Brainscape's Knowledge GenomeTM

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


See full index

Immuno Exam 3 > Lecture 23 Immunologically-mediated diseases > Flashcards

Lecture 23 Immunologically-mediated diseases Flashcards

1
Q

Type II Hypersensitivity reactions involve

A

insoluble antigens

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

Type II Hypersensitivity reactions involve which class of antibodies?

A

IgM or IgG cytotoxic or cytolytic reactions

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

Type II Hypersensitivity reactions involve complement activity?

A

may or may not involve

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

Mechanisms of Type II Hypersensitivity reactions is through either:

A

classical complement pathway activation, opsonic effects mediated by receptors for Fc or C3b, or ADCC

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

examples of Type II Hypersensitivity reactions

A

transfusions reactions, Rh incompatibility, autoimmune disease, drug reaction

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

Alloantigens

A

antigens that are shared as a group by species, but differ between individuals of the same species

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

Examples of alloantigens

A

ABO, Rh

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

Alloantigens are

A

surface glycolipid antigens

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

People that are known as “secretors”

A

secrete A and B alloantigen mucopolysaccharides in slavia, sweat, etc

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

Isohemaglutinins

A

naturally occurring IgM antibodies that occur with deliberate sensitization against them (Anti-A and Anti-B)

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

How does one obtain anti-B and anti-A antibodies without sensitization?

A

result of colonization of the gut over time with normal intestinal flora inducing a cross-reacting antibody against ABO antigens

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

Do newborns have anti-A and anti-B IgM?

A

No, their NF of the gut has not been colonized

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

What class of Ig are isohemaglutinins

A

IgM

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

Do you humans have naturally occurring Rh antibodies?

A

No

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

Are Rh antigens dense or sparse on the surface of RBCs

A

Sparse

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

Are ABO antigens present on cells other than RBCs? Rh?

A

Yes; No

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

The d/D antigen confers

A

Rh phenotype

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

Hemolytic Diseases of the newborn

A

Rh+ RBCs of the infant induce IgG anti-Rh antibodies in the mother

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

Anti-Rh antibodies are of what class?

A

IgG

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

If the mother’s anti-Rh antibodies cross the placenta, this will cause:

A

anemia (RBC destruction), Leukopenia and thrombocytopenia (bone marrow erythropoeisis crowds out other progenitors), hepatomegaly and jaundice, splenomegaly, ascites and edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Is it rare for HDN to occur during the first pregnancy?

A

Yes, it requires sensitization which generally occurs from a previous birth, but occasionally happens as a result of transfusions, leaky placenta, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Is it rare for HDN to be attributable to ABO blood group incompatibility between mother and child?

A

Yes, Anti-A and Anti-B are IgM antibodies, these do not cross the placental barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why is C’ fixation is not normally a major mechanism of HDN even though they are bound to IgG antibody?

A

Anti-Rh is IgG which is capable of complement fixation, but the concentration of Rh on a RBC is so sparse and the complement activation system requires 2 molecules of IgG, therefore it does to normally occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Prevention of HDN

A

Serotype parents, administer Rhogam before birth or in some cases throughout pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

RhoGam

A

anti-Rh IgG given to the mother 72 hours before birth, it binds and removes fetal RBCs before the mother’s immune system can initiate an immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

If HDN is present -

A

exchange transfusion with O negative blood

27
Q

Administration of RhoGam should occur within __________ of birth

A

72 hours

28
Q

ABO transfusion reactions are mediated by

A

isohemaglutinins of the IgM subclass

29
Q

IgM are efficient at

A

complement fixing

30
Q

ABO transfusion reaction mechanism

A

release of anaphylatoxins, damaged RBCs, free heme complex in circulation

31
Q

Manifestations of ABO transfusion reaction

A

fever, chills, angina, hypotension, shock, DIC, renal failure

32
Q

Non-Immune transfusion reactions include

A

transfusion of contaminated blood

33
Q

Hemolytic blood transfusion reactions include

A

Major incompatibility, Minor incompatibility, delayed

34
Q

Major incompatibility means

A

recipient has pre-existing antibodies against donor RBCs

35
Q

Minor incompatibility means

A

donor serum/plasma contains antibodies to recipient’s RBCs

36
Q

Delayed hemolytic transfusion reaction

A

antibodies to donor’s cells form after transfusion, 7-10 days for response

37
Q

Non-hemolytic transfusion reaction

A

Recipient antibody to WBC (anti-HLA)

38
Q

Anti-IgA of the IgE class may be present when

A

individual has a IgA deficiency, plasma given with IgA may cause anaphylaxis

39
Q

Type III Hypersensitivities is mediated by

A

deposition of immune complexes with the activation of complement

40
Q

Antigen in Type III Hypersensitivities is

A

SOLUBLE

41
Q

Arthus Reaction

A

a localized reaction caused by aggregates of antigen and antibody (Immune Complex)

42
Q

Arthus reaction mechanism

A

individual is sensitized to antigen, has high levels of IgG, subQ or intradermal dose causes reaction

43
Q

Time of earliest onset of an Arthus Reaction

A

1-2 hours after injection

44
Q

Examples of Type III Hypersensitivities

A

Arthus Reaction and serum sickness

45
Q

Manifestations of an Arthus Reaction

A

local swelling at injection site (redness, edema, hemorrhage, necrosis), acute inflammation (neutrophils, slowed BF, hemorrhage and necrosis

46
Q

C5a role

A

increase capillary permeability causing edema, C5a attracts neutrophils

47
Q

Neutrophils at the injection site try to ingest immune complexes but cannot, this is called

A

frustrated phagocytosis

48
Q

Neutrophils and platelets at injection site release

A

proteases, collagenases, ROS, and vasoactive substances

49
Q

Example of an Arthus reaction is

A

intramuscular booster immunization into deltoid resulting in soreness

50
Q

Serum Sickness

A

systemic reaction to an antigen administered intravenously

51
Q

Manifestations of Serum Sickness

A

fever, enlarged lymph nodes, splenomegaly, red and urticarial rashes, painful joints, transient albuminuria, and edema

52
Q

Onset of Serum Sickness in sensitized patients

A

3-4 days

53
Q

Onset of Serum Sickness in non-sensitized patients

A

7-14 days

54
Q

Serum Sickness mechanism

A

antigen is present in plasma when antibody is present of antibody formation is initiated, ICs deposit in blood vessels, glomeruli, joint fluid, etc

55
Q

Serum CH50 concentrations

A

lowest level at height of disease (all of it is bound) fixing the complement

56
Q

Serum sickness is a model for

A

autoimmune diseases (RA, lupus)

57
Q

Type IV Hypersensitivities (delayed) mediated by

A

Cell-mediated immune responses of the CD4 T helper cell

58
Q

Type IV Hypersensitivities (delayed) mechanism

A

memory T cells become effector T cells on second exposure, releasing mediators and cytokines that attract and activate other mononuclear cells and macrophages

59
Q

Onset of Type IV Hypersensitivities (delayed)

A

24-48 hours in a sensitized individual

60
Q

Manifestation of Type IV Hypersensitivities (delayed)

A

erythema at site and induration

61
Q

induration

A

cutaneous and subcutaneous hardening

62
Q

Example of Type IV Hypersensitivities (delayed)

A

tuberculin reaction or PDD skin test for TB, contact dermatitis

63
Q

Type II Hypersensitivity reactions involve

A

insoluble antigens

Immuno Exam 3 (6 decks)

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