immunopath 3

Question 1

describe the mechanism of tissue damage for arthrus rxn and serum sickness

Answer 1

1) immune complexes (antibody + antigen) stuck in basement membrane
2) activate complement

Question 2

why is tissue damage called innocent bystander injury

Answer 2

when activate complement, surrounding tissue is damaged by complement (neutrophils + histamine release)

Question 3

Critical size when immune complexes stuck in basement membrane

Answer 3

Stuck if too small to be cleared by RE system but large enough to activate complement

~ 1,000,000 Daltons

Question 4

Describe one-shot serum sickness

Answer 4

1) animal antisera injected IV/IM
2) antibody production against antisera (XS antisera compared to antibody)
3) antisera decr, antibody incr
4) before equilvalence, little antisera excess forms complex with antibody to stick in basement membrane
5) activate complement until enough antibody to form larger complex with antisera to be eliminated

Question 5

when do serum sickness-like symptoms occur?

Answer 5

after treatment with murine, chimeric, or humanized monoclonal antibodies OR after viral infexn

Question 6

In which tissues does damage occur from deposition of immune complexes?

Answer 6

tissues with net outflow of fluid

• joints
• pleura
• peritoneum
• skin, choroid plexus,
  kidney

Question 7

Mechanism of type 3 disease with exogenous antigen

Answer 7

1) exogenous antigen enters blood –> forms complexes
2) complex moves to basement membrane
3) stuck in membrane –> activates complement

Question 8

Three conditions to illicit type 3 disease

Answer 8

ONLY ONE NEEDS TO BE MET

1) enough antigen introduced, so sufficient antigen to form complexes of right size to get stuck in basement membrane
2) antigen stored in depot so enough antibody made for complex
3) antigen self-replicating to produce enough of itself for complex

Question 9

How could urticaria from interaction of antigen with either IgE or IgG?

Answer 9

Urticaria = hives

when IgG and antigen complex activate complement, C3a/C5a anaphylaxotoxins cause release of histamines released from mast cells

or IgE in IgE/antigen complex bind through Fc end to mast cells and basophils –> release histamine

Question 10

Table for human immune complex diseases

Answer 10

see notes

Question 11

what is fluffy white precipitate?

how does fluffy white precipitate form?

Answer 11

mixed cryoglobulin

immune complex less soluble in cold so precipitate out of solution

Question 12

what does fluffy white precipitate in patient’s serum after 1 day in fridge mean?

Answer 12

means antibody-antigen complex formation and possible type 3

Question 13

What is rheumatoid factor and what are its components?

Answer 13

RF = IgM autoantibody to Fc portion patient’s own IgG

in RA

Question 14

Pathogenesis of post-streptococcal glomerulonephritis

Answer 14

1) immune complex form btwn antibody-antigen from Strep Pyogenes
2) stuck in basement membrane of kidney
3) activate complement

Question 15

how to diagnose glomerulonephritis by fluorescent antibody?

Answer 15

1) biopsy of pt kidney
2) add anti-IgG antibody
3) immune complex appear in clumps = LUMPY BUMPY

Question 16

pathogenesis of hypersensitivity pneumonitis (Farmer’s Lung)

Answer 16

1) individual has IgG antibody to antigen from chronic inhalation
2) enough antigen inhaled –> immune complex with IgG
3) complex diffuse to alveoli
4) activate complement + PMN

Question 17

Farmer’s lung

Answer 17

hypersensitivity pneumonitis example

antigen = Actinomycetes in moldy hay/silage

when damp hay dries, spores aerosolized