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Pharmacology Exam 3 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Seizure begins at a single site in the cortex (only a few electrodes show synchronous activity)

A

Partial seizure

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2
Q

Seizure in both hemispheres of the brain (all electrodes go off simultaneously)

A

Generalized seizure

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3
Q

Type of seizure:
No loss in consciousness
Short duration (20-60 seconds)
Ex: one side of face may twitch

A

Simple seizure (partial)

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4
Q

Type of seizure:

Sudden loss of consciousness
Less than 30 seconds
Person may be staring and blinking (3 blinks per second)
More common in children than adults

A

Petit mal (absence seizure) (generalized)

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5
Q

Gradual loss of consciousness (30seconds to 2 minutes)

Starts with simple seizure and hallucinations then there are strong automatisms (lip smacking)

A

Complex seizure (partial)

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6
Q

Sudden loss of consciousness (1.5-2.5minutes)

20 seconds of muscle rigidity, then 1-2 minutes of rhythmic muscle contractions

A

Tonic-clinic (generalized)

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7
Q

Single shock like contraction in the whole body that lasts less than 1 second
More in children than in adults

A

Myoclonic (generalized)

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8
Q

Starts with a partial seizure and progresses to generalized seizure

A

Secondarily generalized seizure

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9
Q

Sodium and potassium bromide Use

A

Less seizures because of severe sedation

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10
Q

Sodium and potassium bromide ADRs

A

Severe sedation

Severe skin rash and/or lesions

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11
Q

First anti seizure drug (1912)

A

Phenobarbital (Luminal)

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12
Q

Barbiturate metabolized to phenobarbital and PEMA

A

Primidone

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13
Q

Animal model where repeated low intensity, electrical stimulation to the amygdala

A

Kindling model for partial and generalized seizures

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14
Q

Animal model where there were injections of excitatory neurotransmitters

A

Model for tonic clonic seizures

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15
Q

MOA: Potentiation of synaptic inhibition via GABAa receptor

Use: Monotherapy used for generalized tonic-clonic and partial seizures

A

Phenobarbital (Luminal)

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16
Q

MOA: Potentiation of synaptic inhibition via GABAa receptor

Use: Monotherapy for generalized tonic clonic, partial and adolescent Myoclonic seizures (*less effective than phenobarbital)

A

Primidone

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17
Q

MOA: prolong rate of recovery for voltage gated Na channels from inactivation (inactivated for longer)

Use: Monotherapy for generalized tonic clonic and partial seizures

A

Phenytoin (Dilantin)

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18
Q

Drug concentration for this drug increases disproportionately as the dosage is increased and is bound 90% to plasma protein

A

Phenytoin (Dilantin)

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19
Q

Side effects for phenobarbital

A

*Induction of CYP3A4 so increased drug metabolism of certain drugs like oral contraceptives
Sedation in adults
Hyperactivity/irritation in children

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20
Q

Side effects for Primidone

A

Induction of CYP3A4 so increased drug metabolism of certain drugs like oral contraceptives
Sedation in adults
Hyperactivity/irritation in children

PLUS 
dizziness 
Nausea
Nystagmus 
Ataxia
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21
Q

Side effects for phenytoin

A
  • Increases drug metabolism of drugs that are metabolized by the same enzyme (CYP2C9) because these enzymes are saturable (warfarin)
  • Induces CYP3A4 so increased metabolism of drugs like contraceptives
  • Gingival hyperplasia
  • Steven johns syndrome
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22
Q

Adverse immune reaction

Blistering of skin and mucous membranes after flu like symptoms and a persistent fever

A

Steven johns syndrome

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23
Q

Treatment for Steven johns syndrome

A

*Discontinuation of drug

Possible immunosuppressants

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24
Q
  • MOA: Inhibit T-type Ca channels

* Uses: Monotherapy for absence seizures

A

Ethosuximide

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25
Q

MOA: prolong the rate of recovery of Na channels from inactivation

Uses: Monotherapy for generalized Tonic clonic and partial seizures
Also for Manic depressive patients

A

Carbamazepine

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26
Q

MOA: prolong rate of recovery of Na channels from inactivation

Uses: Monotherapy in treatment of partial seizures 4-16 years old
Adjunctive treatment for partial seizures

A

Oxcarbazepine

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27
Q

Not bound to plasma protein so few drug-drug interactions

A

Ethosuxomide

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28
Q

Induces own metabolism so have to wait 3 weeks to get a good steady level to be reached

A

Carbamazepine

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29
Q

A prodrug that is converted to active metabolite in the Iiver

*does not autoinduce like carbamazepine

A

Oxcarbazepine

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30
Q

Phenobarbital, phenytoin, and valproic acid increase the metabolism for this drug

A

Carbamazepine

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31
Q

Side effects for carbamazepine

A

Chronic side effects
*induces drug metabolism of OCs from CYP3A4
Drowsiness, vertigo, ataxia, blurred vision

Acute side effects:
Stupor, coma, hyper irritability convulsions

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32
Q

Side effects for oxcarbazepine

A

*Increases drug metabolism of CYP3A4 enzyme like OCs. Not as much as carbamazepine though
Dizziness, nausea, ataxia

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33
Q

Side effects for ethosuximide

A

Nausea, vomiting, anorexia
CNS drowsiness, lethargy, euphoria
SJS, aplastic anemia

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34
Q

MOA: *inhibits T-type Ca channels
prolongs inactivation of Na and increases GABA synthesis

Use: *used as monotherapy for absence, myoclonic, partial, and tonic-clonic seizures. “broad spectrum” anti epileptic

A

Valproic acid (Depakote)

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35
Q

ADRs for Valproic Acid (Depakote)

A

increase in hepatic blood enzymes, increases hepatic toxicity

inhibits CYP2C9 so increased concentration of phenytoin & phenobarbital

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36
Q

MOA: starts synaptic inhibition via GABAa receptors

Use: adjuncitve treatment for absence seizures and juvenile myoclonic seizures

A

benzodiazepines (clonazepam and clorazepate)

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37
Q

ADRs for benzodiazepines

A

Drowsiness, lethargy

In children, aggression, hyperactivity, irritability

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38
Q

MOA: unknown…even though binds to Ca channels, nothing happens and nothing happens with GABA either

Use: adjunctive treatment for partial with and without secondary generalized seizures

A

Gabapentin (Neurontin)

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39
Q

this drug is not metabolized but excreted unchanged in the urine so renal function must be determined before dosing

A

gabapentin (Neurontin)

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40
Q

Gabapentin side effects

A

fatigue and ataxia

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41
Q

GABA molecule bound to lipophilic hexane ring but doesnt interact with GABA receptors at all

A

gabapentin (Neurontin)

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42
Q

GABA molecule bound to isobutane

A

pregabalin (Lyrica)

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43
Q

MOA: unknown

Use: adjunctive therapy for partial onset seizures and fibromyalgia

A

pregabalin (Lyrica)

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44
Q

MOA: inhibits Ca, Na, NMDA, and AMPA-kainate receptors

Use: monotherapy and adjunctive therapy for LGS, partial and generalized seizures in adults

A

felbamate (Felbatol)

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45
Q

Felbatol side effects

A

GI upset, anorexia, and insomnia

may have aplastic anemia and hepatotoxicity

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46
Q

childhood onset of epilepsy that can causes severe cognitive dysfunction
multiple seizure types including atonic or “drop” seizures and is resistant to drug therapy

A

LGS (Lennox-Gustaut syndrome)

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47
Q

this drug was taken off the market for causing hepatotoxicity and aplastic anemia but was later brought back as a last resort drug for resistant seizures

A

flebamate (Felbatol)

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48
Q

MOA: prolongs the rate of recovery of Na channels from inactivation. To a small extent, inhibits Ca

Use: *a monotherapy and adjunctive treatment for partial and generalized tonic/clonic seizures like LGS.

considered a broad spectrum anti epileptic

A

Lamotrigine (Lamictal)

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49
Q

when used with other anti epileptics, can get rash and SJS

A

Lamotrigine (Lamictal)

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50
Q

Lamotrigine side effects

A

dizziness, ataxia, blurred vision, nausea

rash and SJS when combined with other anti epileptics

51
Q

MOA: inhibit Na channels and AMPA-kainate receptors enhance GABA receptors

Use: *monotherapy and adjunctive treatment for partial and tonic clonic seizures (LGS). considered a broad spectrum anti epileptic

A

Topiramate (Topamax)

52
Q

side effects for Topiramate:

A

ataxia, fatigue, somnolence, weight loss

53
Q

Reduces plasma levels of OCs and estradiol

A

Topiramate (Topamax)

54
Q

MOA: inhibit GABA reuptake at synapse and prolong GABA action

Use: treats partial with and without secondarily generalized tonic clonic seizures

A

Tiagabine (Gabitril)

55
Q

side effects for tiagabine (Gabitril)

A

dizziness, somnolence, tremor (mild after initial treatment)

56
Q

MOA: unknown

Uses: *adjunctive treatment for partial and tonic clonic seizures in adults

  • myoclonic seizures in children.
  • IV prep for status epilepticus
A

Levitracatem (Keppra)

57
Q

highest safety of margin in animal studies

rapid dose titration makes this drug useful in adjunctive therapy

A

Levitracatem (Keppra)

58
Q

MOA: prolong rate of recovery for Na channels.
inhibit T-type Ca channels

Uses: adjunctive treatment for partial seizures in adults

A

Zonisamide

59
Q

Side effects for Zonisamide

A

somnolence, dizziness, anorexia, fatigue

1% get renal calculi

60
Q

What are the following drugs used to treat?

Lacosamide (Vimpat)
Rufinamide (Benzel)
Vigabatrin (Sabril)
Egozabine (Potiga)

A

epilepsy

61
Q

drug of choice for a partial seizure secondarily generalized

A

carbamazepine and phenytoin

62
Q

alternative drugs for partial secondarily generalized seizures

A

lamotrigine and valproic acid

63
Q

drugs of choice for generalized absence seizures

A

ethosuximide and valproic acid

64
Q

alternative drug of choice for generalized absence seizures

A

clonazepam

65
Q

drug of choice for generalized tonic clonic seizures

A

carbamazepine, phenytoin, valproic acid

66
Q

alternative drug of choice for generalized tonic clonic seizures

A

lamotrigine and topiramate

67
Q

a disease in which there are a series of seizures and where a full recovery doesnt occur before there is an onset of second seizure

A

status epilepticus

68
Q

how to treat status epilepticus

A

give either diazepam or lorazepam IV (lorazepam is preferred). avoid hypoventilation and hypotension. then give IV fosphenytoin (water soluble prodrug for phenytoin) or Levitracatem, phenobarbital or valproic acid

69
Q

what do long term use of AEDs cause?

A

osteoporosis

70
Q

true/false

women on OCs have a higher failure rate. if yes, by what 3?

A

true. they have a 3X higher failure rate.

71
Q

AEDs are safe to take while pregnant

true or false

A

false. there is a 2-3X higher increase in birth defects

72
Q

how to reduce the likelihood of neuronal rube defecfts from AEDs?

A

0.4mg/day of folate throughout pregnancy

give vitamin K during the last month

73
Q

which drug to completely avoid during pregnancy

A

valproic acid…teratogenic

74
Q

are generic drugs ok to give for seizures?

A

No because switching even from brand to generic can cause major seizures

75
Q

what are the 4 phases of migraines?

A

premonitory, aura, headache, and resolution

76
Q

what is the premonitory phase of a migraine?

A

can have neurologic symptom (photophobia and phonophobia), psychological symptoms (anxiety and depression), constitutional symptoms (stiff neck, yawning, thirst, food cravings)

77
Q

when is the premonitory phase?

A

hours to days before the actual migraine

78
Q

what is the aura phase of a migraine?

A

an aura refers to focal, neurological symptoms (vision or other sensations) occurs in ~31% of people with migraine

79
Q

how do migraines work (the headache part)

A

start from a dull ache in frontotemporal region and extends to the back of the skull and goes on to intense pulsations (usually unilateral) and these worsen over time. ~90% of patients have GI symptoms as well like nausea, vomiting and also photphobia and phonophobia

80
Q

how long does a migraine normally last?

A

4-72 hours

81
Q

what is a tension headaches

A

a muscle contraction headache.

a dull persisting, non pulsating and non debilitating bilateral pain. no nausea/vomiting and no aura or photophobia/phonophobia

82
Q

what is a cluster headache

A

brief episodes of extremely excruciating unilateral pain that come in clusters with periods of remission (months to years)

83
Q

what to migraines result from?

A

inappropriate dilation of intracranial extracerebral blood vessels

84
Q

what is the serotonergic abnormality theory for migraines?

A

drugs that deplete serotonin from tissue stores can induce migraines and so an intravenous injection of 5-HT can abort spontaneous migraines

85
Q

name a couple drugs that are known to deplete serotonin levels from the tissue stores thus causing migraines

A

reserpine and fenfluramine

86
Q

what is a rebound headache and why does it occur?

A

a rebound headache is a medication overuse headache and occur if you use the drug too much which induces a higher headache frequency

87
Q

what does the abortive therapy include?

A

combination analgesics, opiates, ergotamine tartrates, and triptans

88
Q

how do you avoid rebound headaches?

A

use abortive therapy no more than 2 times a week

89
Q

possible triggers for migraines (food)

A

alcohol
chocolate (phenylethylamine)
beer, red wine, cheese (tyramine)
frozen dinners, canned food, chinese food (MSG)
processed meats and fish (sodium nitrate)

90
Q

possible triggers for migraines (general)

A

irregular sleep pattern
stress
environmental changes
hormonal changes

91
Q

what is the first line therapy for mild to moderate migraines?

A

analgesiscs (NSAIDS, Midrin, Opiates)

92
Q

MOA: blocks prsotaglandin synthesis which prevent inflammation in the trigeminovascular system and lessens pain sensitization

A

NSAIDS

93
Q

a combination therapy that is as effectice as oral ergotamine in some patients with lower side effects

A

Midrin

94
Q

what are the 3 ingredients used in midrin?

A

Isomethoheptene,
dichlorophenazone
acetaminophen

95
Q

this drug should be used with extreme caution in patients with peptic ulcer disease, renal disease or hypersensitivity to aspirin

A

NSAIDS

96
Q

what is isomethoheptene do?

A

Mild vasocontrictor activity

97
Q

what does dichlorophenazone do?

A

sedative action

98
Q

this drug is used for severe, infrequent headaches where conventional therapies either do not work or are contraindicated so a rescue medication is needed

A

opiates (Butorphanol…a nasal spray)

99
Q

what are the ADRs for butorphanol?

A

dizziness, nauseam vomiting, drowsiness, and bad taste

100
Q

what are ergotamine tartrates used for?

A

they are used in the acute treatment of moderate to severe migraines

101
Q

where are ergot-like compounds found in nature?

A

found in rye contaminated with the fungus claviceps purperea

102
Q

what is ergotism?

A

gangrenous mummified limbs and spontaneous abortions

103
Q

what are the 3 dosage forms ergotamine are available in?

A

oral, sublingual and suppository

104
Q

what is the maximum dose of oral/sublingual ergotamine?

A

not to exceed 6mg/attack or 10mg/week

105
Q

___ is added to some ergotamine containing products for vasoconstriction and to help it absorb in the intestines

A

caffeine

106
Q

why is ergotamine called a dirty drug?

A

it interacts with serotonin, dopamine, and adrenergic receptors

107
Q

how do ergotamines work?

A

activation of 5-HT1b receptors and by causing vasoconstriction. in addition, it may reduce neurologic inflammation by decreasing vasodilators

108
Q

___ is a powerful vasoconstricor and a contraindication in patients with peripheral vascular disease

___ may potentiate the vasoconstriction that is caused by ergotamines

A

ergotamine

B blocker

109
Q

one of the side effects of ergotamines include GI upset. How does this happen and what needs to be added to counteract it?

A

there is an activation of central dopamine receptors in the chemoreceptor trigger zone. we need to add metoclopramide to the regimen as an antiemetic

110
Q

___ (antibiotic) can interferew with the liver metabolism of ergotamine and cause ergot toxicity

A

erythromycin

111
Q

Aside from peripheral vascular disease, what is one contraindication of ergotamine?

A

cardiovascular disease

112
Q

MOA: direct vasoconstriction of dilated intracranial arteries, reduced neurologic inflammation by decreasing the release of vasodilators and proinflammatory neuropeptide transmitter (works like ergotamine)

A

Dihydroergotamine (DHE45)

113
Q

true/false

DHE45 needs to be administered parenterally

A

true it is not absorbed in the GI tract at all

114
Q

1st line treatment for the acute treatment of moderate to severe migraines

A

Dihydroergotamine (DHE45)

115
Q

what is the only thing that is different between ergotamine and DHE45 (dihydroergotamine) regarding ADRs

A

DHE45 is less likely to have vasospasms because of less arterial vasoconstrictor activity. with DHE45 there is more alpha blocking activity

116
Q

what are triptans used for?

A

they are used for the acute treatmetn of moderate to severe migraines

117
Q

sumatriptan is a derivative of _____ and can be administered by _____, _____, and _____ (routes).

it is metabolized by _____

can be administered up to ____ hours after onset of attack and be effective

A

serotonin (5-HT)

SQ injection, oral tablets, or nasal spray

MAO-A

4 hours

118
Q

how does sumatriptan work?

A

causes constriction of inflamed/dilated intracranial arteries and inhibits the release of vasodilator/proinflammatory mediators

119
Q

what side effects of migraines does sumatriptan relieve?

A

nausea, vomiting, photophobia, and phonophobia

120
Q

what is the one huge contraindication in using sumatriptan and why?

A

contraindicated in pateints with cardiovascular disease. many fatalities are reported in patients who have cardiovascular disease and use SQ sumatriptan. High chance of getting MIs so do not give IV

121
Q

True/false

it is ok to give sumatriptan and another ergot-type compound together

A

false!!!! do not give them within 24 hours of each other!!

122
Q

common triptan symptoms

A

chest and throat tightness, difficulty breathing, panic/anxiety

123
Q

this drug is contraindicated with the use of an MAO inhibitor

A

sumatriptan

124
Q

these have a greater bioavailability than triptans

they act at the peripheral components of the trigeminovascular system

act centrally to inhibit pain transmission in he trigeminal nucleus (greater lipid solubility)

A

second generation triptans

Pharmacology Exam 3 (1 decks)

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