Hypersensitivity And The Lung

Question 1

Slide 13

Question 2

The immune system- cells

Answer 2

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

Question 3

The immune system- humoral

Answer 3

Immunoglobulins

Complement (form membrane attack complex)

Cytokines (allow communication between leukocytes and tissue cells)

Question 4

Antibodies

Answer 4

Produced by B-lymphocytes (plasma cells)

Neutralises or eliminates pathogens

In wrong circumstances May also cause disease

Question 5

IgM

Answer 5

Circulating tetramers made at the beginning of infection

Question 6

IgG

Answer 6

Monomer highly specific antibodies targeting single epitopes.

Question 7

IgE

Answer 7

Likely to have developed in response to parasitic threats.

Implicated in allergy, particularly alongside eosinophils

Question 8

IgA

Answer 8

Expressed in mucosal tissue. Forms dimers. Protects the neonatal gut (expressed in breast milk)

Question 9

IgD

Answer 9

Monomers, induction of antibodies in B cells, activates basophils and mast cells

Question 10

What is Hypersensitivity- Gell and Coombs classification?

Answer 10

Recognition of foreign antigen can cause collateral tissue damage

Question 11

Slide 25

Question 12

Type I

Answer 12

Antigen interacts with IgE bound to mast cells or basophils
This causes Degranulation of mediators lead to local effects

Histamine the predominant mediator

Question 13

Anaphylaxis

Answer 13

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.

Question 14

Type II

Answer 14

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

Question 15

Anti Glomerular Basement Membrane Disease

Answer 15

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

Question 16

Mycoplasma Pneumonia

Answer 16

“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

Question 17

Type III

Answer 17

Antigen-immunoglobulin complexes are formed on exposure to the allergen

These are deposited in tissues and cause local activation of complement and neutrophil attraction

Question 18

Hypersensitivity pneumonitis

Answer 18

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

Question 19

Type IV

Answer 19

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

Question 20

Checkpoint

Answer 20

On ppt

Question 21

Consequences of t-cell hyperactivity

Answer 21

Diabetes
Thyroid disease
Hepatitis
Nephritis
Myositis
Any –itis!
Life threatening pneumonitis
MUST STOP DRUG
Steroids may be helpfu

Question 22

Asthma

Answer 22

Characterised by airway hyper-reactivity
Characterised by disease phenotypes
Different pathological mechanisms respond to different treatments