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Lab 10

Multiple sclerosis is an autoimmune disorder characterized by CNS demyelination and axonal damage, leading to various symptoms such as vision changes, balance issues, and cognitive difficulties. Treatment options include acute relapse management with corticosteroids and long-term disease-modifying therapies like beta interferons and monoclonal antibodies. Complications may include mobility issues, memory loss, and emotional disturbances, necessitating symptomatic therapies for comprehensive care.

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Hossam Mohamed Ahmed ahmed
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11 views32 pages

Lab 10

Multiple sclerosis is an autoimmune disorder characterized by CNS demyelination and axonal damage, leading to various symptoms such as vision changes, balance issues, and cognitive difficulties. Treatment options include acute relapse management with corticosteroids and long-term disease-modifying therapies like beta interferons and monoclonal antibodies. Complications may include mobility issues, memory loss, and emotional disturbances, necessitating symptomatic therapies for comprehensive care.

Uploaded by

Hossam Mohamed Ahmed ahmed
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Multiple

sclerosis
Presented by: Menna-Allah Sakr
01
INTRODUCTION
❑ Autoimmune disorder with areas of CNS demyelination and axonal
transaction.

❑ Damages the protective myelin the protective covers (sheaths) that


surround brain and spinal cord nerves.
SYMTOMS
Change in vision
Loss of balance

Difficulty with cognitive


function Difficulty with bladder
regulation
Numbness or pain
Muscle stiffness and muscle
spasms (tremors) Difficulty in speech and
swallowing

Mood changes
COMPLICATIONS
• Difficulty walking without assistance

• Loss of bowel or bladder control

• Memory loss

• Sexual dysfunction

• Depression and anxiety


02
PATHOPHYSIOLOGY
03
TYPES
❑Relapsing :

Episodes of acute worsening

❑Remitting :

varying degree of recovery, with a stable course


between attacks (remissions)
TYPES

Relapsing
04
Treatment
1. Treatment of Acute relapses
IV Methylprednisolone: 1 gm / Day
(1 Dose or Divided doses for 3 -5
days)

Oral prednisone : 1250 mg/day


given every other day for five doses

Intravenous adrenocorticotropic
hormone
2. Long Term: (Disease-modifying therapies)
I. Beta interferons
II. Glatiramer acetate
III. Fingolimod
IV. Mitoxantrone
V. Dimethyl fumarate
VI. Antibody therapy (monoclonal antibody)
I. Beta interferons
M.O.A:
● Suppress t-cell activity
● Increase anti-inflammatory cytokines, and decrease inflammatory
cytokines
Interferon beta-1a
(Avonex):
30mcg , IM
once weekly

Interferon beta-1a
Beta (Rebif):
interferons 44 mcg, SC ,
3 times / week

Interferon beta-1b
(Betaseron):
0.25 mg, SC ,
Every other day
Adverse reactions

● Injection site reactions ✓ Bring a drug to room temperature


before injection.
✓ Ice the injection site.
✓ Rotate injection sites.

● Flulike symptoms ✓ Inject the dose in the evening.


✓ Begin at the 0.25–0.5 dose and
slowly increase.
✓ Use ibuprofen or acetaminophen.
II. Glatiramer acetate

M.O.A
● Decreases type 1 helper T cells
● Increases type 2 helper T cells
● Increases production of nerve growth factors.
Adverse reactions

● Injection site reactions Icing the site pre- and post-


injection may help

● Systemic reactions: - Flushing


- Chest tightness,
- Palpitations,
- Anxiety
- Shortness of breath
III. Fingolimod
First oral agent for multiple sclerosis treatment

M.O.A
● Binds to the S1P receptor 1 expressed on T cells, prevents
activation of T cells.

Contraindication
• Avoid pregnancy during treatment and for 2 months after treatment.
• Vaccines – less effective during and 2 months after fingolimod
treatment; avoid live attenuated vaccines.
Adverse reactions
● Bradycardia
✓ Patients must be monitored for bradycardia for 6 hours after the first dose.
✓ ECG is within 6 months for the following patients:
Using antiarrhythmics, With cardiac risk factors, With slow or irregular heartbeat

● Decrease in lymphocytes

✓ A recent CBC count before starting therapy.


✓ Infections may be more common. (Discontinue therapy for serious infections)
✓ Test patients without varicella zoster vaccine or infection history for varicella
zoster virus antibodies And immunize antibody negative patients (wait 1 month
to begin fingolimod).
IV. Mitoxantrone
● Potential for toxicity, reserved for patients with rapidly
advancing disease whose other therapies have failed.
● MOA:
Decreases monocytes and macrophages, inhibits T and B cells.
● No Live vaccines, other vaccines should be held for 4–6 weeks
post dose.
Adverse reactions

● Cardiotoxicity is the lifetime Echocardiograms or several


dose-limiting toxicity (140 gated acquisition scans must
mg/m2) be performed:
- at baseline and
- every 6 –12 months
thereafter
- before each infusion after
100 mg/m2 is reached.

● Therapy-related acute leukemia occurs in about 0.8% of


patients.
V. Dimethyl fumarate
● M.O.A:
Antioxidant and cytoprotective+ inhibits proinflammatory cytokines+
increases anti-inflammatory cytokines.
● Adverse reactions:
- Skin flushing: aspirin may block flushing + taking with food.
- GI events
- Lymphocytes decrease by 30% in the first year of therapy and then
stabilize.
VI. Monoclonal antibody
Natalizumab Alemtuzumab
Block T-cell entry into the CNS Binds to CD52 >cell surface antigen on T cells, B
cells, natural killer cells, monocytes, and
macrophages lead to lysis of T and B cells
For patients with relapsing-remitting disease Avoid live virus vaccines during treatment;
whose other treatment has failed complete all vaccines 6 weeks before initiation of
therapy
Adverse reactions: Adverse reactions:
• Progressive multifocal leukoencephalopathy • Thyroid disorders, immune
• Hypersensitivity reactions thrombocytopenia, glomerular nephropathies
• Infusion reactions, Increased infections
• May increase risk of thyroid cancer,
melanoma, and lymphoma
VII. Teriflunomide
● MOA:
Prevents activation of lymphocytes
● Adverse reactions:
✓ Hepatotoxicity
✓ GI effects
✓ Dermatologic effects: Alopecia, rash
✓ Infection
✓ Teratogenic: negative pregnancy test at baseline; adequate
contraception should be ensured.
3. Symptomatic therapies

● Fatigue, spasticity, urinary incontinence, pain, depression, cognitive


impairment, fecal incontinence, constipation, and sexual dysfunction; -
Treatment should be with standard therapies.

● Fatigue:

Nonpharmacologic (rest, cooling strategies, exercise, stress management).

Pharmacologic (amantadine, methylphenidate).


• Walking impairment
● Spasticity
Dalfampridine:
Therapies must be centrally
acting: ✓ improving walking speed.
i. First line: baclofen, ✓ Potassium channel blocker.
tizanidine ✓ Dose: 10 mg orally 2
ii. Second line: dantrolene, times/day; extended-release
diazepam tablets.
iii. Third line: intrathecal ✓ Contraindicated in patients
baclofen with history of seizures or
moderate or severe renal
iv. Focal spasticity: botulinum
impairment
toxin
05
Case study
● S.F. is a 36-year-old woman with a history of MS. This morning, her
left arm became progressively weaker over about 3 hours. She was
previously healthy except for a broken radius when she was 13
years old and a case of optic neuritis when she was 25. Her current
medications include metoprolol 100 mg orally twice daily and
fluoxetine 10 mg orally daily.
1. Which would be best for treating S.F.’s exacerbation?
A. Interferon beta-1a.
B. Glatiramer acetate.
C. Methylprednisolone.
D. Fingolimod.
2. Which would be best for S.F. to prevent further exacerbations?
A. Methylprednisolone.
B. Baclofen.
C. Glatiramer acetate.
D. No treatment
"You may not control all the events that
happen to you, but you can decide not to
be reduced by them."
—Maya Angelou
Thank you

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