Exam 3 Flashcards
medulla fxn
involuntary (autonomic fxn)
-breathing, cardiac, vasomotor response, reflexes (like coughing)
pons fxn
relays signal from forebrain to cerebellum
midbrain fxn
SN: delivers dopamine to striatum
-some voluntary movement control and some cognitive fxn
cerebellum fxn
motor coordination for smooth movements
cortex fxn
processing and interpreting information
thalamus fxn
relay signals to and from cortex
astrocytes role
-provide neurons with growth factors and antioxidants
-remove excess glutamate (excess glutamate can cause excitotoxicity that can cause harm to neurons, astrocytes regulate this)
-support BBB
oligodendrocytes role
-produce myelin sheath that insulates axons
microglia role
-provides growth factors
-clears debris by phagocytosis (similar to macrophages)
-can cause inflammatory response that may damage nearby neurons
GABA (aa) role in CNS disorders
-major inhibitory neurotransmitter in the brain (CNS depressants)
-lowers neuronal excitability by increasing Cl- ions into the neuron
glycine (aa) role in CNS disorders
similar to GABA but acts in the spinal cord
glutamate (aa) role in CNS disorders
-major excitatory aa neurotransmitter in the brain
-excess glutamate can lead to excess Ca2+ influx into the neuron, causing damage
do GABA and glutamate oppose each other or work together
sort of oppose each other (act as an on and off switch to regulate each other)
acetylcholine (non-aa)
-both muscarinic and nicotinic receptors
-drug include cholinesterase inhibitors like Aricept (for Alzheimer’s)
loss of dopamine signaling happens in what disease
PD
excessive dopamine signaling happens in what disease
schizophrenia
NET inhibitors treat what disease state
depression
Common sx of MS: just be familiar with these
-keep in mind no 2 MS patients will have the same Sx
visual problems
numbness/tingling
fatigue
difficulty walking/gait problems/falls/ataxia
pain
spasticity
stiffness
vertigo/dizziness
sexual dysfunction
bladder problems
constipation
depression or mood changes
MS drugs that only act in periphery (including BBB)
IFN beta
glatiramer acetate
natalizumab
mitoxantrone
teriflunomide
clabridine
rituximab (ocralizumab)
ATL1102 (ASO)
drugs that have PML as AE (or increase risk of PML)
-fingolimod
-dimethyl fumarate, diroximel fumarate, monomethyl fumarate
-natalizumab
drugs that act in periphery and CNS
-fingolimod, siponimod, ozanimod, ponesimod
-dimethyl fumarate, diroximel fumarate and monomethyl fumarate
drugs that act at BBB
-IFN beta
-natalizumab
-ATL1102 (ASO)
drugs that act via cytotoxic effect
-mitoxantrone
-teriflunomide
-clabridine
only drug used to treat PPMS
rituximab (ocrelizumab)
dissemination in time (DIT)
time between evidence of new lesions on subsequent MRIs (damaged that has happened more than once)
dissemination in space (DIS)
lesions in at least two of four MS-typical CNS regions: cortical, preventricular, infratentorial, spinal cord (damage that is in more than one place)
CIS (clinically isolated syndrome)
first demyelinating events, most pts with this develop MS within 20 years
EDSS (expanded disability status scale)
1-4: independent
5-7: still mobile but need assistance (cane, walker, wheelchair)
8-9: bedridden
10: death
tx of acute MS attacks
oral or IV high dose corticosteroid is 1st choice
-methylprednisolone 500-1000mg IV daily for 3-7 days, w/wo oral taper over 1-3 weeks
-if outpatient: oral prednisolone 1250mg QOD for 5 days, no taper (this means 25 50mg tabs - take w food and counsel patients that fatigue is common)
what pts must be tested for JCV before starting meds for MS
All of them
Varicella should be given to what pts who have MS
those who have not had chicken pox
how does phenytoin, carbamazepine, valproate (and some other anticonvulsants) work? (MOA)
by binding and stabilizing the inactivated state of sodium channels
type of PK phenytoin has on graph
non-linear
-because its elimination is dose dependent
important SE of phenytoin
arrhythmias
blurry vision
ataxia
GI upset
hirsutism (hair growth)
skin rashes
phenytoin is metabolized by what?
CYP P450 enzymes
-this can increase the metabolism of other drugs such as carbamazepine
tricyclic compound structure is characteristic of what drugs
drugs used to treat Bipolar depression
carbamazepine SE (or toxicity, as named by Yang)
blurry vision
ataxia
GI upset
sedation at high doses
SJS
DRESS
lacosamide (Vimpat) MOA
enhances activation of voltage gated Na+ channels
lacosamide SE (or toxicity, as named by Yang)
skin reactions/rashes
cardiac risks (PR interval prolongation)
visual disturbances
barbiturates and benzos bind which site on GABAA receptor?
-active site
-allosteric site
-binding site
-gamma site
allosteric site
phenobarbital MOA
binds allosteric site of GABAA receptor to increase duration (as opposed to frequency like we see in diazepam and clonazepam) of Cl- channel opening events (this enhances GABA inhibitory signaling)
primidone MOA
similar to phenytoin, binds inactivated Na+ channels
SE/toxicity of phenobarbital
sedation
physical dependence
diazepam (Valium) and clonazepam (Klonopin) MOA
binds allosteric site of GABAA receptor to increase frequency (as opposed to duration like we see in phenobartbital) of Cl- channel opening events (this enhances GABA inhibitory signaling)
SE/toxicity of benzos
sedation
physical dependence
diazepam is used in
tonic-clonic status epilepticus
clonazepam is used in
acute treatment of epilepsy and absence seizures
Which of the following is true?
a. tiagabine inhibits GABA transaminase
b. gabapentin increases Cl- influx in postsynaptic neurons
c. topiramate is an NMDA receptor antagonist
d. phenytoin is stabilized by the co-administration of carbamazepine
b
