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Z-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
Describe the use of benzodiazepines in chronic seizure states and status epileticus?
* 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
What are the primary treatments in infantile spasms?
* Palliative - make them comfortable/sleepy to reduce seizures * IM prednisone * Vigabatrin - GABA analog blocking enzymatic hydrolysis
27
What are the primary considerations in status epilepticus?
* Preservation of organ functioning via BLS/ACLS * Stopping the seizure activity asap with IV benzos
28
What are alternative therapies for seizures?
* Awake craniotomy * Ketogenic diet * Vagus nerve stimulation
29
What some anesthetic considerations when patients have seizure disorders or are taking AED?
* Chronic phenytoin therapy makes patients resistant to NMB * Acute phenytoin levels will enhance NMB * Avoid drugs that enchance seizure activity (sevoflurane, methohexital, demerol)
30
Define sedation and hypnosis?
* **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
What are the sedative-hypnotic benzodiazepines and their receptor target?
* Diazepam and midazolam * GABAa receptors
32
What are the sedative-hypnotic barbituates and their receptor target?
* Phenobarbital, thiopental, methohexital * GABAa receptor at level of cell wall
33
What are the sleep aids and their receptor target?
* Zolpidem (ambien) and Lunesta * GABAa receptor
34
What are the anxiolytics and their receptor target?
* Buspirone * 5HT1A receptors
35
What is ethanol's target receptor?
* Increases action of GABA at GABAa receptors * Inhibits glutamate to open NMDA channels
36
Describe the effects on sleep stages with sedative-hypnotics?
* Desirable: Decreases time to fall asleep, increases stage 2 NREM sleep * Undesirable: Decreased REM sleep, decreased stage 4 NREM slow-wave sleep
37
Describe/draw the biochemical metabolism of ethanol?
* Normal pathway is alcohol dehydrogenase pathway * Chronic users also utilize the microsomal ethanol-oxidizing system (MEOS)
38
Where does disulfram work in the ethanol methabolism pathway? What are its effects?
* 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
Explain the pharmacodynamics of ethanol at differing levels of intoxication?
* **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
What are the pharmacokinetics of ethanol?
**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
What are the toxic effects of acute ethanol ingestion?
* Sedation * Vasodilation * Tachycardia * GI upset * Severe electrolyte imbalances and hypoglycemia * Can aspirate own vomit * Causes weight gain (beer belly)
42
What are the toxic effects of chronic ethanol ingestion?
* 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
Describe tolerance, addiction, and dependence?
* 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
What is the management of acute alcohol intoxication?
* Prevent aspiration of vomit * Correct electrolyte and fluid imbalances * Monitor hypoglycemia
45
What is the treatment in acute alcohol withdrawl syndrome?
* Prevent seizures, delirium, and arrhythmias * Replace electrolytes * Thiamine therapy * Substitute alcohol with long acting sedative/hypnotic (benzo), then taper
46
What is the management of alcohol-use disorders?
* Alcohol counseling * Naltrexone (long acting opioid antagonist) * Acamprosate - decrease desire for alcohol * Disulfram (antabuse) - causes toxic effects of acetaldehyde rapidly
47
What cautions associated with sedative-hypnotics?
* 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
What are the common automatisms seen with seizures?
Lip smacking, swallowing, fumbling, scratching, walking about
49
Describe the difference in free and therapeutic doses for phenytoin? What causes this?
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
Whatis the reversal drug for benzos and its MOA?
Flumazenil Out-competes benzo binding sites on GABAa receptors preventing activation and opening of the receptor, preventing chloride entry and hyperpolarization

Z-Advanced Pharmacology (17 decks)

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