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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
Q

Remyelination

A

mechanism of repair

patch over damage, not perfect (worse than pre-demyelination)

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26
Q

Demyelination causes

A

axonal injury and loss over time

significant injury –> decreased # of fibres

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27
Q

Brain of MS patient

A

periventricular lesions

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28
Q

Causes of MS

A

Genes and environment interact to cause MS

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29
Q

Environmental triggers include

A
  • infections
  • smoking
  • salt
    = things that trigger inflammation
  • lack of sun exposure (low vit D)
    Triggers facilitate disease progression
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30
Q

Genetic contribution to MS risk

A

HLA complex marker–Markers of immunity
Not genetically transmissible
Genetic contribution is low

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31
Q

MS thought to be

A

IMMUNE MEDIATED
Although the initiating etiological factors are unknown,
the destruction within the CNS is thought to be
immune-mediated

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32
Q

MS as immune-mediated evidence

A
  • 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
Q

EAE

A

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
Q

Mice EAE

A

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
Q

MBP

A

Myelin basic protein (protein of myelin)

36
Q

Immunology of EAE

A

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
Q

How models of molecular mimicry can cause MS

A

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
Q

Naive T cells types

A 
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
Q

Goal of therapeutics on cytokines

A

pro-inflammatory factors cause auto-immune response so want to increase the anti-inflammatory side

40
Q

T-cells action in brain

A

get in brain (trans-migration through BBB) –> activated inflammatory cells in CNS will be re-stimulated –> look for myelin (MBP) –> attack

41
Q

Perivacular inflammatioon in MS plaques

A

perivascular infiltrate of the lymphocyte that surrounds the vessel then infiltrates the brain parenchyma causing injury

42
Q

Transection of Axons: longterm effect

A

Accumulation of transected axons causes disaease symptoms

goal in treatment: prevent transection

43
Q

Transection of axons correlated well with disease progression TRUE or FALSE

A

TRUE

44
Q

Brain atrophy: HOW

A

loss of axons –> complete atrophy –> widening of venticles

45
Q

2 approaches to MS treatment

A

Disease-modifying treatment

Symptom treatment

46
Q

Disease-modifying treatment

A

Long-term treatments to modify disease course, delay
accumulation of disability
No direct impact on symptoms

47
Q

Symptom treatment

A

Treatments to settle symptoms

No direct impact on disease

48
Q

Spasms in MS–why

A

b/c lesions affect the corticospinal tract

Loss of inhibitory signals = muscle continuously contracted –> spasticity (+ main and functional loss)

49
Q

Most used drug for spasms

A

Baclofen

50
Q

Baclofen

A

most relevant drug for MS-related spasticity
GABA agonist
Side effects: Sedation, drowsiness, muscle weakness

51
Q

Benzos

A

used for spasticity in MS
Facilitate postsynaptic effect of GABA and increase presynaptic inhibition
Side effects: Fatigue, drowsiness, dry mouth, postural hypotension

52
Q

Drugs for spasticity

A

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
Q

For severe spasticity use….

A
  • Intratechal baclofen
  • Chemodenervation (Botox injections)
  • Delta9-tetrahydrocannabinol (Sativex)
54
Q

Intrathecal baclofen

A

Pump baclofen into spinal CSF
continuous
Used in severe spasticity

55
Q

Botox

A

Used in severe spasticity to relax muscles

56
Q

Fatigue–definition

A

a feeling of physical tiredeness and
lack of energy distinct from sadness or
weakness

57
Q

Severe fatigue is seen in ___ % of patients

A

Severe in up to 74 % of pts, the worst symptom of the disease in 50-60 % of pts

58
Q

Drugs to treat fatigue

A

Amantadine (MA, Ach and Glut effects on CNS)
Modafinil (CNS stimulant)
Pemoline (CNS stimulant)
4-Aminopyridine (Blocks K+ channels –> longer APs, more NT)

59
Q

Amantadine

A

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
Q

Main side effect from anti-fatigue drugs

A

tend to be stimulants, cause lack of sleep

61
Q

Bladder dysfunction–3 types

A

Bladder overactivity: urgency, frequency, urge incontinece.
Bladder inefficiency: incomplete emptying, residual, urine.
Detrusor-sphyncter dyssinergia: co-contraction of bladder and urethral sphyncter

62
Q

Bladder overactivity

A

urgency, frequency, urge incontinece.

63
Q

Bladder inefficiency

A

incomplete emptying, residual, urine.

64
Q

Detrusor-sphyncter dyssinergia

A

co-contraction of bladder and urethral sphyncter (can’t let urine down from bladder)

65
Q

Bladder dysfunction affects ___% of patients

A

75%

66
Q

Treatment of Bladder dysfunction: 2 categories to treat

A 
Storage dysfunction (Bladder inefficiency, Bladder overactivity)
Voiding dysfunction  (Detrusor-sphyncter dyssinergia)
67
Q

Treating bladder storage dysfunction

A 
• Behavioural therapy
• Antimuscarinic agents (oxybutynin, tolterodine, solifenacin)
• Desmopressin
• Botox
• Beta3-adrenoceptor agonists (mirabegron)
• Bladder augmentation
• Sacral deafferentation/anterior root
stimulation
68
Q

Treating Bladder Voiding dysfunction

A
  • Intermittent catheterization
  • Indwelling catheterization
  • Alpha-adrenoceptor blockers
69
Q

Pain 2 types in MS

A
  • Persistent neurogenic pain
  • Paroxismal neurogenic pain (trigeminal
    neuralgia)
70
Q

Persistent neurogenic pain

A

burning dysestesia of the limbs and/or trunk attributed to disruption of the spinothalamic pathway usually within the spinal cord

71
Q

Paroxysmal neurogenic pain (trigeminal

neuralgia)

A

episodes of excruciating facial pain.
triggered by light touch to face
shooting pain

72
Q

Pain affects __ % of patients

A

40-50%

73
Q

To induce bladder relaxation

A

use anticholinergics to blocks Ach cascade

74
Q

Main drug type for bladder storage dysfunction

A 
Antimuscarinic agents (oxybutynin, tolterodine, solifenacin) 
act on mAchRs
75
Q

SC control of pain main NTs

A

NE and 5HT

76
Q

Treatment of trigeminal neuralgia: 2 categories

A

Anti-epileptics (stabilize cell memb)

Surgical interventions

77
Q

Pharmaceutical treatment of trigeminal neuralgia

A
  • Carbamazepine
  • Oxacarbazepine
  • Lamotrigine
  • Gabapentin
78
Q

Surgical treatment of trigeminal neuralgia

A

used when especially bad
• Radiofrequency thermocoagulation
• Glycerol rhizothomy
• Balloon compression

79
Q

Treatment of persistent neuropathic pain

A
  • Tricyclic antidepressant (amitryptiline, nortriptiline)
  • Gabapentin
  • pregabalin
  • Serotonin or norepinephin reuptake inhibitors (SNRIs–duloxetine, venlafaxine)
  • cannabinoids

PMCOL 412 (35 decks)

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