hypersensitivity II-IV

Question 1

type II hypersensitivity reactions are mediated by-

Answer 1

antibody

Question 2

type III hypersensitivity reactions are mediated by-

Answer 2

immune-complexes

Question 3

type IV hypersensitivity reactions are mediated by-

Answer 3

T cells

Question 4

3 steps in type II hypersensitivity reaction

Answer 4

1- anti-tissue antibody (other than IgE) binds to tissue
2- complement and antibody mediates recruitment and activation of inflammatory cells
3- neutrophils and macrophages cause tissue injury

Question 5

autoimmune hemolytic anemia

Answer 5

auto-antibodies against RBC antigens that promote their destruction via lysis or phagocytosis
tx- splenectomy or IVIG

Question 6

hemolytic disease of the newborn

Answer 6

problem for Rh- mothers carrying Rh+ babies
sensitization during first pregnancy and subsequent production of anti-Rh antibodies, upon 2nd pregnancy with Rh+ baby, anti-Rh antibodies attack and can cause erythroblastosis fettles or HDN, treat with RhoGAM

Question 7

describe RhoGAM schedule

Answer 7

1st dose at 28 weeks

2nd dose after birth if baby is Rh+

Question 8

goodpasteur’s syndrome

Answer 8

LINEAR deposition of autoantibodies (IgG) against collagen type IV- affects kidneys, lungs
activation of complement and compression of glomerulus

Question 9

graves disease

Answer 9

antibody to TSH receptor acts as agonist
Thyroid hormone release not regulated by circulating levels
clinically hyperthyroid

Question 10

myasthenia gravis

Answer 10

antibodies to Ach receptor are antagonistic
decrease mm response to stimulation
clinically flaccid paralysis

Question 11

autoimmune/idiopathic thrombocytopenic purpura

Answer 11

autoantibody against platelet membrane proteins

clinically- bleeding

Question 12

pemphigus vulgaris

Answer 12

autoantibody against epidermal cell junction protein (cadherin), clinically- blisters

Question 13

pernicious anemia

Answer 13

autoantibody against intrinsic factor of gastric parietal cells, clinically- B12 def

Question 14

rheumatic fever

Answer 14

autoantibody against strep cell wall antigen, antibody cross-reacts with myocardial antigen
clinically- myocarditis, arthritis

Question 15

3 steps in the process of type III hypersensitivity reactions

Answer 15

1- circulating immune complexes (not IgE) are deposited in blood vessel walls
2- complement and Fc receptor medicated recruitment of inflammatory cells
3- vasculitis develops

Question 16

arthus reaction mechanism

Answer 16

localized reaction in which an antigen is locally injected and forms immune complexes with IgG, immune complexes stimulate complement , C5a sensitizes mast cells to respond to the immune complexes and FcgRIII on mast cells are activated, degranulation is triggered upon binding

Question 17

consequences of arthus reaction (4)

Answer 17

local inflammation
increase in fluid and protein release
phagocytosis
blood vessel occlusion

Question 18

when was serum sickness first described?

Answer 18

when anti-pneumococcal antibodies from horses were used to treat pneumonia

Question 19

process for serum sickness

Answer 19

first injection of “serum” causes the formation of anti-serum IgG, second injection causes memory response; complexes cause fever, vasculitis, nephritis, arthritis and urticaria

Question 20

currently, serum sickness is sometimes induced by the injection of what? (4)

Answer 20

anti-lymphocyte serum (transplants)
horse antivenin
anti-TNFa mab (RA)
bacterial streptokinase (blood thinner for MI, CVA)

Question 21

biggest difference between arthus run and serum sickness

Answer 21

arthus reaction is localized

serum sickness is systemic

Question 22

subacute bacterial endocarditis

Answer 22

failure to clear microbe from heart valves results in continuous antibody production and subsequent formation of immune complexes

Question 23

farmer’s lung

Answer 23

inhaled antigens related to farm work cause the formation of antigen-antibody (IgG) complexes in the lungs

Question 24

which “type” of immune complex is more likely to be deposited in blood vessel walls?

Answer 24

antigen excess, bc they are smaller

Question 25

reaction that occurs when antibodies precipitate soluble antigen

Answer 25

precipitin reaction

Question 26

how does complement remove antigen-antibody complexes from the blood?

Answer 26

- C3b is deposited on circulating antigen-antibody complexes - complement receptor (CR1) on RBCs bind C3b (and thus binds the immune complex) - RBC travels to spleen or liver where phagocytes remove the bound immune complexes from the RBC surface

Question 27

polyarteritis nodosa

Answer 27

immune complexes with microbial antigens (like HBV antigen), cause vasculitis

Question 28

post-streptococcal glomerulonephritis

Answer 28

immune complexes with streptococcal cell wall antigens, cause nephritis

Question 29

process of type IV hypersensitivity reactions

Answer 29

1- CD4 cells cause tissue injury through activation of macrophages and inflammatory cells 2- CD8 cells mediate direct killing of cells

Question 30

type IV hypersensitivity reactions are also called-

Answer 30

delayed

Question 31

in allergic contact dermatitis, modification of intracellular protein will trigger activity of ___ vs. extracellular protein will trigger ___

Answer 31

intracellular protein- CD8 | extracellular protein- CD4

Question 32

how does poison ivy cause Type IV reaction?

Answer 32

urushiol penetrates skin, modifies intracellular proteins, modified proteins are displayed on MHC-I and CD8 T cells are activated

Question 33

how does nickel cause type IV reaction?

Answer 33

mediated by TLR4 that increases transcription of IRF3 and NFKB, and later IFN and proinflammmatory molecules

Question 34

what are the DCs of the skin?

Answer 34

langerhan's cells

Question 35

what HLA type is assoc with 95% of celiac disease

Answer 35

HLA-DQ2

Question 36

proposed mechanism for development of celiac disease (3)

Answer 36

1-peptides from gluten digestion move across IECs 2- ttg modifies peptides and they then bind MHC-II 3- MHC-II binding causes activation of gluten-specific CD4 cells

Question 37

3 mechanisms of tissue damage in celiac disease

Answer 37

1- activated T cels kill IECs by binding fas 2- activated T cells secrete IFNg to activate IEC (inflammation) 3- IECs release IL-15 to induce MIC-A expression, CD8 cells expressing NKG2D receptors will then kill IECs expressing MIC-A

Question 38

all pts with celiac disease have ___ against ___

Answer 38

IgA against TTg

Question 39

clinical triad of chronic bronchial asthma

Answer 39

1- intermittent airway obstruction 2- chronic inflammation with eosinophils 3- smooth mm hyper-reactivity to bronch-constrictors

Question 40

what is not used in the treatment of asthma?

Answer 40

anti-histamines have NO role in the treatment of asthma