Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

immuno final > hypersensitivity II-IV > Flashcards

hypersensitivity II-IV Flashcards

1
Q

type II hypersensitivity reactions are mediated by-

A

antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

type III hypersensitivity reactions are mediated by-

A

immune-complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

type IV hypersensitivity reactions are mediated by-

A

T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 steps in type II hypersensitivity reaction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

autoimmune hemolytic anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

hemolytic disease of the newborn

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe RhoGAM schedule

A

1st dose at 28 weeks

2nd dose after birth if baby is Rh+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

goodpasteur’s syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

graves disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

myasthenia gravis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

autoimmune/idiopathic thrombocytopenic purpura

A

autoantibody against platelet membrane proteins

clinically- bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

pemphigus vulgaris

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

pernicious anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

rheumatic fever

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

3 steps in the process of type III hypersensitivity reactions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

arthus reaction mechanism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

consequences of arthus reaction (4)

A

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

18
Q

when was serum sickness first described?

A

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

19
Q

process for serum sickness

A

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

20
Q

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

A

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

21
Q

biggest difference between arthus run and serum sickness

A

arthus reaction is localized

serum sickness is systemic

22
Q

subacute bacterial endocarditis

A

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

23
Q

farmer’s lung

A

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

24
Q

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

A

antigen excess, bc they are smaller

25
Q

reaction that occurs when antibodies precipitate soluble antigen

A

precipitin reaction

26
Q

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

A
  • 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
27
Q

polyarteritis nodosa

A

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

28
Q

post-streptococcal glomerulonephritis

A

immune complexes with streptococcal cell wall antigens, cause nephritis

29
Q

process of type IV hypersensitivity reactions

A

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

30
Q

type IV hypersensitivity reactions are also called-

A

delayed

31
Q

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

A

intracellular protein- CD8

extracellular protein- CD4

32
Q

how does poison ivy cause Type IV reaction?

A

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

33
Q

how does nickel cause type IV reaction?

A

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

34
Q

what are the DCs of the skin?

A

langerhan’s cells

35
Q

what HLA type is assoc with 95% of celiac disease

A

HLA-DQ2

36
Q

proposed mechanism for development of celiac disease (3)

A

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

37
Q

3 mechanisms of tissue damage in celiac disease

A

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

38
Q

all pts with celiac disease have ___ against ___

A

IgA against TTg

39
Q

clinical triad of chronic bronchial asthma

A

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

40
Q

what is not used in the treatment of asthma?

A

anti-histamines have NO role in the treatment of asthma

immuno final (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions