Multiple Sclerosis Flashcards

(93 cards)

1
Q

What is multiple sclerosis (MS)?

A

A chronic immune-mediated inflammatory disease causing CNS demyelination and degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Primary pathology of MS

A

Loss of myelin sheath in CNS with scarring (gliosis) and axonal loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Key features of MS

A

Inflammation; demyelination; plaque formation; gliosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where does MS primarily occur?

A

White and gray matter of brain and spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are MS plaques?

A

Areas of scar tissue from demyelination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is gliosis?

A

Scarring from glial cell activity in CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Function of myelin sheath

A

Allows rapid nerve signal transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Effect of demyelination

A

Slows or blocks nerve impulse transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ultimate effect of MS progression

A

Neuron death and brain atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Comparison disease (PNS demyelination)

A

Guillain-Barré syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Etiology of MS

A

Unknown; likely genetic + immune + environmental trigger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Common trigger theory for MS

A

Infection activating immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Typical age of onset

A

20–40 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Sex prevalence

A

More common in females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MS severity in males

A

Often more severe and progressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Geographic risk factor

A

Higher prevalence in cooler climates (northern regions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Latitude association

A

Higher above and below 40th parallels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Ethnic risk factor

A

More common in White individuals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Family history risk

A

Increases likelihood of MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Other possible risk factors

A

Smoking; vitamin D deficiency; obesity; infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Immune cells involved in MS

A

T lymphocytes and antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Pathophysiology step 1

A

T cells cross blood-brain barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Step 2 of MS pathophysiology

A

Inflammation increases; myelin breakdown begins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Step 3 of MS pathophysiology

A

Antigen-antibody reaction attacks myelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Step 4 of MS pathophysiology
Loss of oligodendrocytes (myelin-producing cells)
26
Step 5 of MS pathophysiology
Demyelination and plaque formation
27
Step 6 of MS pathophysiology
Axonal damage and death
28
Result of myelin destruction
Delayed then lost nerve signals
29
Early MS nerve changes
Inflammation with preserved signal transmission
30
Intermediate MS changes
Myelin detachment and axon damage
31
Late MS changes
Complete signal blockage and permanent function loss
32
Why MS diagnosis is often delayed
Early symptoms are mild and insidious
33
General pattern of MS symptoms
Depend on which nerves are affected
34
What are exacerbations (relapses)?
Temporary worsening of symptoms
35
Duration of relapses
Days to weeks
36
Goal of MS treatment
Reduce relapse frequency and severity; slow progression
37
Benign MS course
Relapse followed by full return to baseline
38
Relapsing-remitting MS (RRMS)
Most common; periods of relapse and remission
39
RRMS prevalence
80–90% of MS cases
40
RRMS recovery pattern
Partial recovery with slight decline over time
41
Primary progressive MS (PPMS)
Steady worsening without relapses/remission
42
Secondary progressive MS (SPMS)
Starts RRMS → becomes progressive
43
Progressive relapsing MS (PRMS)
Progressive disease with occasional relapses
44
Key factor in MS classification
Frequency of relapses and duration of remission
45
Common initial MS symptom
Paresthesia (numbness/tingling)
46
Other early MS symptoms
Weakness; vision problems; gait issues
47
Example of nerve-specific symptom
Optic neuritis causing unilateral vision loss
48
Bladder-related MS symptoms
Incontinence or urinary retention
49
Cognitive symptom of MS
"Cog fog" (difficulty thinking/concentrating)
50
Difference between cog fog and memory loss
Not memory loss but impaired thinking clarity
51
Common psychological symptom
Depression
52
Cause of depression in MS
Loss of function and disease burden
53
Common physical symptom
Fatigue
54
Pain types in MS
Chronic or acute (burning or stabbing)
55
Bowel dysfunction in MS
Constipation or incontinence
56
Mobility issues in MS
Balance problems; gait disturbance; fall risk
57
Advanced mobility impairment
May require wheelchair
58
Sexual dysfunction in MS
Possible due to nerve involvement
59
Vertigo in MS
Can occur due to CNS involvement
60
Main pharmacotherapy goals
Slow disability; reduce relapses; extend remission; reduce lesions
61
Types of MS treatments
Disease-modifying; relapse treatment; symptom management
62
Interferon beta example
Avonex
63
Mechanism of interferons
Prevent pro-inflammatory cells crossing BBB
64
Effectiveness of interferons
Reduce relapse rate by ~30%
65
Interferon adverse effects
Flu-like symptoms; liver toxicity; bone marrow suppression; depression
66
Glatiramer acetate (Copaxone) mechanism
Increases anti-inflammatory T cells
67
Glatiramer adverse effects
Injection reactions; flushing; chest pain; palpitations; rash; laryngeal constriction
68
Duration of glatiramer reaction
Usually transient (10–20 minutes)
69
Fingolimod mechanism
Traps lymphocytes in lymph nodes
70
Use of fingolimod
Common in RRMS
71
Dimethyl fumarate mechanism
Suppresses immune cells; reduces inflammation
72
Natalizumab mechanism
Prevents T cells from crossing BBB
73
Natalizumab effectiveness
Reduces relapse rate by ~68%
74
Natalizumab major risk
Progressive multifocal leukoencephalopathy (PML)
75
Natalizumab program
TOUCH prescribing program required
76
Natalizumab adverse effects
Headache; fatigue; liver toxicity; hypersensitivity
77
Risk factor for PML
Use with other immunosuppressants
78
Natalizumab use
Monotherapy for RRMS
79
Alemtuzumab use
Reserved for poor response to ≥2 therapies
80
Mitoxantrone use
SPMS; PRMS; worsening RRMS
81
Treatment for acute MS relapse
High-dose IV glucocorticoids (pulse therapy)
82
Typical steroid dose
500 mg–1 g daily for 3–5 days
83
Steroid complications
Hyperglycemia; requires monitoring
84
Alternative relapse treatment
IV immunoglobulin (IVIG)
85
ACTH gel use
For relapse if steroids ineffective/intolerable
86
Plasmapheresis use
Removes plasma and replaces with donor plasma
87
Purpose of plasmapheresis
Remove harmful immune components
88
Symptom management approach
Individualized based on presentation
89
Urinary symptom treatment
Anticholinergic (frequency); cholinergic (retention)
90
Constipation management
Hydration; fiber; bulk laxatives
91
Fatigue treatment
Amantadine; rest planning
92
Muscle spasm treatment
Muscle relaxants
93
Cognitive symptom treatment
Donepezil (Aricept)