Brainscape's Knowledge GenomeTM

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


See full index

Immuno Final > 4 Hypersensitivity I > Flashcards

4 Hypersensitivity I Flashcards

1
Q

What is the normal function of the immune system?

A

defend against microbial infections by differentiating from the self and non-self and eliminating the non-self.

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

What are disorders caused by immune responses where they cause tissue injury and/or disease?

A

hypersensitivity

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

What are the 3 mechanisms by which immune responses can cause tissue injury?

A
  1. reaction against microbes
  2. reactions against environment antigens
  3. reactions against self
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 ways immune reactions against microbes can cause tissue damage?

A
  1. Immune response is excessive or persistent
  2. Antibodies produces against microbes bind antigen and the complex deposits in tissue
  3. Antibodies or T cells agains microbe cross-react with normal tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T-F—most healthy individuals have some reaction against common environmental substances?

A

False—most have no reaction

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

How much of the population have an abnormal response to one or more substances?

A

20%

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

What is the failure of the normal mechanisms of self-tolerance?

A

Autoimmunity—> reactions against self antigens

[5% of population most common between 20-40 years old]

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

Are the mechanisms of tissue injury are the same as those that are normally used to eliminate infections?

A

yes– but they are triggered and maintained inappropriately

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

What are the 4 types of hypersensitivity?

A

I=Immediate
II= Antibody mediated
III= immune complex mediated
IV=T cell mediated

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

What antibody mediates immediate Type I hypersensitivity?

A

IgE

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

What cells play a large role in Type I hypersensitivity?

A

Mast Cells and their mediators

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

What is the pathologic immune system of Type II hypersensitivity?

A

IgM, IgG against cell surface or extracellular matrix antigens

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

What is the pathologic immune response of Type III hypersensitivity?

A

Immune complexes of CIRCULATING ANTIGENS and IgM or IgG

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

What it is the pathologic immune mechanism of Type IV hypersensitivity?

A
  • CD4 T cells- cytokine mediated inflammation

- CD8 CTLS- direct cytolysis

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

What are the two ways antibodies can cause disease in tissues?

A
  1. Ig binds to particular cells/tissue [Type II]

2. Antigen-Ig complexes deposit in tissue/VESSEL [Type III]

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

What would a micrograph of a glomerulonephritis induced by an antibody against the glomerular basement membrane look like?

A

-glomerular inflammation
-smooth deposits of Ig along basement membrane
[Type II response]

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

What would a micrograph look like of glomerulonephritis induced by the deposition of immune complexes look like?

A

Neutrophilic inflammation and coarse deposits of antigen-Ig complexes along the basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What might be a treatment for a patient with IgG against protein antigens on the surface of RBCs?

A

Immunosuppression (glucocorticoids)—-may need a splenectomy too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

T-F–Type II hypersensitivity response antibodies are usually systemic that affect cells/tissues?

A

False–they are usually affected where the antigen is particularly present at

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the 3 effector mechanism of tissue injury?

A
  1. opsonization
  2. Antibody deposition in tissue
  3. Antibody binding to cellular receptos or proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What effector mechanism is described by phagocytosis?

A

Opsonization- [Directly or through complement cascade]

22
Q

What effector mechanism is described as recruitment of PMNs/Mac mediator release?

A

Antibody deposition in the tissue

23
Q

What effector mechanism is described as interference with normal function of the cell without inflammation or damage?

A

Antibody binding to cellular receptors or proteins

24
Q

What disease—nonsuppurative sequela 2-4 weeks after strep pharyngitis in 5-15 year old children?

A

Acute rheumatic fever

25
Q

What are some signs of acute rheumatic fever?

A

carditis, arthritis, chorea, rash

26
Q

What is the immunologic cause of acute rheumatic fever?

A

Ig and T cells against GAS [strep] antigens cross react with host antigens–[host mimicry of strep M protein and myosin]

27
Q

What is the most common cause of acquired valvular heart disease worldwide?

A

rheumatic heart disease

28
Q

Most patients with post streptococcal glomerulonephritis have very low serum levels of what? It is the most common cause of what?

A

1.C3

Acute nephritis worldwide

29
Q

Immune complexes deposited into tissues in Type III hypersensitivity activate what?

A

complement- and Fc receptor-mediated inflammation —–> this leads to injury of the vessels and adjacent tissues

30
Q

What are the particularly susceptible Type III response locations?

A

nephritis, arthritis, vasculitis

[remember that the plasm is ultra filtered in glomeruli and synovia of joints]

31
Q

Small complexes that form when antigen is in excess tend to deposit where?

A

in the blood vessels

[the larger aggregates fix complement and are cleared by circulating phagocytes]

32
Q

What classic prototype of antigen-antibody complex reaction—localized form of immune complex-mediated vasculitis, subcutaneous injection, antibodies binding rapidly, immune complex deposits in walls of arteries and local cutaneous vasculitis with tissue necrosis ensues?

A

Arthus Reaction

33
Q

What classic prototype of antigen-antibody complex reaction— systemic immune-complex mediated reaction, starts 7-10 days after exposure, symptoms are fever chills rash arthritis and glomerulonephritis?

A

Serum Sickness

34
Q

What illness is described as complexes deposited in small vessels and activating complement and phagocytes, inducing fever and the symptoms of vasculitis, nephritis, and arthritis?

A

serum sickness

35
Q

What are the 2 ways T lymphocytes injure tissues in Type IV hypersensitivity?

A

Trigger inflammation

or directly killing target cells

36
Q

What CD4 T cell cytokine activates macrophages?

A

IFN-y

37
Q

What CD4 T cell cytokine activates neutrophils?

A

IL-17

38
Q

Besides activating macrophages and neutrophils, what else does CD4 T cells release that causes inflammation and damage?

A

ROS
lysosomal enzymes
NO
Pro-inflammatory cytokines

39
Q

T-f–responses to viral infection by CD8 T cells can lead to killing infected cells even if the virus has no cytopathic effects?

A

True

40
Q

delayed type hypersensitivity takes about how long to develop after antigen challenge?

A

24-48

41
Q

About how many hours in delayed type hypersensitivity does it take for neutrophils to form around post capillary venues? For T cells and monocytes to surround venues? For induration to be detectable?

A

4
12
18

Peaks at 48 hours

42
Q

What forms in chronic DTH reaction when infection activates macrophages but fails to eliminate the phagocytksed microbes?

A

nodules of inflammatory tissue called granulomas

43
Q

What is a multinucleate giant cell?

A

fusion of activated macrophages that form in chronic DTH reaction

44
Q

What happens in chronic DTH reactions after prolonged cytokine signals?

A

cycle of injury and chronic inflammation followed by replacement with connective tissue
[fibrosis]

[in tuberculosis, it is the fibrosis that actually does the damage and not the microbes itself]

45
Q

Contact dermatitis to plant toxins is an example of what type of hypersensitivity reaction?

A

Type IV

46
Q

What is the pathway of initial exposure of poison ivy?

Re-Exposure?

A
  1. allergens penetrate epidermis—>APC processes—>regional lymph node—> clonally expanded T cells circulate.
  2. cytokine release occurs, clinical symptoms, in 12-48 hours
47
Q

What is the treatment for poison ivy?

A

topical corticosteroids

[for severe cases of the face and genitalia you could use systemic corticosteroids i.e. prednisone]

48
Q

T-F—contact dermatitis can be caused by many other allergens?

A

True

49
Q

There are a few slides that have tons of examples of each type of hypersensitivity…I don’t think they are going to be tested on and didn’t want to make tons of useless slides, but I would go back and look over.

A

:)

50
Q

There are a few slides that have tons of examples of each type of hypersensitivity…I don’t think they are going to be tested on and didn’t want to make tons of useless slides, but I would go back and look over.

A

:)

Immuno Final (7 decks)

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