Exam 3 Flashcards

(49 cards)

1
Q

medulla fxn

A

involuntary (autonomic fxn)
-breathing, cardiac, vasomotor response, reflexes (like coughing)

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2
Q

pons fxn

A

relays signal from forebrain to cerebellum

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3
Q

midbrain fxn

A

SN: delivers dopamine to striatum
-some voluntary movement control and some cognitive fxn

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4
Q

cerebellum fxn

A

motor coordination for smooth movements

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5
Q

cortex fxn

A

processing and interpreting information

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6
Q

thalamus fxn

A

relay signals to and from cortex

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7
Q

astrocytes role

A

-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

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8
Q

oligodendrocytes role

A

-produce myelin sheath that insulates axons

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9
Q

microglia role

A

-provides growth factors
-clears debris by phagocytosis (similar to macrophages)
-can cause inflammatory response that may damage nearby neurons

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10
Q

GABA (aa) role in CNS disorders

A

-major inhibitory neurotransmitter in the brain (CNS depressants)
-lowers neuronal excitability by increasing Cl- ions into the neuron

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11
Q

glycine (aa) role in CNS disorders

A

similar to GABA but acts in the spinal cord

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12
Q

glutamate (aa) role in CNS disorders

A

-major excitatory aa neurotransmitter in the brain
-excess glutamate can lead to excess Ca2+ influx into the neuron, causing damage

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13
Q

do GABA and glutamate oppose each other or work together

A

sort of oppose each other (act as an on and off switch to regulate each other)

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14
Q

acetylcholine (non-aa)

A

-both muscarinic and nicotinic receptors
-drug include cholinesterase inhibitors like Aricept (for Alzheimer’s)

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15
Q

loss of dopamine signaling happens in what disease

A

PD

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16
Q

excessive dopamine signaling happens in what disease

A

schizophrenia

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17
Q

NET inhibitors treat what disease state

A

depression

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18
Q

Common sx of MS: just be familiar with these
-keep in mind no 2 MS patients will have the same Sx

A

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

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19
Q

MS drugs that only act in periphery (including BBB)

A

IFN beta
glatiramer acetate
natalizumab
mitoxantrone
teriflunomide
clabridine
rituximab (ocralizumab)
ATL1102 (ASO)

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20
Q

drugs that have PML as AE (or increase risk of PML)

A

-fingolimod
-dimethyl fumarate, diroximel fumarate, monomethyl fumarate
-natalizumab

21
Q

drugs that act in periphery and CNS

A

-fingolimod, siponimod, ozanimod, ponesimod
-dimethyl fumarate, diroximel fumarate and monomethyl fumarate

22
Q

drugs that act at BBB

A

-IFN beta
-natalizumab
-ATL1102 (ASO)

23
Q

drugs that act via cytotoxic effect

A

-mitoxantrone
-teriflunomide
-clabridine

24
Q

only drug used to treat PPMS

A

rituximab (ocrelizumab)

25
dissemination in time (DIT)
time between evidence of new lesions on subsequent MRIs (damaged that has happened more than once)
26
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)
27
CIS (clinically isolated syndrome)
first demyelinating events, most pts with this develop MS within 20 years
28
EDSS (expanded disability status scale)
1-4: independent 5-7: still mobile but need assistance (cane, walker, wheelchair) 8-9: bedridden 10: death
29
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)
30
what pts must be tested for JCV before starting meds for MS
All of them
31
Varicella should be given to what pts who have MS
those who have not had chicken pox
32
how does phenytoin, carbamazepine, valproate (and some other anticonvulsants) work? (MOA)
by binding and stabilizing the inactivated state of sodium channels
33
type of PK phenytoin has on graph
non-linear -because its elimination is dose dependent
34
important SE of phenytoin
arrhythmias blurry vision ataxia GI upset hirsutism (hair growth) skin rashes
35
phenytoin is metabolized by what?
CYP P450 enzymes -this can increase the metabolism of other drugs such as carbamazepine
36
tricyclic compound structure is characteristic of what drugs
drugs used to treat Bipolar depression
37
carbamazepine SE (or toxicity, as named by Yang)
blurry vision ataxia GI upset sedation at high doses SJS DRESS
38
lacosamide (Vimpat) MOA
enhances activation of voltage gated Na+ channels
39
lacosamide SE (or toxicity, as named by Yang)
skin reactions/rashes cardiac risks (PR interval prolongation) visual disturbances
40
barbiturates and benzos bind which site on GABAA receptor? -active site -allosteric site -binding site -gamma site
allosteric site
41
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)
42
primidone MOA
similar to phenytoin, binds inactivated Na+ channels
43
SE/toxicity of phenobarbital
sedation physical dependence
44
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)
45
SE/toxicity of benzos
sedation physical dependence
46
diazepam is used in
tonic-clonic status epilepticus
47
clonazepam is used in
acute treatment of epilepsy and absence seizures
48
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
49