Type II & III hypersensitivity Flashcards

1
Q

Type II hypersensitivity is mediated by?

A

antibodies

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2
Q

Which antibodies mediated in Type II hypersensitivity? against what?

A

IgM and IgG against tissue Antigens(Ag)

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3
Q

Type III hypersensitivity is mediated by?

A

IgM and IgG immune complexes

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4
Q

what so bad about immune complexes?

A

deposition in glomeruli

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5
Q

C3b does what?

A

opsonisation

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6
Q

C5b and C5a do what?

A

C5a: enhance inflammation/phagocytes
C5b: MAC

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7
Q

2 main outcomes for Type II hypersensitivity?

A
  1. injury due to MAC

2. abnormal physiology (activation/inhibition)

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8
Q

2 example of abnormal physiology Type II hypersensitivity?

A

Graves Disease

Myasthenia Gravis

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9
Q

Classic Type II hypersensitivity injury?

A

transfusion reactions

tissue rejection

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10
Q

what are some transfusion reactions?

A

haemolysis, shock, nausea, vomiting, pain

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11
Q

why are erythrocytes targets for Type II hypersensitivity responses for drug allergies?

A

drugs like penicillin bound to RBCs/platelets, get targeted by immune system = splenic macrophages causing haemolytic anaemis or thrombocytopenia

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12
Q

what is haemolytic disease of newborn?

A

Mom is Rh -ve, baby is Rh +ve, mom makes antibodies against baby during birth. 2nd birth, mom’s antibodies attack fetus RBCs if they are Rh+ve

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13
Q

How to treat haemolytic disease of newborn?

A

Give mother anti-Rh antibodies within 24 hrs of delivery to remove fetal RBCs in circulation

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14
Q

What is Goodpasture syndrome?

A

antibodies made against type IV collagen: basement membrane > glomerular disease

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15
Q

What happens in Type II hypersensitivity for Graves disease?

A

TSH negative feedback loop is useless because antibodies are made that continuously activate the TSH receptor = hyperthyroidism (

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16
Q

What happens in Type II hypersensitivity for Myasthenia Gravis disease?

A

antibodies attack acetylcholine receptors in neuromuscular junction, internalized and degraded (inhibit function)

17
Q

Type III hypersensitivity immune complexes occurs why? 2 reasons

A

complexes excessively produced

inefficiently cleared

18
Q

How are immune complexes normally dealth with?

A

cleared by splenic macrophages

19
Q

good efficient immune complexes are usually made up of what antibodies?

A

IgG with fixed complement

20
Q

which are better? large or smaller immune complexes? why?

A

large complexes better because they activate complement better, removed from circulation efficiently by RBCs

21
Q

3 reasons why immune complexes not cleared?

A

excess antigen
law affinity Ab
inefficient complement activation

22
Q

How do immune complexes cause pathology?

A

deposition on vessel walls > inflammation >complement > activate mast, basophils, platelets

23
Q

3 common outcomes of Type III hypersensitivity?

A

vasculitis
glomerulonephritis (BMs)
arthritis (joint synovium)

24
Q

Farmer’s Lung is e.g. of what kind of hypersensitivity?

A

Type III hypersensitivity

25
Q

how do you get immune complexes deposited in lungs?

A

inhaled antigen: mould, plant, animal antigen

26
Q

how do you get kidney, joint, arteries, skin immune complex deposition usually?

A

autoimmunity

27
Q

Farmer’s lung from exposure to?

A

mouldy hay dust/bacteria (actinomyces)

28
Q

SLE is? what kind of hypersensitivity?

A

systemic lupus erythematosis, Type III hypersensitivity

29
Q

2 big features seen in SLE? females or males more?

A

anti-DNA autoantibodies
immune complexes in BMs of kidneys
more females

30
Q

Antibodies against self reasons? 2 reasons

A

antigen receptor rearrangement is random

tolerance is not perfect

31
Q

2 kinds of tolerance

A

central: in bone marrow, removal during development
peripheral: T-Regs