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Fall 2024 > Pharm Test 3 > Flashcards

Pharm Test 3 Flashcards

1
Q

List the main types of siezures

A

focal
complex focal
focal secondarily generalized
Generalized
generalized tonic-clonic
generalized absent
tonic
atonic
clonic and myoclonic
infantile spasms

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2
Q

What are the symptoms of simple focal seizures?

A

Minimal spread of discharge
Does not affect consciousness or awareness
EEG may show normal discharge

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3
Q

what is the difference between focal and generalized seizures?

A

focal begins and stays in one area of the brain
generalized covers the entire brain

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4
Q

What are the symptoms of complex focal seizures?
Where do these originate?

A

May become unresponsive or lose consciousness
Most arise from temporal lobes

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5
Q

What are the symptoms of focal seizures secondarily generalized?

A

Begin as simple or complex focal seizures, but then spread to rest of brain
Look like generalized tonic-clonic seizures

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6
Q

What does generalized seizures have that focal seizures do not?

A

aura and post-ictal phase

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7
Q

What are the symptoms of a generalized tonic-clonic (grand mal) seizure?

A

Person falls to ground
Entire body stiffens
Muscles jerk or spasm
Tongue or cheek may be bitten
Urinary incontinence

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8
Q

What are the symptoms of a generalized absent seizure?

A

Stare into space
Wake-up, no notice of seizure
Some automatisms possible

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9
Q

What are the symptoms of a generalized tonic seizure?

A

Muscles suddenly contract and stiffen (“sudden tone”)
Often causes falls
Another form of drop attack

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10
Q

What are the symptoms of a generalized atonic seizure?

A

Sudden loss of muscle tone
Patient falls without warning
A drop attack

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11
Q

What are the symptoms of a generalized clonic and myoclonic seizure?

A

Make the body jerk like it is being shocked

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12
Q

What are the symptoms of infantile spasms?

A

Muscle spasms that affect a child’s head, torso, and limbs
Usually begins before age of 6 months

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13
Q

what are the 3 general mechanisms of action that are targets for antiepileptic drugs?

A
  1. Modification of ion conductance
    Na+, K+, Ca++
  2. Enhancing inhibition
    Increasing inhibitory response by increasing activity at GABA receptors
  3. Inhibiting excitation
    Inhibit excitation response by inhibiting glutamate transmission, either at glutamate receptor or through release of glutamate itself
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14
Q

What are the most common automatisms seen with seizures

A

Lip smacking
Rapid blinking of eyes
Swallowing
Fumbling
Scratching
Stumbling about

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15
Q

What is tonic?

A

increase in tone of muscles; muscles contract and stiffen

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16
Q

what is clonic?

A

muscle jerks/spasms; rapid movement back and forth

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17
Q

What is the oldest non-sedative anti seizure drug?

A

phenytoin

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18
Q

what is the most effective drug for tonic-clonic seizures?

A

phenytoin

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19
Q

What is important to know about the pharmacokinetics of phenytoin?

A

It is highly bound to albumin.
It is really easy to overdose on when in it’s free form
have to be careful with other drugs that compete for albumin or kick phenytoin off albumin

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20
Q

What drug kicks phenytoin off of albumin?

A

valproic acid

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21
Q

what is the therapeutic level of phenytoin?

A

10-20mcg/mL

only 10% is typically in the free form in the body

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22
Q

what is the toxic and lethal level of phenytoin?

A

30-50mcg/mL

> 100mcg/mL

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23
Q

what are drugs that compete for albumin binding sites?

A

carbamazepine
sulfonamides
Valproic acid

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24
Q

What are the toxicity symptoms of phenytoin?

A

vision changes
sedation
gingival hyperplasia
hirsuitism

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25
Q

what is the MOA of carbamazepine?

A

blocks Na+ channels

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26
Q

what drug class is carbamazepine?

A

TCA

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27
Q

what is the drug of choice for focal seizures?

A

carbamazepine (tegretol)

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28
Q

what does carbamazepine treat besides focal seizures?

A

trigeminal neuralgia

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29
Q

What is special about the pharmacokinetics of carbamazepine?

A

It increases it’s own metabolism by increasing CYP450
named autoinducer

This increased metabolism also increases the metabolism of other drugs:
phenytoin
phenobarbital
ethosuxemide
valproic acid
clonazepam

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30
Q

locasamide(Vimpat) is widely used for what?

A

focal seizures

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31
Q

what is the MOA of lacosamide(Vimpat)?

A

blocks Na+ channels

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32
Q

toxicity of lacosamide (Vimpat)?

A

HA, nausea, dizziness

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33
Q

what is the safest sedative anti epileptic drug?

A

phenobarbital

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34
Q

what is the MOA of phenobarbital?

A

unknown
may enhance GABA

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35
Q

what is the drug of choice for seizures in infants?

A

phenobarbital

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36
Q

which anti seizure drug is the closest to the “miracle drug” that works for most seizures?

what types of seizures is it not useful to give for and may actually worsen them?

A

phenobarbital

Absence, atonic attacks, infantile spasms

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37
Q

what is the toxicity of phenobarbital?

A

sedation

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38
Q

What is fosphenytoin?

A

More soluble prodrug of phenytoin
“Better” than phenytoin because can be given IV

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39
Q

What are the drugs used for Focal and generalized tonic-clonic seizures?

A

phenytoin (Dilantin)
Carbamazepine
Lacosamide (Vimpat)
Phenobarbital

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40
Q

What are the drugs used for generalized seizures (not tonic-clonic)

A

ethosuximide
valproic acid(depakene)

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41
Q

what is the drug of choice for absence seizures?

A

ethosuximide

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42
Q

Ethosuximide has a good safety and efficacy index which is why it is often used for

A

children

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43
Q

what is the MOA of ethosuximide?

A

Ca++ channel inhibition

44
Q

what is the MOA of valproic acid?

A

unknown
some effects on Na+ currents
increases GABA
Increases K+ conductance at high levels

45
Q

what is known as a “broad spectrum AED”?

A

valproic acid (Depakene)

46
Q

What is the drug interactions to know for valproic acid (depakene)?

A

Displaces Phenytoin from proteins

inhibits metabolism of many other drugs:
phenobarbital
phenytoin
carbamazepine

47
Q

what are some common benzodiazepines?

A

Diazepam (valium)
Lorazepam (ativan)
Clonazepam (klonipin)
Chlorazepate dipotassium (tranxene)

48
Q

what is the MOA of benzodiazepines?

A

Increases GABA action to depress all levels of CNS

49
Q

clonazepam (klonipin) is only available in the _______ form.
It is good for

A

oral

absence seizures and myoclonic seizures

50
Q

diazepam (Valium) is effective in stopping _______ but ________ therapy is not considered effective

A

continuous seizure activity

chronic

51
Q

Lorazepam (ativan) is more effective than diazepam for ________

A

status epilepticus

52
Q

what is the treatment options for infantile spasms?

A

palliative (keep sedated)
Prednisone
Vigabatrin (GABA analog)

53
Q

what are the treatment options for epilepsy?

A

AED
resection of foci
vagus nerve stimulation
ketogenic diet (children)
medical marijuana

54
Q

Status epilepticus is a

A

medical emergency.

55
Q

treatment for status epilepticus

A

IV antiseizure meds
ABC’s
Possibly intubation and sedation

56
Q

chronic phenytoin therapy makes patients resistant to ___________

A

neuromuscular blocking agent

57
Q

phenytoin can enhance neuromuscular blockades when

A

there is a high level in the system at the time the NMB is given

58
Q

what is the only narcotic drug that can stimulate seizure activity?

A

Meperidine (demerol)

59
Q

What is the MOA of Lamotrigine (Lamictal)

A

ion channel blocker

60
Q

What is Lamotrigine (Lamictal) used for?

A

focal seizures

61
Q

what is the MOA of GABA analogs?

A

increase GABA

62
Q

what drugs are known as GABA Analogs?

A

gabapentin
pregabalin
vigabatrin

63
Q

what are gaba analogs used for?

A

adjunct, neuralgia, infantile spasms

64
Q

which category does GABA analogs fall under on the major seizure drugs chart?

A

focal and generalized tonic-clonic

65
Q

Why are benzodiazepines rarely used in chronic therapy of seizure states but are valuable in status epilepticus?

A

They are sedative hypnotics which is great for stopping a seizure but you don’t want the patient to be sleepy or sedated all the time

66
Q

what is the difference between sedation and hypnosis?

A

Sedation:
Calming effect, decreased anxiety
Depressant effects on psycho-motor function

Hypnosis:
Deep sleep
Lack of memory

67
Q

What are the major subgroups of sedative-hypnotics?

A

Benzodiazepines
barbituates
sleep aids
anxiolytics
ehtanol

68
Q

What are the major drugs in the Benzodiazepine sedative-hypnotic subgroup?

A

diazepam
midazolam

69
Q

What are the major drugs in the Barbituates sedative-hypnotic subgroup?

A

phenobarbital

70
Q

What are the major drugs in the sleep aids sedative-hypnotic subgroup?

A

zolpidem

71
Q

What are the major drugs in the anxiolytic sedative-hypnotic subgroup?

A

buspirone

72
Q

what receptor does sedative-hypnotic drugs work on and what does it do?

what is special about ethanol in this regard?

A

GABA
it increases permeability to Chloride

ethanol enhances GABA as well as inhibits glutamate from opening cation channels.

73
Q

what are the 4 phases of sleep and the important changes seen when taking sedative-hypnotics.

A
  • Stage 1 (NREM): when we are first going to sleep
  • Stage 2 (NREM): with hypnotics, there is an increase in this stage. This is desirable
  • Stage 3 (NREM, used to be known as stage 3 and 4): this is our deepest sleep
    undesirable effects is a decrease stage 4 NREM slow-wave sleep
  • REM sleep. associated with dreaming. We are close to being awake at this point.
    undesirable effect is decreased REM

The time it takes for us to actually go to sleep is known as SOL (sleep onset latency). The last desirable effect that hypnotics have is it decreases the time it takes for us to go to sleep

74
Q

Describe ethanols effects on sleep

A
  • Gives us more vivid dreams
  • Not sleeping good
  • Fall asleep faster and sleep longer but the sleep is not as restful as it could be because they do not spend as much time in REM sleep
75
Q

Describe the Alcohol dehydrogenase pathway (AD)

A

Ethanol is broken down by alcohol dehydrogenase (ADH) into acetaldehyde.

If we are drinking at moderate levels, acetaldehyde is broken down by aldehyde dehydrogenase → then produced into acetate → acetate can be broken down into lipids/glucose or it can be breathed out

Alcohol dehydrogenase and Acetaldehyde both utilizes NAD (nicotinamide adenine dinucleotide) → NAD is converted into NADH → NADH goes through electron transport chain to make ATP/energy

76
Q

what drug can inhibit alcohol dehydrogenase?

What is the result of this?

A

Fomepizole

increases our ethanol levels

77
Q

Because you can get energy/calories from alcohol, it is viewed as similar to which biomolecule?

A

More similar to lipids than it is to glucose

78
Q

Acetaldehyde is a toxic compound that produces what symptoms?

A

headaches, N/V

Associate acetaldehyde with hangover symptoms

79
Q

Why do people get a “beer belly”?

A

This alcohol dehydrogenase pathway causes more calorie intake d/t the biproducts of acetaldehyde being broken down by aldehyde dehydrogenase to produce acetate
then acetate being broken down into lipids/glucose

80
Q

Disulfiram (antabuse) MOA

Who is a target for this drug and why?

A

inhibits aldehyde dehydrogenase that converts acetaldehyde into acetate (so you’ll have more acetaldehyde in the body)

This can be given to chronic alcoholics. Within minutes of drinking alcohol, they have these hangover symptoms
The goal is to make them feel bad so they stop drinking

81
Q

Which ethanol breakdown pathway is the common pathway?
Why is it called common?

A

alcohol dehydrogenase pathway

It is used by most people who are not chronic alcoholics

82
Q

If someone drinks a wood alcohol (methanol: can cause death) which drug do you want to give?

A

Fomepizole.

Can block wood alcohol metabolism by blocking Alcohol dehydrogenase converting Ethanol into acetaldehyde.

83
Q

Associate fomepizole with

A

toxic concentrations of poisonous alcohol, as opposed to ethanol

84
Q

Describe the Microsomal ethanol-oxidizing system (MEOS) pathway

A

This pathway produces NADPH as a byproduct, instead of NAD/NADH
These individuals get less calories from alcohol. They tend to be thinner as well (this is because they aren’t having the conversion of NAD → ATP → calories)
This pathway still produces acetaldehyde

85
Q

Which pathway is going to increase in activity with people who have chronic alcohol use?

A

Microsomal ethanol-oxidizing system (MEOS)

86
Q

What percent of alcohol is metabolized by the liver?

A

90%

87
Q

How much alcohol does the adult metabolize in 1 hr to prevent going into zero order kinetics?

A

7-10grams/hr
(1 standard drink)

88
Q

What are the toxic effects of chronic ethanol ingestion?

A

Fatty liver → hepatitis → cirrhosis → liver failure

Neurotoxicity
Symmetrical peripheral nerve injury
Gait disturbances, ataxia
Optic nerve degeneration
Dementia, demyelinating disease

Wernicke-Korsakoff syndrome
Thiamine deficiency
Treatment: replenish thiamine
Paralysis of external eye muscles, ataxia, confusion, psychosis

89
Q

What are the molecular targets of ethanol?

A

GABA (gamma-aminobutyric acid): main brain inhibitory neurotransmitter
Alcohol enhances the action of GABA at GABAA receptors

Glutamate NMDA: (from a&p) one of our pain receptors. Remember we talked about how alcohol is one of the things that can inhibit NMDA!
Ethanol inhibits the ability of glutamate to open this channel
Glutamate is excitatory, so ethanol inhibits this action

90
Q

What is the difference between physiologic and psychological dependence?

A

Alcohol dependence (physiologic):
Body is now reliant on the drug - if you stop taking it you’ll have withdrawals

Addiction (psychological dependence)
Will seek out the drug regardless of negative consequences
Associated with dopamine

91
Q

What is alcohol abuse?

A

Alcohol abuse- Use in dangerous situations and despite adverse consequences

92
Q

How to manage acute alcohol intoxication?

A

Goal= patient safety
Prevent respiratory depression and aspiration of vomit
correct electrolyte imbalance and hypoglycemia
(banana bag for chronic alcoholics)

93
Q

What are the treatment options for alcohol withdrawal syndrome and alcohol-use disorders?

A

Detoxification: Taper sedative to benzodiazepines
Alcohol counseling

Meds:
Naltrexone
Acamprosate
Disulfiram

94
Q

How does Naltrexone work?

A

Long acting opioid antagonist
Patients must be opioid free before initiating because it could cause acute withdrawal syndrome from opioids

95
Q

How does Acamprosate work?

A

Deals with the desire for alcohol
GABA channels in CNS decrease over time → patient has withdrawals and does not have normal brain function → acamprosate increases GABA activity
Adjunct therapy, not effective alone

96
Q

How does Disulfiram work?

A

Inhibits aldehyde dehydrogenase - acetaldehyde accumulation
Causes extreme discomfort in patients that drink alcohol

97
Q

What is the treatment for acute anxiety?

A

treat underlying causes first (disease, situational)
benzodiazepines (sedative/hypnotic)

98
Q

What is the treatment for chronic anxiety?

A

buspirone (5-HT1A receptor agonist, which is G inhibitory and decreases cAMP)

99
Q

What is the treatment for sleep disorders?

A

Non pharmacologic first: proper diet/exercise, stimulant (caffeine) avoidance, comfortable sleep environment

Pharmacologic:
Benzos/barbiturates: this is less effective sleep because you have decreased REM sleep and decreased stage 4 NREM sleep
Zolpidem (ambien) and eszopiclone (lunesta): helpful for sleep but high abuse potential
OTC: most are histamines (benadryl)

100
Q

What is the major routes that sedative-hypnotic drugs are excreted?

A

Some of the sedative-hypnotics are excreted through the liver via alcohol dehydrogenase pathway (AD) and microsomal ethanol-oxidizing system (MEOS)

Others are excreted through the urine unchanged.

101
Q

Where do most sedative-hypnotics work?

A

GABAA

102
Q

How does a GABAA work?

A

GABA binds to receptor (has two binding sites for GABA)→ channel opens and chloride comes into the cell → hyperpolarized cell → harder to excite

103
Q

What is the proposed mechanisms of action of benzodiazepines, barbiturates, and zolpidem?

A

GABAA
activation

104
Q

What are some cautions associated with sedative-hypnotic drugs?

A

Drowsiness, impaired judgment, diminished motor skills
Somnambulism (sleep walking): with ambien and lunesta
“Date-rape “ drugs: benzos
In elderly pts, possibly use half dose to avoid overdose
Intentional overdose with these drugs: coma/death
Interactions with other CNS depressants can cause poor outcomes (coma/death): including alcohol and ambien

105
Q

MOA of phenytoin?

A

alters sodium, GABA and Glutamate conductance

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