Immunopathology Type 3, Immune Complex Disease Flashcards

1
Q

____ and ____ attract neutrophils, which release cathepsin G, elastase, and hydrogen peroxide, causing degradation of the BM.

A

C3a; C5a

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2
Q

What are the treatments of Type 3 immunopathologies?

A

anti-inflammatory drugs, immunosuppressants, antihistamines, plasmapheresis

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3
Q

What is post-strep glomerulonephritis?

A

immune complexes in the kidney 10-14 days after a strep infection

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3
Q

What is Hypersensitivity Pneumonitis?

A

actinomycetes bacteria exposure causes development of IgG antibodies; on 2nd exposure, antigen/antibody complexes form in the lungs

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5
Q

How large is IgM?

A

750,000 daltons

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5
Q

What pathology of SLE makes it a type 3 disease?

A

pt makes IgG antibody to ds DNA; immune complexes deposit in the kidneys

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6
Q

What is the reticuloendothelial system (RES)?

A

all the macs/phagocytes of the tissues

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7
Q

As anaphylatoxins, C3a and C5a release ____ and other mediators from mast cells, increasing the inflammatory rxn.

A

histamine

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7
Q

What cells cause the symptoms of Hypersensitivity Pneumonitis?

A

neutrophils and complement initially; Th1 and Th2 in chronic cases

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7
Q

What pathology of RA makes it a type 3 disease?

A

an IgM autoantibody to one’s own IgG

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8
Q

What is the Arthus reaction?

A

immune complex formation from booster immunizations- activates complement and neutrophils; causes soreness at injection site

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10
Q

As anaphylatoxins, ___ and ____ release histamine and other mediators from mast cells, increasing the inflammatory rxn.

A

C3a; C5a

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11
Q

What is an immune complex formation from booster immunizations that activates complement and neutrophils; causes soreness at injection site?

A

the Arthus reaction

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12
Q

How do immunocomplexes activate complement?

A

they bind C1q to initiate the classical cascade

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13
Q

As anaphylatoxins, C3a and C5a release histamine and other mediators from ____, increasing the inflammatory rxn.

A

mast cells

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13
Q

What disease is caused by actinomycetes bacteria exposure causing development of IgG antibodies; on 2nd exposure, antigen/antibody complexes form in the lungs?

A

Hypersensitivity Pneumonitis

15
Q

How is the risk of serum sickness minimized?

A

by affinity purification and by cutting off the Fc portion of the protein and only using the F(ab) or F(ab2)

16
Q

How can you test for the presence of immune complexes?

A
  1. total hemolytic complement will be low; check lysis of RBCs using pts serum as compared to a standard 2. bind serum to complement C1q to look for complex agglutination 3. check for RF by adding pt’s serum to IgG coated microbeads 4. perform a renal biopsy, immunotag, and look for lumpy bumpy appearance
18
Q

What is serum sickness?

A

the binding of antibody to exogenous serum, forming immune complexes that accumulate until large enough that the RES can clear it out

20
Q

C3a and C5a attract _____, which release cathepsin G, elastase, and hydrogen peroxide, causing degradation of the BM.

A

neutrophils

21
Q

What is IgA nephropathy?

A

deposition of IgA and IgG bound to IgA1 in the renal glomerulus

22
Q

What size immunocomplex can activate complement but is too small to be removed by the RES?

A

1 million daltons

23
Q

Name 6 places immune complexes can lodge.

A
  1. joints 2. pleura 3. peritoneum 4. skin 5. choroid plexus 6. kidneys
24
Q

C3a and C5a attract neutrophils, which release ____, ____, and ____, causing degradation of the BM.

A

cathepsin G, elastase, and hydrogen peroxide

25
Q

What does RES stand for?

A

reticuloendothelial system

26
Q

What is a type 3 immunopathology?

A

immune complexes get stuck in basement membranes