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PMCOL 412 > MS I > Flashcards

MS I Flashcards

1
Q

Global distribution of MS–risk and lattitude

A

Increased MS risk as you move away from the equator

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2
Q

Areas most affected by MS

A

includes: Canada, northern Europe, New Zealand, South Africa

Places far from the equator and having northern European descent

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3
Q

MS prevalence in canada

A

High in Canada,

esp. in prairies and Atlantic

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4
Q

MS in alberta ___ cases/100 000 people

A

340 cases/100 000 population

effects ~15 000 people in Alberta

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5
Q

Most affected ages

A

most patients between the ages of 15-45

can also have pediatric cases or late onset

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6
Q

Pediatric MS makes up ___% of total MS patients

A

6%

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7
Q

__ % of MS patients are under 18 years old

A

3-10%

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8
Q

Sex differences in MS

A

MS, like other autoimmune diseases effect females more

3:1 ratio of females to males

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9
Q

Clinical manifestations of MS

A
  • ocular manifestations
  • cerebellar manifestations
  • Autonomic manifestations
  • Motor manifestations
  • sensory manifestations
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10
Q

ocular manifestations examples

A

Blurred vision, diplopia

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11
Q

cerebellar manifestations examples

A

Ataxia, vertigo, nystigmus

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12
Q

Autonomic manifestations examples

A

urinary incontinence, sexual disorders

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13
Q

Motor manifestations examples

A

Reduced strength and activity
muscle spasms
muscle weakness and loss of strength

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14
Q

Sensory manifestations examples

A

sensory changes, hypoesthesia, progressive sensory los

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15
Q

MRI imaging in MS

A

help see issues prior to clinical manifestation

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16
Q

2 stages of MS

A

relapsing-remitting and secondary progression

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17
Q

Relapsing-remitting

A

Symptoms will almost completely disappear and then return (altering on/off of symptoms)
- Goes on until recovery from symptoms is incomplete

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18
Q

Secondary progression

A

Once recovery from symptoms is incomplete and the subject can no longer relapse –> accumulate disability and get gradually worse

Usually 15-17 years into the disease, fewer relapses start 2nd progressive MS

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19
Q

T/F: there is a disconnect between the neurodegenerative and inflammatory aspects of the disease

A

TRUE

Will get progressively worse but maintain relapsing and remitting until a certain point

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20
Q

Expanded disability status scale (EDSS)

A

The scale used to measure disability over time
looks at motor, sensory, cerebellar systems and score them –> get score
0 = normal
10 = death

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21
Q

6 on EDSS

A

assistance required to walk

use of cane

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22
Q

7 on EDSS

A

restricted to wheelchair

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23
Q

MS

A

Demyelination causes damage to nerve can have two outcomes:
Transection (not-desired)
Remyelination (and therefore repair)
get a mix of the two

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24
Q

Transection

A

Disconnection over time

axons cut

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25
Remyelination
mechanism of repair | patch over damage, not perfect (worse than pre-demyelination)
26
Demyelination causes
axonal injury and loss over time | significant injury --> decreased # of fibres
27
Brain of MS patient
periventricular lesions
28
Causes of MS
Genes and environment interact to cause MS
29
Environmental triggers include
- infections - smoking - salt = things that trigger inflammation - lack of sun exposure (low vit D) Triggers facilitate disease progression
30
Genetic contribution to MS risk
HLA complex marker--Markers of immunity Not genetically transmissible Genetic contribution is low
31
MS thought to be
IMMUNE MEDIATED Although the initiating etiological factors are unknown, the destruction within the CNS is thought to be immune-mediated
32
MS as immune-mediated evidence
- Many inflammatory cell types are localized to lesion sites in the CNS - The activity of several inflammatory cell types is dysregulated - Levels of several inflammatory cytokines are increased in the serum, CSF and CNS of patients with MS
33
EAE
Experimental autoimmune encephalomyelitis (EAE) is a T-cell-mediated autoimmune disease of the CNS that causes the CNS myelin to be recognized as an exogenous immunogen and subsequently be attacked by T-cells
34
Mice EAE
EAE injected into muce --> diseases mediated by myelin basic protein-specific Th1 cells --> can transmit EAE through transfer of injected T-cells into healthy mice
35
MBP
Myelin basic protein (protein of myelin)
36
Immunology of EAE
Inject MBP into mice --> MBP-recognizing T-cell (in a pool of naive T-cells) is usually silent but will pick up antigen and present it to lymphocyte --> expansion of MBP-reactive T-cells --> enter CNS --> reactivated in CNS --> CNS pathology attacking myelin
37
How models of molecular mimicry can cause MS
virus with molecular similarly to MBP --> in a pool of naive T-cells both a virus recognizing cell and the MBP-recognizing cell are activated --> antigen presentation of virus to naive T-cells --> expansion of both virus-speicifc and cross-reactive MBP-specific T cells --> enter CNS where they recognize MBP and initiate inflammatory damage
38
Naive T cells types
``` Pro-inflammatory: - TH1 cytokine (IL-2, IL-12, IFN-gamma, TNF-alpha) - TH17 cytokines (IL-17, IL-23) Anti-inflmamatory: - Th2 (IL-4,5,10,13,25; TGF-beta) - Treg (TGF-beta, IL-10, IL35) ```
39
Goal of therapeutics on cytokines
pro-inflammatory factors cause auto-immune response so want to increase the anti-inflammatory side
40
T-cells action in brain
get in brain (trans-migration through BBB) --> activated inflammatory cells in CNS will be re-stimulated --> look for myelin (MBP) --> attack
41
Perivacular inflammatioon in MS plaques
perivascular infiltrate of the lymphocyte that surrounds the vessel then infiltrates the brain parenchyma causing injury
42
Transection of Axons: longterm effect
Accumulation of transected axons causes disaease symptoms | goal in treatment: prevent transection
43
Transection of axons correlated well with disease progression TRUE or FALSE
TRUE
44
Brain atrophy: HOW
loss of axons --> complete atrophy --> widening of venticles
45
2 approaches to MS treatment
Disease-modifying treatment | Symptom treatment
46
Disease-modifying treatment
Long-term treatments to modify disease course, delay accumulation of disability No direct impact on symptoms
47
Symptom treatment
Treatments to settle symptoms | No direct impact on disease
48
Spasms in MS--why
b/c lesions affect the corticospinal tract | Loss of inhibitory signals = muscle continuously contracted --> spasticity (+ main and functional loss)
49
Most used drug for spasms
Baclofen
50
Baclofen
most relevant drug for MS-related spasticity GABA agonist Side effects: Sedation, drowsiness, muscle weakness
51
Benzos
used for spasticity in MS Facilitate postsynaptic effect of GABA and increase presynaptic inhibition Side effects: Fatigue, drowsiness, dry mouth, postural hypotension
52
Drugs for spasticity
Baclofen (GABA agonist) Tizanidine (Alpha2 agonist) Dantrolene (reduces Ca2+ release) Benzos (increases Cl- channel opening, increase GABA) Gabapentine (Decreses release of gluatmate presynaptic terminal)
53
For severe spasticity use....
- Intratechal baclofen - Chemodenervation (Botox injections) - Delta9-tetrahydrocannabinol (Sativex)
54
Intrathecal baclofen
Pump baclofen into spinal CSF continuous Used in severe spasticity
55
Botox
Used in severe spasticity to relax muscles
56
Fatigue--definition
a feeling of physical tiredeness and lack of energy distinct from sadness or weakness
57
Severe fatigue is seen in ___ % of patients
Severe in up to 74 % of pts, the worst symptom of the disease in 50-60 % of pts
58
Drugs to treat fatigue
Amantadine (MA, Ach and Glut effects on CNS) Modafinil (CNS stimulant) Pemoline (CNS stimulant) 4-Aminopyridine (Blocks K+ channels --> longer APs, more NT)
59
Amantadine
Drug to treat fatigue Monoaminergic, cholinergic and glutamatergic effects of the CNS Side effects: Anorexia, nausea, insomnia, hallucinations, blurred vision, peripheral edema, urinary retention
60
Main side effect from anti-fatigue drugs
tend to be stimulants, cause lack of sleep
61
Bladder dysfunction--3 types
Bladder overactivity: urgency, frequency, urge incontinece. Bladder inefficiency: incomplete emptying, residual, urine. Detrusor-sphyncter dyssinergia: co-contraction of bladder and urethral sphyncter
62
Bladder overactivity
urgency, frequency, urge incontinece.
63
Bladder inefficiency
incomplete emptying, residual, urine.
64
Detrusor-sphyncter dyssinergia
co-contraction of bladder and urethral sphyncter (can't let urine down from bladder)
65
Bladder dysfunction affects ___% of patients
75%
66
Treatment of Bladder dysfunction: 2 categories to treat
``` Storage dysfunction (Bladder inefficiency, Bladder overactivity) Voiding dysfunction (Detrusor-sphyncter dyssinergia) ```
67
Treating bladder storage dysfunction
``` • Behavioural therapy • Antimuscarinic agents (oxybutynin, tolterodine, solifenacin) • Desmopressin • Botox • Beta3-adrenoceptor agonists (mirabegron) • Bladder augmentation • Sacral deafferentation/anterior root stimulation ```
68
Treating Bladder Voiding dysfunction
* Intermittent catheterization * Indwelling catheterization * Alpha-adrenoceptor blockers
69
Pain 2 types in MS
- Persistent neurogenic pain - Paroxismal neurogenic pain (trigeminal neuralgia)
70
Persistent neurogenic pain
burning dysestesia of the limbs and/or trunk attributed to disruption of the spinothalamic pathway usually within the spinal cord
71
Paroxysmal neurogenic pain (trigeminal | neuralgia)
episodes of excruciating facial pain. triggered by light touch to face shooting pain
72
Pain affects __ % of patients
40-50%
73
To induce bladder relaxation
use anticholinergics to blocks Ach cascade
74
Main drug type for bladder storage dysfunction
``` Antimuscarinic agents (oxybutynin, tolterodine, solifenacin) act on mAchRs ```
75
SC control of pain main NTs
NE and 5HT
76
Treatment of trigeminal neuralgia: 2 categories
Anti-epileptics (stabilize cell memb) | Surgical interventions
77
Pharmaceutical treatment of trigeminal neuralgia
* Carbamazepine * Oxacarbazepine * Lamotrigine * Gabapentin
78
Surgical treatment of trigeminal neuralgia
used when especially bad • Radiofrequency thermocoagulation • Glycerol rhizothomy • Balloon compression
79
Treatment of persistent neuropathic pain
* Tricyclic antidepressant (amitryptiline, nortriptiline) * Gabapentin * pregabalin * Serotonin or norepinephin reuptake inhibitors (SNRIs--duloxetine, venlafaxine) * cannabinoids

PMCOL 412 (35 decks)

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