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Advanced Pharmacology > Exam 3 -Seizures, Sedatives, Hypnotics > Flashcards

Exam 3 -Seizures, Sedatives, Hypnotics Flashcards

1
Q

Describe simple focal seizures?

A
  • Originates at a foci in the brain and has minimal spread
  • Does not affect conciousness or awareness
  • EEG may be normal if foci is not captured
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2
Q

Describe complex focal seizures?

A
  • Most arise from temporal lobes
  • May become unresponsive/unconcious
  • Involves automatisms

Focal seizures can spread and become generalized tonic-clonic seizures

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3
Q

Describe generalized seizures?

A
  • Begin over the entire surface of the brain
  • May involve in aura
  • Can be tonic or atonic
  • Possible incontinence
  • Have post-ictal state
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4
Q

Describe an abscence seizure?

A
  • Staring into space
  • No remembrance of seizure
  • May have automatisms
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5
Q

Describe tonic and atonic seizures?

A
  • Tonic: muscles contract and stiffen, often causes falls
  • Atonic: Sudden loss of muscle tone, falling without warning
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6
Q

Describle infantile spasms (West’s syndrome)?

A
  • Muscle spasms that affects a child’s head, torso, and limbs.
  • Usually begins before age of 6 months.
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7
Q

Describe clonic and myoclonic seizures?

A

Myoclonic: The body jerks quickly like it is being shocked
Clonic: Rhythmic jerking motions

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8
Q

Describe the MOA and uses for phenytoin (Dilantin)?

A
  • Oldest non-sedative antiseizure drug
  • Alters Na+, K+, Ca++, glutamate, and GABA
  • Used for Generalized tonic-clonic and focal seizures
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9
Q

Describe the MOA and uses for carbamazepine (Tegretol)?

A
  • Is a TCA
  • Similiar to phenytoin, blocks Na+ channels
  • Drug of choice for focal seizures, also used in generalized tonic-clonic
  • Used to treat trigeminal neuralgia and bipolar disorder
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10
Q

Describe the MOA and uses of lacosamide (Vimpat)?

A
  • Blocks Na+ channels
  • Used for focal seizures
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11
Q

Describe the MOA and uses of phenobarbital?

A
  • Oldest and one of the safest sedating antiepileptics
  • Enhances GABA, decresaes glutamate
  • Used in focal and generalized tonic clonic
  • Drug of choice in infants
  • Can worsen absence, atonic, and infantile spasms seizures
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12
Q

Describe the MOA and uses for GABA analogs?

A

Gabapentin, pregabalin, vigabatrin
* Increases GABA
* Used as an adjunct
* Treats neuralgia and infantile spasms

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13
Q

Describe the MOA and uses for ethosuximide?

A
  • Blocks Ca++ channels
  • Drug of choice for abscence seizures
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14
Q

Describe the MOA and uses for valproic acid (depakene)?

A
  • MOA: All, effects GABA, Na+ currents, and K+ conductance
  • Broad spectrum antiepileptic
  • Also used in bipolar and migraine prophylaxis
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15
Q

Describe the MOA and use for benzodiazepines?

A
  • Increases GABA
  • Used in status epilepticus and abscence seizures
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16
Q

Define tonic and clonic?

A
  • Tonic: increase in muscle tone (stiffness)
  • Clonic: rapid muscle movement (jerking)
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17
Q

List the drugs of choice for focal seizures, generalized tonic-clonic seizures, absence, myoclonic seizures, and status epilepticus

A
  • Abscence – ethosuximide
  • Focal – carbamazepine (tegretol)
  • Generalized tonic-clonic – Phenytoin (dilantin)
  • Myoclonic – Valproic acid or clonazepam (klonopin)
  • Status epilepticus – IV benzodiazepam
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18
Q

Describe the pharmacokinetics and adverse effects of phenytoin?

A
  • Highly bound to albumin
  • Accumulates in the ER of brain, muscle, liver, and fat
  • Toxicity: Increases with dose -Gingival hyperplasia, hirsuitism, nystagmus
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19
Q

Describe the pharmacokinetics and adverse effects of carbamazapine?

A
  • Competes for binding sites on albumin, does not displace other drugs.
  • Induces heptaic enzymes, increasing its own metabolism as well as other antiepileptics.
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20
Q

Describe the pharmacokinetics and adverse effects of lacosamide?

A
  • Has equal efficacy at different doses
  • Toxicity: dizziness, HA, nausea, minimal drug interactions
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21
Q

Describe the pharmacokinetics and adverse effects of phenobarbital?

A
  • Very safe
  • Causes sedation
22
Q

Describe the pharmacokinetics and adverse effects of ethosuximide?

A
  • Good safety and efficacy
  • Toxicity: GI upset, lethargy
23
Q

Describe the pharmacokinetics and adverse effects of valproic acid?

A
  • Toxicity: GI upset
  • Inhibits metabolism of many drugs
  • Displaces phenytoin from plasma proteins
24
Q

Describe albumin binding site competition and relation to phenytoin levels?

A
  • Drugs that are protein bound compete for the same inert binding sites on albumin
  • If multiple drugs are competing for the same site, one drug will be displaced and have an increased plasma concetration
  • This occurs when valproic acid and phenytoin are given together. Valproic acid will displace the phenytoin bound to albumin, increasing the plasma concentration to potentially fatal levels.
25
Q

Describe the use of benzodiazepines in chronic seizure states and status epileticus?

A
  • Benzos are rarely used in chronic seizure states because they depress all levels of the CNS leading to sleepiness/sedation
  • They are valuable in status epilepticus because they can quickly stop the seizures by inducing sedation. This is important because S.E. is a lifethreatening emergency.
26
Q

What are the primary treatments in infantile spasms?

A
  • Palliative - make them comfortable/sleepy to reduce seizures
  • IM prednisone
  • Vigabatrin - GABA analog blocking enzymatic hydrolysis
27
Q

What are the primary considerations in status epilepticus?

A
  • Preservation of organ functioning via BLS/ACLS
  • Stopping the seizure activity asap with IV benzos
28
Q

What are alternative therapies for seizures?

A
  • Awake craniotomy
  • Ketogenic diet
  • Vagus nerve stimulation
29
Q

What some anesthetic considerations when patients have seizure disorders or are taking AED?

A
  • Chronic phenytoin therapy makes patients resistant to NMB
  • Acute phenytoin levels will enhance NMB
  • Avoid drugs that enchance seizure activity (sevoflurane, methohexital, demerol)
30
Q

Define sedation and hypnosis?

A
  • Sedation – Relief of anxiety and calming effect. Depressant effect on psycho motor function.
  • Hypnosis – Encourages sleep and leads to deep sleep. Adjunct to anesthesia or at high doses it can be used to induce anesthesia.
31
Q

What are the sedative-hypnotic benzodiazepines and their receptor target?

A
  • Diazepam and midazolam
  • GABAa receptors
32
Q

What are the sedative-hypnotic barbituates and their receptor target?

A
  • Phenobarbital, thiopental, methohexital
  • GABAa receptor at level of cell wall
33
Q

What are the sleep aids and their receptor target?

A
  • Zolpidem (ambien) and Lunesta
  • GABAa receptor
34
Q

What are the anxiolytics and their receptor target?

A
  • Buspirone
  • 5HT1A receptors
35
Q

What is ethanol’s target receptor?

A
  • Increases action of GABA at GABAa receptors
  • Inhibits glutamate to open NMDA channels
36
Q

Describe the effects on sleep stages with sedative-hypnotics?

A
  • Desirable: Decreases time to fall asleep, increases stage 2 NREM sleep
  • Undesirable: Decreased REM sleep, decreased stage 4 NREM slow-wave sleep
37
Q

Describe/draw the biochemical metabolism of ethanol?

A
  • Normal pathway is alcohol dehydrogenase pathway
  • Chronic users also utilize the microsomal ethanol-oxidizing system (MEOS)
38
Q

Where does disulfram work in the ethanol methabolism pathway? What are its effects?

A
  • Inhibits aldehyde dehydrogenase, preventing metabolism of acetaldehyde to acetate
  • This causes someone to get the toxic effects of acetaldehyde rapidly after drinking (headache, N/V)
39
Q

Explain the pharmacodynamics of ethanol at differing levels of intoxication?

A
  • Acute intoxication causes sedation, relief of anxiety, slurred speech, impaired judgement.
    -Acute tolerance occurs within hours
    -Chronic drinkers require a higher concentration
  • At moderate levels inhibition of attention and information processing skills and motor vehicle operation
    -The legal alcohol limit to drive is less than 0.08%
  • In high concentrations: coma, respiratory depression, and death
40
Q

What are the pharmacokinetics of ethanol?

A

A: Rapid, water soluble, peaks in 30 mins
D: rapid, tissue levels will match blood levels. Concentrations rise in the CNS quicly.
M: 90% by liver, the rest in the stomach and lungs. See above for the metabolism pathways.
E: Body can handle one standard drink per hour, more than that the body switches to zero order elimination.

41
Q

What are the toxic effects of acute ethanol ingestion?

A
  • Sedation
  • Vasodilation
  • Tachycardia
  • GI upset
  • Severe electrolyte imbalances and hypoglycemia
  • Can aspirate own vomit
  • Causes weight gain (beer belly)
42
Q

What are the toxic effects of chronic ethanol ingestion?

A
  • Liver disease/death
  • Tolerance, dependence, and addiction.
  • Generalized symmetric peripheral nerve injuries, ataxia, dementia, and optic nerve degeneration.
  • Causes weight loss d/t conversion to MEOS metabolism
  • Wernicke-Korsakoff syndrome: causes paralysis of the external eye muscles, confusion, psychosis, coma, and death due to thiamine deficiency
43
Q

Describe tolerance, addiction, and dependence?

A
  • Tolerance: more of the drug is needed to achieve the same initial effect
  • Dependence: the body is physiologically dependent on the drug.
  • Addiction: psychological dependence on the drug that changes behavior (drug seeking)
44
Q

What is the management of acute alcohol intoxication?

A
  • Prevent aspiration of vomit
  • Correct electrolyte and fluid imbalances
  • Monitor hypoglycemia
45
Q

What is the treatment in acute alcohol withdrawl syndrome?

A
  • Prevent seizures, delirium, and arrhythmias
  • Replace electrolytes
  • Thiamine therapy
  • Substitute alcohol with long acting sedative/hypnotic (benzo), then taper
46
Q

What is the management of alcohol-use disorders?

A
  • Alcohol counseling
  • Naltrexone (long acting opioid antagonist)
  • Acamprosate - decrease desire for alcohol
  • Disulfram (antabuse) - causes toxic effects of acetaldehyde rapidly
47
Q

What cautions associated with sedative-hypnotics?

A
  • Drowsiness and impaired motor skills
  • Somnambulism (sleep walking)
  • Benzos used as “date rape” drugs
  • Use half dose in the elderly
  • Overdoses
  • Excessive CNS depression when multiple are combined.
48
Q

What are the common automatisms seen with seizures?

A

Lip smacking, swallowing, fumbling, scratching, walking about

49
Q

Describe the difference in free and therapeutic doses for phenytoin?
What causes this?

A

Therapeutic: 10-20 mcg/mL
Free: 1-2.5 mcg/mL
phenytoin is mostly bound to albumin, only about 10% is in the free form

50
Q

Whatis the reversal drug for benzos and its MOA?

A

Flumazenil
Out-competes benzo binding sites on GABAa receptors preventing activation and opening of the receptor, preventing chloride entry and hyperpolarization

Advanced Pharmacology (11 decks)

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