Neurologically Active drugs Flashcards
(145 cards)
1
Q
Movement disorders are classified as either
A
Hypo or Hyper kinetic
2
Q
Voluntary movements come from
A
Corticospinal (pyramidal) tracts
Basal Ganglia
Cerebellum (motor coordination center)
3
Q
Extrapyramidal system is modulated by
A
Basal ganglia
Cerebellum
Cerebral Cortex
4
Q
In the Extrapyramidal system, direct output is through the
A
Cerebral Coretx
5
Q
Extrapyramidal system involves
A
Involuntary Actions
Reflexes
Locomotion
Complex movements
Postural control
Neural lesions causing movement (Extrapyramidal disorders)
6
Q
Notable characteristics of Parkinson’s Disease
A
Resting tremor
Stiffness & Rigidity
Bradykinesia
Gait & Postural Instability
7
Q
Juvenile Parkinsonism occurs
A
Early onset 21-40 years
8
Q
General Parkinson’s occurs
A
Mean age of 57 years
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
10
Q
Parkinson’s is often characterized as this in the system
A
Lewy Bodies
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
12
Q
Dopamine is ______in the Extrapyramidal system
A
Inhibitory
13
Q
Acetylcholine is ______in the Extrapyramidal system
A
Excitatory
14
Q
In Parkinson’s, there is generally a loss of______action and an overproduction of ________
A
Inhibitory; Excitatory
15
Q
80% of the brains dopamine is in the
A
Basal Ganglia
16
Q
In Parkinson’s, the percentage of dopamine in the basal ganglia can be as low as
A
10%
17
Q
Excess excitatory cholinergic activity can cause
A
Progressive Tremor
Muscle Rigidity
Bradykinesia
Postural Disturbances
18
Q
Common treatments of Parkinson’s
A
Restore Dopamine function
Levodopa/ Carbidopa
Dopamine Agonists
MAO-B inhibitors
Amantadine
19
Q
Stereotactic deep brain stimulation targets the
A
Thalamus
Subthalamic Nucleus
Globus Pallidus
20
Q
Autonomic dysfunctions of Parkinson’s
A
Ortho HOTN
Poor temperature control
Sialorrhea
Maintain Volume Status
21
Q
Parkinson’s suffer from pulmonary dysfunction such as
A
Bradykinesia
Rigidity of Respiratory Muscles
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
23
Q
Parkinson’s can cause cognitive impairment, leading to
A
Postop delirium
24
Q
GABA inhibition in the basal ganglia can worsen or abolish
A
Microelectrode recordings (MER)
25
What medication should be avoided if testing for tremors
Beta Blockers
26
When should DBS be discontinued?
15 minutes before MER
27
Dexmedetomidine may abolish
MER, HOTN, & paradoxical agitation
28
Propofol depresses
Neuronal discharge & induced dyskinesia
29
Fentanyl & Remifentanil May
Worsen rigidity & suppress tremor
30
Benzodiazepines May
Abolish MER, suppress tremor & induce dyskinesia
31
Levodopa crosses
BBB & is a dopamine precursor
32
Levodopa is converted by
Enzyme to dopamine in basal ganglia
( Dopa decarboxylase)
33
Can dopamine pass BBB?
No it does not and it’s elevated levels can cause side effects
34
Of levodopa, ___% is rapidly converted to dopamine during___________
95%; first hepatic pass
35
Levodopa metabolites are converted to ________&_________
Dopamine & Homovanillic Acid which metabolizes further into NE & E
Requires adequate levels of COMT to metabolize excess catecholamines (methionine from diet)
36
Levodopa/Carbidopa inhibits______in the peripheral tissues
Decarboxylase
37
Levodopa/Carbidopa inhibits
Levodopa breakdown
(Levodopa + decarboxylase inhibitors)
38
Levodopa/ Carbidopa maximizes
The amount of levodopa reaching the brain before conversion to dopamine, which allows lower levodopa dose
39
Levodopa adverse effects on GI
N/V-dopamine stimulation of CRT
Carbidopa may decrease N/V
Avoid dopamine antagonists antiemetics (promethazine & metoclopramide)
40
Levodopa adverse effects on Endocrine
Inhibits prolactin secretion
Increased aldosterone leading to hypokalemia
41
Levodopa adverse effects on CV
Potential adrenergic receptor activation from dopamine, Epi & NE (increased inotropy)
ORTHO HOTN
Tachy, PVCs/PACs, Afib, VTach
Skin flushing
42
Levodopa adverse effects on neuromuscular
Abnormal involuntary movements (facial tics & grimacing, rocking of extremities & trunk)
Irregular gasps (diaphragmatic dyskinesia)
Change in mobility
43
Levodopa psychiatric adverse effects
Confusion
Hallucination
Paranoia
Impulsive/ compulsive behavior
AVOID HALDOL
44
What is Parkinsonism-Hyperpyrexia Syndrome
Life threatening related to abrupt withdrawal or dose reduction
Resembles Neuroleptic Malignant Syndrome
45
Signs and symptoms of Parkinsonism Hyperpyrexia Syndrome
Rigidity
Pyrexia
Autonomic Instability
Depressed Consciousness
46
Risk for Parkinsonism Hyperpyrexia Syndrome
DVT/PE
Renal Failure
Aspiration PNA
47
Treatment of Parkinsonism Hyperpyrexia Syndrome
Give antiparkinsonian therapy
Levodopa PO or NGT
Supportive measures
48
Levodopa adverse effects with antipsychotics
Antagonize effects of dopamine
49
Levodopa adverse effects with MAOIs
Interfere with inactivation of dopamine causing HTN & hyperthermia
50
Levodopa adverse effects with Anticholinergic drugs
Synergism improves symptoms
51
Levodopa adverse effects with Vitamin B6
enhances decarboxylase activity (levodopa metabolism)
52
Common dopamine agonists
Bromocriptine
Pramipexole
Ropinirole
Rotigotine
53
Characteristics of Dopamine Agonists
Mimic Dopamine at receptor site
Synthetic
Don’t require transformation or transport across BBB
54
Adverse effects of Dopamine Agonists
Hallucinations
HOTN
Dyskinesia
Pulmonary Fibrosis
Vertigo
Nausea
55
Amantadine is also a/an
Antiviral for influenza A
56
Amantadine can
Improve PD symptoms like muscle rigidity & Bradykinesia
57
Adverse effects of Amantadine
Anticholinergic effects
Peripheral edema
Confusion
Psychosis
58
MAO-B inhibitors…
Breaks down dopamine in the CNS
59
MAO-B, Selegine, is
Highly selective
Irreversible Inhibitor
Doesn’t alter peripheral metabolism or NE
60
MAO-B adverse effects include
Insomnia
Confusion
Hallucination
Paranoia
61
Rasa filing is a
MAO-A & MAO-B
62
COMT inhibitors examples are
Tolcapone
Entacapone
63
COMT is partially responsible for the ______________________
Peripheral breakdown of levodopa
64
COMT Inhibitors block
Enzyme activity in the GIT
65
COMT inhibitors slow
Elimination of Carbidopa- Levodopa
66
COMT inhibitors adverse effects
Worsened Dyskinesia
Nausea/ Diarrhea
Hepatotoxicity
Rhabdomyolysis
67
Anticholinergic drug medications are
Benztropine
Trihexyphenidyl
68
Anticholinergic blocks the effects of
Excitatory ACh
69
When Anticholinergics are used, excitatory ACh is blocked, which…
Corrects balance between DA & ACh
Controls tremors
Decreases excess salvation
Minimal effects on muscle rigidity & Bradykinesia
70
Adverse effects of Anticholinergics
Confusion
Hallucination
Sedation
Mydriasis
Ileus
Urinary Retention
71
Anti-Parkinson’s medications are usually_________morning of surgery for DBS
Held
72
In the Parkinson’s population DO NOT GIVE THESE FOR PONV
NO phenothiazines
NO Dopamine Antagonists
73
CNS activity anesthetic considerations
Risks for AMS
Confusion
Hallucinations
Somnolence
Insomnia
Involuntary movements
Dystonia
74
Seizures come from the
Cortical gray matter
75
Possible symptoms of seizure disorders
Altered Awareness
LOC
Abnormal Sensation
Focal involuntary movements
Convulsions (widespread violent involuntary muscle contractions)
76
Common causes of seizures in PEDS
Fever
Congenital disorders
Birth injury
Idiopathic
77
Common causes of seizures in ADULTS
Cerebral Trauma
ETOH Withdrawl
Tumors
Stroke
Unknown
78
Epilepsy is defined as
Recurrent 2+ not related to stressors
>24 hours apart
Chronic
Idiopathic
May be caused by malformations, strokes, & tumors
Various types
79
An Aura is
Something that precedes seizure
Can be sensory, autonomic, or psychic sensation or motor activity
80
How long can the postictal state last
Minutes to hours
81
Postictal state is characterized by
Deep sleep
HA
Confusion
Muscle soreness
82
How is status epileptics defined
Seizure lasting >5-10 minutes or serial seizures without return to baseline
83
Most seizures appear
Neurologically normal between seizures and antiepileptic drugs may cause sedation
84
Most seizures only last
1-2 min
85
If there is no known cause or acute symptomatic (breakthrough seizure) then give
Anti seizure medication
Commonly give fosphenytoin, Keppra, calorific acid, Propofol
86
What increases the chances of seizure activity
Sleep wake pattern changes w/ anesthesia
Anesthetic
Electrolyte abnormalities
Hypoglycemia
Medication withdrawl
Changing anti seizure regimen
Age
Hyperventilation
87
Factors promoting spread of seizure foci
Serum glucose
PaO2, PaCO2, pH
Electrolyte & metabolic imbalance (increase sodium & calcium; blocked potassium channels)
Endocrine function
Stress
Fatigue
88
Hypoalbuminemia ________concentrations of free anti seizure drugs
Increases
89
Anti-seizure medication induce
Hepatic p450 enzyme
90
Anti-seizure medications interacts with
Various receptors & NT
91
Anti-seizure medications requires an increase in these medications
Propofol
Thiopental
Midazolam
Opioids
Non depolarizing MR
92
MOA of Anti-seizure medications
Alters Na, K, Ca currents across membranes
Alter synaptic activity of inhibitory NT
93
What 2 medications treat tonic clonic status epilepticus
Lorazepam
Diazepam
94
Broad spectrum antiseizure medications
Valproic Acid
Clonazepam
95
Antiseizure adjuncts
Lamotrigine
Gabapentin
96
This drug class is used in short term treatment of acute seizure, status epilepticus & ETOH withdrawal
Benzodiazepines
97
These two medications are particularly effective for status epilepticus
Diazepam
Nasal midazolam
98
________for local anesthetic toxicity
0.1mg/kg IV Q 10-15min MAX DOSE 30mg
Diazepam
99
Epilepsy & myoclonic seizure treated with this may cause tolerance if treated with this
Clonazepam
100
Benzodiazepines are a ___________allosteric modulator of___________
Positive; GABA inhibition
101
Adverse effects of Benzodiazepines
Ataxia
Hyperactivity
Irritability
Personality change
Skeletal muscle incoordination
Sedation
Tolerance
Withdrawal seizures w/abrupt discontinuation
102
Phenobarbital is a
Barbiturate
103
Phenobarbital is _______acting & effective for_________
Long acting
Most seizures
104
Phenobarbital limits________& _____________
Spread of activity & increases seizure threshold
105
MOA of barbiturates
Increased GABA inhibition
Decreased glutamate excitation
Depressed sensory, motor cortex & cerebellum
106
Why is phenobarbital rarely used
Cognitive & behavioral side effects
107
Adverse effects of Phenobarbital
Sedation (adults)
Hyperactivity (PEDS)
Depression
Slowed ability to process tasks
Teratogenicity
Fetal malformations
Respiratory depression
108
Gabapentin is structurally related to
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
Adverse effects of Gabapentin
Sedation
Drowsiness
Ataxia
Dizziness
Vertigo
110
Keppra is used to treat
Myoclonic epilepsy, partial & generalized seizures
111
Dose of Keppra
500-1000mg IV
Dilute IV solution in 100mL NS/LR
Infuse over 15min
112
What is the MAYBE of Keppra MOA
May inhibit Ca channels & decrease NT release
May increase GABA inhibition
113
Perioperetive considerations of Keppra
Seizure prophylaxis during crani
No serum level Monitoring
Given at start of surgery
114
Adverse effects of Keppra
HA
Increased BP
Somnolence & sedation
115
Valproic acid is often used to treat
All generalized & convulsive epilepsies
116
MOA For Valproic acid
Limits sustained repetitive neuronal firing
May increase GABA levels
Mimics GABA
Inhibits Na & Ca channels (membrane stabilization)
117
Adverse effects of Valproic Acid
Black box- fatal hepatotoxicity (esp. under 2 years)
Teratogenicity-malformations
N/C & dyspepsia
Increased bleeding time
Thrombocytopenia
Sedation
Enzyme inhibition
118
Phenytoin is used to treat
Partial & generalized seizures
119
Phenytoin MOA
Na membrane transport regulation (promoted Ed flux & decreased influx) in motor cortex neurons
Stabilizes neuronal membrane
120
Phenytoin therapeutic range
10-20 mcg/mL
Slow IV Infusion (<50 mg/min)
121
Black box warning for Phenytoin
Risk HOTN & arrhythmias (asystole)
122
Adverse effects of Phenytoin
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
MOA of carbamazepine
Stabilizes Na channels in inactivated state
Neuron less excitable
124
Adverse effects of carbamazepine
Liver dysfunction
Thrombocytopenia
Dizziness
Vertigo
N/v
125
Black box warning of carbamazepine
Fatal dermatological reactions & aplastic anemi
126
MOA of lamotrigine
Inhibits release of glutamate
Inhibits (stabilizes) voltage gated Na Channels
127
Adverse effects of lamotrigine
Dizziness
Diplopia
Blurred Vision
HA
Sedation
Ataxia
128
Black box for lamotrigine
Severe, life threatening rash SJS
129
Ethosuximide (Zarontin) is the drug of choice for
Absence (petit mal) epilepsy
130
MOA of Ethosuximide (Zarontin)
Block voltage gated Ca conductance in thalami’s neurons
131
Adverse effects of Ethosuximide (Zarontin)
GI intolerance (n/v)
Lethargy
Dizzy
Ataxia
Hyponatremia
Bone marrow suppression
132
Analeptics do what?
Stimulate the CNS & used to treat a variety of conditions with CNS depression
133
MOA of analeptics
Block inhibition or enhance excitation
134
Analeptics have ______influence with a ___________maintained
Excitatory & inhibitory influences
Narrow range
135
Amphetamine & methylphenidate are used to treat
ADHD, narcolepsy & obesity
( cause euphoria)
136
MOA of Amphetamine & methylphenidate
NE release from central & peripheral nerve terminals
Stimulate respiratory centers
Increases alertness & concentration
Increases muscle strength
137
Amphetamine & methylphenidate anesthetic considerations
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
DoXapram is used to treat
COPD related acute hypercapnia & postop respiratory depression & drug induced CNS depression
139
MOA of Doxapram
Stimulates medulla through peripheral carotid chemoreceptors
Increases TV
Increases O2 consumption
140
Adverse effects of Doxapram
HTN, Tachy, Arrhythmias
Increased body temp & vomiting
141
Methylxanthines include
Caffeine, theophylline, & theobromine
142
MOA of Methylxanthines
Antagonism at adenosine receptors
Phosphodiesterase inhibition
143
Methylxanthines physiological effects
CNS stimulation
Diuretics
Increased myocardial contractility
Smooth muscle relaxation
144
Methylxanthines uses
Primary apnea r/t prematurity
Bronchospasm r/t asthma
Postural puncture HA (caffeine)
Promote wakefulness
145
BZ
