Type II and III hypersensitivity Flashcards

1
Q

What is the pathogenesis of goodpasture’s syndrome?

A

Ab binds to type IV collagen in glomeruli causing complement act. and phagocyte recruitment > glomeruli damage

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1
Q

What hormone is mimicked in grave’s disease?

A

TSH

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1
Q

How can self reactive ab form when there is a tolerance mechanism in place in the primary lymphoid tissue?

A

Self ab’s sneak through the system!

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3
Q

Which type of hypersensitivity involved immune complexes?

A

III

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4
Q

What is targeted in goodpasture’s syndrome?

A

A variant of collagen IV - particularly on glomeruli

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5
Q

What are the two possible outcomes ab binding to host ag in type II hypersensitivity?

A
  1. Complement activation > Inflammation > Damage
  2. Ab binding to proteins or receptors interfering with their function - can stimulate or inhibit
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6
Q

After which pregnancy (in a single mother) does haemolytic disease occur in newborns?

A

The 2nd pregnancy (if both children are Rh+)

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6
Q

Which hormone is overproduced in grave’s disease?

A

Thyroid hormones

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6
Q

Which organs are commonly affected in systemic lupus erythematosis?

A

Kidney

Skin

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7
Q

How can some drugs initiate a type II hypersensitivity response?

A

Drug bind to RBCs or platelets > anti-drug ab’s target the RBC/platelet+drug > damage

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7
Q

What happens to receptors in myasthenia gravis?

A

Aberrant self ab bind to them, blocking ligands from binding and causing them to be internalised

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8
Q

What is characteristic of immune complexes that are most effectively cleared?

A

They act complement well

They ab is high affinity

Their makeup is relatively high in ab’s

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9
Q

T/F Immune complexes in type III HS have self ag only

A

False, they can have self or foreign ag’s

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11
Q

What type of hypersensitivity occurs when blood transfusions are mismatched?

A

Type II

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12
Q

Which type of hypersensitivity II or III, targets cell bound or extracellular matrix protein?

A

II

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13
Q

What is an example of a type II HS disease where there is activation by the aberant ab

A

Grave’s disease

13
Q

Are self ab’s generally high or low affinity to their ag

A

Low affinity

14
Q

What must the ag status of the mother and baby be for haemolytic disease of newborns to occur?

A

Mother: Rh-

Baby: Rh+

16
Q

Which blood groups is the universal donor?

A

O

16
Q

Which receptors are targeted in myasthenia gravis?

A

Acetylcholine receptors

17
Q

Are small or large complexes better cleared?

A

Large

19
Q

Which blood group is the universal acceptor?

A

AB

20
Q

Where are immune complexes deposited in farmer’s lung?

A

Alveolar air spaces - leads to fibrosis and scarring

22
Q

What is example of a type II HS disease where there is inactivation by the aberrant ab

A

Myasthenia gravis

23
Q

What mediates type II hypersensitivity?

A

Antibody (particularly IgG and IgM)

24
Q

Describe the classical pathway for complement activation

A

Ab bound to a cell’s surface

C1 > C4 > C2 = C3 Convertase

C3 Convertase cleave C3 in C3a and C3b

25
Q

What are some examples of disease mediated by type III HS?

A

Farmers lung

Serum sickness

Glomerulonephritis

Rheumatic fever

Endocarditis

Arthritis

27
Q

How can you prevent haemolytic disease of newborns?

A

Give anti-Rh ab to the mother right after birth so she can’t develop an immune response to that ag.

28
Q

When do complexes in type III HS becomes probematic?

A

When are they overproduced or not effectively cleared and complement is activated and a strong inflammatory response is attracted in small vessels

29
Q

Which ag mediates haemolytic disease in newborns?

A

Rh (Rhesus)

30
Q

What do you find in kidneys in SLE?

A

Immune complexes and anti-DNA ab’s

32
Q

When do maternal antibodies against Rh form in haemolytic disease of newborns?

A

During the first pregnancy, the fetal blood enters the mother and the mother mounts an immune response to it

33
Q

What is the name of the bacteria in farmer’s lung?

A

Actinomyces