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Respiratory system > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is hypersensitivity?

A

Altered state of immune responsiveness which causes excess or inappropriate immune response, leading to tissue damage

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2
Q

Which types of hypersensitivity are antibody mediated?

A

1-3, 4 is cell mediated

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3
Q

Type 1 hypersensitivity

A

Allergic/immediate hypersensitivity
IgE antibodies in response to antigens
Exposure - inhalation, ingestion, injection, direct contact

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4
Q

Systemic hypersensitivity

A

Anaphylaxis

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5
Q

Localised hypersensitivity

A

Allergic rhinitis, asthma

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6
Q

Sensitisation type 1 hypersensitivity

A
  • Allergen enters body, recognised by antigen presenting cells, breaks up allergen and presents on MHC II to T helper cells which activate B lymphocytes to differentiate = IgE antibodies which enter through blood to find mast cells and stick to their surface on Fc receptors (Bind to constant region of antibody)
  • IgE antibodies coat surface of mast cell = sensitised mast cell
  • Next time encountered, allergen binds to IgE antibodies on mast cell
  • When 2 antibodies bind to one antigen, cross linking occurs - signal activates mast cell to degranulate
  • Smooth muscle contraction, blood vessel contraction, mucous gland secretion, platelets activated, infiltration of eosinophils
  • Re-activating T cells which activates more B cells = more IgE cells = replenishes B cells
  • Smooth muscle - bronchospasm, cramps, rhinitis, hypovolaemia, hypoxia
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7
Q

Blood vessels

A

Erythema, oedema, pulmonary oedema

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8
Q

Eosinophils

A

Eosinophilia - damage of tissue

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9
Q

Pathophysiology type 1 hypersensitivity

A

IgE as a result of prior sensitisation
Subsequent encounter with antigens results in IgE-mediated reaction by preformed IgE antibodies
Free antigens binds to two adjacent IgE antibodies
Cells degranulate
Histamines and other mediators released

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10
Q

Type 3 hypersensitivity

A
  • Immune complex hypersensitivity
  • Onset usually 2-6 hours
  • Can be local or systemic
  • Antigens causing injury can be exogenous or endogenous
  • Resultant disease depends where complex forms and deposits
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11
Q

Pathophysiology of type 3 hypersensitivity

A

Immune complexes formed when antibodies bind to soluble antigens
Immune complexes deposit in basement membrane of blood vessels
Complement system activated
Release of anaphylatoxins which increase vascular permeability - oedema
Chemokines attract neutrophils - degranulation and inflammation

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12
Q

Examples of type 3 hypersensitivity

A

Lupus, polyarteritis nodosa, poststreptococcal glomerulonephritis, serum sickness

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13
Q

Symptoms of lupus and antigens involved

A

Nephritis, arthritis, vasculitis

DNA, nucleoproteins

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14
Q

Symptoms of polyarteritis nodosa and antigens

A

Vasculitis, hep B virus surface antigen

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15
Q

Symptoms of post streptococcal glomerulonephritis and antigens

A

Nephritis and streptococcal wall antigens

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16
Q

Symptoms of serum sickness and antigens

A

Arthritis, vasculitis, nephritis

Various antigens

17
Q

Type 4 hypersensitivity

A
  • Delayed hypersensitivity reaction - inflammation by 2-6 hours, peaks by 24-48 hours
  • Result from interaction of T-cell initiated inflammation and don’t involve antibodies
  • Inflammatory response results from manner in which T cells encounter and respond to antigen
  • Can be transferred by sensitised T cells but not serum
18
Q

Pathophysiology of type 4 hypersensitivity

A

T cell mediated
T helper cells: antigen penetrates skin - uptake by Langerhans cells - migration to lymph nodes and formation of sensitised T lymphocytes
Secretion of lymphokines and cytokines by sensitised T lymphocytes - macrophage activation and inflammatory reaction in tussle
Killer T cells release perforin and granzymes

19
Q

Examples of type 4 hypersensitivity

A 
Rheumatoid arthritis
MS
Type 1 diabetes
IBD
Psoriasis
20
Q

Principle mechanism of tissue injury of rheumatoid arthritis

A

Inflammation mediated by TH1 and TH17 cytokines

21
Q

Principle mechanism of tissue injury for MS

A

Inflammation mediated bey TH1 and TH17 cytokines - myelin destruction by macrophages

22
Q

Principle mechanism of tissue injury for IBD

A

Inflammation mediated by TH1 and TH17 cytokines

23
Q

Principle mechanism of tissue injury for type 1 diabetes

A

T cell mediated inflammation - destruction of islet cells by CTLs

24
Q

Principle mechanism of tissue injury for psoriasis

A

Inflammation mediated by T cell derived cytokines

25
Q

Anaphylaxis

A

Type 1 - mast cells and IgE

26
Q

Grave’s

A

Type 2 - antibody-antigen complex, IgM

27
Q

Lupus

A

Type 3 - IgG and IgM

28
Q

MS

A

Type 4 - T-cell mediated

29
Q

Rheumatoid arthritis

A

type 4/3

T cell driven

30
Q

Farmer’s lung

A

Type 3

Soluble antigens inhaled - mold

31
Q

1) hypersensitivity 2

A

1) antigen on healthy cell IgG or IgM bind to antigen = antigen-antibody complex on host tissue
Complement cascade activated and antibody dependent cell mediated toxicity
Complement binds to Fc portion of antibody. Some of the cascade becomes cleaved and chemotaxic (attracts neutrophils). Neutrophils undergo degranulation and release enzymes e.g. peroxidase, myeloperoxidase and proteinase 3 which generates oxygen radicals (cytotoxic to cell)

32
Q

2) Hypersensitivity 2

A

Antigen on healthy cell IgG or IgM binds to antigen = antigen-antibody complex on host tissue
Complement cascade activated and antibody dependent cell mediated cytotoxicity
Opsonisation and phagocytosis, again due to complement cascade. Phagocytes engulf cells in spleen

33
Q

3) hypersensitivity 2

A

Antigen on healthy cell IgG or IgM bind to antigen = antigen-antibody complex on host tissue
Complement cascade activated and antibody dependent cell mediated cytotoxicity
Ag-AB complex recognised by NK cells and binds to AB. Release perforins (form pores in cell). Granzymes and granulysin enter = apoptosis

34
Q

4) hypersensitivity 2

A

antigen on healthy cell IgG or IgM bind to antigen = antigen-antibody complex on host tissue
Complement cascade activated and antibody dependent cell mediated cytotoxicity
AB mediated cellular dysfunction. AB bound to antigen blocks normal receptor activator from getting to receptor e.g. myasthenia. Or cause overactivatioj of receptor e.g. Graves

Respiratory system (23 decks)

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