Type 3 Hypersensitivity Reactions:

Front 1

What are 3 other names of Type III hypersensitivity reactions?

Back 1

-immune complex mediated
-indirect target
-innocent bystander

Front 2

What is type III hypersensitivity a result of?

Back 2

-formation of circulating antigen-antibody complexes that deposit in vessel walls and activate complement

Front 3

Can Type III reactions form IC's that are both within circulation and in situ?

Back 3

YES

Front 4

What are three types of systemic TYPE III hypersensitivity reactions and 1 type of localized immune complex disease?

Back 4

systemic: serum sickness, systemic lupus arythematosis, post-infectious (post-streptococcus glomerulonephritis)

local: Arthus reaction

Front 5

Describe the history of discovery of serum sickness:

Back 5

Von pirquet in 1911 injected horse seru (horses exposed to diphtheria) into children; 10 days afterward found sickness in children from horse serum injected (whether horse was exposed or not exposed previously to diphtheria)

Front 6

What clinical findings did Von Pirquet discover in children injected with horse serum? (4)

Back 6

joint inflammation (arthritis and arthralgia); skin rash (urticaria); fever; glomerulonephritis

Front 7

What caused these symptoms?

Back 7

antigen-antibody deposition in vasculature

Front 8

-When do IC's become deposited in tissues and cause disease?

Back 8

-ICs produced in excessive amounts
-not efficiently cleared by phagocytic system

Front 9

What are three physicochemical properties of Ags and Abs that can determine the extent and location of IC deposition?

Back 9

-charge, valence, and antibody avidity
-local vascular factors (filtering at high pressure; urine and synovial fluid)
-affinity of Ag to tissue compartments

Front 10

What are two clinical outcomes for patients who developed serum sickness?

Back 10

-acute serum sickness (if single large exposure the IC's are catabolized)

-chronic serum sickness: repeated or prolonged exposure to an antigen

Front 11

Describe the three phases in the pathogenesis of Type III hypersensitivity disease:

Back 11

1.) Phase 1: immune complex formation
2.) Phase II: immune complex deposition via complement and Fc receptor-mediated leukocyte recruitment and activation
3.) Phase III: immune complex-mediated inflammation and tissue injury

Front 12

Reconstruct the robbins flow chart image of the pathogenesis of type III reactions:

Back 12

Front 13

What is this a picture of? and what type of necrosis is it?

Back 13

picture of immune complex vasculitis; necrotic vessel wall is replaced by smudgy, pink "fibrinoid" material: fibrinoid necrosis caused by protein deposition

Front 14

deposition of IC in vessel wall leads to activation of ______ and recruitment of _____

Back 14

complement, polys

Front 15

What is SLE and what organs does it affect an in what age group/ sex?

Back 15

systemic lupus erythematosis (SLE): chronic autoimmune inflammatory disease that affects every organ of the body;
-most prevalent in women from 16-64 years of age ; waxing and waning course

Front 16

What kind of antibodies does SLE make?

Back 16

antinuclear antibodies

Front 17

What two reasons explain the development of autoantibodies in SLE? What is the fundamental defect?

Back 17

-susceptibility genes -> B an T cells specific for self-nuclear antigens

-external triggers (UV radiation ) --> defective clearance of apoptotic bodies and increased burden of nuclear antigens
fundamental defect = failure of mechanisms that maintain self-tolerance

Front 18

What three factors may promote the development of ANA:

Back 18

genetic factors; immunologic factors; environmental factors:

Front 19

what are four categories of antinuclear antibodies and OTHER additional antibodies in SLE?

Back 19

-antibodies to DNA, histones, non-histone proteins bound to RNA, nucleolar antigens

-others: against RBC, WBC, platelets; and antiphospholipid antibodies produced in 40-50% of patients with SLE

Front 20

what is the principle screening test for SLE? How sensitive and specific is it? What antibodies are SPECIFIC for SLE?

Back 20

positive ANA lab test: 95% sensitive but not specific because 5-15 of healthy people have positive ANA

-antibodies to DS DNA and anti-smith ABS (small nuclear ribosomal Ag = specific for SLE)

Front 21

give four sample clinical manifestations of SLE:

Back 21

1.) skin rashes, arthritis, glomerulonephritis and CNS involvement

Front 22

What is the most commonly involved visceral organ in SLE?

Back 22

kidney (50% patients develop renal disease)

Front 23

What is difference between glomerulonephritis in Goodpasture's vs SLE?

Back 23

in SLE, antibody deposits along the glomerulus not specific whereas for Goodpasture's, the complexes is specific to the basement membrane collagen type IV

Front 24

Give two other systemic immune complex diseases not already mentioned:

Back 24

1.) poststrep glomerulonephritis
2.) polyarthritis nodosa with viral hepatitis

Front 25

describe classic scenario of post-strep glomerulonephritis (clinical presentation, time of appearance, labs, kidney appearance)

Back 25

-malaise, nausea, oliguria, hematuria, proteinuria 1-4 weeks after strep infection
-occurs only in nephritogenic strains -immune complexes may be circulating or antigen may be planted
-low complement lab levels and granular deposits of IgG on the GBM

Front 26

When does post-infectious polyarteritis nodosa occur and in what age group?

Back 26

-occurs following infection with Hep B or C virus infection; systemic vasculitis of medium size arteries
-average of of 40;

Front 27

What is the treatment of post-infectious polyarteritis nodosa and what happens if no treatment occurs?

Back 27

-immunosuppressive treatment
-if no treatment, death in 2-5 years

Front 28

What is the Arthus reaction and when does it occur/peak? Give example of type of reaction.

Back 28

-it is a localized area of tissue necrosis resulting from acute immune complex vasculitis
-peaks 4-10 hours after injection
-example is a tetanus booster