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Neurologically Active drugs Flashcards

1
Q

Movement disorders are classified as either

A

Hypo or Hyper kinetic

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2
Q

Voluntary movements come from

A

Corticospinal (pyramidal) tracts

Basal Ganglia

Cerebellum (motor coordination center)

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3
Q

Extrapyramidal system is modulated by

A

Basal ganglia

Cerebellum

Cerebral Cortex

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4
Q

In the Extrapyramidal system, direct output is through the

A

Cerebral Coretx

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5
Q

Extrapyramidal system involves

A

Involuntary Actions

Reflexes

Locomotion

Complex movements

Postural control

Neural lesions causing movement (Extrapyramidal disorders)

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6
Q

Notable characteristics of Parkinson’s Disease

A

Resting tremor

Stiffness & Rigidity

Bradykinesia

Gait & Postural Instability

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7
Q

Juvenile Parkinsonism occurs

A

Early onset 21-40 years

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8
Q

General Parkinson’s occurs

A

Mean age of 57 years

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9
Q

In Parkinson’s, this aggregates and causes cell death, which accumulated in nigrostriatal system

This property is also neuronal & a glial cell protein

A

Synuclein

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10
Q

Parkinson’s is often characterized as this in the system

A

Lewy Bodies

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11
Q

In Parkinson’s there is _______& a loss of substantia nigra neurons, which causes a depletion in ________in the ____________

A

Degeneration; Dopamine; Basal Ganglia

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12
Q

Dopamine is ______in the Extrapyramidal system

A

Inhibitory

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13
Q

Acetylcholine is ______in the Extrapyramidal system

A

Excitatory

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14
Q

In Parkinson’s, there is generally a loss of______action and an overproduction of ________

A

Inhibitory; Excitatory

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15
Q

80% of the brains dopamine is in the

A

Basal Ganglia

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16
Q

In Parkinson’s, the percentage of dopamine in the basal ganglia can be as low as

A

10%

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17
Q

Excess excitatory cholinergic activity can cause

A

Progressive Tremor

Muscle Rigidity

Bradykinesia

Postural Disturbances

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18
Q

Common treatments of Parkinson’s

A

Restore Dopamine function

Levodopa/ Carbidopa

Dopamine Agonists

MAO-B inhibitors

Amantadine

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19
Q

Stereotactic deep brain stimulation targets the

A

Thalamus

Subthalamic Nucleus

Globus Pallidus

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20
Q

Autonomic dysfunctions of Parkinson’s

A

Ortho HOTN

Poor temperature control

Sialorrhea

Maintain Volume Status

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21
Q

Parkinson’s suffer from pulmonary dysfunction such as

A

Bradykinesia

Rigidity of Respiratory Muscles

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22
Q

Parkinson’s suffer from swallowing impairment & dysphasia which is caused by _______& can lead to_______

A

Bradykinesia (rigidity of pharyngeal muscles)

Exacerbated by ET intubations

Risk for Aspiration

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23
Q

Parkinson’s can cause cognitive impairment, leading to

A

Postop delirium

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24
Q

GABA inhibition in the basal ganglia can worsen or abolish

A

Microelectrode recordings (MER)

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25
Q

What medication should be avoided if testing for tremors

A

Beta Blockers

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26
Q

When should DBS be discontinued?

A

15 minutes before MER

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27
Q

Dexmedetomidine may abolish

A

MER, HOTN, & paradoxical agitation

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28
Q

Propofol depresses

A

Neuronal discharge & induced dyskinesia

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29
Q

Fentanyl & Remifentanil May

A

Worsen rigidity & suppress tremor

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30
Q

Benzodiazepines May

A

Abolish MER, suppress tremor & induce dyskinesia

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31
Q

Levodopa crosses

A

BBB & is a dopamine precursor

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32
Q

Levodopa is converted by

A

Enzyme to dopamine in basal ganglia
( Dopa decarboxylase)

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33
Q

Can dopamine pass BBB?

A

No it does not and it’s elevated levels can cause side effects

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34
Q

Of levodopa, ___% is rapidly converted to dopamine during___________

A

95%; first hepatic pass

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35
Q

Levodopa metabolites are converted to ________&_________

A

Dopamine & Homovanillic Acid which metabolizes further into NE & E

Requires adequate levels of COMT to metabolize excess catecholamines (methionine from diet)

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36
Q

Levodopa/Carbidopa inhibits______in the peripheral tissues

A

Decarboxylase

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37
Q

Levodopa/Carbidopa inhibits

A

Levodopa breakdown

(Levodopa + decarboxylase inhibitors)

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38
Q

Levodopa/ Carbidopa maximizes

A

The amount of levodopa reaching the brain before conversion to dopamine, which allows lower levodopa dose

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39
Q

Levodopa adverse effects on GI

A

N/V-dopamine stimulation of CRT

Carbidopa may decrease N/V

Avoid dopamine antagonists antiemetics (promethazine & metoclopramide)

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40
Q

Levodopa adverse effects on Endocrine

A

Inhibits prolactin secretion

Increased aldosterone leading to hypokalemia

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41
Q

Levodopa adverse effects on CV

A

Potential adrenergic receptor activation from dopamine, Epi & NE (increased inotropy)

ORTHO HOTN

Tachy, PVCs/PACs, Afib, VTach

Skin flushing

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42
Q

Levodopa adverse effects on neuromuscular

A

Abnormal involuntary movements (facial tics & grimacing, rocking of extremities & trunk)

Irregular gasps (diaphragmatic dyskinesia)

Change in mobility

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43
Q

Levodopa psychiatric adverse effects

A

Confusion

Hallucination

Paranoia

Impulsive/ compulsive behavior

AVOID HALDOL

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44
Q

What is Parkinsonism-Hyperpyrexia Syndrome

A

Life threatening related to abrupt withdrawal or dose reduction

Resembles Neuroleptic Malignant Syndrome

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45
Q

Signs and symptoms of Parkinsonism Hyperpyrexia Syndrome

A

Rigidity

Pyrexia

Autonomic Instability

Depressed Consciousness

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46
Q

Risk for Parkinsonism Hyperpyrexia Syndrome

A

DVT/PE

Renal Failure

Aspiration PNA

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47
Q

Treatment of Parkinsonism Hyperpyrexia Syndrome

A

Give antiparkinsonian therapy

Levodopa PO or NGT

Supportive measures

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48
Q

Levodopa adverse effects with antipsychotics

A

Antagonize effects of dopamine

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49
Q

Levodopa adverse effects with MAOIs

A

Interfere with inactivation of dopamine causing HTN & hyperthermia

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50
Q

Levodopa adverse effects with Anticholinergic drugs

A

Synergism improves symptoms

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51
Q

Levodopa adverse effects with Vitamin B6

A

enhances decarboxylase activity (levodopa metabolism)

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52
Q

Common dopamine agonists

A

Bromocriptine

Pramipexole

Ropinirole

Rotigotine

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53
Q

Characteristics of Dopamine Agonists

A

Mimic Dopamine at receptor site

Synthetic

Don’t require transformation or transport across BBB

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54
Q

Adverse effects of Dopamine Agonists

A

Hallucinations

HOTN

Dyskinesia

Pulmonary Fibrosis

Vertigo

Nausea

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55
Q

Amantadine is also a/an

A

Antiviral for influenza A

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56
Q

Amantadine can

A

Improve PD symptoms like muscle rigidity & Bradykinesia

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57
Q

Adverse effects of Amantadine

A

Anticholinergic effects

Peripheral edema

Confusion

Psychosis

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58
Q

MAO-B inhibitors…

A

Breaks down dopamine in the CNS

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59
Q

MAO-B, Selegine, is

A

Highly selective

Irreversible Inhibitor

Doesn’t alter peripheral metabolism or NE

60
Q

MAO-B adverse effects include

A

Insomnia

Confusion

Hallucination

Paranoia

61
Q

Rasa filing is a

A

MAO-A & MAO-B

62
Q

COMT inhibitors examples are

A

Tolcapone

Entacapone

63
Q

COMT is partially responsible for the ______________________

A

Peripheral breakdown of levodopa

64
Q

COMT Inhibitors block

A

Enzyme activity in the GIT

65
Q

COMT inhibitors slow

A

Elimination of Carbidopa- Levodopa

66
Q

COMT inhibitors adverse effects

A

Worsened Dyskinesia

Nausea/ Diarrhea

Hepatotoxicity

Rhabdomyolysis

67
Q

Anticholinergic drug medications are

A

Benztropine

Trihexyphenidyl

68
Q

Anticholinergic blocks the effects of

A

Excitatory ACh

69
Q

When Anticholinergics are used, excitatory ACh is blocked, which…

A

Corrects balance between DA & ACh

Controls tremors

Decreases excess salvation

Minimal effects on muscle rigidity & Bradykinesia

70
Q

Adverse effects of Anticholinergics

A

Confusion

Hallucination

Sedation

Mydriasis

Ileus

Urinary Retention

71
Q

Anti-Parkinson’s medications are usually_________morning of surgery for DBS

72
Q

In the Parkinson’s population DO NOT GIVE THESE FOR PONV

A

NO phenothiazines

NO Dopamine Antagonists

73
Q

CNS activity anesthetic considerations

A

Risks for AMS

Confusion

Hallucinations

Somnolence

Insomnia

Involuntary movements

Dystonia

74
Q

Seizures come from the

A

Cortical gray matter

75
Q

Possible symptoms of seizure disorders

A

Altered Awareness

LOC

Abnormal Sensation

Focal involuntary movements

Convulsions (widespread violent involuntary muscle contractions)

76
Q

Common causes of seizures in PEDS

A

Fever

Congenital disorders

Birth injury

Idiopathic

77
Q

Common causes of seizures in ADULTS

A

Cerebral Trauma

ETOH Withdrawl

Tumors

Stroke

Unknown

78
Q

Epilepsy is defined as

A

Recurrent 2+ not related to stressors

> 24 hours apart

Chronic

Idiopathic

May be caused by malformations, strokes, & tumors

Various types

79
Q

An Aura is

A

Something that precedes seizure

Can be sensory, autonomic, or psychic sensation or motor activity

80
Q

How long can the postictal state last

A

Minutes to hours

81
Q

Postictal state is characterized by

A

Deep sleep

HA

Confusion

Muscle soreness

82
Q

How is status epileptics defined

A

Seizure lasting >5-10 minutes or serial seizures without return to baseline

83
Q

Most seizures appear

A

Neurologically normal between seizures and antiepileptic drugs may cause sedation

84
Q

Most seizures only last

85
Q

If there is no known cause or acute symptomatic (breakthrough seizure) then give

A

Anti seizure medication

Commonly give fosphenytoin, Keppra, calorific acid, Propofol

86
Q

What increases the chances of seizure activity

A

Sleep wake pattern changes w/ anesthesia

Anesthetic

Electrolyte abnormalities

Hypoglycemia

Medication withdrawl

Changing anti seizure regimen

Age

Hyperventilation

87
Q

Factors promoting spread of seizure foci

A

Serum glucose

PaO2, PaCO2, pH

Electrolyte & metabolic imbalance (increase sodium & calcium; blocked potassium channels)

Endocrine function

Stress

Fatigue

88
Q

Hypoalbuminemia ________concentrations of free anti seizure drugs

89
Q

Anti-seizure medication induce

A

Hepatic p450 enzyme

90
Q

Anti-seizure medications interacts with

A

Various receptors & NT

91
Q

Anti-seizure medications requires an increase in these medications

A

Propofol

Thiopental

Midazolam

Opioids

Non depolarizing MR

92
Q

MOA of Anti-seizure medications

A

Alters Na, K, Ca currents across membranes

Alter synaptic activity of inhibitory NT

93
Q

What 2 medications treat tonic clonic status epilepticus

A

Lorazepam

Diazepam

94
Q

Broad spectrum antiseizure medications

A

Valproic Acid

Clonazepam

95
Q

Antiseizure adjuncts

A

Lamotrigine

Gabapentin

96
Q

This drug class is used in short term treatment of acute seizure, status epilepticus & ETOH withdrawal

A

Benzodiazepines

97
Q

These two medications are particularly effective for status epilepticus

A

Diazepam

Nasal midazolam

98
Q

________for local anesthetic toxicity

0.1mg/kg IV Q 10-15min MAX DOSE 30mg

99
Q

Epilepsy & myoclonic seizure treated with this may cause tolerance if treated with this

A

Clonazepam

100
Q

Benzodiazepines are a ___________allosteric modulator of___________

A

Positive; GABA inhibition

101
Q

Adverse effects of Benzodiazepines

A

Ataxia

Hyperactivity

Irritability

Personality change

Skeletal muscle incoordination

Sedation

Tolerance

Withdrawal seizures w/abrupt discontinuation

102
Q

Phenobarbital is a

A

Barbiturate

103
Q

Phenobarbital is _______acting & effective for_________

A

Long acting

Most seizures

104
Q

Phenobarbital limits________& _____________

A

Spread of activity & increases seizure threshold

105
Q

MOA of barbiturates

A

Increased GABA inhibition

Decreased glutamate excitation

Depressed sensory, motor cortex & cerebellum

106
Q

Why is phenobarbital rarely used

A

Cognitive & behavioral side effects

107
Q

Adverse effects of Phenobarbital

A

Sedation (adults)

Hyperactivity (PEDS)

Depression

Slowed ability to process tasks

Teratogenicity

Fetal malformations

Respiratory depression

108
Q

Gabapentin is structurally related to

A

GABA but has NO EFFECT on GABA binding, uptake & metabolism

Presence of Gabapentin binding sites in brain

Binds Ca channels (inhibits excitatory NT release)

109
Q

Adverse effects of Gabapentin

A

Sedation

Drowsiness

Ataxia

Dizziness

Vertigo

110
Q

Keppra is used to treat

A

Myoclonic epilepsy, partial & generalized seizures

111
Q

Dose of Keppra

A

500-1000mg IV

Dilute IV solution in 100mL NS/LR

Infuse over 15min

112
Q

What is the MAYBE of Keppra MOA

A

May inhibit Ca channels & decrease NT release

May increase GABA inhibition

113
Q

Perioperetive considerations of Keppra

A

Seizure prophylaxis during crani

No serum level Monitoring

Given at start of surgery

114
Q

Adverse effects of Keppra

A

HA
Increased BP
Somnolence & sedation

115
Q

Valproic acid is often used to treat

A

All generalized & convulsive epilepsies

116
Q

MOA For Valproic acid

A

Limits sustained repetitive neuronal firing

May increase GABA levels

Mimics GABA

Inhibits Na & Ca channels (membrane stabilization)

117
Q

Adverse effects of Valproic Acid

A

Black box- fatal hepatotoxicity (esp. under 2 years)

Teratogenicity-malformations

N/C & dyspepsia

Increased bleeding time

Thrombocytopenia

Sedation

Enzyme inhibition

118
Q

Phenytoin is used to treat

A

Partial & generalized seizures

119
Q

Phenytoin MOA

A

Na membrane transport regulation (promoted Ed flux & decreased influx) in motor cortex neurons

Stabilizes neuronal membrane

120
Q

Phenytoin therapeutic range

A

10-20 mcg/mL

Slow IV Infusion (<50 mg/min)

121
Q

Black box warning for Phenytoin

A

Risk HOTN & arrhythmias (asystole)

122
Q

Adverse effects of Phenytoin

A

CNS toxicity (>20mcg/mL)

Peripheral neuropathy

Gingival hyperplasia

Inhibition of insulin secretion leading to hyperglycemia

Hepatotoxicity

Skin reactions

Increased metabolism of NDMRs- mild blocking effects at NMJ, up regulation of ACh receptors & increased dose requirements

123
Q

MOA of carbamazepine

A

Stabilizes Na channels in inactivated state

Neuron less excitable

124
Q

Adverse effects of carbamazepine

A

Liver dysfunction

Thrombocytopenia

Dizziness

Vertigo

N/v

125
Q

Black box warning of carbamazepine

A

Fatal dermatological reactions & aplastic anemi

126
Q

MOA of lamotrigine

A

Inhibits release of glutamate

Inhibits (stabilizes) voltage gated Na Channels

127
Q

Adverse effects of lamotrigine

A

Dizziness

Diplopia

Blurred Vision

HA

Sedation

Ataxia

128
Q

Black box for lamotrigine

A

Severe, life threatening rash SJS

129
Q

Ethosuximide (Zarontin) is the drug of choice for

A

Absence (petit mal) epilepsy

130
Q

MOA of Ethosuximide (Zarontin)

A

Block voltage gated Ca conductance in thalami’s neurons

131
Q

Adverse effects of Ethosuximide (Zarontin)

A

GI intolerance (n/v)

Lethargy

Dizzy

Ataxia

Hyponatremia

Bone marrow suppression

132
Q

Analeptics do what?

A

Stimulate the CNS & used to treat a variety of conditions with CNS depression

133
Q

MOA of analeptics

A

Block inhibition or enhance excitation

134
Q

Analeptics have ______influence with a ___________maintained

A

Excitatory & inhibitory influences

Narrow range

135
Q

Amphetamine & methylphenidate are used to treat

A

ADHD, narcolepsy & obesity
( cause euphoria)

136
Q

MOA of Amphetamine & methylphenidate

A

NE release from central & peripheral nerve terminals

Stimulate respiratory centers

Increases alertness & concentration

Increases muscle strength

137
Q

Amphetamine & methylphenidate anesthetic considerations

A

Increases BP

Tachy

Reflex Brady

Bronchodilation

Acute intoxication leading to increased MAC

chronic exposure decreases MAC

Catecholamine depletion (use DIRECT acting vasopressors like epi, norepi & Vaso)

138
Q

DoXapram is used to treat

A

COPD related acute hypercapnia & postop respiratory depression & drug induced CNS depression

139
Q

MOA of Doxapram

A

Stimulates medulla through peripheral carotid chemoreceptors

Increases TV

Increases O2 consumption

140
Q

Adverse effects of Doxapram

A

HTN, Tachy, Arrhythmias

Increased body temp & vomiting

141
Q

Methylxanthines include

A

Caffeine, theophylline, & theobromine

142
Q

MOA of Methylxanthines

A

Antagonism at adenosine receptors

Phosphodiesterase inhibition

143
Q

Methylxanthines physiological effects

A

CNS stimulation

Diuretics

Increased myocardial contractility

Smooth muscle relaxation

144
Q

Methylxanthines uses

A

Primary apnea r/t prematurity

Bronchospasm r/t asthma

Postural puncture HA (caffeine)

Promote wakefulness

Pharmacology Exam 3 (3 decks)

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