Lecture 18 - autoimmune conditions pharmaceutical care Flashcards

1
Q

describe the difference between antibodies vs autoantibodies

A

antibody types are
IgM, IgG, IgA, IgD, IgE, attacks foreign antigens, cause infections agents to be targeted by other immune cells and destroyed

autoantibodies; mainly IgM, attack self antigens, in healthy individuals they target dead cells and waste products and in pathology they target specific self antigens in the body, developing autoimmune diseases

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2
Q

what are examples of autoimmune disorders?

A

neurological; Multiple Sclerosis
Myasthenia Gravis
Guillain-Barre Syndrome
Systemic Lupus Erythematosus
Chronic Inflammatory Demylenating Polyneuropathy

Rheumatoid Arthritis
Type 1 Diabetes
Ulcerative colitis
Psoriasis
Vasculitis
Coeliac disease

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3
Q

what are risk factors of autoimmune diseases?

A

Women twice as likely as men
Ethnicity
Genetic
Diet
Bacterial/viral infection
Adverse drug effects
Chemical Toxins/environmental pollutants
Prior medical history

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4
Q

what are signs and symtoms of an autoimmune disease

A

Fatigue
Fever
Swelling/Pain
Numbness/tingling in extremities
Rash
Muscle pain/weakness

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5
Q

what is the diagnosis f an autoimmune disease

A

No specific test
Difficult to diagnose
Magnetic resonance imaging (MRI)
Lumbar puncture (LP)
Antinuclear Antibody Test
Physical examination/Symptoms

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6
Q

what are treatments for autoimmune diseases?

A

Immunosuppressants
Steroids
Monoclonal antibody
Disease modifying therapies

Plasma exchange

Immunoglobulins

Analgesics

Lifestyle
- Diet
- Exercise
- Supplements

no cure

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7
Q

describe myasthesia

A

Myasthenia Gravis, Ocular Myasthenia, and Lambert-Eaton Myasthenic Syndrome are conditions related to autoimmune neuromuscular transmission issues.
T
he disease is characterized by autoantibodies targeting self-antigens at the acetylcholine (ACh) receptors.

Symptoms include weakness and fatigue in muscles, which worsen after exertion and towards the end of the day.

Myasthenia Gravis can affect individuals of any age and gender.
The disease may have periods of relapse and remission.

Treatments include anticholinesterase drugs, steroids, immunosuppressants, plasma exchange (plasmapheresis), intravenous immunoglobulin (IVIG), and surgical removal of the thymus gland (thymectomy).

There are certain drugs that individuals with Myasthenia Gravis should avoid such as drugs which affect nerve muscle transmission can make myasthenia worse

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8
Q

what is the treatment for myasthenia gravis ?

A

Pyridostigmine. It Inhibits acetylcholinesterase enzyme. There is a higher bioavailability of Acetylcholine and enhances nerve signal transmission

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9
Q

describe guillan barre syndrome

A

Often occurs 1-3 weeks after an infection

Self-antigen targeted by autoantibodies – Nodal proteins

Has been linked to Zika virus infection
More common in adult males

Affects the myelin coating of peripheral nerves causing weakness/numbness and pain in hands, feet and limbs. Can lead to breathing and swallowing issues in severe cases

Most people will make a full recovery although it can be quite serious and life threatening

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10
Q

what are the treatments for guillan barre syndrome ?

A

Intravenous immunoglobulin (IVIG). this is Made from donated blood that contains healthy antibodies. It Stops autoantibodies from damaging the nerves

Plasma exchange (plasmapheresis)
Filters blood to remove harmful antibodies then returning it to body

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11
Q

describe multiple sclerosis

A

multiple sclerosis affecst 3 times as many women than men.

it is caused by self-antigen targeted by autoantibodies myelin protein eg myelin nasic protein, myelin oligodendrocyte glycoprotein). The immune cells attacks the myelin coating that protect the nerve in the brain and spinal cord becomign damaged

Symptoms can include Optic neuritis, numbness, fatigue, Uhtoff’s phenomenon etc.

there can be 3 subtypes: relapsing, primary progressive, secondary progressive.

Treatment of disease modifying therapies (DMTs)

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12
Q

what are treatments for multiple sclerosis ?

A

Alemtuzumab (Lemtrada)
Anti-CD52 antibody (present on most immune cells)
Long-lasting depletion of B-cells (producers of antibodies) and T-cells
Restores healthy immune cell population

Ocrelizumab (Ocrevus)
Anti-CD20 antibody
Helps kill B-cells, stopping them from entering the brain where they can attack myelin

Beta interferons (e.g Betaferon)
Increases production of anti-inflammatory cytokines and downregulates production of proinflammatory cytokines

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13
Q

what are challenges of autoimmune condition treatment ?

A

New drugs

High cost therapies

Difficult diagnosis

Trial and error /risk vs benefit treatment

Debilitating conditions/no cure

Often require prompt treatment/life threatening

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