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Stage 2: Supporting Life > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is hypersensitivity?

A

An immunologically driven host tissue-damaging/tissue-irritating process

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2
Q

What are the 4 types of hypersensitivity?

A

1) Immediate hypersensitivity
2) Antibody-mediated
3) Immune complex mediated
4) Cell mediated (delayed)

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3
Q

Describe immediate hypersensitivity (type 1)

A
  • Non-microbial environmental antigens that are innocuous
  • Response within minutes
  • Mediated by IgE mast cells and their mediators
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4
Q

Describe antibody-mediated hypersensitivity (type 2)

A
  • IgM, IgG antibodies against cell surface/ECM
  • Complement mediated
  • The binding of antibody to antigen on cells/tissues activates complement and recruits immune cells
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5
Q

Describe immune complex mediated (type 3) hypersensitivity

A
  • Soluble immune complexes antigen-IgM or antigen-IgG
  • Complement mediated
  • Antibodies are important but it is the actual accumulation of antibody-antigen complex that drives illness
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6
Q

Describe cell mediated (delayed) hypersensitivity (type 4)

A
  • CD4 and CD8 cells (antibody independent)
  • Cell killing and cytokine-mediated inflammation
  • 24-48h after antigen challenge → takes longer to develop, delayed inflammation
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7
Q

What are the hallmarks of type 1 hypersensitivity?

A

IgE production and activation of Th2 cells

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8
Q

Describe the action of mast cells

A

1) Cross-linking of 2 adjacent IgE molecules triggers mast cell activation and degranulation
2) This releases cytokine cell mediators which create atopy and hypersensitivity

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9
Q

What cells other than mast cells also release granules?

A

Eosinophils

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10
Q

What are the two types of storage granules?

A

Histamine and tryptase

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11
Q

What is the action of histamine?

A
  • Increased vascular permeability → to collect more components of the immune system
  • Smooth muscle contraction
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12
Q

What is the action of tryptase?

A
  • Tissue remodelling
  • Increased mucus secretion
  • Fibrinogen alpha chain
  • C3a + C5a
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13
Q

What substances are produced de novo during degranulation of mast cells and what are their action?

A

Prostaglandins, leukotrienes and cytokines →

  • Increased vascular permeability
  • Smooth muscle contraction
  • Vasodilation (brain + flushing - PGD2)
  • Systemic anaphylaxis
  • Hypotension (bradykinin)
  • Bronchospasm (leukotrienes)
  • Swelling (b+l)
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14
Q

Why is systemic anaphylaxis lethal if not treated in minutes?

A

Because it is basically a massive vascular leak in whole body

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15
Q

What is an allergen?

A

An antigen that drives type 1 hypersensitivity bc it creates an allergic response

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16
Q

What are the two characteristics of the main allergens?

A

1) Individuals are repeatedly exposed to them
2) They do not induce macrophage/dendritic cell typical responses driving Th1/Th2 like microbes do → they need to induce Th2

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17
Q

What are the 4 types of main allergens?

A

1) Inhaled e.g. pollen, spores, dander, dust mite
2) Ingested e.g. peanut, egg, fruits, sesame
3) Venoms e.g bee, wasp strings and bites (Hymenoptera)
4) Drugs e.g. antibiotics, chemotherapeutics

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18
Q

What are inhaled antigens usually associated with?

A

Asthma hypersensitivity

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19
Q

What are examples of indoor inhaled allergens?

A 
Dust mites 
Animal dander (skin flakes) e.g. cats, dogs
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20
Q

What are examples of outdoor inhaled allergens?

A

Fungi - mould spores e.g. penicillin

Pollen e.g. grass or tree

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21
Q

Are patients often allergic to more than one allergen?

A

Yes

22
Q

What % of people in the UK are allergic

A

20%

23
Q

What are examples of type 1 hypersensitivity?

A
  • Pruritus (itch)
  • Urticaria (hives)
  • Allergic rhinitis (hay fever)
  • Asthma → immediate asthma (but asthma and allergy do not always co-exist)
  • Systemic anaphylaxis (whole body)
24
Q

What is wheal and flare?

A

Vasodilation + vascular leakage of plasma and protein (oedema)

25
Q

What is the late response of hypersensitivity?

A

Release of cytokines but basophils causing inflammation

26
Q

What is the effect of PAF (platelet activating factor)?

A

Vasodilation

27
Q

What are the (rapid onset) symptoms, by organ, of type 1 hypersensitivity?

A
  • Lung → asthma, wheezing
  • Nose → rhinitis, sneezing, runny nose
  • Eye → conjunctivitis
  • Skin → atopic dermatitis
  • Gut → food allergy
28
Q

What tests do you do to diagnose type 1 hypersensitivity?

A

1) Skin prick test → >3mm wheal (swelling) - prick contains a bit of the antigen
2) Total IgE → > 100 IU/ml
3) Specific IgE raised against specific antigen e.g. RAST
4) Tryptase levels → transient (24-48h), so need to take at the right time
5) RAS test
6) BAT/MAT test (basophil and mast cell activation tests)

29
Q

What is the RAS test?

A

Radio-AllergoSorbent Test

  • Detection of label → proportionate to the amount of IgE specific for the antigen
  • On the surface, fix the specific antigen and put it in touch with the serum of the patient to test if there is IgE specific to the antigen
30
Q

What are the types of type II hypersensitivity?

A

1) Complement activation and opsonisation → phagocytosis
2) Complement and Fc receptor mediated inflammation → neutrophils and macrophages are recruited and bind to Ab or complement via IgG Fc or complement R
3) No cell/tissue injury → activation of abnormal processes

31
Q

What are examples of complement activation and opsonisation type II hypersensitivity?

A

1) Autoimmune haemolytic anaemia
2) Autoimmune thrombocytopenia purpura
3) Haemolysis in transfusion reactions (incompatible e.g. different blood types)

32
Q

What are examples of complement and Fc receptor mediated inflammation type II hypersensitivity?

A

1) Glomerulonephritis

2) Vasculitis caused by ANCA (anti-neutrophil cytoplasm antibody)

33
Q

What are examples of no cell/tissue injury type II hypersensitivity?

A

1) Grave’s disease (TSH receptor)
2) Insulin-resistant diabetes
3) Myasthenia gravis (Ab-ACh)

34
Q

What are the key features of type III hypersensitivity?

A
  • Binding of antibody to antigen (self or foreign)
  • Soluble complexes not cleared leading to immune complexes of circulating antigens and IgM/G antibodies
  • Activation of complement and recruitment of neutrophils and macrophages
  • Pathologic features reflect the site of deposition (deposit in middle sized blood vessels) → multiple tissues
35
Q

What causes serum sickness in type III hypersensitivity?

A

Accumulation of complexes

36
Q

What are the types of complexes involved in type III hypersensitivity?

A

1) Small complexes
2) Complexes that activate mast cells/leukocytes → cytokines, vasoactive mediators
3) Deposited complexes → inflammation

37
Q

Describe small complexes involved in type III hypersensitivity?

A
  • Not phagocytosed bc relatively small
  • Deposed in vessels
  • Ab-Ag+ : BM and glomeruli- → deposited here bc they have positive charge and BM/glomeruli have negative charge
  • Severe, long lasting injury
38
Q

What are 3 examples of diseases involving type III hypersensitivity?

A

1) SLE (nuclear Ag-Ab) → nephritis, arthritis, vasculitis (complexes in small arteries, synovial joints and renal glomeruli)
2) Polyarteritis nodosa (Hep B Ag-Ab) → vasculitis
3) Poststreptococcal glomerulonephritis (streptococcal Ag-Ab) → nephritis

39
Q

What is BSA?

A

A protein used to mimic hypersensitivity

40
Q

What are the two types of type IV hypersensitivity?

A

1) Cytokine-mediated inflammation → APC presents Ag to T cell, leading to activation of Th1, Th17 and Th2 cells
→ (CD4) T cells secrete cytokines leading to macrophage activation and inflammation (delayed type hypersensitivity)
2) T cell mediated cytotoxicity → CD8 T cells directly kill tissue cells, direct target cell lysis

41
Q

What are examples of diseases involving cytokine-mediated inflammation in type IV hypersensitivity?

A

1) IBD → Th1/Th17 = Crohn’s, Th2 → ulcerative colitis
2) Contact sensitivity/dermatitis (Ni2+)
3) Asthma
4) RA?

42
Q

What are examples of diseases involving T cell mediated cytotoxicity in type IV hypersensitivity?

A

1) Autoimmune myocarditis → myosin heavy chain protein

2) Type 1 diabetes mellitus → destruction of islet cells

43
Q

What two types of hypersensitivity are most linked to asthma?

A

Type I and type IV

44
Q

What is the immune mechanism in type II hypersensitivity?

A

IgM and IgG antibodies to cell surface ECM antigen

45
Q

What causes type I allergic reactions?

A

Allergen + allergen-specific IgE + mast cell

46
Q

What are the stages of anaphylaxis (type I immediate hypersensitivity, systemic allergic reaction)?

A

I) Generalising itching, urticaria
II) Swelling away from the sting e.g. sting on cheek to swelling in eye
III) Difficulty breathing
IV) Fall in BP, loss of consciousness

47
Q

What pro-inflammatory mediators are released by degranulation?

A

1) Short lived = histamine and serotonin

2) Sustained inflammatory drives = cytokines and leukotrienes

48
Q

What are the actions of pro-inflammatory mediators released by degranulation?

A

1) Vasoactive - increased local blood flow and vascular permeability leads to fluid accumulation and influx of blood cells
2) Smooth muscle cell contraction causes expelling e.g. vomiting and diarrhoea, increase in mucus and cough in bronchial constriction
3) Cytokines e.g. IL-4 and TNFalpha cause a sustained inflammatory signal

49
Q

Describe the skin prick test for diagnosis of type I hypersensitivity

A
  • Put some allergen on skin and prick it into the CT below the skin where the mast cells are
  • If you are allergic, you will have IgE coated mast cells there and so this prick will cause the release of the inflammatory mediators leading to wheal and flare
50
Q

Describe the immunoassay radioallergosorbent test (RAST) for diagnosis of type I hypersensitivity

A

Measure antibody in serum but need to be v sensitive assays bc most allergen-specific IgE is attached to mast cells in CT so there are v low levels of circulating IgE in the blood stream

Stage 2: Supporting Life (30 decks)

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