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Therapeutics 3 - Spring 2018 > Exam 3 - Rochet (CNS/MS Drugs) > Flashcards

Exam 3 - Rochet (CNS/MS Drugs) Flashcards

1
Q

3 main parts of brain

A

hindbrain
midgrain
forebrain

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2
Q

main parts of hindbrain

A

medulla

pons, cerebellum

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3
Q

main parts of midbrain

A

substantia nigra (SN)

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4
Q

main parts of forebrain

A

cerebral cortex
basal ganglia (minus SN)
limbic system
diencephalon

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5
Q

what makes up limbic system

A

hippocampus

amygdala

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6
Q

what makes up basal ganglia

A

striatum
globus pallidus
subthalamic nucleus

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7
Q

what makes up the diencephalon

A

thalamus

hypothalamus

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8
Q

is it in the hindbrain, midbrain, forebrain?

medulla

A

hindbrain

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9
Q

is it in the hindbrain, midbrain, forebrain?

substantia nigra

A

midbrain

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10
Q

is it in the hindbrain, midbrain, forebrain?

pons, cerebellum

A

hindbrain

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11
Q

is it in the hindbrain, midbrain, forebrain?

cerebral cortex

A

forebrain

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12
Q

is it in the hindbrain, midbrain, forebrain?

basal ganglia

A

forebrain

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13
Q

is it in the hindbrain, midbrain, forebrain?

limbic system

A

forebrain

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14
Q

is it in the hindbrain, midbrain, forebrain?

diencephalon

A

forebrain

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15
Q

is it in the hindbrain, midbrain, forebrain?

hippocampus

A

in limbic system — therefore in FOREBRAIN

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16
Q

is it in the hindbrain, midbrain, forebrain?

amygdala

A

in limbic system — therefore in FOREBRAIN

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17
Q

is it in the hindbrain, midbrain, forebrain?

hypothalamus

A

in diencephalon — therefore in FOREBRAIN

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18
Q

is it in the hindbrain, midbrain, forebrain?

thalamus

A

in diencephalon — therefore in FOREBRAIN

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19
Q

what is the overall function of medulla

A

autonomic functions

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20
Q

what is overall function of pons

A

a “bridge”

relays signal from forebrain to cerebellum

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21
Q

Pons: relays signal from ______ to _______

A

from forebrain to cerebellum

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22
Q

main function of cerebellum

A

“little brain”

governs motor coordination for producing SMOOTH movements

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23
Q

Medulla does conscious or non-conscious actions?

A

NON-conscious/autonomice

reflexes, respiration, cardiac function etc…

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24
Q

_________ undergoes neurodegeneration in spinocerebellar ataxias

A

cerebellum

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25
Q

Substantia Nigra: Pars Compacta

provides _____ to basal ganglia (supplies _______ to the ______

A

provides INPUT

supplies DOPAMINE to STRIATUM

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26
Q

what are the two parts of substantia nigra

A

pars COMPACTA

or pars RETICULATA

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27
Q

Substantia Nigra: Pars Reticulata
has ______ function
relays signal from _________ to ______

A

OUTPUT function

from basal ganglia; to thalamus

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28
Q

Pars Compacta or Pars Reticulata?

has input function

A

compacta

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29
Q

Pars Compacta or Pars Reticulata?

has output function

A

reticulata

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30
Q

Pars Compacta or Pars Reticulata?

provides signal to basal ganglia

A

compacta

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31
Q

Pars Compacta or Pars Reticulata?

provides signal to thalamus

A

reticulata

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32
Q

Pars Compacta or Pars Reticulata?

supplies dopamine to striatum

A

compacta

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33
Q

Pars Compacta or Pars Reticulata?

involved with voluntary motor control

A

compacta (b/c dopamine)

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34
Q

main function of cortex

A

processing/interpreting information (executive function)

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35
Q

other name for cortex

A

cerebrum

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36
Q

main role of basal ganglia

A

voluntary motor control

some cognitive functions

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37
Q

main role of limbic system

A

emotions and memory

emotions - amygdala; memory - hippocampus

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38
Q

what is the role of amygdala

A

emotions

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39
Q

what is the role of hippocampus

A

memory

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40
Q

main role of diencephalon

A

relay station to AND from cortex
regulating internal homeostasis, emotions, hormonal control, and direct regulation

(relaying - thalamus; hypothalamus does the rest (aka lots of regulation)

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41
Q

main role of thalamus

A

relay station to AND from cortex

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42
Q

main role of hypothalamus

A

regulating internal homeostasis, emotions, hormonal control, and direct regulation

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43
Q

Decisions are made in “______________” about how to interpret and act on the incoming sensory information

A

cortico-thalamic loops

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44
Q

Schizophrenia is considered a disease of the _______

A

frontal cortex

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45
Q

damage to the cortex can affect what things?

A

movement, speech, personality

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46
Q

T or F: when there is damage to the cortex, drugs are not typically available to treat these deficiencies

A

True!!

exception is Schizophrenia tho

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47
Q

Afferent or Efferent Neuron Tracts?

transmit signals from cortex to periphery

A

efferent

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48
Q

Afferent or Efferent Neuron Tracts?

transmit signals from periphery to cortex

A

afferent

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49
Q

brain is surrounded by layers of membranes collectively known as the ______

A

meninges

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50
Q

3 main layes of meninges

A

dura
arachnoid
pia

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51
Q

Dura, Arachnoid, Pia layer of meninges?

us closest to bone

A

dura

dura = hard next to bone

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52
Q

Dura, Arachnoid, Pia layer of meninges?

is closest to brain

A

pia

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53
Q

Dura, Arachnoid, Pia layer of meninges?

is the middle layer

A

arachnoid

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54
Q

Dura, Arachnoid, Pia layer of meninges?

is the outer layer

A

dura

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55
Q

Dura, Arachnoid, Pia layer of meninges?

is the inner layer

A

pia

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56
Q

what fills the space b/w arachnoid and pia layers?

A

CSF - cerebrospinal fluid

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57
Q

blood enters brain via the ________

A

carotid artery

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58
Q

once carotid artery enters the brain… it branches into what things?

A

4 arteries total…
opthalmic artery;
anterior, middle, and posterior cerebral arteries

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59
Q

CNS consists of ______ and _____ cells

A

neurons;

glial cells

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60
Q

which is more abundant?

neurons or glial cells

A

glial cells

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61
Q

3 main glial cells

A

astrocytes
Oligodendrocytes
Microglia

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62
Q

Role of Astrocytes
provide neurons w/ _________ & _______
remove excess __________
support the _________

A

provide growth factors and anti-oxidants
remove excess GLUTAMATE
support BLOOD BRAIN BARRIER

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63
Q

Role of Oligodendrocytes

A

produce myelin sheath that insulates axons

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64
Q

Role of Microglia

A

Clear debris!!
also provide growth factors

(if too many microglia => inflammation)

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65
Q

why is it good astrocytes remove excess glutamate

A

too much glutamate can damage neurons

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66
Q

Astrocytes, Oligodendrocytes, or Microglia?

remove debris

A

Microglia

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67
Q

Astrocytes, Oligodendrocytes, or Microglia?

remove excess glutamate

A

astrocytes

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68
Q

Astrocytes, Oligodendrocytes, or Microglia?

make myelin sheath for axon insulation

A

oligodendrocytes

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69
Q

Astrocytes, Oligodendrocytes, or Microglia?

support blood brain barrier

A

astrocytes

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70
Q

Astrocytes, Oligodendrocytes, or Microglia?

provide growth factors

A

astrocytes (mainly)

also microglia

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71
Q

Astrocytes, Oligodendrocytes, or Microglia?

provide anti-oxidants

A

astroyctes

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72
Q

Blood Brain Barrier:

stabilized by ________ in the ______ cell layer of blood vessels in the brain

A

tight junctions

in endothelial cell layer

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73
Q

Neurotransmission is triggered by ______ of the neuron

A

electrical depolarization (shocking…)

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74
Q

Neurotransmission occurs when a influx of ______ changes polarity of membrane

A

Na+ ions…

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75
Q

T or F:

smaller axon diameter leads to faster firing

A

false!

bigger diameter = faster firing

76
Q

depolarizing neurons = excitatory or inhibitory?

A

excitatory

77
Q

polarizing neurons = excitatory or inhibitory?

A

inhibitory

78
Q

T or F: action potentials for a SINGLE neuron are always the same magnitude

A

true!

“all or none” type thing

79
Q

bundle of axons aka _______

A

nerve fiber

80
Q

currents carrier by a nerve fiber are higher because of the result of ________

A

summation

81
Q

what is EPSP

A

excitatory postsynaptic potential

82
Q

______ neurotransmitters will induce EPSP

A

excitatory…

83
Q

Excitatory neurotransmitters act on (chronotropic or ionotrpic?) receptor allowing ____ ions to cross the membrane

A

ionotropic; Na+

84
Q

Inhibitory neurotransmitters induce _________ by allowing ____ ions to cross the membrane

A

hyperpolarizing; Cl- ions

85
Q

T or F: IPSP can decrease the magnitude of a subsequent EPSP

A

true!
if lots of hyperpolarizing (hella negative), it can prevent a action potential the next time (aka like refractory period)

86
Q

what are the common amino acid neurotransmitters

A

GABA
Glycine
Glutamate

87
Q

what are the common non-amino acid neurotransmitters

A

Ach
DA (dopamine)
NE
Serotonin (5-HT)

88
Q

GABA:

is a excitatory or inhibitory neurotransmitter?

A

inhibitory

89
Q

GABA:

decrease neuronal excitability by doing what?

A

increasing the influx of Cl- ions into the neuron

90
Q

what are types of GABA receptors?

A

GABA-A and GABA-B

91
Q

drugs that normally interact with GABA pathways are known as CNS ________

A

depressants

92
Q

what drug classes are known to be related to the GABA pathway

A
  • Sedative hypnotics (BZDs, Barbituates)
  • Anticonvusalnts
  • Anxiolytics
93
Q

______ is similar to GABA but it works in the spinal cord

A

glycine

94
Q

glycine is similar to GABA but it works in the _______

A

spinal cord

95
Q

GABA-A receptor is a ______
and
GABA-B receptor is a _______

A

A: ion channel
B: GPCR

96
Q

GABA-A or GABA B receptor is more relevant in seizures

A

A!

97
Q

Glutamate:

is a excitatory or inhibitory neurotransmitter?

A

excitatory

98
Q

Excess glutamate leads to neuronal damage by allowing excessive _____ into neuron

A

Ca2+ influx

99
Q

what are the glutamate receptors?

A

AMPA/NMDA

mGluR

100
Q

Glutamate receptors are ______tropic or ______tropic

A

metabotropic
or
ionotropic

101
Q

Ach receptors are?

A

muscarinic (mAchR)
or
nicotinic (nAchR)

102
Q

what parts of the brain does Ach have an effect?

A

basal forebrain!!

Pons, Cortex, Basal Ganglia

103
Q

Ach

is a excitatory or inhibitory neurotransmitter?

A

excitatory

104
Q

Glutamate works in what parts of the brain?

A

throughout the whole brain

105
Q

GABA works in what parts of the brain?

A

throughout the whole brain

106
Q

Ach or DA?

works in basal forebrain

A

Ach

107
Q

Ach or DA?

works in midbrain

A

DA

108
Q

Dopamine Drug Targets

A

D1 - D5 GPCR receptors
and
DAT (dopamine transporter)

109
Q

DA neurons arise from where?

A

VTA and SN

```
VTA = ventral tegmental area
(SN = substanta nigra)
~~~

110
Q

Drugs that block DAT lead to (decrease or increase) in DA?

A

increase!!

111
Q

what drugs block DAT

A

amphetamine and cocaine = more dopamine = euphoria = addiction

112
Q

DA Receptors:
D1 like is G___ coupled
D2 like is G____ coupled

A

D1: Gs

D2: Gi

113
Q

NE works where in the brain?

A

Pons

114
Q

drug targets for NE

A

adrenergic receptors (alpha and beta)
and
NET (NE transporter)

115
Q

NET inhibitors are used to treat _______

A

depression

116
Q

D2 receptor antagonists are used as _______ drugs

A

Antipsychotics

117
Q

Drug targets for 5-HT

A

GPCRs and
Gated Ion channel and
SERT (serotonin transporter)

118
Q

5-HT axons arise from a group of cell bodies in the brain stem called __________

A

Raphe Nuclei

119
Q

5-HT(2A) antagonists are known as _______

A

atypical antipsychotics

120
Q

5-HT(1D) agonists are used for ______

A

migraines

121
Q

SERT uptake inhibitors are used for ______

A

depression (SNRIs??)

122
Q

5-HT(2A) agonists are known as ________

A

hallucinogenic

(2A - antag used as antipsych…
2A- agonist used to create hallucinogens…)

123
Q

what is Charcot’s Triad used for?

A

its the 3 key signs of MS

124
Q

what makes up Charcot’s Triad?

A

1 - Nystagmus
2 - intention tremor
3 - telegraphic speech

125
Q

what is nystagmus

A

uncontrolled eye movement

126
Q

what the common symptoms of MS

Rochet lists 10…

A
  • Visual problems
  • Numbness/Tingling
  • fatigue/motor weakness
  • Problems walking/gait problems
  • pain
  • spasticity
  • dizziness/vertigo
  • Sexual dysfunction
  • Bladder problems/Constipation
  • Emotional/Cognitive changes/depression
127
Q

Viral/bacterial infections may increase risk of MS by activating _________ cells

A

autoreactive immune

128
Q

What evidence supports the idea that viral/bacterial infections can lead to MS (autoreactive immune cells cause it)

  • increased ______ synthesis in CNS of MS pts
  • increased ______ to certain viruses
  • epidemiological data suggests that _____ infection increases MS risk
A

IgG;
antibody titers
childhood

129
Q

EBV and MS:

- sequence similarities b/w EBV and self peptides –> activation of ___________ (aka _________)

A

activating autoreactive T or B Cells; molecular mimicry

130
Q

Genetic Influences in MS:

Risk is ______ in twins/siblings and _____ in children/half siblings

A

higher; lower

131
Q

Genes linked to MS encode the following immune related proteins:

  • MHC/HLA______
  • interleukin ____ receptor
  • interleukin ____ receptor
A
  • MHC/HLA: DR15/Dr6

2(alpha)

7(alpha)

132
Q

List the Clinical Forms of MS:

A 
RRMS (relapsing remitting) 
SPMS (secondary progressive)
PPMS (primary progressive)
CIS (clinically isolated syndrome)
Marbug Variant
133
Q

SPMS:

has less ________ but does have progressive _____

A

less inflammation

progressive decline

134
Q

RRMS or PPMS:

which one has later onset

A

PPMS (primary progressive)

probs bc RRMS has inflammatory episodes surpass symptomatic threshold

135
Q

what is CIS

A

clinically isolated syndrome;
initial episode of neurologic syndrome > 24 h
involves inflamm. and demyelination in optic nerve/cerebrum,cerebellum, brainstem, or spinal cord

136
Q

what is Marburg Variant of MS

A

aggressive MS — hella inflammation; may resemble brain tumor

137
Q

MS consists of what 2 phases

A

autoimmune and degenerative

138
Q

MS Autoimmune Phase:

_____ cells present CNS antigens and activate ____ cell responses in the peripheral ________ tissue

A

Dendritic cells
T cells
lymphoid

139
Q

MS Autoimmune Phase:

activated B and T cells proliferate and infiltrate CNS (it involves _______ mediated binding and penetration of _____)

A

involves alpha-4 integrin

penetrate BBB (blood brain barrier)

140
Q

MS Autoimmune Phase:
after re-encountering their specific antigen in CNS, B cells mature into ________ and release ______ to target the antigen on expressing cells

A

mature into PLASMA CELLS

release IgG antibodies

141
Q

CD8 T Cells or CD4 T Cells?

interact with target ligands on oligodendrocytes

A

CD8 T cells

142
Q

CD8 T Cells or CD4 T Cells?

interact with target ligands on microglia

A

CD4 T cells

143
Q

CD8 T Cells or CD4 T Cells?

interact with MHC Class I molecules

A

CD8 T cells

144
Q

MS Autoimmune Phase:

T cells being activated leads to what things?

A

cytokine release + macrophage stimulation –> damage to myelin sheath

145
Q

what cytokines are released by T cells

A

IFN- gamma
TNA-alpha
perforin
granzyme

146
Q

MS Autoimmune Phase:

antibodies trigger activation of ________ on oligodendrocytes that result in _____ formation/cell damage

A

activated COMPLEMENT

result in PORE

147
Q

MS Autoimmune Phase:

Macrophages get recruited to the _________ and release _______ that will harm _________

A

to the inflamm. lesion
release toxins
harm oligodendrocytes

148
Q

Node of Ranvier have ____ channels
vs
Myelin sheath have _____ channels

A

Ranvier: Na+ Channels

Myelin: K+ Channels

149
Q

T or F: Action potentials travel faster if myelin sheath isn’t there

A

False…. need the sheath for insulation (duh why demyleination is bad..)

150
Q

when there is damage in MS and a lesion has occurred, what two things migrate to the lesion?

A

neuronal stem cells and OPCs (oligodendrocyte progenitor cells)

151
Q

what is astrogliosis

A

invasion/propagation of astrocytes resulting in gliotic plaques/scars (done when demyelination occurs)

152
Q

Remyelination in MS:

1st Demyelination has to happen, this will cause the activation of what two cells?

A

microglia and astrocytes

153
Q

Remyelination in MS:

when astrocytes/microglia get activated the end up releasing what? to recruit what?

A

pro-migratory factors and mitogens

recruit OPCs

154
Q

3 possible targets/therapeutic interventions in MS

A
  • immune system targets
    (T cell binding and BBB penetration; T cell/APC interactions; Cytokines)
  • targeting remyelination
  • targeting neurodegeneration
155
Q

why is gadolinium (Gd) important to MS

A

when injected it penetrates the regions where the blood brain barrier is comprosmised
MS lesions are enhanced when GD is given

156
Q

Guillain Barre Syndrome:

usually preceded by what?(for about 50% of pts)

A

GI or Respiratory infection

157
Q

Guillain Barre Syndrome:

Pathophys?

A

autoimmune attack on peripheral nerves by circulation Abs –> leads to myelination

158
Q

Tx of Guillain Barre Syndrome?

A
  • ventilation (when resp. distress)
  • Plasmapheresis (eliminate auto-Abs)
  • IV immunoglobulin administration
159
Q

Sx of Guillain Barre Syndrome?

A

weakness starts in distal muscles/lower extremities goes to upper extremities

can progress to total paralysis w/ death from respiratory failure

160
Q

Progression of Guillain Barre Syndrome can peak in how long?

A

10 - 14 days

161
Q

what drugs are used for acute MS attacks?

A

Methylprednisolone
Prednisone
ACTH (adrenocorticotropic hormone)

162
Q

Interferon Beta Drugs:

first line or second line?

A

first

163
Q

Interferon Beta Drugs:

act in the _______ and ______

A

periphery and BBB

164
Q

Interferon Beta Drugs:

inhibit what?

A

inhibit autoreactive lymphocytes
and
inhibit BBB penetration (by decreasing matrix metalloproteinase - MMP)

165
Q

Interferon Beta Drugs:

efficacious at neutralizing ________

A

antibodies

166
Q

Glatiramer:

first line or second line

A

first line

167
Q

MOA of Glatiramer?

A

synthetic polypeptide
mimics antigenic properties of myelin basic protein
inhibits T cell - APC/Dendritic interaction

168
Q

MOA of Fingolimod

A

S1P receptor agonist (sphingosine 1 - phosphate)

169
Q

Fingolimod MOA:

  • stimulate ___________
  • interference w/ ____________
A
  • stimulate oligodendrocyte survival (remylenination)

- lymphocyte movement out of lymphoid organs

170
Q

Fingolimoid:

first or second line?

A

first line

171
Q

Natalizumab:

first line or second line?

A

second

172
Q

MOA of Natalizumab?

A

Monoclonal Ab specific for a-4 integrin

173
Q

Mitoxantrone:

first or second line

A

second line

174
Q

MOA of Mitoxantrone

A

anthracenedione with CYTOTOXIC activity (reduce lymphocyte numbers)

175
Q

special feature about Mitoxantrone

A

first cytotoxic drug licenced for SPMS

176
Q

Teriflunomide:

first or second line agents

A

uhh…. NEW DRUG! but also used a lot so…?

177
Q

MOA Teriflunomide:

A

CYTOTOXIC agent that inhibits dihydroorotate dehydrogenase (aka prevents de novo pyrimidine biosynthesis)

178
Q

notable part of dimethyl fumarte’s structure?

A

its simple AF (very small..)

179
Q

MOA for dimethyl fumarate

A

gets metabolized by esterases in GI tract, blood, tissues and activates Nrf2 mediated cellular anti-ox responses and anti-inflamm. pathyway

180
Q

In Normal Circumstances,

_______ is an antagonist to Nrf2 by promoting Nrf2 ________

A

Keap1; ubiquitylation

181
Q

Keap1 dissociates from Nrf2 when cell is exposed to _________ or _____________

A

electrophilic toxins or oxidative stress

182
Q

for Nrf2 Pathway:

Keap 1 gets covanlently modified on key ______ residues and then Nrf2 is not ubiquitylated anymore

A

cysteine

183
Q

for Nrf2 Pathway:
once Nrf2 is not ubiquitlyated anymore it accumulates and enters ________ to activate ________ that are regulated by _________

A

enters NUCLEUS
to activate gene transcription of genes
regulated by ARE (antiox response element)

184
Q

what genes are under control of ARE?

A

enzymes for glutathione biosynthesis
and
detoxification
(aka some Phase II enzymes)

185
Q

Glial cells will release _________ and _______ to create neuroprotection and regeneration

A

release Neurotrophin/antioxidant

186
Q

Nrf2 antiox response pathway induces _______ upregulation in neurons through astrocyte-neuron communication

A

GSH

187
Q

Firtaegrast: MOA and notable part of struc

A

MOA: targest a-4 integrin

small molecule

Therapeutics 3 - Spring 2018 (20 decks)

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