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JKC Pharm- Spring '24 > CNS- Exam 2 > Flashcards

CNS- Exam 2 Flashcards

1
Q

_____ Integrates sensory information and generates motor output and other behaviors necessary to interact with the environment

A

Central Nervous System

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2
Q

_____ electrically excitable cells that process and transmit information via electrochemical processes

A

Neurons

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3
Q

_____ nonneuronal support cells that perform a variety of functions in the CNS such as maintaining extracellular ion concentration, providing nutrients to neurons, and insulating/controlling the speed of conduction in neurons

A

Neuroglia

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4
Q

_____ protective separation of the circulating blood from extracellular fluid in the CNS that limits penetration of substances including most medications

A

Blood Brain Barrier: BBB

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5
Q

______ characterized by an aura of variable duration that may involve nausea, vomiting, visual scotomas or even hemianopsia and speech abnormalities

A

Classic migraine

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6
Q

How are classic and common migraine different?

A

Common migraines lacks the aura phase, the headache is similiar

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7
Q

What is the main way to treatment a migraine?

A

NSAIDs

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8
Q

_____ is an area of partial alteration in thefield of visionconsisting of a partially diminished or entirelydegeneratedvisual acuitythat is surrounded by a field of normal vision

A

Scotoma

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9
Q

Serotonin neurons are in involved with numerous functions in the body, name a few

A

mood, sleep, appetite, temperature regulation, perception of pain, regulation of blood pression and vomiting

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10
Q

What is the specific serotonin receptor?

A

5-HT

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11
Q

What serotonin migraine related triptan receptor is located in substantia nigra and globus pallidus?

A

5-HT1B

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12
Q

What serotonin migraine related triptan receptor is located in the brain?

A

5-HT1D

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13
Q

Name a few Serotonin 5-HT1B/1D Agonists. What is the main one?

A

Triptans:
almotriptan
eletriptan
rizatriptan
**sumatriptan
zolmitriptan

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14
Q

Triptans MOA?

A

acts on intracranial blood vessels and peripheral sensory nerve endings, resulting in vasoconstriction and decreased release of inflammatory neuropeptides

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15
Q

What ingestible routes of sumatriptan? Which ones are faster?

A

Injectable, nasal, oral, rectal, transdermal

Injectable and nasal are faster than oral

injectable is the fastest

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16
Q

What is first line therapy for acute severe migraine attacks?

A

Injectable or nasal Sumatriptan

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17
Q

When should you NOT use Sumatriptan?

A

CAD, angina, stroke

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18
Q

Define angina. What can it induce?

A

a type of chest pain caused by reduced blood flow to the heart

Coronary vasospasm

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19
Q

Ergot alkaloid MOA. Specifically what receptor?

A

causes vasoconstriction of vascular smooth muscle working mostly at alpha receptors

Alpha receptors

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20
Q

Are Ergot alkaloids more or less effective for treatment of acute migraine than triptan meds?

A

Less effective

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21
Q

Ergot alkaloids are (more/less) effective when taken early in a migraine attack

A

MORE

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22
Q

When Ergot Alkaloids are used frequently, ______ can occur. What are they often combined with ?

A

rebound headache

Caffeine

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23
Q

What are some side effects of ergotamine?

A

cyanosis, ischemia, prolonged vasospasm

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24
Q

What is the max dose of ergotamine in an attack and week

A

no more than 6mg per attack or 10mg weekly

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25
Q

What are some common prophylaxis meds that are commonly used for migraines?

A

Commonly prescribed:

Propranolol – (beta-blocker: non-selective and lipophilic = passes through BBB)
Topiramate – (anticonvulsant)
Valproic acid – (anticonvulsant)

Less common:
Amitriptyline - (tricyclic antidepressant)
verapamil – (calcium channel blocker)

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26
Q

For Sumatriptan when is it best give an additional dose?

A

1-2 hours after the initial dose

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27
Q

For Sumatriptan, ____ hours until time of onset

A

1.5 hours

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28
Q

For subq Sumatriptan, ___ hours until time of onset

A

0.2 hours

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29
Q

______ is the progressive loss of structure or function ofneurons, including death ofneurons

A

Neurodegeneration

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30
Q

Name 4 neurodegenerative diseases

A

Amyotrophic Lateral Sclerosis (ALS), Parkinson’s, Alzheimer’s, and Huntington’s

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31
Q

Tremor at rest is characteristic of _____

A

Parkinsonism

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32
Q

_____ consists of irregular, unpredictable, involuntary muscle jerks that occur in different parts of the body and impair voluntary activity

A

Chorea

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33
Q

_____ abnormal movements may be slow and writhing in character

A

Athetosis

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34
Q

_____ sustained slow abnormal movements that are regarded as abnormal postures

A

Dystonia

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35
Q

_____ are sudden coordinated abnormal movements that tend to occur repetitively, particularly about the face and head,

A

Tics

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36
Q

______ syndrome is characterized by chronic multiple tics

A

Gilles de la Tourette

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37
Q

Name two common tics

A

Repetitive sniffing

shoulder shrugging

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38
Q

______ is characterized by a combination of rigidity, bradykinesia, tremor, and postural instability

A

Parkinson’s Disease

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39
Q

_______ is present before a diagnosis of Parkinson’s disease is made

A

bradykinesia

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40
Q

Name a few other non-motor symptoms of Parkinson’s Disease

A

affective disorders (anxiety or depression)
confusion
cognitive impairment
personality changes
apathy
fatigue
abnormalities of autonomic function (e.g., sphincter or sexual dysfunction, dysphagia and choking, sweating abnormalities, sialorrhea, or disturbances of blood pressure regulation)
sleep disorders
sensory complaints or pain

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41
Q

In Parkinson’s, there is a loss of ____ neurons in the substantia nigra that normally inhibit the output of ____ in the corpus striatum

A

dopamine

GABAergic cells

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42
Q

What type of neurotransmitter is GABA?

A

Inhibitory

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43
Q

In Parkinson’s, _____ is expressed instead of being blocked in a normal person

A

GABA

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44
Q

What are the two treatment strategies for Parkinson’s

A

Increase dopamine levels

Inhibit Ach

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45
Q

______ does not cross the blood-brain barrier and if given into the peripheral circulation has no therapeutic effect in Parkinsonism

A

Dopamine

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46
Q

_____ is the immediate metabolic precursor of dopamine. Is it able to cross the BBB?

A

Levodopa

YES

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47
Q

How does Levodopa cross the BBB? Then what happens?

A

via anL-amino acid transporter, LAT

decarboxylated to dopamine

48
Q

Levadopa on its own, what percentage enters the brain unaltered? What happens to the rest of it?

A

1-3%

metabolized extra-cerebrally, predominantly by decarboxylation to dopamine, which does not penetrate the blood-brain barrier.

49
Q

Does a dopa-decarboxylase inhibitor cross the BBB?

A

NO, but it does allow for more Levodopa to get to the brain without being metabolized first

50
Q

Using carbidopa reduces the daily requirements of Levodopa by ____%

A

75%

51
Q

_____ will delay the effects of Levodopa

A

Taking it with food

Need to take Levodopa on an empty stomach

52
Q

What are some side effects of Levodopa/Carbidopa?

A

dizziness, nausea, dyskinesia, constipation

53
Q

What is the common starting dose of Levodopa/Carbidopa? How many times a day? Take it with or without food?

A

Carbidopa 25mg/Levodopa 100mg TID, with or without food

54
Q

Carbidopa/Levodopa: What is the dose you eventually work up towards? How many times a day?

A

Carbidopa 25mg/Levodopa 250mg tid-qid

55
Q

_____ of levodopa dose will alleviate dyskinesia, but motor symptoms of parkinsonism then ____

A

Reduction

Get worse

56
Q

In the on-off phenomenon, off-periods of marked _____ alternate over the course of a few hours with on-periods of _______

A

akinesia

improved mobility but often marked dyskinesia

57
Q

______ may help to reduce more troublesome dyskinesia.

A

Amantadine (antiviral)

58
Q

Are levodopa holidays recommended? Why or why not?

A

NO, carries the risks of aspiration pneumonia, venous thrombosis, pulmonary embolism, and depression resulting from the immobility accompanying severe Parkinsonism

59
Q

What is the argument in favor of a levodopa holiday? What does it not help with?

A

may temporarily improve responsiveness to levodopa and alleviate some of its adverse effects

on-off phenomenon

60
Q

____ enhance the extracerebral metabolism of levodopa and may therefore prevent its therapeutic effect unless a peripheral decarboxylase inhibitor is also taken

A

Vitamin B6 (Pyridoxine)

61
Q

Levodopa should not be given to patients taking _____ or within 2 weeks of their discontinuance

A

monoamine oxidase A (MAO) inhibitors

62
Q

What would happen if Levodopa and monoamine oxidase A (MAO) inhibitors are taken together?

A

hypertensive crises

63
Q

Pramipexole, ropinirole, Bromocriptine and Pergolide all are ???? What does it do?

A

Dopamine Receptors Agonist

act on the dopamine receptors in the brain

64
Q

Selegiline and Rasagiline are what type of drug? What does it do?

A

common MAO-B inhibitors used in Parkinsons

Stop the breakdown of Dopamine

65
Q

Tolcapone and Entacapone are _____. What does it do? Which one is preferred?

A

COMT inhibitors

prolong the action of levodopa by diminishing its peripheral metabolism

Entacapone is preferred (Tolcapone is associated with hepatotoxicity)

66
Q

What does Stalevo a combination of?

A

combination of levodopa with both carbidopa and entacapone.

67
Q

Stalevo has been associated with ______ and ______

A

Earlier occurrence and increased frequency of dyskinesia

68
Q

_____ finite episodes of brain dysfunction caused by abnormal discharge of cerebral neurons

A

Seizure

69
Q

____ chronic recurrent seizures

A

Epilepsy

70
Q

Infection, tumor, head injury, hypocalcemia, degenerative diseases, genetic mutations, epilepsy are all causes of _____

A

Seizures

71
Q

What are the two cellular mechanisms of too MUCH neural excitation in seizures?

A

Increase in intracellular flow of Na or Ca causes depolarization of the neuron making it more likely to fire

Increase in excitatory neurotransmitter release (glutamate)

72
Q

What are the two cellular mechanisms of too LITTLE neural excitation in seizures?

A

-Decrease in intracellular flow of Cl or efflux of K

  • Decrease in release of inhibitory neurotransmitters (GABA)
73
Q

What are the “clinical pearls” with regards to dosing seizure medications?

A

“Start low, go slow”

Controlled and sustained release products result in lower peaks and higher troughs

When discontinuing, always slowly taper

74
Q

If you do NOT slowly taper seizure medications, what are the associated risks?

A

risk of breakthrough seizures increases

75
Q

What is a normal taper schedule for a patient who has been on therapy for LESS than 8 weeks?

A

25% per week reduction in dosage for two weeks then taper remaining dosage over next 7 days

76
Q

What is a normal taper schedule for a patient who has been on therapy for MORE than 8 weeks?

A

Taper over 3-4 weeks

77
Q

What is a normal taper schedule for a patient who has been on therapy for MORE than 6 months?

A

Taper over 6-8 weeks

78
Q

What are the 6 types of generalized seizures?

A

Tonic clonic
Absence
Myoclonic
Atonic
Tonic
Clonic

79
Q

What type of seizure originates from both hemispheres of the brain, movements are bilateral and symmetric

A

Generalized seizures

80
Q

Types of seizures:

_____ sustained muscle contraction

A

Tonic

81
Q

Types of seizures:

_____ rhythmic jerking involving the same muscle groups on both sides or may be asymetric

A

Clonic

82
Q

Types of seizures:

_____ Grand-mal seizure. Loss of contience and all muscle movements

A

Tonic Clonic

83
Q

Types of seizures:

_____ sudden onset and interrupts ongoing activities, blank stare or eyes roll up in head for a few seconds to half a minute during which the patient is nonresponsive

A

Absence

84
Q

Types of seizures:

_____ jerk a little. Sudden brief involuntary muscle contractions

A

Myoclonic

85
Q

Types of seizures:

_____ loss of consiousness. Limpness of head trunk jaw or limbs

A

Atonic

86
Q

Carbamazepine**
Lamotrigine**
Levetiracetam**
Phenobarbital**
Perampanel**
Phenytoin**
Topiramate**
Valproic acid**
Oxcarbazepine
Zonisamide
^ These medications are used in _____ seizures

A

Tonic Clonic

87
Q

Ethosuximide**
Valproic acid**
Lamotrigine
Zonisamide
^Medications used in ____ seizures

A

Absence seizures

88
Q

Lamotrigine**
Levetiracetam**
Topiramate
Valproic acid
Zonisamide
^ Medications used in _____ seizures

A

Myoclonic seizures

89
Q

Lamotrigine
Valproic acid
Zonisamide
^Medications used in ____ seizures

A

Atonic seizures

90
Q

______ seizures do NOT have any FDA approved medications. What else is also recommended?

A

Atonic

diet, surgery, vagus nerve stimulation (implanted device), laser ablation of epilepsy foci, thalamus stimulation, trigeminal nerve stimulation

91
Q

Measured drug level = ______ + ______

A

level of UNbound drug + bound drug

92
Q

Phenytoin is subject to what 3 things?

A
  1. Michaelis-Menten kinetics
  2. Protein binding
  3. Narrow therapeutic range
93
Q

This is a _______

A

Michaelis-Menten curve

94
Q

Phenytoin binds to ___ in the blood

A

albumin

95
Q

What do 1 and 2 represent?

A
  1. Drug level in the blood
  2. 50% of max metabolism
96
Q

What do 3 and 4 represent?

A
  1. Max (Vmax)
  2. Rate of metabolism
97
Q

The Michaelis-Menten curve will be linear until ____ is reached

A

Km- 50% metabolism of drug

98
Q

What does this graph represent?

A

Michaelis-Menten levels of Phenytoin

99
Q

According to the Michaelis-Menten saturation graph a small change in Phenytoin dose with result in ?

A

BIG changes in levels in the body

100
Q

What organ helps to metabolize phenytoid?

A

Liver

101
Q

What is the normal range for TOTAL serum phenytoin?

A

10-20 ug/mL

102
Q

What is the normal FREE phenytoin levels?

A

0.75-1.25 ug/mL

103
Q

What is the formula to adjust total serum phenytoin?

A
104
Q

Carbamazepine is both an inducer and substrate of 3A4. What does this mean?

A

It induces and eats up the drug but it will stabilize after 3-4 weeks, so need to wait a month before checking the level to get an accurate reading

105
Q

Carbamazepine, Oxcarbazepine, Phenobarbital and Phenytoin. What do they all have in common?

A

are inducers and are metabolized by many things so always need to check for drug interactions with these drugs

106
Q

Describe MOA for stimulants. What are the 2 types? Which one typically works a little better?

A

increase catecholamine release
Inhibit monoamine oxidase

amphetamine > methylphenidate

107
Q

Short acting stimulants typically work for how long?

A

4-6 hours

108
Q

Intermediate acting medications typically works for how long?

A

6-8 hours

109
Q

Long acting medications typically works for how long?

A

8-12 hours

110
Q

Which stimulant is typically dosed at night because it is released approximately 10 hours later? What drug class is it?

A

Jornay PM

Methylphenidate

111
Q

______ are less likely to have drug interactions compared to the other stimulant

A

Methylphenidates are LESS likely to have drug interactions when compared to Mixed amphetamines

112
Q

Stimulants are metabolized via _____. What happens when they are taken together with bupropion, fluoxetine and paroxetine?

A

2D6

Bioavailability and ½ life can be 4-8x greater in those taking

113
Q

______ can delay absorption and decrease bioavailability for stimulants

A

Food

114
Q

What are common side effects of stimulants?

A

Reduced appetite, stomachache, insomnia, headache, rebound symptoms, irritability

115
Q

Name some rare but serious stimulants side effects

A

Dysphoria, zombie-like state, tics, hypertension, hallucinations

116
Q

What are the 3 broad classes of adverse effects of stimulants?

A

psychosis or mania
aggression or violent behavior
severe anxiety or panic attacks

117
Q
A

JKC Pharm- Spring '24 (18 decks)

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