Lecture DetailsEdit

James Goding; Week 12 MED1011; Immunology

Lecture ContentEdit

Non-immunological tissue damage is caused by body's reaction to injury. Excessive scarring is fibrosis, associated with chronic inflammation and ongoing tissue damage eg cirrhosis. Most common causes are hepatitis B and C, consequences are bleeding due to lack of clotting factors, jaundice due to decreased bilirubin and brain disturbances.

Keloid is excessive scarring of skin wounds, genetic predisposition and due to foreign body (eg dirt) in wounds. Damage to abnormal tissues is a normal immune response, can occur in foreign tissues or infected tissues. Damage to normal tissues is abnormal immune response, can be due to an unusual type of response (allergy) or an unusual specificity of response (auto-immunity).

Autoimmune disease has a histological presentation of chronic inflammation (lymphocyte infiltration). Is more common in females than males. Some are organ specific such as diabetes, RA, thyrotoxicosis, MS. Some such as SLE affect multiple organs. Primary defect thought to be in T cells, risk factors associated with certain HLA types. An environmental trigger is likely but few have been identified. HLA B27 increases risk of ankylosing spondylitis by 90 fold, HLA DR3/4 increased IDDM 25 fold.

Type 1 hypersensitivity is immunological damage to normal tissues is IgE responses causing allergy, hay fever, hives etc. Mast cells are cross-linked by IgE causing degranulation and immediate hypersensitivity (bronchoconstriction, increased vascular permeability, mucus production). Hives is also known as urticaria.

Anaphylaxis is massive generalised tissue damage around the body, due to IgE mediated degranulation of mast cells. Causes low BP (circulatory collapse), itching, rash, asthma, swelling of eyelids, tongue, throat and other sites. Can be life threatening. Important to maintain airway, circulation and inject adrenaline subcutaneously.

Type 2 hypersensitivity is destroying cells by antibody and complement. Haemolysis is bursting of RBCs due to incompatible blood transfusion (normal response to abnormal cells) or autoimmune haemolytic anaemia (abnormal response to normal cells). Antibodies to these cells bind complement and induce haemolysis. Signs of an incompatible blood transfusion are urticaria, pain in back/chest/headache, shivering, fever, rapid pulse, sense of impending doom.

Type 3 hypersensitivity reaction is Arthus reaction; antigen-antibody complexes provoke inflammation via activation of complement or other mechanisms. Tissue damage by circulating antibody/antigen complexes are SLE and serum sickeness. Can cause skin rash, arthritis or kidney damage.

Type 4 hypersensitivity is delayed type, damage is caused by T cells. Examples are graft rejection, hypersensitivity to nickel, Mantoux test for TB.

IDDM has beta cells destroyed in pancreas, HLA DR3/4 increases risk 25 fold.

Type 5 hypersensitivity reaction is where antibodies to cellular receptors can stimulate cells or block signalling pathways. For example, in thyrotoxicosis antibodies to TSH receptors cause excessive release of thyroxine. Myasthenia gravis has antibodies to ACh receptors that keep it stimulated, causing tetany.


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