front 42

This benzodiazepine has no active metabolites

Back 42

Lorazepam (Ativan)

Front 43

Metabolism and clearance of benzodiazepines

Back 43

Metabolized by CYP in the liver, and excreted in urine as glucoronides

Front 44

This drug has high lipid solubility, and therefore a higher volume of distribution and therefore shorter duration of action in status epilepticus

Back 44

Diazepam

Front 45

T/F: Lorazepam has a longer half-life than Diazepam

Back 45

False. Diazepam has a longer half life even though it has a shorter duration of action due to its lipid solubility

Front 46

Cimetidine inhibits the metabolism of these drugs, thereby increasing their duration of activity

Back 46

Benzodiazepines

Front 47

These are the side effects of benzodiazepines

Back 47

Sedation, disinhibition (esp in the demented), falls, tolerance & dependence

Front 48

These drugs should be withdrawn gradually

Back 48

Phenobarbital, Benzodiazepines

Front 49

This is the drug of choice for partial and secondarily generalized seizures

Back 49

Carbamazepine

Front 50

This drugs makes some types of primary generalized seizures worse

Back 50

Carbamazepine

Front 51

This drug is very useful for the treatment of trigeminal neuralgia and painful peripheral neuropathy

Back 51

Carbamazepine

Front 52

This drug is a good second line drug (after lithium and Valproate (Divalproex)) for chronic treatment of bipolar disorder

Back 52

Carbamazepine

Front 53

Mechanism of carbamazepine

Back 53

Blocks Na+ channels

Front 54

This drug has variable oral absorption; it is very insoluble and there is no IV preparation

Back 54

Carbamazepine

Front 55

Because this drug is not available in IV formation, it is not a treatment for acute seizures

Back 55

Carbamazepine

Front 56

Half-life of carbamazepine

Back 56

12 hrs (short)

Front 57

Metabolism of carbamazepine

Back 57

Hepatic (CYP)

Front 58

This drug induces its own metabolism, so blood levels and effectiveness may fall after several weeks of use

Back 58

Carbamazepine

Front 59

10-11 epoxide is an active metabolite of this drug

Back 59

Carbamazepine

Front 60

Excretion of carbamazepine and its metabolite

Back 60

Renal, after glucoronidation

Front 61

This drug decreases the effectiveness of birth-control pills

Back 61

Carbamazepine

Front 62

Macrolide (lactone) antibiotics are best avoided in patients taking this drug

Back 62

Carbamazepine

Front 63

Erythromycin and CEB's raise levels of this drug in the blood

Back 63

Carbamazepine

Front 64

These are the side effects of carbamazepine

Back 64

Sedation, ataxia, blurred vision, hyponatremia and SIADH, neutropenia, allergic reactions

Front 65

This is a wide spectrum drug that is effective in treating all seizure types

Back 65

Valproate (Divalproex)

Front 66

This is the drug of choice for absence seizures and all other primary generalized seizures

Back 66

Valproate (Divalproex)

Front 67

This AED is also used to treat bipolar disorder

Back 67

Valproate (Divalproex)

Front 68

This AED is also used in prophylactic treatment of migraines

Back 68

Valproate (Divalproex)

Front 69

Mechanism of Valproate (Divalproex)

Back 69

Not well understood. Possibly Na channels, indirect GABA agonist, Ca and K conductances

Front 70

Half-life of Valproate (Divalproex)

Back 70

15 hours

Front 71

Administration of Valproate (Divalproex)

Back 71

IV and oral. Valproate (Divalproex) is well-absorbed orally

Front 72

Metabolism and clearance of Valproate (Divalproex)

Back 72

Hepatic metabolism, also excreted renally without metabolism after glucoronidations

Front 73

These drugs tends to drop levels of Valproate (Divalproex)

Back 73

Phenytoin, phenobarbital

Front 74

These are the side effects of Valproate (Divalproex)

Back 74

GI upset, acute pancreatitis, wt gain, tremor, hair loss, thrombocytopenia, menstrual irregularities

Front 75

Retarded children are susceptible to liver damage caused by this drug

Back 75

Valproate (Divalproex)

Front 76

This drug can cause elevated ammonia levels and encephalopathy

Back 76

Valproate (Divalproex) (in retarded children)

Front 77

This is used to treat elevated ammonia levels and encephalopathy when they occur in the context of Valproate (Divalproex)

Back 77

Carnitine supplementation

Front 78

This drug was developed as a GABA receptor agonist, but it is not

Back 78

Gabapentin

Front 79

Mechanism of gabapentin

Back 79

Unknown

Front 80

This drug is weakly effective against partial and secondarily generalized seizures

Back 80

Gabapentin

Front 81

This drug may make absence and myoclonic seizures worse

Back 81

Gabapentin

Front 82

This AED is relatively safe-it has a benign side effect profile, and almost no drug interactions

Back 82

Gabapentin

Front 83

This AED is useful for neuropathic pain and fibromyalgia, and may also be effective against tremor

Back 83

Gabapentin

Front 84

This drug has a short half-life and therefore requires 3-4 times a day dosing

Back 84

Gabapentin

Front 85

Administration of gabapentin

Back 85

Well absorbed orally

Front 86

Metabolism and clearance of gabapentin

Back 86

Excreted renally without metabolism

Front 87

These are the side effects of gabapentin

Back 87

Sedation, esp in the elderly; behavioral problems in retarded children

Front 88

This AED is also used to treat mood disorders and sleep disturbances

Back 88

Lamotrigine

Front 89

This drug is effective against all seizure types

Back 89

Lamotrigine

Front 90

This drug is a weak anti-folate, but its main mechanism is probably interaction with Na channels to decrease sustained repetitive firing, and prevention of abnormal release of glutamate

Back 90

Lamotrigine

Front 91

Half-life of lamotrigine

Back 91

24 hrs

Front 92

Metabolism and clearance of lamotrigine

Back 92

Renal, after glucoronidation. Not significantly metabolized

Front 93

This drug has its levels doubled by interactions with this drug, which itself is unaffected

Back 93

Lamotrigine levels are doubled by Valproate (Divalproex)

Front 94

These are the side effects of lamotrigine

Back 94

Allergic rash (dose dependent, which is unusual among allergies); also dizziness, HA, diplopia, ataxia, nausea, etc

Front 95

The side effects of this drug are circumvented by introducing the drug slowly over 4-8 weeks

Back 95

Lamotrigine

Front 96

Mechanism of topiramate

Back 96

Multiple: GABA and glutamate receptors, blockage of Na channels

Front 97

Half-life of topiramate

Back 97

24 hrs

Front 98

These are the side effects of topiramate

Back 98

Can cause paresthesias, kidney stones and wt loss; confusion, speech problems

Front 99

These are novel, new drugs with a broad spectrum of use for focal and generalized seizures

Back 99

Topiramate, levetiracetam

Front 100

Mechanism of levetiracetam

Back 100

Unknown (may block Ca channels, bind to vessicles to block release)

Front 101

Metabolism and clearance of levetiracetam

Back 101

Excreted renally without metabolism

Front 102

Half-life of levetiracetam

Back 102

12 hrs (short)

Front 103

Administration of levetiracetam

Back 103

IV and oral

Front 104

This drug is metabolized by an enzyme found in RBC membranes

Back 104

Levetiracetam

Front 105

These are the side effects of levetiracetam

Back 105

Virtually no physical side effects; mental side effects include cognitive effects and behavioral problems

Front 106

This drug was developed as an analog of piracetam which is a brain stimulant and anti-myoclonus drug

Back 106

Levetiracetam

Front 107

These AED's are Na channel blockers

Back 107

Phenytoin, carbamazepine, valproate, topiramate and lamotrigine.

Front 108

T-type Ca channels are found here

Back 108

Thalamus

Front 109

This drug blocks Na channels, and is a GABA agonist and glutamate antagonist

Back 109

Topiramate

Front 110

These drugs are GABA agonists

Back 110

Barbiturates, benzodiazepines, topiramate

Front 111

These drugs are (direct and indirect) glutamate antagonists

Back 111

Lamotrigine (blocks glutamate release), topiramate (glutamate antagonist)

Front 112

This drug blocks Na channels, and blocks glutamate release

Back 112

Lamotrigine