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MS Flashcards

1
Q

what is MS?

A

MS: chronic, immune-mediated inflame disease of CNS
- Demyelinating neuroinflam condition which affects CNS  brain and spinal cord

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2
Q

who is most likely to get MS?

A

females
20s-40s

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3
Q

what is the aetiology?

A

though to be abnormal immune reaction to unknown environmental trigger in genetically predisposed individual
- Genetics: plays slight role

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4
Q

what are the RF for MS?

A

viral infections
geography
vit D
obesity during adolescence
smoking

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5
Q

what viral infection is linked to MS onset?

A

EBV

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6
Q

where are you are most at risk from MS and why?

A

further from equator
vitD deficiency link

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7
Q

what is the pathophysiology of MS?

A

inflame
demyelinating disease characterised by presence of plaques
oligodendrocytes are destroyed –> demylination axonal loss
immune dsyregulation

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8
Q

what do oligodendrites do?

A

type of glial cell important in the formation of myelin sheath

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9
Q

what is the autoimmune aspect of the pathophysiology of MS?

A
  1. Activation of myeline-reactive T lymphocytes and disruption of BBB
  2. Pro-inflam recruiting B cells. microglia (macrophages of CNS) mediate cytokine, phagocytosis and APC cells
  3. Marked immune response including AB-mediated with Immunoglobulins (oligobands in CSF)
  4. Continued reaction causes damage to oligodendrites  subsequent demyelination  formation of MS plaques
  5. Focal areas of demyelination/ plaques – inflame,s carring (gliosis), axonal injury
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10
Q

what are the MS plaques made up of?

A

hypercellular
containing reactive T, B and macrophages

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11
Q

where are classic plaque sites?

A
  • Optic nerve – affects 40% of those with disease
  • Spinal cord – 50-75%, majority associated with concomitant brain lesions
  • Brainstem: may present with ophthalmoplegia
  • Cerebellum: ataxia and gait disturbances
  • Juxtacortical white matter: near cerebral cortex
  • Periventricular white matter: near ventricles
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12
Q

what is the most common type of MS?

A

90% have relapsing- remitting disease

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13
Q

what is relapsing remitting disease?

A
  • Episodes of exacerbation are followed by periods of recovery
  • As disease progresses they are likely to retain damage with each relapse
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14
Q

10-15% of MS is primary progressive, what is it?

A
  • Sustained progression of disease severity from onset
  • May have periods of active or non progressive
  • No evidence of clinical remission
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15
Q

how many RRD progress to secondary progressive?

A

50% of relapsing will develop this within 15yrs

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16
Q

what is secondary progressive?

A
  • Disease gradually worsens
  • Relapses may occur but without remission
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17
Q

what is clinically isolated syndrome?

A

first episode of suspected MS

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18
Q

what is seen within clinically isolated syndrome?

A
  • No previous evidence of demyelination clinically or neuroimaging
  • Oligobands in CSF  support diagnosis
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19
Q

what is a MS exacerbation?

A

relapse/ episode of new or worsening symptoms for at least 24hrs that can either spontaneously resolve or resolve with management

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20
Q

how do symptoms within MS differ?

A

determined by plaque locations within CNS

21
Q

what are the most common visual pathologies of MS?

A

optic neuritis and eye movement abnormalities

22
Q

what is optic neuritis?

A

inflame of optic nerve and characteristically presents with partial or total unilateral visual loss that develops over days

23
Q

what visual symptoms can be seen within MS?

A

optic neuritis
- Visual loss, blurred vision
- Pain: especially on eye movement
scotoma
poor colour differentiation, relative afferent pupillary defect, optic nerve swelling seen on fundoscopy

24
Q

what is scotoma?

A

partial visual field loss

25
Q

how do eye movement disorders arise?

A

due to brainstem lesions that affect cranial nerves or pathways

26
Q

what eye movement disorders can occur?

A

INO
abducens palsy

27
Q

what motor and coordination signs may manifest within MS?

A

weakness and ataxia  upper motor neurone signs eg spasticity, reduced power and hyper-reflexia

28
Q

what is transverse myelitis?

A

focal inflame within spine – sensory and motor symptoms below level of lesion eg bladder/ bowel involvement

29
Q

what is cerebellar syndrome?

A

ataxia, slurred speech, intension tremor, nystagmus

30
Q

what is nystagmus?

A

(uncontrolled, repetitive eye movements – side to side , up and down or circular pattern)

31
Q

what sensory and autonomic manifestations may occur within MS?

A

paraesthesia, pain, heat sensitivity (uhtoff phenomenon), sexual dysfunction, bladder and bowel

32
Q

what cognitive and psychological symptoms may arise within MS?

A

cognitive impairment, depression, fatigue

33
Q

how is MS diagnosed?

A

clinical judgement with MRI to support
lumbar puncture

34
Q

what general care is involved within MS management?

A
  • Bladder dysfunction: may require anticholinergic seg oxybutynin for detrusor overactivity, retention  intermittent self -catheterisation or long term catheters
  • Depression: duloxetine may be preferred if co-existing neuropathic pain/ fatigue. SSRIs
  • Fatigue: physical activity and treat co-morbidity eg modafinil
  • Gait disturbance: occupational and physio
  • Pain: neuropathic pain is significant issue  amitriptyline, gabapentin/ pregabalin
  • Spasticity: can lead to functional disability  may need physio and baclofen (skeletal muscle relaxants)
35
Q

how do you manage an acute relapse of MS?

A
  1. Need to rule out infection
  2. Need to distinguish from fluctuations in disease course or pregressive disease
    - Steroids: oral methylpred 500mg for 5days or IV 1g OD for 3-5days
    - Gastroprotection: PPI
    - Discuss risk/ benefit or treatment: acute changes in blood glucose/ mental health
36
Q

how long can it take to recover from a relapse?

A

Recovery may be 2-3months byt in some cases can be 12months
- If severe can lead to residual functional disability

37
Q

what are DMTs?

A

Disease modifying therapies: immunomodulatory meds that aim to decrease the number of relapses and slow progression

38
Q

what is the MOA of teriflunomide - DMT?

A

Inhibits pyrimidine synthesis  antiproliferative and anti inflame

38
Q

what is the MOA of glatirameter acetate - DMT?

A

Induce and activate T suppressor cells for myelin antigen

38
Q

what is the MOA of interferon - beta (DMT)?

A

Modulates immune response

38
Q

when is DMTs indicated?

A

no evidence of non-relapsing and sustained disability

39
Q

what is the MOA of alemtuzumab?

A

Monoclonal AB targeting CD52 – found in many immune cell lines – immunomodulatory

40
Q

what is the MOA of cladribine - DMT?

A

Purine nucleoside analogue – cytotoxic effects on B and T lymphocytes preventing DNA synthesis

41
Q

what is the MOA of natalizumab - DMT?

A

Monoclonal AB against alpha 4 subunit of integrin molecules. Prevents migration of leucocytes across BBB

42
Q

what is linked to worse prognosis?

A

primary rather than relapsing-remitting
not recovering from first attack
having pyramidal, brainstem, cerebellar path symptoms
more lesions and cerebral atrophy

43
Q

how is pregnancy linked to MS?

A

pregnancy - protective
postpartum: increased risk of relapse

44
Q

what are complications of MS?

A
  • fatigue
  • mobility balance problems
  • spasticity
  • bowel and bladder dysfunction
  • emotional lability
  • ophthalmic complications
  • pain
  • cognition including memory
45
Q
A

neuro (12 decks)

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