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A Haematology and Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is hypersensitivity?

A

A group of disorders where the normally beneficial components of the immune response act in an exaggerated or inappropriate fashion to environmental antigens which do not normally cause tissue damage.

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2
Q

What is responsible for tissue damage in hypersensitivity reactions?

A

The exaggerated response directed at the antigen rather than the antigen itself is responsible for the tissue damage which results.

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3
Q

What are the 4 types of hypersensitivity reaction?

A

Type 1:
Allergy/anaphylaxis

Type 2:
Cytotoxic (blood)

Type 3:
Immune complex (complement)

Type 4:
Delayed

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4
Q

What mediates type 1 reactions?

A

IgE

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5
Q

What elements are involved in type 1 reactions?

A
  • Allergen (antigen_
  • IgE
  • Mast cell/basophil
  • Th2 cells
  • Eosinophils
  • Genes
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6
Q

Give examples of allergens involved in type 1 reactions.

A

Airborne
-Pollen, house dust mitre, animal products

Ingested
-Milk, egg, fish, shellfish, cereals, nuts

Occupational
-Latex, drugs, industrial

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7
Q

When do type 1 reactions occur?

A

Immediate reaction to stimulus

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8
Q

What are type 1 reactions due to?

A

Hypersensitive Th cells

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9
Q

What is atopy?

A
  • Genetic potential to produce allergic reactions

- Genetic tendency to produce IgE to normally innocuous environemental allergens (40%)

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10
Q

What is allergy?

A

A clinical expression of atopic tendency (15-20%)

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11
Q

What are the 2 phases in type 1 reactions?

A
  • Sensitisation phase

- Reaction phase

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12
Q

What is the pathogenesis of type 1 reactions?

A
  • Allergen exposure
  • Mast cell activation and IgE
  • Leads to degranulation and release of preformed mediators
  • Synthesis of new mediators
  • Results in mucosal oedema, capillary leakage, secretions, smooth muscle contraction and vasodilation
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13
Q

What are the 2 response phases in type 1 reactions?

A
  • Early phase response (within minutes of allergen exposure)

- Late phase response (hours)

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14
Q

What is the early phase response of type 1 reactions due to?

A

Preformed mediators

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15
Q

What is the late phases response of type 1 reactions due to?

A
  • Due to newly synthesise mast cell -Th2 cytokines

- Eosinophil mediators

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16
Q

What mast cells mediators are preformed in type 1 reactions?

A
  • Histamine
  • Heparin
  • Tryptase
  • Chymase
  • ECF
  • NCF
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17
Q

What mast cell mediators are newly synthesised in type 1 reactions?

A
  • Prostaglandins

- Leukotrienes

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18
Q

How can allergy present clinically?

A
  • Allergic rhino conjunctivitis
  • Some asthma
  • Urticaria, angioedema, eczema
  • Food allergies
  • Anaphylaxis
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19
Q

What are some common precipitants of anaphylaxis?

A

-Foods: fish, shellfish, eggs, milk, nuts, wheat

Insect venoms: bee, wasp

Drugs: antibiotics, anaesthetic agents, antisera

Latex, seminal plasma

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20
Q

How is allergy diagnosed?

A
  • History and examination
  • Skin prick tests
  • Patch testing
  • RAST test (IgE levels)
  • Serum histamine, tryptase, leukotriene
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21
Q

How is allergy treated?

A

-Avoidance
-Antihistamines
-Steroid
-Adrenaline
-Patient education
-Sodium cromoglycate
-Leukotriene antagonist
-Desensitisation therapy
Specific treatment for asthma and anaphylaxis

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22
Q

What mediates type 2 reactions?

A

IgG or IgM directed against antigens on cell surface or within tissues

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23
Q

What is the pathogenesis of type 2 reactions?

A
  • Antibody binds to antigen
  • Complement activation
  • Fc binding and stimulation of phagocytes
  • Antibody dependent cellular toxicity
  • Inhibits or stimulates target cells
24
Q

How can type 2 reactions present clinically?

A
  • Haemolytic reactions (Autoimmune/blood transfusions)
  • Haemolytic disease of the new-born
  • Hyperacute graft rejection
  • Some organ specific autoimmune disease
25
Q

Give examples of organ specific autoimmune disease classed as type 2 reactions.

A
  • Grave’s disease (TSH receptor)
  • Myasthenia gravis (acetylcholine receptor)
  • Goodpasture’s syndrome (Type IV collagen)
  • Pemphigus (desmosomes)
26
Q

How are type 2 reactions treated?

A

Prevention

  • Cross matching of blood
  • Tissue typing
  • Detection of rhesus incompatibility in pregnancy

Immune suppression

  • Autoimmune disease
  • Transplant rejection
27
Q

What are type 3 reactions mediated by?

A

By actions of antibody: condition arises as a result of antigen/antibody complex deposition in tissues

28
Q

What is the physiology of a normal immune complex?

A
  • Immune complex undergoes opsonisation either directly or via complement activation
  • Uptake by phagocytes via Fc and complement receptors
  • Destruction of immune complex
29
Q

What is the pathophysiology of a type 3 reaction?

A
  • Excessive or abnormal immune complex formation
  • Complement activation and recruitment of inflammatory cells
  • Tissue damage
30
Q

What can type 3 reactions occur as a result of?

A

Antigen factors

  • Chronic persistence of antigen
  • An abnormal ratio of antigen to antibody
  • Rate of immune complex formation

Host response factors

  • Antibody defects
  • Complement defects
  • Fc or phagocyte defects
31
Q

How do type 3 reactions present?

A

Systemic illness where immune complexes form in the circulation and are deposited in a widespread fashion throughout many tissues (serum sickness)

More localised disorder where complexes are actually formed locally in tissues rather than being deposited from the blood (arthus reaction)

32
Q

When do symptoms occur in type 3 reactions?

A

4-10 hours after antigen exposure

33
Q

What clinical disorders can type 3 reactions manifest as?

A
  • Extrinsic allergic alveolitis
  • Post-streptococcal glomerulonephritis (complexes of streptococcal and anti-strep antibody)
  • Chronic infections such as leprosy and malaria
  • Tumours
  • SLE
34
Q

How are type 3 reactions diagnosed?

A
  • Clinical features
  • Tissue biopsy
  • Circulating immune complex tests
  • Precipitating antibody tests
35
Q

How are type 3 reactions treated?

A
  • Antigen elimination (e.g. infection, tumour)
  • Removal of immune complexes
  • Immunosuppressive therapy
36
Q

What mediates type 4 reactions?

A

No detectable Ab component and are mediated by Th1 and/or Th17 and the cytokines they secrete

37
Q

What do type 4 reactions occur in response to?

A

Occur in response to contact with inert environmental substances or as a reaction to infection with certain micro-organisms

38
Q

Why do type 4 reactions occur?

A

Generally take place as the immune system finds it difficult to destroy the agents. Due to:

  • Structure of the agent
  • Evolved ability of the organism to evade, confound or counteract the immune response
39
Q

What is the pathogenesis of type 4 reactions?

A
  • Exogenous low molecular weight antigen (hapten) binds to endogenous protein (carrier) or a micro-organism
  • Presented to antigen presenting cell (HLA-2)
  • Th1 (Th17) cytokine produce, dysregulation and overactivity
40
Q

What are the clinical presentations of type 4 reactions?

A
  • Tissue damage which occurs during mycobacterial infections or autoimmune disease
  • Mantoux test (skin test of delayed type hypersensitivity to mycobacterial peptides)
  • Contact dermatitis
41
Q

What can trigger contact dermatitis?

A
  • Metals
  • Drugs
  • Plastics
  • Rubber
  • Plants
  • Cosmetic
42
Q

What is the treatment for type 4 reactions?

A
  • Prevention and avoidance of contact with antigens
  • Antimicrobial therapy as required for specific infections
  • Anti-inflammatory drugs including corticosteroids
  • Immunosuppressive drugs in autoimmune disease where antigen cannot be avoided
  • Drugs that exploit knowledge of the immune response e.g. block TNF, IL6, B cells, often monoclonal antibodies
43
Q

Hapten

A

Low weight environmental stimlus

44
Q

What is a ‘carrier’ in type 4 reactions?

A

Host protein

45
Q

When do type 4 reactions manifest?

A

Clinical effects occur 48-72 hours after antigen exposure

46
Q

Why do type 4 reactions occur?

A

• The environmental stimulus generally does not cause any adverse effects, it is the immune system itself which causes the tissue damage

47
Q

Give examples of autoimmune disease associated with type 4 reactions.

A

T1DM
-Th1 respond to pancreatic islet cell antigens

MS
-Th1 and Th17 initiate damage but B cells and Abs also involved

Rheumatoid arthritis
-Many features of DTH with Th1 and Th17 and the TNF secretion but also autoantibodies involved

48
Q

Why do haptens need carriers?

A

Environmental agents involved are generally too small to produce an immune responses so they bind to host proteins to produce an antigenic stimulus that is big enough to cause a response

49
Q

What type of reaction is associated with atopic dermatitis?

A

Type 1

50
Q

What type of reaction is associated with contact dermatitis?

A

Type 4

51
Q

What is the cause of atopic dermatitis?

A

Degranulation of basophils and mast cells in response to sensitised IgE

52
Q

Who is atopic dermatitis common in?

A

Children

53
Q

Where does atopic dermatitis commonly affect?

A

Exposed and flexor surfaces

54
Q

Why does the skin get dry and itchy in atopic dermatitis?

A

Leaky skin allows more allergen in and water out

55
Q

What is the pathogenesis of contact dermatitis?

A
  • Haptens cross stratum corneum and act as antigen
  • Langerhans cells present TNF alfa and IL-1, 13 and 18 to Th1 cells
  • LCs become differentiated dendritic cells presenting allergenic epitope and multiply
56
Q

How does the 2nd time response in contact dermatitis compare to the first exposure?

A

More aggressive response 2nd time

A Haematology and Immunology (20 decks)

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