Immunopathology - Allergy & Hypersensitivity Flashcards

1
Q

Which immunoglobulin types are involved in type II and III hypersensitivity?

A

IgM and IgG

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2
Q

What is the target of the antibodies in type II hypersensitivities?

A

cell bound or extracellular matrix antigens

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3
Q

What happens in type III hypersensitivities?

A

there is an immune complex deposition that can’t be cleared efficiently

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4
Q

What is the main damage caused by complement in immunopathology?

A

the inflammation due to the production of C3a and C5a

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5
Q

What are the two outcomes of type II hypersensitivity?

A

injury due to activation of effector mechanisms e.g. recruitment of inflammatory mediators and abnormal physiological responses due to activating or inhibiting receptors

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6
Q

What is a transfusion reaction?

A

a type II hypersensitivity where the antibodies in the blood attack antigens on the red blood cells that have been transfused

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7
Q

What are the consequences of a transfusion reaction?

A

RBC haemolysis, shock, nausea, vomiting, pain

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8
Q

What antibodies are in the blood of a type A?

A

B

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9
Q

What happens in a type II mediated drug allergy?

A

the drug will bind to RBCs and platelets and if the body produces antibodies against the drug then the splenic macrophages will phagocytose the cells resulting in haemolytic anemia or thrombocytopenia

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10
Q

What happens in haemolytic disease of the newborn?

A

In the first pregnancy the mother is Rh-ve and the baby is Rh+ve, when the baby is born foetal blood cells enter the mother’s circulation and the mother makes antibodies against them. In the second pregnancy if the baby is Rh+ve the antibodies that the mother has made will cross the placenta and attack the RBCs of the foetus

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11
Q

How is haemolytic disease of the newborn treated?

A

Give antibodies to the mother to clear the foetal RBCs from circulation before she makes an immune response

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12
Q

What is Goodpasture’s syndrome?

A

where antibodies are generated against type IV collagen and the complement and phagocyte activation causes glomerular disease

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13
Q

What is Grave’s disease?

A

where antibodies are generated which activate the receptor on the thyroid gland and cause hyperthyroidism

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14
Q

What is myasthenia gravis?

A

where antibodies block the ability of ACh to bind to the NMJ causing muscle wasting

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15
Q

What does the pathology of type III hypersensitivities depend on?

A

where the immune complexes are deposited

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16
Q

How are immune complexes usually removed?

A

in the spleen by resident macrophages

17
Q

Why are immune complexes not cleared?

A

when there is an excess of antigens, the antibodies are low affinity and there is poor complement activation

18
Q

What is the mechanism of type III hypersensitivity?

A

there is a gradual deposition of immune complexes, and once it reaches a threshold there is enough to activate complement which leads to the induction of inflammatory mediators and an inflammatory response

19
Q

What is the outcome if the immune complexes deposit on blood vessel walls?

A

vasculitis

20
Q

What is the outcome of the immune complexes deposit on glomerular basement membranes?

A

glomerulonephritis

21
Q

What is the outcome if the immune complexes deposit on joint synovium and vessels?

A

arthritis

22
Q

What are the causes of type III hypersensitivity?

A

either persistent infection, autoimmunity or an inhaled antigen

23
Q

What is farmer’s lung?

A

localised immune complex in the lung due to exposure to bacteria in mouldy hay (actinomyces) - causes alveolitis leading to inflammation and fibrosis

24
Q

What is systemic lupus erythematosis?

A

defined by presence of anti-DNA autoantibodies and immune complex deposition in kidney - involves multiple body systems - cause is unknown

25
Q

Why do we make antibodies against self?

A

because antigen receptors are generated in a random way and although there are mechanisms to remove receptors that are reactive to self sometimes these dont work

26
Q

What are the two forms of immunological tolerance?

A

central tolerance - removal of self reactive lymphocytes at the site of development and peripheral tolerance - removal of self reactive lymphocytes outside site of development