Exam 3 Flashcards

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
Q

dissemination in time (DIT)

A

time between evidence of new lesions on subsequent MRIs (damaged that has happened more than once)

26
Q

dissemination in space (DIS)

A

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
Q

CIS (clinically isolated syndrome)

A

first demyelinating events, most pts with this develop MS within 20 years

28
Q

EDSS (expanded disability status scale)

A

1-4: independent
5-7: still mobile but need assistance (cane, walker, wheelchair)
8-9: bedridden
10: death

29
Q

tx of acute MS attacks

A

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
Q

what pts must be tested for JCV before starting meds for MS

A

All of them

31
Q

Varicella should be given to what pts who have MS

A

those who have not had chicken pox

32
Q

how does phenytoin, carbamazepine, valproate (and some other anticonvulsants) work? (MOA)

A

by binding and stabilizing the inactivated state of sodium channels

33
Q

type of PK phenytoin has on graph

A

non-linear
-because its elimination is dose dependent

34
Q

important SE of phenytoin

A

arrhythmias
blurry vision
ataxia
GI upset
hirsutism (hair growth)
skin rashes

35
Q

phenytoin is metabolized by what?

A

CYP P450 enzymes
-this can increase the metabolism of other drugs such as carbamazepine

36
Q

tricyclic compound structure is characteristic of what drugs

A

drugs used to treat Bipolar depression

37
Q

carbamazepine SE (or toxicity, as named by Yang)

A

blurry vision
ataxia
GI upset
sedation at high doses
SJS
DRESS

38
Q

lacosamide (Vimpat) MOA

A

enhances activation of voltage gated Na+ channels

39
Q

lacosamide SE (or toxicity, as named by Yang)

A

skin reactions/rashes
cardiac risks (PR interval prolongation)
visual disturbances

40
Q

barbiturates and benzos bind which site on GABAA receptor?
-active site
-allosteric site
-binding site
-gamma site

A

allosteric site

41
Q

phenobarbital MOA

A

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
Q

primidone MOA

A

similar to phenytoin, binds inactivated Na+ channels

43
Q

SE/toxicity of phenobarbital

A

sedation
physical dependence

44
Q

diazepam (Valium) and clonazepam (Klonopin) MOA

A

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
Q

SE/toxicity of benzos

A

sedation
physical dependence

46
Q

diazepam is used in

A

tonic-clonic status epilepticus

47
Q

clonazepam is used in

A

acute treatment of epilepsy and absence seizures

48
Q

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

A

b

49
Q
A