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Pharmacology Exam 3 > Neurology Part 1 > Flashcards

Neurology Part 1 Flashcards

1
Q

EPILEPSY

A

EPILEPSY

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2
Q

In short, what is epilepsy?

Primary vs secondary epilepsy?

A

-Recurrent seizures, neurons are synchronously active when they shouldn’t be
-Primary- unknown cause, accounts for >50% of cases (idiopathic)
Secondary- in children: injury at birth,metabolic diseas
in adults: TBI

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3
Q
  • What is the main CNS inhibitory neurotransmitter?
  • What is the main CNS excitatory neurotransmitter?
  • How do these neurotransmitters relate to seizure activity?
A
  • GABA
  • Glutamine
  • To little GABA or too much Glutamine will cause too much excitation, causing neurons to be active when they shouldn’t be.
    • GABA-inhibitory
    • Glutamine-excitatory
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4
Q

What are the two types of epilepsy?

A

Partial seizure

Generalized seizure

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5
Q
  • A partial seizure is localized in one ______ ________

- Partial seizures can either be _______ or ______ partial seizure. Whats the difference?

A
  • cerebral hemishpere
  • simple or complex
  • The difference is that a simple partial seizure is a primary sensory component without LOC. In a complex partial seizure LOC may occur.
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6
Q

What cerebral hemisphere is involved in a generalized seizure?

A

-Both, LOC

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7
Q

What are the 6 types of seizures?

Which is the most common?

A
  • Tonic-clonic
  • Tonic
  • Clonic
  • Absence
  • Atonic
  • Myoclonic

-Tonic-clonic

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8
Q

Tonic-clonic

  • Tonic phase: rigid ______ spasm * 10-30 seconds, _______ stops, defication/micturition/salivation may occur
  • Clonic phase: rhythmic _____ spasm * 2-4 minutes, continued LOC, alertness slowly occurs

Tonic and clonic seizures are the same as the phases for the tonic-clonic seizure except for what?

A
  • extensor, respiration
  • flexor

-dont have others phases and only last a few seconds

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9
Q

Absence seizure

  • Most common in ______
  • Less _______ but more _______ than tonic-clonic. Involves a breif ____
A
  • children
  • dramatic, frequent
  • LOC, amnesia of event
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10
Q

Atonic seizures

  • Also known as __________
  • Seddun reduction in muscle tone resulting in ________ of head/limb. Lasts about ___-____
A
  • drop attacks

- dropping, 10-30 seconds

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11
Q

Myoclonic

-Single or multiple brief _________ of face, trunk, or extremities. Lasts for _______

A
  • contractions

- few seconds

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12
Q

What are the treatment options?

A
  • Daily medication (anticonvulsants)
  • Surgery
  • Nerve stimulation: stimulate vagus nerve
  • Ketogenic diet
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13
Q
  • What are the antieleptic medications referred to as?

- What does drug selection depend on?

A

-AED, ASD, or anticonvulsants

-Patient specific factors-age, pregnant, etc.
Type of seizures
Response to previous meds

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14
Q

Medications are split into what?

What is good about the 3rd generation medications?

A
  • 1st, 2nd, and 3rd generation

- possible less side effects

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15
Q

What is the MOA of the medications for epilepsy?

A
  • not fully understood

- either decreases excitatory or increases inhibatory signaling

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16
Q

People with epilepsy tend to have fast or long lasting activation of ________ receptors (NMDA) or a dysfunction in ______ receptors. This neuron is then considered __________ which may cause seizures.

A
  • Glutamate
  • GABA
  • hyperexcitable

-can also be caused by a decrease in GABA or an increase in Glutamate

17
Q

5 MOA for medications for epilepsy:

  1. ) Block __, ___ entry
  2. ) Block _______ release
  3. ) Block ________ binding
  4. ) Block ____ and ______
  5. ) Prolong opening of ______ channels
A
  • Na+, Ca2+
  • glutamate
  • glutamate
  • GAT1 and GABA-T
  • GABA-A
18
Q

What are the acute vs chronic AE of epilepsy medication?

A

Acute- may be concentration dependent or idiosyncratic

Chronic- due to duration of use

19
Q
  • What are the AE associated with epilepsy medications?
  • Which of these AE is associated with all epilepsy medication?
  • What is a rare AE associated with these drugs?
A
  • Neurotoxicity
    • sedation, ataxia, confusion, dizziness, blurred vision
  • Weight gain (a few cause weight loss)
  • Hypothyroidism
  • Rash
  • Idiosyncratic: mild to severe hypersensitivity reactions; may have more severe Stevens-Johnson Syndrome rash
  • neurotoxicity
  • aplastic anemia
20
Q

What is key with epilepsy drugs?

A

Monitoring because many are NTI and they also have MANY DDI

21
Q

What are the at risk populations and why?

A

Elderly

  • changes in body mass can change volume of distribution and med half life
  • hypoalbuminemia- can increase free drug in plasma if drug is typically highly protein bound
  • greater sensitivity to neuro effects
  • polypharmacy- DDI interactions

Children
-hepatic/renal activity changes during childhood means an increase in drug monitoring and dose adjustments

Women
-fluctuating -estrogen/progesterone may change risk of seizures throughout the menstrual cycle

Pregnant Women

  • increased risk of seizures and increased risk of maternal and fetal complications
  • risk vs benefit
22
Q

Therapeutic Concerns with Epileptic Drugs:

  • The primary AE of this class of drugs (______,______,_____) have direct impacts on patients participation in PT.
  • If patient is referred to PT for gait instability, what could this be due to?
A
  • sedation, dizziness, ataxia

- could be the medication

23
Q

ADHD

A

ADHD

24
Q

What are the three subtypes of ADHD?

A
  • Inattentive type
  • Hyperactive-impulsive type
  • Combined type
25
Q
  • The etiology (cause) of ADHD is ________: environmental, genetic, biologic
  • Pre and perinatal exposure to cigarettes/alcohol increases risk _-_x
A
  • multifactorial

- 2-3x

26
Q

In order to be diagnosed with ADHD, they have to be classified into _ of the 3 settings.

A

2 of the 3

27
Q

Neurochemical and Anatomic Anomalies of ADHD:

  • Mostly unclear- no particulat sole defect in the ______ associated with ADHD
  • MRI studies have shown _____________, it is unknown where this causes ADHD or is a result of ADHD
  • There is a ________ dysfunction in adults with ADHD
  • Appears that motor (__________) and cognitive (________) result from dysfunction of different cortical sites
A
  • brain
  • decreased brain volume
  • dopamine
  • hyperactivity, inattention
28
Q

What are the 2 main treatments for for ADHD?

Stimulants act on both _______ and _________ while atomoxetine only acts on _________

A
  • Stimulants, Atomoxetine

- norepinephrine and dopamine, norepinephrine

29
Q

Methylphenidate (________) and Mixed Amphetamine Salts (__________)

  • What class of drugs are these?
  • What is the MOA?
  • What is IR and XR?
  • What happens if theye are taken with food?
A

-Ritalin, Adderral
-Stimulant
-Methylphenidate: blocks dopamine and norepinephrine reruptake
Amphetamine: block dopamine and norepinephrine reuptake; ALSO increase dopamine and NE release
-IR= immediate release; onset of 15-30 minutes, lasts 2-6hrs
ER= extended release, lasts 8-12 hrs
-Slower onset and decreased absorption buy may decrease AE

30
Q

What are the common AE associated with stimulant medications __________ (Ritalin) and _______________ (Adderral)?

A

-methylphenidate, mixed amphetamine salts

  • decreased appetite/weight loss
  • stomachache
  • insomnia
  • HA
  • irritability/jitteriness
31
Q

What are the uncommon to rare AE associated with methylphenidate (_______) and mixed amphetamine salts (__________)?

A

-Ritalin, Adderral

  • dysphoria
  • “spacey”/ zombie like status
  • tics
  • HTN, HR fluctuations
  • hallucinations
  • skin discoloration with methyphenidate patch
32
Q

What are the boxed warnings associated with some stimulants?

A
  • CV risk

- Abuse potential

33
Q

atomoxetine (_________)

  • What is its MOA?
  • Is it more effective than stimulants and does it have a decreased abuse potential?
  • Is atomoxetine used as a monotherapy?
  • What is the onset time and when do we see the full benefit?
  • How are the AE different than stimulants?
  • What is an important boxed warning with this drug?
A
  • Strattera
  • selective NE reuptake inhibitor
  • less effective than stimulants but has less abuse potential
  • Yes, but can be used with a stimulant
  • 2-4 weeks for onset and full benefit at 6-12 weeks
  • Generally similar but more fatigue, sedation, and dizziness
  • increrased risk of suicidal ideation in children/adolescents
34
Q

-What other drug class is also used for ADHD?
-What is the MOA?
-Are these more of less effective than stimulants?
-Are they used as a monotherapy?
What are the most common AE?
What happens when either med is abruptly stopped?

A
  • alpha2 adrenergic agonists (guanfacine, clonidine)
  • mimic NE which improves working memory and behavioral inhibition
  • less effective but less potential for abuse
  • Yes, but also used with stimulants
  • dose-dependent sedation, hypotension, constipation
  • rebound hypertension
35
Q

What are 3 other drugs used for ADHD?

A
  • bupropion
  • lithium
  • antipsychotics
36
Q

Therapeutic Concerns with ADHD Drugs:

  • Monitor _________ (especially in ______)
    • stimulant therapy can increase __ and __
  • Be aware of loss of ________ and _________
  • Monitor behavior and attention span
A
  • vital signs (especially in adults)
  • HR,BP
  • appetite, insomnia

Pharmacology Exam 3 (10 decks)

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