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Pharmacotherapy III > MS-Rochet > Flashcards

MS-Rochet Flashcards

1
Q

What is MS?

A

Immune-mediated disorder

Destroys myelin sheath of neurons

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2
Q

What is sclerosis?

A

Scars in white matter of MS patients

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3
Q

What are 3 key signs of MS - Charcot’s triad?

A

Nystagmus (eye problems)
Intention tremor
Telegraphic speech

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4
Q

MS is more common in men/women?

A

Women

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5
Q

What are common symptoms of MS?

A 
Visual problems
Numbness/tingling
Fatigue, motor weakness
Difficulty walking/gait problems
Pain
Spasms
Dizziness/vertigo
Sexual dysfunction
Bladder problems/constipation
Emotional changes/depression
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6
Q

The most prominent symptoms of an MS patient reflect what?

A

The regions of the brain with the most severe damage

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7
Q

Where is MS most prevalent in the world?

A

above the 37th parallel

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8
Q

There is an increased MS risk with decrease ____

A

Vit D levels

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9
Q

What are some risk factors of MS?

A 
Age (40's)
Decreased Vit D
Viral infections
Environmental insults
Cigarette smoking
genes
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10
Q

How can bacterial infections induce MS?

A

Activating autoreactive immune cells

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11
Q

MS patients have increased ___ synthesis in the CNS

A

IgG

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12
Q

MS patients have increased _______ to certain viruses

A

antibody titers

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13
Q

What virus might be involved with MS?

A

Epstein-Barr Virus (MONO)

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14
Q

Why would EBV be involved with MS?

A

Sequence similarities between self-peptides and EBV –> activation of immune cells against self

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15
Q

Does EBV cause MS?

A

Not directly

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16
Q

Risk distribution in families indicates a ____ mode of inheritance

A

Polygenic – >50 genomic regions involved

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17
Q

What proteins are linked to MS?

A

Major histocompatibility complex (HLA)
Interleukin 2a
Interleukin 7a

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18
Q

RRMS is ???

A

Relapsing Remitting MS, where symptoms come and go (remission and relapse)

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19
Q

RRMS usually eventually enters into ____

A

SPMS - secondary progressive MS, where symptoms don’t go away

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20
Q

What is PPMS?

A

Primary progressive MS - never has relapses/remission periods

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21
Q

Mean onset is later for PPMS or RRMS?

A

PPMS

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22
Q

What does CIS stand for?

A

clinically isolated syndrome

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23
Q

What is CIS?

A

First episode of MS symptoms lasting >24 hours

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24
Q

T/F: Most cases of CIS progress to MS

A

True

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25
What is the Marburg variant of MS?
Aggressive MS involving inflammation- resembles brain tumor
26
What is the progressive phase?
Constantly occurring cytodegeneration (loss of myelin/oligodendrocytes)
27
T/F: Progressive phase is faster with PPMS
FALSE: occurs at similar rate in all different forms of MS
28
The relapse phases are more determined by ______
immune activity/inflammation
29
What happens in autoimmune phase of MS?
Antigens released from CNS or foreign antigens that look like CNS activate aB and T cells B and T cells migrate to CNS where they carry out immune functions at CNS sites
30
What happens in the degenerative phase of MS? - CNS damage is triggered by ___ - Antigens released from CNS ______ in the periphery
- Triggered by activated B and T cells, or stroke/infection/etc - Further prime immune cells
31
Does degenerative trigger autoimmune or autoimmune trigger degenerative?
Not clear
32
So two theories of MS development are:
- Inside-out: CNS antigens are entering periphery and activating immune cells - Outside in: Autoimmunity in periphery is developing and immune cells are entering CNS
33
____ cells that present CNS antigens activate ___ in peripheral lymphoid tissue
Dendritic cells; activate T-cell responses
34
What protein is important for B and T cells to get through the BBB into the CNS?
alpha-4-integrin!!
35
CD8+T cells interact with ligands presented by ____ on MHC class __
Oligodendrocytes or neurons | Class I
36
CD4+T cells interact with ligands presented by ___ on MHC class __ molecules
``` Microglia MHC class II ```
37
T cell activation results in ___ release and ___ stimulation, leading to damage to the ________
cytokine release macrophage stimulation damage to myelin sheath
38
How do CD8 T cells damage Oligodendrocytes?
``` Release cytokines IFN-gamma TNF-alpha perforin granzyme ```
39
How do antibodies damage oligodendrocytes?
Trigger complement activation --> pore formation
40
How do macrophages damage oligodendrocytes?
Release toxic ROS/Nitrogen that harm oligodendrocytes
41
How do macrophages damage the myelin sheath?
Phagocytosis
42
In demyelinated axons, AP is faster/slower?
slower
43
Normally, how are Na/K channels arranged?
Separated-- Na found in Nodes K found under myelin sheath
44
How are N/K channels arranged with MS?
Mixed together in areas of demyelination - Na channels move
45
How can damaged neurons and oligodendrocytes be replaced?
Neuronal stem cells and oligodendrocyte progenitor cells migrate to the lesion!
46
Why does remyelination usually fail in MS?
Lack of OPCs or failure of OPCs to differentiate to oligodendrocytes
47
What is astroglisosis? | Invasions and propagation of ___ resulting in irreversible formation of ____
astrocytes | gliotic plaques/scars
48
Demyelination activates __ and ___
Microglia and astrocytes
49
What produces pro-migratory factors that recruits OPCs?
Activated microglia and astrocytes
50
T/F: Myelin sheaths that result from remyelination are just as strong as the original sheaths
False: they are thinner and shorter
51
Remyelination in MS fails because of ___
ongoing inflammation
52
What target to prevent T cell binding/penetration of BBB?
a4-integrin antibodies | IFN-Beta
53
What are the targets for MS treatment?
- Immune system - Remyelination (OPC recruitment/differentiation) - Neurodegeneration
54
What are the immune system targets for MS?
T cell binding/penetration T cell/APC interactions Cytokines
55
What agent is used to visualize MS brain lesions w/MRI?
gadolinium
56
Where does gadolinium penetrate?
Regions where BBB is compromised
57
What are active lesions?
MS lesions that exhibit enhancement after gadolinium
58
What is Guillain-Barre syndrome?
Inflammatory neuropathy
59
What precedes Guillain-Barre syndrome?
GI or respiratory infection
60
Symptoms of Guillain-Barre?
- Weakness in distal muscles | - Can become total paralysis w/DEATH
61
Pathophysiology of Guillain Barre?
Autoimmune attack on peripheral nerves --> DEMYELINATION
62
Treatment of Guillain Barre?
Ventilation Plasmapheresis (get rid of auto-abs) IV Immunoglobulin administration
63
How long does recovery from Guillain-barre take?
months to years

Pharmacotherapy III (12 decks)

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