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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

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2
Q

Type II Hypersensitivity reactions involve which class of antibodies?

A

IgM or IgG cytotoxic or cytolytic reactions

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3
Q

Type II Hypersensitivity reactions involve complement activity?

A

may or may not involve

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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

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5
Q

examples of Type II Hypersensitivity reactions

A

transfusions reactions, Rh incompatibility, autoimmune disease, drug reaction

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6
Q

Alloantigens

A

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

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7
Q

Examples of alloantigens

A

ABO, Rh

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8
Q

Alloantigens are

A

surface glycolipid antigens

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9
Q

People that are known as “secretors”

A

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

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10
Q

Isohemaglutinins

A

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

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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

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12
Q

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

A

No, their NF of the gut has not been colonized

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13
Q

What class of Ig are isohemaglutinins

A

IgM

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14
Q

Do you humans have naturally occurring Rh antibodies?

A

No

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15
Q

Are Rh antigens dense or sparse on the surface of RBCs

A

Sparse

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16
Q

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

A

Yes; No

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17
Q

The d/D antigen confers

A

Rh phenotype

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18
Q

Hemolytic Diseases of the newborn

A

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

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19
Q

Anti-Rh antibodies are of what class?

A

IgG

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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

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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

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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

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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

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24
Q

Prevention of HDN

A

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

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25
RhoGam
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
26
If HDN is present -
exchange transfusion with O negative blood
27
Administration of RhoGam should occur within __________ of birth
72 hours
28
ABO transfusion reactions are mediated by
isohemaglutinins of the IgM subclass
29
IgM are efficient at
complement fixing
30
ABO transfusion reaction mechanism
release of anaphylatoxins, damaged RBCs, free heme complex in circulation
31
Manifestations of ABO transfusion reaction
fever, chills, angina, hypotension, shock, DIC, renal failure
32
Non-Immune transfusion reactions include
transfusion of contaminated blood
33
Hemolytic blood transfusion reactions include
Major incompatibility, Minor incompatibility, delayed
34
Major incompatibility means
recipient has pre-existing antibodies against donor RBCs
35
Minor incompatibility means
donor serum/plasma contains antibodies to recipient's RBCs
36
Delayed hemolytic transfusion reaction
antibodies to donor's cells form after transfusion, 7-10 days for response
37
Non-hemolytic transfusion reaction
Recipient antibody to WBC (anti-HLA)
38
Anti-IgA of the IgE class may be present when
individual has a IgA deficiency, plasma given with IgA may cause anaphylaxis
39
Type III Hypersensitivities is mediated by
deposition of immune complexes with the activation of complement
40
Antigen in Type III Hypersensitivities is
SOLUBLE
41
Arthus Reaction
a localized reaction caused by aggregates of antigen and antibody (Immune Complex)
42
Arthus reaction mechanism
individual is sensitized to antigen, has high levels of IgG, subQ or intradermal dose causes reaction
43
Time of earliest onset of an Arthus Reaction
1-2 hours after injection
44
Examples of Type III Hypersensitivities
Arthus Reaction and serum sickness
45
Manifestations of an Arthus Reaction
local swelling at injection site (redness, edema, hemorrhage, necrosis), acute inflammation (neutrophils, slowed BF, hemorrhage and necrosis
46
C5a role
increase capillary permeability causing edema, C5a attracts neutrophils
47
Neutrophils at the injection site try to ingest immune complexes but cannot, this is called
frustrated phagocytosis
48
Neutrophils and platelets at injection site release
proteases, collagenases, ROS, and vasoactive substances
49
Example of an Arthus reaction is
intramuscular booster immunization into deltoid resulting in soreness
50
Serum Sickness
systemic reaction to an antigen administered intravenously
51
Manifestations of Serum Sickness
fever, enlarged lymph nodes, splenomegaly, red and urticarial rashes, painful joints, transient albuminuria, and edema
52
Onset of Serum Sickness in sensitized patients
3-4 days
53
Onset of Serum Sickness in non-sensitized patients
7-14 days
54
Serum Sickness mechanism
antigen is present in plasma when antibody is present of antibody formation is initiated, ICs deposit in blood vessels, glomeruli, joint fluid, etc
55
Serum CH50 concentrations
lowest level at height of disease (all of it is bound) fixing the complement
56
Serum sickness is a model for
autoimmune diseases (RA, lupus)
57
Type IV Hypersensitivities (delayed) mediated by
Cell-mediated immune responses of the CD4 T helper cell
58
Type IV Hypersensitivities (delayed) mechanism
memory T cells become effector T cells on second exposure, releasing mediators and cytokines that attract and activate other mononuclear cells and macrophages
59
Onset of Type IV Hypersensitivities (delayed)
24-48 hours in a sensitized individual
60
Manifestation of Type IV Hypersensitivities (delayed)
erythema at site and induration
61
induration
cutaneous and subcutaneous hardening
62
Example of Type IV Hypersensitivities (delayed)
tuberculin reaction or PDD skin test for TB, contact dermatitis
63
Type II Hypersensitivity reactions involve
insoluble antigens

Immuno Exam 3 (6 decks)

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