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Pharmacology II > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

What is receptor is responsible for excitatory?

A

Glutamate

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2
Q

What receptor is responsible for inhibitory?

A

GABA

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3
Q

How is a seizure defined?

A

The clinical manifestation resulting from an abnormal or excessive discharge of a set of neurons in the brain.

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4
Q

How is epilepsy defined?

A

A chronic condition characterized by recurrent (>2) epileptic seizures, unprovoked by any immediate identifiable cause

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5
Q

What are alterations of consciousness, motor, sensory, automatic or psychic events?

A

Clinical manifestations

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6
Q

What can cause a seizure?

A 
Fever
Withdrawal from CNS depressants
Metabolic abnormalities
Uremia
Encephalitis/meningitis
Head trauma
Brain tumor
Stroke
Lead poisoning
Sleep deprivation
Medications
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7
Q

What drugs are known to cause seizures?

A 
Antimicrobials
Anesthetics and analgesics
Immunosuppressants
Psychotropics
Radiographic contrast agents
Theophylline
Sedative hypnotic drug withdrawal
Drugs of abuse
Flumazenil
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8
Q

Epidemiology of epilepsy

A

Increases in people >70 y/o
Most common neurological disorder in children
70% of patients can be seizure free with appropriate therapy

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9
Q

Pathophysiology of seizures involves what?

A

Origination from the gray matter of any cortical area (neurons fire abnormally)
Due to excessive excitation or disordered inhibition of neurons (normal membrane function breakdown, excess excitability)

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10
Q

What are the physiologic consequences of a seizure?

A

Increased consumption of oxygen & glucose
Increased production of lactate and CO2
Increased cerebral blood flow is generally sufficient to compensate for changes
Brief seizures rarely cause long-term seqeulae

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11
Q

Why don’t you want a seizure to occur over a long period of time?

A

Seizures cost a lot and take a lot out of a person depriving the brain of oxygen and glucose after a long period of time

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12
Q

What are the physiological consequences of a seizure?

A

Sympathetic discharge results in tachycardia, HTN, and hyperglycemia
Difficulty maintaining the airway

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13
Q

What results when an airway is not maintained during a seizure?

A

Hypoxia, hypercarbia, and respiratory acidosis

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14
Q

What results from a prolonged seizure?

A

Lactic acidosis, rhabdomyolosis, hyperkalemia, hyperthermia, and hypoglycemia.

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15
Q

Diagnosis can be made based on:

A

Patient hx
PE- neurological findings, cranial nerves, motor function, cerebellar function, and sensory function
Lab- metabolic causes- glucose, electrolytes, calcium, and renal function, also drugs/ETOH screen
EEG
MRI

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16
Q

What is an EEG and what is its significance?

A

An EEG confirms the presence of electrical activity, classifies the seizure type, and indicates the location of focus.
These are performed w/in 48 hrs of a seizure
More than 1/2 of epileptics initially have normal EEGs

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17
Q

What defines a primary seizure?

A

No specific anatomic cause and involves chronic treatment

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18
Q

How is secondary epilepsy caused?

A

Tumors, head injury, hypoglycemia, meningitis, or rapid withdrawal from ETOH. Drugs are used for tx until primary cause is corrected

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19
Q

What is the difference between a focal (partial) and generalized seizure?

A

The location of the cerebrum where the seizure originates

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20
Q

What is the difference between a simple and complex seizure?

A

Impairment of consciousness (whether the patient looses consciousness or not.

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21
Q

A seizure that begins in one hemisphere of the brain, has symptoms classified as motor, autonomic, or sensory, has ASYMMETRIC MANIFESTATIONS, and accounts for 80% of all adult epilepsies is what type of seizure?

A

Focal Seizure

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22
Q

A seizure that begins in BOTH hemispheres of the brain and has BILATERAL MANIFESTATIONS is what type of seizure?

A

Generalized Seizure

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23
Q

A seizure that does not result in loss of consciousness is a?

A

Simple focal seizure

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24
Q

A seizure that results in a loss or alteration of consciousness is what type of seizure?

A

Complex focal seizure

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25
Q

A focal onset evolving to generalized tonic-clonic seizures is what type of seizure?

A

Secondary generalized focal seizure

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26
Q

Tonic seizure is defined as?

A

A generalized seizure that consists of continuos muscle contraction

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27
Q

Clonic seizure is defined as?

A

A generalized seizure that consists of rhythmic muscle contractions

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28
Q

Tonic-clonic seizure is defined as?

A

A generalized seizure that involves an alteration b/w tonic and clonic

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29
Q

Myoclonic seizure is defined as?

A

A generalized seizure involving sudden, brief muscle spasm

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30
Q

Atonic seizure is defined as?

A

A generalized seizure consisting of a sudden brief loss of muscle tone

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31
Q

Absence seizure is defined as?

A

A generalized seizure that involves Impaired awareness or interaction

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32
Q

What is the clinical presentation of a focal seizure?

A

Asymmetrical manifestation
Symptoms of the motor (any part of the body), autonomic (pallor, flushing, vomiting, sweating, vertigo, or tachycardia), and sensory (visual, auditory, or olfactory)

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33
Q

What is the clinical presentation of a complex seizure?

A

Prodrome, aura, and automatisms

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34
Q

What is an awareness of an impending seizure such as HA, insomnia, irritability, feeling of impeding doom?

A

Prodrome

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35
Q

What is a simple focal seizure consisting of autonomic or sensory symptoms?

A

Aura

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36
Q

What is lip smacking, chewing, swallowing, abnormal tongue movements, thrashing, fumbling or snapping of fingers?

A

Automatisms

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37
Q

What is the clinical presentation of a generalized seizure?

A

Bilateral motor manifestations
Tonic-clonic (Grand Mal)- sometimes w/ aura, LOC, sudden tonic contractions followed by rigidity and clonic movements, cries or moans, loss of sphincter control, and unconsciousness followed by a deep sleep.

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38
Q

What type of seizure involves sometimes w/ aura, LOC, sudden tonic contractions followed by rigidity and clonic movements, cries or moans, loss of sphincter control, and unconsciousness followed by a deep sleep.

A

Tonic-Clonic (Grand Mal)

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39
Q

What is the clinical presentation of a absence (petit mal) seizure?

A

Sudden onset, interruption of activity

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40
Q

What is the clinical presentation of a complex seizure?

A

Prodrome, aura, and automatisms

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41
Q

What is an awareness of an impending seizure such as HA, insomnia, irritability, feeling of impeding doom?

A

Prodrome

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42
Q

What is a simple focal seizure consisting of autonomic or sensory symptoms?

A

Aura

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43
Q

What is lip smacking, chewing, swallowing, abnormal tongue movements, thrashing, fumbling or snapping of fingers?

A

Automatisms

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44
Q

What is the clinical presentation of a generalized seizure?

A

Bilateral motor manifestations
Tonic-clonic (Grand Mal)- sometimes w/ aura, LOC, sudden tonic contractions followed by rigidity and clonic movements, cries or moans, loss of sphincter control, and unconsciousness followed by a deep sleep.

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45
Q

What type of seizure involves sometimes w/ aura, LOC, sudden tonic contractions followed by rigidity and clonic movements, cries or moans, loss of sphincter control, and unconsciousness followed by a deep sleep.

A

Tonic-Clonic (Grand Mal)

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46
Q

What is the clinical presentation of a ansence (petit mal) seizure?

A

Sudden onset, interruption of activity

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47
Q

What is the clinical presentation of myoclonic seizure?

A

Brief shock-like contraction of face, trunk, and upper extremities.

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48
Q

What is the clinical presentation of an atonic seizure?

A

Head dropping, slumping to the ground

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49
Q

What is the clinical presentation of a febrile seizure?

A

Generalized seizure
Illness accompanied with a high fever
3 mo. to 5 y/o
Benign; rarely required medication

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50
Q

What are the goals of treatment for seizures?

A

Accurate diagnosis
Suppress seizure activity
Minimize adverse drug reactions
Optimize QOL

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51
Q

GABA Neurotransmitter

A

Major inhibitory amino acid
Alters the conductance of ion-selective channels -> K+ efflux or Cl- influx results in membrane hyperpolarization
Drugs- BZDP and barbituates

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52
Q

Glutamate Neurotransmitter

A

Primary excitatory amino acid
Influx of Na+ ions or reduced outflow of K+ ions depolarize membrane
Drugs- mostly experimental

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53
Q

Drugs that modulate GABA receptors affect what?

A 
Arousal and attention
Memory formation
Anxiety
Sleep
Muscle tone
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54
Q

What is GABAs metabolism?

A

Glutamate synthesis and metabolism intertwined with GABA synthesis and metabolism.
Synthesis: decarboxylation of glutamate -> GABA.
Packaged into vesicles and in response to the action potential exocytosis of the vesicle with the release of GABA into the synaptic cleft occurs.
Termination of GABA action is via uptake by neurons and glia cells (GABA transporters), GABA-transminase converts GABA to succinic semiadehyde which is oxidized to succinic acid and then via the krebs cycle to a-ketoglutarate, GABA-transaminase regenerated glutamate from a-ketoglutarate. Then it is diffused out of the synaptic cleft.

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55
Q

What are the two types of GABA receptors?

A

Ionotropic and metabotropic

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56
Q

What do ionotropic receptors bind and what is there mechanism?

A

BInd GABAa and GABAb.

Binds GABA and opens intrinsic chloride ion channels

57
Q

What do metabotropic receptors bing and what is there mechanism?

A

BInd GABAb

G-protien-coupled receptors that affect neuronal ion current through 2nd messenger system.

58
Q

What is the biggest difference between ionotropic and metabotropic receptors?

A

Ionotropic occur really fast and metabotropic are slower to terminate. Metabotropic uses second messenger systems slowing the mechanism down.

59
Q

What are the two pathways that metabolism occurs in glutamatergic neurotransmission?

A

a-ketoglutarate formed in Krebs cycle transaminated to glutamate in CNS nerve terminal.
Glutamine produced and secreted by glial cells transported into nerve and converted into glutamate.

60
Q

Which anticonvulsants work by prolonged inactivation of the voltage-sensitive sodium channel?

A

Phenytoin, carbamazepine, and iamotrigine

61
Q

Which anticonvulsants work by enhancing GABA-mediated inhibition? Directly and indirectly?

A

Direct-BZDP, barbiturates, topiramate

Indirect-Gabapentin, tiagabine, vigabatrin

62
Q

Which anticonvulsants work by reduction of glutaminergic excitation?

A

AMPA- PB, topiramate

63
Q

What is the general treatment approach to an epileptic patient?

A

Accurate dx of seizure type
Idenitify patient specific treatment goals
Monotherapy
If seizures not controlled, add on a drug with a different MOA
Patient education (dose titration, compliance, ADRS)

64
Q

What are the 8 ideal pharmacokinetic characteristics of anticonvulsants?

A 
Good oral bioavailability
Penetration through BBB
Long half life
Low binding to plasma protiens
Lack of metabolism
Renal elimination
Linear pharmacokinetics
No drug interactions
65
Q

What are the first line DOC based on seizure type for partial seizures?

A 
Carbamzepine
Phenytoin
Lamotrigine
Oxcarbazepine
Topiramate
66
Q

What are the second line DOC based on seizure type for partial seizures?

A 
Gabapentin
Levetiracetam
Phenobarbital
Pregabalin
Primidone
Tiagabine
Valproic acid
67
Q

What are the first line DOC based on seizure type for absence seizures?

A

Ethosuximide
Lamotrigine
Valproic acid

68
Q

What are the first line DOC based on seizure type for myoclonic and atonic seizures?

A

Valproic acid

Lamotrigine

69
Q

What are the first line DOC based on seizure type for tonic-clonic seizures?

A

Valproic acid
Carbamazepine
Oxcarbazepine
Lamotrigine

70
Q

Phenytoin (Dilantin) MOA and Indications

A

Blocks voltage gated Na+ channels reducin the propogation of abnormal impulses in the brain.
Indications- simple and complex partial sz, generalized tonic-clonic sz, and status epilepticus caused by recurrent tonic-clonic sz.

71
Q

Phenytoin Pharmakokinetics and administration considerations

A

Metabolized by P450 system
Potent non-specific inducer of many drug metabolizing enzymes
Highly protein bound
Nonlinear kinetics
Requires dosing therapeutic monitoring
Enteral feeding reduces oral absorption, oral suspension shake vigoriously.
IV formulation can cause pain, phlebitis, and extravasation.
No IM injection

72
Q

Phenytoin anti arrhythmia and drug interactions

A

Dont stop abruptly
Inducers- carbamazepine, OCP, doxyclycline, quinidine, cyclosporin, methadone, levodopa
Inhibitors- chloramphenicol, CIMETIDINE sulfonamide, and ISONIAZID

73
Q

Phenytoin ADRs

A

Dose related- nystagmus, ataxia, drowsiness, cognitive impairment
Non-dose related- GINGIVAL HYPERPLASIA, hirsutism, acne, rash, hepatotoxicity
Teratogenic- Fetal hydantoin syndrome (cleft lip and palate, congenital heart disease, slowed growth and mental deficiency)

74
Q

Carbamazepine (Tegretol) MOA and indications

A

Blocks Na+ channels

Indications- first line tx of simple partial, complex partial, and generalized tonic-clonic

75
Q

Carbamazepine (Tegretol) Pharmakokinetics

A

Monitoring through autoinduction (first 20-30 days of tx, autoinduction is dose dependent, after complete, steady state concentrations are achieved after 3 days)
Potent non-specidic inducer of many drugs and transporters

76
Q

Carbamazepine (Tegretol) ADRs

A

Dose related- vertigo, ataxia, diplopia, drowsiness, nausea
CNS side effects- HA, paraesthesis, confusion, psychosis
Non-specific- SIADH, leukopenia, thrombocytopenia, stevens johnson syndrome.

77
Q

Phenobarbital (Luminal) MOA, indications, and side effects

A

MOA unknown
Indications- generalized tonic clonic, partial sz, neonatal sz, febrile sz,
Side effects- sedation, irritability, slowed thinking, ataxia, hyperactivity, and rash

78
Q

Phenobarbital (Luminal) pharmacokinetics

A

Extremely long 1/2 life (96 hours)
Time to steady state is 20-30 days
Metabolized by P450 system

79
Q

Primidone (mysoline) MOA and indication

A

Structurally related to phenobarbita l
Efficacy from metabolites (phenobarbital- tonic clonic sz and simple partial sz, and pehnyethylmalonamide- complex partial sz)
Well absorbed orally; poor protein binding, same ADRs as phenobarbital
Indications- alternative choice in partial sz and tonic-clonic sz

80
Q

Valproic acid (Depakene) & Sodium Valproate (Depakote) MOA and indication

A

Na+ blockade and enhancement of GABAergic transmission

Indication- Myoclonic, tonic, atonic, absence

81
Q

Valproic acid (Depakene) Pharmacokinetics

A

Completely absorbed
Saturable protein binding
Hepatic metabolism but DOESN’T induce P450
Inhibits metabolism of phenobarbital, carbamazepine, ethosuximide

82
Q

What drugs does Valproic acid (Depakene) inhibit the metabolism?

A

Phenobarbital, carbamazepine, ethosuximide.

83
Q

Valproic acid side effects

A

Dose related- N/V, Abd pain, diarrhea, sedation, tremor, unsteadiness
Non-dose related- acute hepatic failure, acute pancreatitis.

84
Q

Ethosuximide (Zarontin) MOA and indication

A

MOA- inhibits calcium channels.

Indication- DOC for absence seizures.

85
Q

Ethosuximide (Zarontin) pharmacokinetics and side effects

A

Absorbed orally; not protein bound; metabolized by but not inducer of P450
Side effects dose related- GI, lethargy, HA, dizziness, anxiety

86
Q

What are the second generations anti-epileptic drugs?

A 
Gabapentin (neurontin)
Oxcarbamazepine (Trileptal)
Tiagapine (Gabitril)
Felbamate (Felbatol)
Lamotrigine (Lamictal)
Zonisamide (Zonegran)
Levetiracetam (Keppra)
Pregabalin (Lyrica)
87
Q

Oxcarbamazepine (trileptal) MOA and indication

A

Active metabolite blocks Na+ channels
Indication- partial sz with or w/out secondary generalization
Analogue of cabamazepine w/ fewer side effects than cabamazepine and phenytoin

87
Q

Oxcarbamazepine (trileptal) Side effects

A

Dizziness, ataxia, fatigue, GI, hyponatremia, rash
30% reactivity for rash with CBZ
No PK monitoring; no autoinduction

88
Q

Gabapentin (Neurotin) MOA and indication

A

Analog of GABA; MOA unknown

Indication- adjunct to partial and GTC sz, tx of peripheral neuropathy.

88
Q

Gabapentin (Neurotin) favorable pharmacokinetic profile

A

Dose-dependent oral absorption
Not protein bound
Excreted unchanged via kidneys
No serum level monitoring

89
Q

Gabapentin (Neurotin) Side effects

A

Somnolence, dizziness, ataxia, nystagmus

89
Q

Tiagabine (Gabitril) MOA and Indication

A

Competitive inhibitor of GABA transporter in neurons and glia (inhibitors re-uptake)
Indication- adjunctive tx of partial sz
TAKE WITH FOOD

90
Q

Tiagabine (Gabitril) pharmacokinetics and side effects

A

Quickly and completely absorbed
Increased clearance in peds, with enzyme inducers
Serum concentrations unnecessary
Side effects- Dose related: dizziness, fatigue, nervousness, difficulty concentrating

90
Q

Lamotrigine (lamictal) MOA and indication

A

Blocks Na+ and Ca++ channels
Adjunctive in children and mono therapy in adults
Indications- GTC, partial seizures, absence

91
Q

Lamotrigine (lamictal) adverse side effects

A

Rash (10%), confusion, depression, N/V, diplopia, severe idiosyncratic (skin, blood)
Slow taper essential, initial dose dependent on other meds

91
Q

Topiramate (Topamax) MOA and indication

A

Blocks Na+ channels and binds GABA thus opening Cl- channels

Indication- tx for partial and generalized sz in pediatrics and adults.

92
Q

Topiramate (Topamax) pharmacokinetics and adverse effects

A 
70% renal elimination
1st order kinetics
Clearance increased w/ enzyme inhibitors
AE- dose related- drowsiness, parasthesias, psychomotor slowing, weight loss, renal calculi
NOTE- Maintain adequate fluid levels
92
Q

Felbamate (felbtol) MOA and indication

A

Blocks Na+ channels, competes for NMDA receptor, prevents AMPA receptor stimulation, blocks Ca++ channels
Indication- partial sz and lennox-gastaut syndrome
Use restricted to refractory Lennox-Gastaut syndrome (active metabolism covalently binds liver, bone marrow proteins, and DNA resulting in aplastic anemia and liver failure.

93
Q

Felbamate (felbtol) Side effects

A

Dose related- anorexia, N/V, insomnia, HA

Non-dose related- aplastic anemia, hepatic failure

93
Q

Levetiracetam (Keppra) MOA and indication

A

MOA unknown
Indication- tx of generalized sz
Adjust dose in renal insufficiency

94
Q

Levetiracetam (Keppra) favorable PK profile and Side effects

A

Almost completely absorbed
Metabolism NOT dependent on the P450 system
Minimal protein binding
MInimal drug interactions
Side effects- sedation, behavioral abnormalities

94
Q

Zonisamide (Zonegran) MOA and Indication

A

Sulfonamide derivative: blocks Na+ and Ca++ channels and enhances GABA-receptor function
Indication- adjunctive therapy for partial sz

95
Q

Zonisamide (Zonegran) pharmacokinetics and Side effects

A

Good oral absorption and renally and hepatically eliminated
Side effects: Dose related: sedation, dizziness, cognitive impairment, nausea
Non-dose related- rash, oligohydrosis, kidney stones

95
Q

Pregabalin (lyrica) Indication and side effects

A

Indication- adjunctive tx for partial onset sz, peripheral neuropathy, postherpatic neuralgia, fibromyalgia syndome
Side effects- dizziness, somnolence, dry mouth, PERIPHERAL EDEMA, blurred vision, weight gain.

96
Q

Topiramate (Topamax) MOA and indication

A

Blocks Na+ channels and binds GABA thus opening Cl- channels

Indication- tx for partial and generalized sz in pediatrics and adults.

97
Q

Topiramate (Topamax) pharmacokinetics and adverse effects

A 
70% renal elimination
1st order kinetics
Clearance increased w/ enzyme inhibitors
AE- dose related- drowsiness, parasthesias, psychomotor slowing, weight loss, renal calculi
NOTE- Maintain adequate fluid levels
98
Q

Felbamate (felbtol) MOA and indication

A

Blocks Na+ channels, competes for NMDA receptor, prevents AMPA receptor stimulation, blocks Ca++ channels
Indication- partial sz and lennox-gastaut syndrome
Use restricted to refractory Lennox-Gastaut syndrome (active metabolism covalently binds liver, bone marrow proteins, and DNA resulting in aplastic anemia and liver failure.

99
Q

Felbamate (felbtol) Side effects

A

Dose related- anorexia, N/V, insomnia, HA

Non-dose related- aplastic anemia, hepatic failure

100
Q

What comprises a generalized convulsive status epilepticus sz?

A

Repeated primary or secondary generalized

Persistant postictal state

101
Q

What comprises a nonconvulsive status epilepticus sz?

A 
Persistent state of impaired consciousness
Partial sz (motor or sensory) that may not interfere w/ consciousness
102
Q

Zonisamide (Zonegran) MOA and Indication

A

Sulfonamide derivative: blocks Na+ and Ca++ channels and enhances GABA-receptor function
Indication- adjunctive therapy for partial sz

103
Q

What are the most common etiology for status epilepticus?

A 
Low blood concentration of AED (34%)
Remore symptomatic causes (24%)
Cerebrovascular accidents (22%)
Anoxia or hypoxia (10%)
ETOH or drug withdrawal (10%)
104
Q

Pregabalin (lyrica) Indication and side effects

A

Indication- adjunctive tx for partial onset sz, peripheral neuropathy, postherpatic neuralgia, fibromyalgia syndome
Side effects- dizziness, somnolence, dry mouth, PERIPHERAL EDEMA, blurred vision, weight gain.

105
Q

What is the most important factors in choosing an anti-epileptic drug?

A

Tolerability and long term safety

106
Q

1) If 1st AED poorly tolerated or fails to control sz what should be used?
2) If 1st AED is well tolerated but doesn’t completely control seizures what should be used?

A

1) alternative should be used

2) combo should be tried

107
Q

What four factors are used to determine medication discontinuation?

A
  1. Sz free for 2-5 year and AED
  2. Pt should have single type of partial or generalized tonic-clonic sz
  3. Patient should have a normal neuro-exam and normal IQ test
  4. Patients EEG should have normalized w/ AED tx
    * *Medication should be titrated off over several months if it is discontinued
108
Q

How is status epilepticus (SE) defined?

A

Continuous or intermittent seizures lasting more than 5 minutes, without full recovery of consciousness b/w seizures.

109
Q

Benzodiazepines

A

Act as positive allosteric modulators by enhancing channel gating in presence of GABA
Not indicated if sz already stopped or for maintenance therapy.

110
Q

Benzodiazepines ADRs

A

Infusion rate related to arrhythmias and hypotension
Respiratory depression
Impairment of consciousness

111
Q

Lorazepam (Ativan)

A

DOC for patient w/ IV access
Onset of action 3-5 min
Can cause vein irritation (Dilution of dose)

112
Q

Lorazepam (ativan) vs diazepam (valium)

A

Lorazepam is preferred over diazepam secondary to duration of action
Diazepam highly lipophilic and quickly redistributes out of brain to other fat stores.
Diazepam DOA- 15 min to 2 hrs
Lorazepam DOA- 12-24 hrs

113
Q

Diazepam (valium)

A

Rapid onset, short duration

option if IV route not available (rectally)R

114
Q

Midazolam (versed)

A

Reserved for refractory sz
Buccal, intranasal, IM routes
Give by continuos infusion for refractory SE

115
Q

Hydantoins place in therapy

A 
Second line (loading dose) if sz continue after 2-3 doses of benzos
Consider loading dose and maintenance dose if sz recur or if recurrence anticipated
Initiate maintenance doses 12-14 hrs after loading dose
Less CNS and respiratory depression than benzo and barbituates
116
Q

Hydantoins Side effects

A

Arrhythmias, nystagmus, dizziness, ataxia

117
Q

Phenytoin Onset of action and administration

A

Onset of Action- longer time to stop sz than benzos, less lipid soluable and requres slower administration
Admin- erractic absorption and pain w/ IM injections
Dilute with NS
Contains propylene glycol (result in arrhythmias, hypotension, metabolic acidosis with repeated doses)

118
Q

Fosphenytoin (Cerebyx)

A

H20 soluble prodrug of phenytoin converted by plasma esterases
Available IM and IV
Doesn’t contain propylene glycol
Compatible with most IV solutions w/ less phlebitis
Paresthesias and pruritis are more frequent

119
Q

Benzodiazepines ADRs

A

Infustion rate related to arrhythmias and hypotension
Respiratory depression
Impairment of consciousness

120
Q

Phenobarbital

A

3rd line agent, if sz persists despite 2-3 doses of benzos and loading dose of hydantoin
2nd line agent if sz persists after 2-3 doses of benzos and hydantoins contraindicated
Used in pediatric patients
Onset of action w/in minutes of loading dose administration

121
Q

Phenobarbital ADR

A

More CNS and respiratory depression than hydantoins

Contains propylene glycol

122
Q

Diazepam (valium)

A

Rapid onset, short duration

option if IV route not available (rectally)

123
Q

Midazolam (versed_

A

Reserved for refractory sz
Buccal, intranasal, IM routes
Give by continuos infusion for refractory SE

124
Q

Hydantoins place in therapy

A 
Second line (loading dose) if sz continue after 2-3 doses of benzos
Consider loading dose and maintenance dose if sz recur or if recurrence anticipated
Initiate maintenance doses 12-14 hrs after loading dose
Less CNS and respiratory depression than benzo and barbituates
125
Q

Hydantoins Side effects

A

Arrhythmias, nystagmus, dizziness, ataxia

126
Q

Phenytoin Onset of action and administration

A

Onset of Action- longer time to stop sz than benzos, less lipid soluable and requres slower administration
Admin- erractic absorption and pain w/ IM injections
Dilute with NS
Contains propylene glycol (result in arrhythmias, hypotension, metabolic acidosis with repeated doses)

127
Q

Fosphenytoin (Cerebyx)

A

H20 soluble prodrug of phenytoin converted by plasma esterases
Available IM and IV
Doesn’t contain propylene glycol
Compatible with most IV solutions w/ less phlebitis
Paresthesias and pruritis are more frequent

128
Q

What is more frequent in fosphenytoin than in phenytoin?

A

Paresthesias and pruritis

129
Q

Phenobarbital

A

3rd line agent, if sz persists despite 2-3 doses of benzos and loading dose of hydantoin
2nd line agent if sz persists after 2-3 doses of benzos and hydantoins contraindicated
Used in pediatric patients
Onset of action w/in minutes of loading dose administration

130
Q

Phenobarbital ADR

A

More CNS and respiratory depression than hydantoins

Contains propylene glycol

Pharmacology II (23 decks)

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