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?

16
Q

Which receptors are targeted in myasthenia gravis?

A

Acetylcholine receptors

17
Q

Are small or large complexes better cleared?

19
Q

Which blood group is the universal acceptor?

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
What mediates type II hypersensitivity?
Antibody (particularly IgG and IgM)
24
Describe the classical pathway for complement activation
Ab bound to a cell's surface C1 \> C4 \> C2 = C3 Convertase C3 Convertase cleave C3 in C3a and C3b
25
What are some examples of disease mediated by type III HS?
Farmers lung Serum sickness Glomerulonephritis Rheumatic fever Endocarditis Arthritis
27
How can you prevent haemolytic disease of newborns?
Give anti-Rh ab to the mother right after birth so she can't develop an immune response to that ag.
28
When do complexes in type III HS becomes probematic?
When are they overproduced or not effectively cleared and complement is activated and a strong inflammatory response is attracted in small vessels
29
Which ag mediates haemolytic disease in newborns?
Rh (Rhesus)
30
What do you find in kidneys in SLE?
Immune complexes and anti-DNA ab's
32
When do maternal antibodies against Rh form in haemolytic disease of newborns?
During the first pregnancy, the fetal blood enters the mother and the mother mounts an immune response to it
33
What is the name of the bacteria in farmer's lung?
*Actinomyces*