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CSIM 1: Immunology Strand > CSIM 1.58: Autoimmune Disease 2 > Flashcards

CSIM 1.58: Autoimmune Disease 2 Flashcards

1
Q

Describe how autoimmunity mediated through type II hypersensitivity reactions causes tissue damage

Which diseases are caused by type II hypersensitivity autoimmunity?

A

Antibody-dependent (may have a direct effect by blocking or stimulating receptors). Complement may be involved in tissue destruction

  • Haemolytic anaemia
  • Autoimmune thyroid disease (Grave’s disease)
  • Myasthenia gravis
  • Goodpasture’s syndrome
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2
Q

Describe how autoimmune thyroid disease such as Grave’s disease comes about

A

Antibodies to thyrocytes TSH (thyroid stimulating hormone) receptor are produced, or antibodies that stimulate growth are produced: (IMG 135)
• Thyroid growth stimulating antibodies - this causes the thyroid gland to grow causing goitre
• Thyroid stimulating immunoglobulins - these stimulate the production of excessive thyroid hormone

Other antibodies stimulate the fat cells in the orbit to cause exophthalmos (bulging eyes)

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3
Q

Describe Goodpasture’s syndrome

A

Antibodies recognise type IV collagen in the basement membrane of the lung and kidney glomeruli

This causes renal failure and haemoptysis (coughing up blood)

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4
Q

What are the clinical features of Grave’s disease?

A

Thyroid features:
• Enlarged thyroid
• Lymphocytic infiltrate
• Excess expression of MHC II on thyrocytes
• Raised T4 (thyroxine) and T3 (triiodothyronine)
• Suppressed TSH

Systemic effects:
  •  Tachycardia
  •  Weight loss
  •  Diarrhoea 
  •  Tremor
  •  Exophthalmos (IMG 136)
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5
Q

How is Grave’s disease diagnosed?

A
  • Raised T4, T3
    • Suppressed TSH
    • Presence of anti-thyroid antibodies
    • Increased iodine uptake on scan
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6
Q

What MHC allele is Grave’s disease strongly associated with?

A

HLA-DR3

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7
Q

People with which antibodies present are more likely to develop thyroiditis in their lifetime?

Does thyroiditis increase or decrease thyroid function?

A

Antibodies against thyroid peroxidase

Can go either way

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8
Q

What can cause hypothyroidism?

What are the serological markers of this?

A
  • Antibodies to thyroid peroxidase
    • TSH-blocking antibodies

Low T4 and T3, raised TSH

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9
Q

What clinical features are present in hypothyroidism?

A 
(Opposite to Grave's disease symptoms)
  •  Weight gain
  •  Bradycardia
  •  Lethargic
  •  Constipated
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10
Q

Which autoimmune diseases are associated with autoimmune thyroid disease and are more likely to occur with those with this disease?

A

1) Type 1 diabetes
2) Addison’s disease
3) Pernicious anaemia

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11
Q

How would you diagnose the following diseases?

1) Type 1 diabetes
2) Addison’s disease
3) Pernicious anaemia
4) Ovarian failure

A

1) Glucose tolerance test, raised blood sugar
2) Low cortisol, short synacthen test
3) Low B12, macrocytosis
4) Amenorrhoea, low oestrogen

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12
Q

What are the potential autoimmune causes of the following diseases?

1) Type 1 diabetes
2) Addison’s disease
3) Pernicious anaemia
4) Ovarian failure

A

1) Antibody to islet cells
2) Antibodies to adrenal cortex
3) Antibodies to gastric parietal cells and intrinsic factor
4) Antibodies to steroid-producing cells of the ovary

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13
Q

Describe the pathogenesis of myasthenia gravis

A

Autoimmune antibodies produced against acetylcholine receptors, causing them to be internalised and degraded

This prevents Na+ influx and thus prevents muscle contraction

(IMG 137)

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14
Q

What are the clinical features of Addison’s disease?

A
  • Pigmentation of the gums
    • Pigmentation of the creases in their hands
    • Weight loss
    • Low BP
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15
Q

What eye-related symptoms are seen in myesthenia gravis?

A
  • Weak eyelids and eye muscles

* Double vision

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16
Q

How is myesthenia gravis diagnosed?

A

Tensilon test

17
Q

How is myesthenia gravis treated

A

Acetylcholinesterase inhibitors

18
Q

How is haemolytic anaemia tested for an autoimmune cause?

A 
Coombs test (IMG 139)
  •  Anti-human immunoglobulin antibody is added to red cells 
  •  If agglutination occurs, then haemolytic anaemia has autoimmune cause, agglutination will occur because the anti-human immunoglobulin will bind to the antibodies bound to the RBCs
19
Q

Describe the pathogenesis of autoimmune haemolytic anaemia

A

Autoantibody against red cell membrane antigen (Rhesus)
• If IgM, the antibody binds complement and causes lysis of the red cell
• Ig IgG, the antibody signals for the RBC’s phagocytosis in the spleen

IMG 138

20
Q

How does type III differ from type II autoimmunity/hypersensitivity?

A

Type III involves the formation of immune complexes and so produces more non-tissue specific autoimmunity, and more generalised autoimmunity

21
Q

Describe an immune complex

A

Antibodies bound to soluble antigen

IMG 140

22
Q

What can cause failure to clear immune complexes, and thus deposition?

A
  • Large amounts of antigen
    • Chronic infections (Hep C, bacterial endocarditis, etc.)
    • Systemic Lupus Erythematosus pathogenesis also causes failure to clear immune complexes
23
Q

Describe how immune complexes are normally cleared

A

RBCs bind to them with complement receptors to the liver or spleen where they are phagocytosed (IMG 141)

24
Q

What happens when immune complexes are not properly cleared?

A

They are deposited

25
Q

What is serum sickness? What type of reaction is this and why

What conditions does this relate to closely which use the same hypersensitivity reaction?

A

14 days after a high antigen exposure (e.g. from serum/injection) due to an acute immune complex reaction
• Arthralgia
• Rash
• Fever
• Renal impairment
This is a type III autoimmune hypersensitivity reaction because immune complexes are involved
IMGS 142 & I43

• Mixed essential cryoglobulinaemia
• Rheumatoid arthritis (also type IV)
NB: the only difference is that with these conditions there is a constant supply of the (self) antigen, and so the symptoms never subside

26
Q

What is SLE?

A

A genetically-predisposed condition with unknown environmental triggers which causes widespread autoimmune complexes to antigens released by apoptosing cells, mediated by auto-reactive lymphocytes.

These complexes are deposited throughout the body causing further tissue damage causing masses of symptoms

27
Q

Describe farmer’s lung

A

Inhaled allergens provoke the wrong response (IgG rather than IgE) stimulating the immune system (IgE usually causes typical asthma etc, whereas IgG actually causes immune complexes, etc.)

This causes immune complexes to form and deposit in the lung, followed by fluid, protein and cells (inflammation)

This slows blood gas interchange

28
Q

How can SLE be identified with diagnostic tests?

A
  • Low complement (it’s all being used up)
    • Antinuclear antibodies present
    • Raised IgG
    • Raised ESR (erythrocyte sedimentation rate)
29
Q

Which autoimmune-caused conditions have a type IV hypersensitivity reaction cause?

A
  • Type 1 diabetes
    • Rheumatoid arthritis
    • MS
    • Crohn’s
    • Psoriasis
30
Q

What causes glomerulonephritis in SLE?

A

Immune complex deposition (IMG 144)

31
Q

Describe the pathogenesis of rheumatoid arthritis

A
  • Unknown trigger initiates a focus of inflammation in a synovial membrane
    • This attracts autoreactive leukocytes, which activate macrophages
    • Bone-resorping osteoclasts are activated, while immune attack against synovial membranes begins
32
Q

What is rheumatoid factor?

A

Anti-IgG IgG immunoglobulins

33
Q

How is rheumatoid arthritis diagnosed?

A
  • Symptoms of painful inflammatory joints
    • Raised CRP
    • Raised ESR
    • Presence of rheumatoid factor
34
Q

What extra-articular disease is rheumatoid arthritis often co-morbid with?

A

Sjogren’s syndrome

35
Q

What are the early features of rheumatoid arthritis?

A

• Swelling and erosion of MCP and PIP joints

36
Q

What hypersensitivity types characterise rheumatoid arthritis pathogenesis?

A 
Type II (IMG 146)
Type IV (IMG 145)

CSIM 1: Immunology Strand (17 decks)

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