Hypersensitivity And The Lung Flashcards
Slide 13
The immune system- cells
Phagocytes e.g. monocytes and neutrophils phagocytose (envelop the invader) and some present to other cells
Lymphocytes: make and release antibodies and kill diseased cells
The immune system- humoral
Immunoglobulins
Complement (form membrane attack complex)
Cytokines (allow communication between leukocytes and tissue cells)
Antibodies
Produced by B-lymphocytes (plasma cells)
Neutralises or eliminates pathogens
In wrong circumstances May also cause disease
IgM
Circulating tetramers made at the beginning of infection
IgG
Monomer highly specific antibodies targeting single epitopes.
IgE
Likely to have developed in response to parasitic threats.
Implicated in allergy, particularly alongside eosinophils
IgA
Expressed in mucosal tissue. Forms dimers. Protects the neonatal gut (expressed in breast milk)
IgD
Monomers, induction of antibodies in B cells, activates basophils and mast cells
What is Hypersensitivity- Gell and Coombs classification?
Recognition of foreign antigen can cause collateral tissue damage
Slide 25
Type I
Antigen interacts with IgE bound to mast cells or basophils
This causes Degranulation of mediators lead to local effects
Histamine the predominant mediator
Anaphylaxis
Sudden onset
Systemic degranulation of mast cells and histamine release
Histamine increases vasodilation and vascular permeability
Skin, eyes, lips swelling, hypotension
Bronchospasm can result in airway occlusion and death if not quickly and accurately managed.
Type II
Antibodies reacting with antigenic determinants on the host cell membrane
Usually IgG or IgM
Outcome depends on whether complement is activated and if metabolism of cell is affected
Anti Glomerular Basement Membrane Disease
Rare but deadly type II HS disease
Goodpasture syndrome = alveolar involvement
GBM is made of type IV collagen present in alveoli and kidneys (glomeruli)
Alpha 3 subunit becomes antigenic
Mycoplasma Pneumonia
“Atypical” pneumonia
Cross reacting epitopes
Antibodies to M.Pneumonia also react to I antigen of red cells
Causes agglutination and haemolysis
Up to 50% of cases
Type III
Antigen-immunoglobulin complexes are formed on exposure to the allergen
These are deposited in tissues and cause local activation of complement and neutrophil attraction
Hypersensitivity pneumonitis
Formerly “extrinsic allergic alveolitis” (EAA)
Immune complexes formed with a range of different antigens
Deposited in the acinar airways leading to inflammation acutely and scarring chronically
Treatment by removal of antigen +/- immunosuppression
Type IV
T-cell mediated, releasing IL2, IFᵧ and other cytokines
Requires primary sensitisation
Secondary reaction takes 2-3 days to develop
May result from normal immune reaction – if macrophages cannot destroy pathogen, they become giant cells and form granuloma
Checkpoint
On ppt
Consequences of t-cell hyperactivity
Diabetes
Thyroid disease
Hepatitis
Nephritis
Myositis
Any –itis!
Life threatening pneumonitis
MUST STOP DRUG
Steroids may be helpfu
Asthma
Characterised by airway hyper-reactivity
Characterised by disease phenotypes
Different pathological mechanisms respond to different treatments
