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POD Exam II > Hypersensitivity 1 and 2 > Flashcards

Hypersensitivity 1 and 2 Flashcards

1
Q

Hypersensitivity:

A

An exaggerated response resulting i harm to the host.

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2
Q

Type I hypersensitivity results in:

A

Release of mediators from IgE-sensitized mast cells.

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3
Q

Components of Type I hypersensitivity immediate reaction (5):

A
  1. Allergen specific IgE.
  2. Mast cells.
  3. Allergen.
  4. Eosinophils.
  5. CD4+ Th2 cells
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4
Q

Type I hypersensitivity late-phase:

A

Develops more slowly, characterized by the accumulation of neutrophils, eosinophils and macrophages.

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5
Q

Type I hypersensitivity - sensitization (4):

A
  1. First exposure to allergen.
  2. Antigen activation of Th2 cells and stimulation of IgE class switching in B cells (IL-4).
  3. Production of IgE.
  4. Binding of IgE to FC receptors on mast cells.
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6
Q

Mediators of the Type I hypersensitivity immediate reaction:

A
  • Vasoactive amines (histamine).

- Lipid mediators.

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7
Q

Mediators of the Type I hypersensitivity late-phase reaction:

A

Cytokines.

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8
Q

Biologic effects of histamines (2):

A
  1. Vasodilation.

2. Vascular leak.

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9
Q

Biologic effects of lipid mediators (2):

A
  1. Broncho-constriction.

2. Intestinal hypermotility.

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10
Q

Biologic effects of cytokines:

A

Inflammation.

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11
Q

Biologic effects of enzymes:

A

Tissue damage.

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12
Q

Type I hypersensitivity late phase reaction(3):

A
  • IL-5 from mast cells and Th2 cells recruit and activate eosinophils.
  • Eosinophils release additional mediators.
  • Begins within 4-8 hours and lasts 1-2 days.
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13
Q

Disease states caused or affected by Type I hypersensitivity (6):

A
  1. Allergic rhinitis.
  2. Allergic asthma.
  3. Eczema or atopic dermatitis.
  4. Some food allergy.
  5. Some drug allergy.
  6. Insect venom allergy.
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14
Q

Allergic march:

A

Progression of allergic symptoms with age.

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15
Q

Allergen-specific serum IgE test:

A
  1. Plate (solid phase) coated with allergen.
  2. Patient’s serum added.
  3. Labeled anti-IgE added.
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16
Q

Serum IgE levels - ELISA method:

A
  1. Solid surface coated with anti-IgE antibody.
  2. Patient’s serum added.
  3. Labelled anti-IgE added.
17
Q

Type II hypersensitivity:

A
  • Antibody mediated hypersensitivity.
  • Involves IgM or IgG antibodies.
  • Involves a circulating antibody and its target antigen.
  • Antigen is located either on the surface of a cell in circulation or in a tissue.
18
Q

Antibody-dependent cell-mediated cytotoxicity:

A

ADCC

- IgG antibodies serve as “bridges” to link target cells to effector cells.

19
Q

Mechanisms of Type II hypersensitivity (3):

A
  1. Complement and Fc receptor mediated inflammation (ADCC).
  2. Opsonization and phagocytosis.
  3. Abnormal physiologic responses without cell/tissue injury.
20
Q

Disease associations of Type II hypersensitivity (6):

A
  1. Transfusion reaction.
  2. Hemolytic disease of the newborn.
  3. Autoimmune hemolytic anemia.
  4. Goodpasture syndrome.
  5. Pemphigus vulgaris.
  6. Rheumatic fever.
21
Q

Direct Coombs test:

A

Picks up antibodies directly on the surface of the red blood cell:
- Pt’s blood added to anti-Ig leads to agglutination of RBC.

22
Q

Direct Coombs test is used to diagnose (3):

A
  1. Hemolytic disease of the newborn.
  2. Autoimmune hemolytic anemia.
  3. Transfusion reaction.
23
Q

Indirect Coombs test:

A

Measures anti-RBC antibodies in the serum.

- Uncoated RBCs added to serum from pt with antibodies, anti-Ig added, agglutination of RBC.

24
Q

Main use of indirect Coombs test:

A

Blood banking:

  • Cross-matching.
  • Blood typing.
  • Ab detection.
  • Ab identification.
25
Q

Clinical symptoms of a transfusion reaction (4):

A
  1. Fever.
  2. Low BP.
  3. Nausea and vomiting.
  4. Back and chest pain.
26
Q

Hemolytic disease of the newborn:

A

Erythroblastosis fetalis:

  • Dramatic type II reaction.
  • Antigen present on the surface of the red cell, RhD.
  • Occurs in second pregnancy of woman who is RhD- and has RhD+ baby.
27
Q

Hemolytic disease of the newborn if untreated causes (4):

A
  1. Elevated bilirubin.
  2. Large liver and spleen.
  3. Petechiae.
  4. Positive direct Coombs test.
28
Q

Autoimmune hemolytic anemia:

A

AIHA

  • Pt’s produce anti-RBC antibodies.
  • Can cause hemolysis of RBCs.
  • Positive direct Coombs test.
29
Q

Pemphigus vulgaris:

A
  • Disease of skin and mucous membranes.
  • Causes blisters all over body.
  • Autoantibodies against intercellular cement substance of skin and mucous membranes.
30
Q

Goodpasture’s syndrome:

A
  • Targets basement membranes of kidney glomeruli and lung alveoli.
  • Leads to acute glomerulonephritis and pulmonary hemorrhage.
31
Q

Acute rheumatic fever:

A
  • Follows a throat infection with group A strep.
  • Symptoms present about 2-4 weeks following onset of infection.
  • JONES
  • Molecular mimicry with cardiac antigens.

POD Exam II (20 decks)

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