Week 13/14 Neuro Flashcards
what is main CNS inhibitory neurotransmitter?
GABA
what is main CNS excitatory neurotransmitter?
Glutamate
what is a focal (partial) seizure?
localized in one cerebral hemisphere
what is generalized seizure?
involves both cerebral hemispheres
AE of antiepileptic
- neurotoxicity, sedation, ataxia, confusion, dizziness,
- many DDI
therapeutic concerns with epileptic drugs
- sedation, dizziness, ataxia
- skin rashes - massage may exacerbate
- bone marrow depression and Vit K deficiency - check for bruising/bleeding
3 subtypes associated with ADHD
inattentive, hyperactivity, and impulsivity
stimulant medication MOA
block re-uptake of NE, dopamine, or both
atomoxetine (Strattera) MOA
SNRI - selective NE reuptake inhibitor - blocks NE reuptake
methylphenidate (Ritalin, Concerta) MOA
stimulant - blocks dopamine and NE reuptake
amphetamine (Adderral) MOA
stimulant - blocks dopamine and NE reuptake
common AE of stimulants
decreased appetite/weight loss, stomachache, insomnia, HA, rebound symptoms, jitteriness
boxed warning of stimulants
safe if no baseline CV disease
report signs of abuse/dependence
atomoxetine (Strattera) AE
similar to stimulants (decreased appetite/weight loss, stomachache, insomnia, HA, rebound symptoms, jitteriness) but more fatigue, sedation, and dizziness
- monitor mood changes
Parkinson’s is related to a decrease in what?
dopamine
what is dyskinesia
uncontrolled, involuntary movements
levodopa-carbidopa MOA
Parkinson’s
l-dopa is a precursor to dopamine and can cross BBB and carbidopa stops the breakdown of l-dopa in the periphery so more l-dopa can cross BBB to be converted to dopamine
levodopa-carbidopa AE
Parkinson’s
motor disturbances, end dose wearing off, delayed on, freezing
MAO-B inhibitor MOA
Parkinson’s
inhibit monoamine oxidase B (MAO B) which breaks down dopamine
MAO-B inhibitor AE
Parkinson’s
serotonin syndrome, watch for DDI
COMT inhibitor MOA
Parkinson’s
inhibit COMT which breaks down l-dopa
COMT inhibitor AE
Parkinson’s
involuntary movements, nausea
dopamine agonists MOA
Parkinson’s
bind to and agonize dopamine receptor
dopamine agonists AE
Parkinson’s
drowsiness, dizziness, syncope
2 options for MS treatment
DMT - disease-modifying therapies and symptom management
Interferon B AE and what needs to be monitored
MS
- flu-like symptoms, HA, injection site reaction
- fatigue, depression, pain, nausea, increase LFT, myalgia
- monitor for neuropsychiatric changes, drug-induced hypothyroidism, worsening cardiac function
Glatiramer acetate MOA
MS
reduce autoimmune response to myelin by reducing T-cell response against myelin
Glatiramer acetate AE
MS
injection site reaction, rash, vasodilation, dyspnea, chest pain
Sphingosine 1-Phosphate (S1P) receptor modulator MOA
MS
decrease inflammation
Sphingosine 1-Phosphate (S1P) receptor modulator AE and what should you monitor
MS
HA, increase LFT (liver function tests), macular edema, infection
- monitor bradycardia
dimethyl fumarate AE
MS GI (N/V/D, abdominal pain) and flushing - usually improve with time
common ending for monoclonal antibodies
-mab
monoclonal antibodies MOA
MS
decrease inflammation in CNS
monoclonal antibodies AE and what should you monitor
MS
infusion-related reactions, HA, fatigue, arthralgia
- monitor for infection
serious risk associated with monoclonal antibodies (-mab), dimethyl fumarate, and SP1 receptor modulators
PML - progressive multifocal leukoencephalopathy
PML s/sx
altered mental status (AMS), aphasia, ataxia, hemiparesis, hemiplegia, visual disturbance, seizures
what is the most common and disabling MS symptom
fatigue
what neurotransmitter is depleted with Alzheimer’s
ACh
cholinesterase inhibitor MOA
Alzheimer’s
- inhibits AChesterase which breaks down ACh = increase ACh
cholinesterase inhibitor AE
Alzheimer’s
cholinergic AE
- nausea, vomiting
- SLUDGE
NMDA Antagonists MOA
Alzheimer’s
antagonizes NMDA receptor = stops activation by glutamate = decreases excitation and neuronal death
NMDA Antagonists AE
Alzheimer’s
- usually well tolerated; monitor for falls
what should Alzheimer patients not be taking?
anticholinergic drugs
tizanidine MOA
a2 agonist for spasticity
- bind to a2 receptors in CNS to decrease the release of excitatory neurotransmitters
tizanidine AE
drowsiness, dizziness, asthenia (weakness)
Flexeril AE
spasticity
- sedation and dizziness
- Beer’s list
Baclofen MOA
spasticity
- inhibit effect on alpha motor neurons through inhibition of excitatory neurons
Baclofen AE
spasticity
- abruptly stopping med can lead to: high fever, altered mental status, rebound spasticity, rhabdo
- CNS depressant (sedation, CV depression), muscle weakness, TBI in older adults
therapeutic concerns with antispasticity/muscle relaxant drugs
sedation and weakness
