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Neuro Pharmacology Flashcards

1
Q

How can medications interfere with neuronal regulation?

A

Alter axonal conduction and synaptic transmission

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2
Q

What is a medication agonism?

A

Drug that causes the same effect that naturally occurs (receptor activation)

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3
Q

What is a medication antagonism?

A

Drug reduces or causes opposite effect (receptor deactivation)

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4
Q

What are the steps of synaptic transmission?

A

Neurotransmitter synthesis and storage

Release of neurotransmitter into cleft

Post-synaptic receptor binding

Inactivation of neurotransmitter

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5
Q

Where is the CNS location of acetylcholine?

A

Cerebral cortex, basal ganglia, limbic and thalamic regions, and spinal interneurons

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6
Q

Where is the CNS location of norepinephrine?

A

Neurons originating in brainstem and hypothalamus that project throughout other areas of the brain

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7
Q

Where is the CNS location of dopamine?

A

Basal ganglia and limbic system

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8
Q

Where is the CNS location of serotonin?

A

Neurons originating in brainstem that project upward (to hypothalamus) and downward (to spinal cord)

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9
Q

Where is the CNS location of GABA?

A

Interneurons throughout the spinal cord, cerebellum, basal ganglia, and cerebral cortex

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10
Q

Where is the CNS location of glycine?

A

Interneurons in spinal cord and brainstem

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11
Q

Where is the CNS location of glutamate, aspartate?

A

Interneurons throughout brain and spinal cord

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12
Q

Where is the CNS location of substance P?

A

Pathways in spinal cord

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13
Q

Where is the CNS location of enkephalins?

A

Pain and suppression pathways in brain and spinal cord

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14
Q

What is the effect of acetylcholine?

A

Excitation

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15
Q

What is the effect of norepinephrine?

A

Inhibition

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16
Q

What is the effect of dopamine?

A

Inhibition

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17
Q

What is the effect of serotonin?

A

Inhibition

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18
Q

What is the effect of GABA?

A

Inhibition

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19
Q

What is the effect of glycine?

A

Inhibition

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20
Q

What is the effect of glutamate, aspartate?

A

Excitation

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21
Q

What is the effect of substance P?

A

Excitation

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22
Q

What is the effect of enkephalins?

A

Excitation

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23
Q

What can drugs that affect the CNS do to movement?

A

Limit and cause involuntary movement

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24
Q

What can drugs that affect the CNS do to sleep and arousal?

A

Induce it

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25
Q

What do drugs that affect the CNS treat?

A

Anxiety, depression

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26
Q

What do drugs that affect the CNS increase?

A

Attention and focus (affect memory)

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27
Q

What does the blood brain barrier do?

A

Protects against foreign substances from entering the brain (prevents entry of damaging and therapeutic substances)

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28
Q

How is the BBB achieved?

A

By structure and function of CNS capillaries

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29
Q

What do not pass the BBB easily?

A

Large molecules and highly charged molecules

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30
Q

What do not pass BBB?

A

Low lipid soluble molecules

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31
Q

What can pass the BBB?

A

Lipid soluble molecules

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32
Q

What can cause the BBB to be affected to allow easier entry of molecules?

A

Birth (not fully formed)

Post radiation

Infectious agent present

Trauma (ischemic and inflammation)

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33
Q

What is used to decrease risk of future stroke?

A

Anti-platelet agents (aspirin)

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34
Q

What is the action of aspirin that helps reduce the risk of strokes?

A

Irreversibly acetylates COX-1 to prevent synthesis of TXA2, key to platelet aggregation

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35
Q

What drug is used post stroke thrombolysis?

A

Tissue plasminogen activators (tPA)

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36
Q

What is the action of Tissue plasminogen activators (tPA)?

A

Clot buster

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37
Q

What are side effects of Tissue plasminogen activators (tPA)?

A

Hemorrhage and mild systemic bleeding (GI or GU)

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38
Q

What should you monitor in a patient taking Tissue plasminogen activators (tPA)?

A

Neuro checks every 15 min for 2 hours, every 30 min for 6 hours then every hour until 24 hours (no other anticoagulants every 24 hours)

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39
Q

What is most important to do with an ischemic stroke?

A

Control BP

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40
Q

What are the BP recommendations post ischemic stroke?

A

< 185/110

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41
Q

How can you control BP?

A

With IV medications

Labetalol

Hydralazine

Metoprolol

Sodium nitroprusside

Nicardipine drip

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42
Q

What is there an imbalance in when it comes to spasticity?

A

Excitatory and inhibitory input to alpha motor neuron

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43
Q

What are the motor unit changes with spasticity?

A

Collateral sprouting

Silent synapse activation

Denervation super sensitivity

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44
Q

What happens to the mechanical properties of muscle post stroke?

A

Sarcomere is shorter and stiffer

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45
Q

What are the treatment goals with spasticity?

A

Improvements in positions

Mobility

Contracture prevention

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46
Q

What are managements techniques for spasticity?

A

Ice

Medications

Nerve block

Surgery

Intrathecal meds

Marijuana

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47
Q

What are the side effects of muscle relaxants?

A

CNS depression

Sedation

Anticholinergic side effects (especially in elderly)

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48
Q

Where is Botox injected for contractures?

A

Directly into muscle

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49
Q

How long does Botox last?

A

3-3.5 months

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50
Q

How long does Botox take to take effect?

A

<2 weeks

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51
Q

What side effects are often seen with Botox?

A

Hematoma and muscle weakness near injection site

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52
Q

How is intrathecal baclofen administered?

A

Directly into spinal canal

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53
Q

When is the onset of intrathecal baclofen?

A

1/2-1 hour with peak effect at 4 hours

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54
Q

How does intrathecal baclofen work?

A

A pump that delivers doses when needed and has to be refilled every 3 months

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55
Q

What is the mechanism of action of baclofen?

A

Inhibits transmission of reflexes at spinal cord (anti spasticity agent)

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56
Q

What is the mechanism of action of carisoprodol?

A

Blocks interneuronal activity and depresses poly synaptic neuron transmission

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57
Q

What is the mechanism of action of Chlorzoxazone?

A

Spinal cord and subcortical areas of the brain to inhibit reflex arcs that cause muscle spasms

58
Q

What is the mechanism of action of cyclobenzaprine?

A

Reduces tonic somatic motor activity

59
Q

What is the mechanism of action of diazepam?

A

Agonizes benzodiazepine subunit on GABA receptors in CNS

60
Q

What is the mechanism of action of dantrolene?

A

Interferes with release of calcium ions

61
Q

What is the mechanism of action of metaxalone?

A

Disrupts pain/spasm cycle through general CNS depression

62
Q

What is the mechanism of action of methocarbamol?

A

Muscle relaxation via general CNS depression

63
Q

What is the mechanism of action of orphenadrine?

A

Indirect muscle relaxant through central atrophine-like effects

64
Q

What is the mechanism of action of tizanidine?

A

Decreases spasticity by increasing Presynaptic inhibition resulting in a reduction in spinal motor neuron conduction

65
Q

What is Parkinson’s disease?

A

Degenerative and progressive disorder

66
Q

How does Parkinson’s progress?

A

Unilateral

Bilateral

Balance issues

Restricted to cane or bed

67
Q

What are the non motor effects of Parkinson’s?

A

Cognitive

Behavioral

Dementia

Disturbance of autonomic nervous system

68
Q

What is the most effective drug for Parkinson’s?

69
Q

What are side effects of levodopa?

A

GI

CV

Psych

Hypotension

Dyskinesia

Neuropathy (prolonged use)

70
Q

What happens with prolonged use of levodopa?

A

Decrease response due to controlled release formulation and adding additional medications

71
Q

What is levodopa delayed by?

A

High protein meals

72
Q

Where is most levodopa metabolized at?

A

The periphery (small amounts cross BBB)

73
Q

What does the small amount of levodopa that crosses the BBB cause?

74
Q

What is sinemet?

A

Levodopa combined with carbidopa

75
Q

Where is most of the nausea caused with levodopa?

A

When levodopa is converted into dopamine in the periphery

76
Q

What prevents conversion of levodopa into dopamine in the periphery?

A

Adding carbidopa

77
Q

What does carbidopa allow levodopa to do?

A

Cross the BBB intact with allows the conversion of levodopa into dopamine in the CNS rather than periphery

78
Q

What is end of dose wearing off with sinemet?

A

Effectiveness wears off before next dose is given and there are more frequent doses given

79
Q

What do COMTs do to levodopa?

A

Inhibit enzymes that degrade it to increase its availability

80
Q

What do COMTs extend?

A

Half life of levodopa from 1.5 to 2.5hrs

81
Q

When are COMTs used?

A

Only in combination with levodopa/carbidopa

82
Q

What do COMTs do?

A

Decrease wearing off times

83
Q

What are types of COMTs?

A

Entacapone and tolcapone

84
Q

Why is tolcapone rarely used?

A

Due to liver toxicity

85
Q

What are the adverse effects of COMTs?

A

Nausea, vomiting, diarrhea, abdominal pain, and dyskinesias

86
Q

What is used in early stages of Parkinson’s to reduce symptoms?

A

Dopamine agonisds

87
Q

What do dopamine agonists delay the need for?

88
Q

What is the mechanism of action for dopamine agonists?

A

Stimulates dopamine receptors in the absence of dopamine

89
Q

What are the side effects of dopamine agonists?

A

Orthostatic hypotension

Dizziness

Unsteadiness

90
Q

What line of therapy is a dopamine agonist?

91
Q

What is apomorphine used for?

A

When a patient is stuck (advanced disease)

92
Q

What is apomorphine?

A

Dopamine agonist

93
Q

What is amantadine?

A

Dopamine agonist (glutamate antagonist)

94
Q

What is amantadine effective for?

A

Levodopa induced dyskinesia

95
Q

What is selegiline/eldepryls place in therapy?

A

1st line in patients with mild disease to slow progression and need for levodopa

96
Q

What is the mechanism of action for selegiline/eldepryl?

A

Decreases breakdown of dopamine

97
Q

What happens at too large of doses of selegiline/eldepryl?

A

Loses its specificity (can lead to hypertensive crisis if taken with tyramine)

98
Q

What are helpful for 1/3 of Alzheimer’s patients?

A

Cholinesterase inhibitors

99
Q

What do cholinesterase inhibitors do?

A

Inhibit AChe breakdown which increases level of duration of ACh

100
Q

What are side effects of cholinesterase inhibitors?

A

Indigestion, diarrhea, loss of appetite, slowed HR

101
Q

Why are dopamine agonists created?

A

To reduce side effects of levodopa

102
Q

What may minimize memory loss in Alzheimer’s?

A

Memantine (block effects of plaque production)

103
Q

What is the effect of glutamate?

A

Excitatory

104
Q

What is the effect of acetylcholine?

A

Excitatory

105
Q

What is the effect of GABA?

A

Inhibitory

106
Q

What is the effect of glycine?

A

Inhibitory

107
Q

What is the effect of noradrenaline?

A

Modulatory

108
Q

What is the effect of dopamine?

A

Slows locomotor pattern

109
Q

What does the BBB play a critical role in?

A

Controlling influx and effluent of biological substances

110
Q

What are the four purposes of CNS medications?

A

Minimize secondary damage in the acute stage

Increase or decrease neurotransmission

Try and slow down disease progression

Minimize signs and symptoms secondary to problems that develop with neuro conditions

111
Q

When should TPA be used for a stroke?

A

If the stroke occurred < 4.5 hours ago

112
Q

What does TPA bind to?

A

Fibrin in the thrombus

113
Q

What is TNK derived from?

114
Q

What is the first choice in treatment of ICP due to trauma?

115
Q

What is the mechanism of action of mannitol?

A

Increases serum osmolality, resulting in creation of osmotic gradient that allows fluid from the cerebral parenchyma to be drawn into the serum (reduces cerebral edema and ICP)

116
Q

What are the side effects of mannitol?

A

Hypotension and dehydration

117
Q

What are the key points of levodopa?

A

Treats symptoms most effectively but effects wear off 25-50% within 5 years

118
Q

What are the key points of dopamine agonist?

A

Used with younger people because it can cause confusion and hallucinations

119
Q

What are the key points of COMT inhibitors?

A

Can increase ON time and allows reduction of levodopa (can worsen dyskinesias)

120
Q

What are the highly effective medications used for MS?

A

Methylprednisolone (corticosteroid)

Ocrelizumab

Ofatumumab

Natalizumab

121
Q

What was the first disease-modifying therapy available to treat MS?

A

Interferon beta

122
Q

What are the adverse effects of interferon beta?

A

Injection site reaction and flu-like symptoms

123
Q

What are the 2 medications for ALS that slow the progression?

A

Radicava

Riluzole

124
Q

What is the mechanism of action of radicava?

A

Free-radical scavenger (protects cells from damage inflicted by oxidative stress)

125
Q

What is the mechanism of action of riluzole?

A

Neuroprotective drug that blocks glutamatergic neurotransmission in the CNS

126
Q

How does baclofen help with spasticity?

A

It binds to GABA receptors to act as a GABA agonist to inhibit transmission within the spinal cord

127
Q

How is baclofen often administered?

128
Q

What do you need to watch for if Baclofen is administered intrathecally?

129
Q

What are side effects of baclofen?

A

Drowsiness, confusion, and hallucinations

130
Q

What is baclofen overdose?

A

Leads to hypotonia and flaccid paralysis (respiratory depression and coma)

131
Q

What is baclofen withdrawal?

A

Hyperreflexia and increased spasticity

132
Q

What is the mechanism of action of Botox?

A

Binds to Presynaptic terminal and enters the terminal where it destroys fusion proteins so AcH cannot be released

133
Q

What is the mechanism of action of antiseizure medications?

A

Inhibit excitation or enhance inhibition

134
Q

What does phenytoin do for seizures?

A

Primary drug for most seizures and blocks sodium current

135
Q

What does carbamezepine do for seizures?

A

Blocks sodium current

136
Q

What does phenobarbital do for seizures?

A

Enhances inhibitory GABA receptors

137
Q

What does valproic acid do for seizures?

A

Prevents re-uptake of GABA at synapses

138
Q

What does benzodiazepine do for seizures?

A

Used to treat status epilepticus

139
Q

What is a common side effect of anti seizure medication?

A

CNS depression

140
Q

Why are Antiepileptics after used for neuropathic pain?

A

They appear to interfere with overactive transmission of pain signals

Pharmacology (20 decks)

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