Hypersensitivity Reactions Flashcards

(32 cards)

1
Q

How many types of hypersensitivities?

A

Four types (ABCD)

Anaphylactic and Atopic (antibody-mediated, type I)

AntiBody-mediated (antibody-mediated, type II)

Immune Complex (antibody-mediated, type III)

Delayed (cell-mediated, type IV)

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2
Q

Which hypersensitivity reaction is antibody-mediated?

A

Type I, II, III

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3
Q

Which hypersensitivity reaction is cell-mediated?

A

Type IV

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4
Q

Anaphylaxis (eg, food, drug, or bee sting

allergies) and allergic asthma are which type of hypersensitivity reaction?

A

Type I hypersensitivity

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5
Q

What are the phases of Type I hypersensitivity?

A

Immediate (minutes):
antigen crosslinks
preformed IgE on presensitized mast cells → immediate degranulation → release:
-histamine (a vasoactive amine)
-tryptase (marker of mast cell activation)
-leukotrienes

Late (hours):
chemokines (attract inflammatory cells, eg, eosinophils) and other mediators from mast cells → inflammation and tissue damage.

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6
Q

What is the mechanism of type II hypersensitivity?

A

Antibodies bind to cell-surface antigens causing

→ Cellular destruction
—cell is opsonized (coated) by antibodies, leading to either:
- Phagocytosis and/or activation of complement system
or
- NK cell killing (antibody-dependent cellular
cytotoxicity)

→ Inflammation
—binding of antibodies to cell surfaces → activation of complement system and Fc receptor-mediated inflammation

→ Cellular dysfunction
—antibodies bind to cell surface receptors → abnormal blockade or activation of downstream process.

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7
Q

What is the difference between direct & indirect Coombs test?

A

Direct Coombs test
—detects antibodies attached directly to the RBC surface

Indirect Coombs test
—detects presence of unbound antibodies in the serum

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8
Q

What are some examples of type II hypersensitivity with cellular destruction?

A
  • Autoimmune hemolytic anemia (including drug induced form)
  • Immune thrombocytopenia
  • Transfusion reactions
  • Hemolytic disease of the newborn
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9
Q

What are some examples of type II hypersensitivity with inflammation?

A
  • Goodpasture syndrome
  • Rheumatic fever
  • Hyperacute transplant rejection
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10
Q

What are some examples of type II hypersensitivity with cellular dysfunction?

A
  • Myasthenia gravis
  • Graves disease
  • Pemphigus vulgaris
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11
Q

What is the mechanism of type III hypersensitivity?

A

In type III reaction, imagine an immune complex as 3 things stuck together:
“antigen-antibody-complement”

Immune complex—antigen-antibody (mostly
IgG) complexes → activate complement → attracts neutrophils which release → lysosomal enzymes.

Can be associated with vasculitis and systemic manifestations.

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12
Q

What is serum sickness?

Which type of hypersensitivity reaction?

A

Prototypic immunecomplex disease. Antibodies to foreign proteins are produced and 1–2 weeks later, antibody-antigen complexes form and deposit in tissues → complement activation → inflammation and tissue damage (↓ serum C3, C4)

Type III hypersensitivity

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13
Q

What is Arthus reaction?

Example?

Which type of hypersensitivity reaction?

A

Local subacute immune complex-mediated hypersensitivity reaction.
Intradermal injection of antigen into a presensitized (has circulating IgG) individual leads to immune complex formation in the skin

(eg, enhanced local reaction to a booster vaccination).

Characterized by

  • edema
  • fibrinoid necrosis
  • activation of complement

Type III hypersensitivity

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14
Q

Examples of Type III hypersensitivity?

A
  • SLE
  • Rheumatoid arthritis
  • Reactive arthritis
  • Polyarteritis nodosa
  • Poststreptococcal glomerulonephritis
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15
Q

Features of serum sickness?

What are some causes?

A
  • Fever
  • urticaria
  • arthralgia
  • proteinuria
  • lymphadenopathy occur 1–2 weeks after antigen exposure

Associated with:
- drugs (may act as haptens, eg, penicillin, monoclonal
antibodies)

  • infections (hepatitis B)
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16
Q

What is the mechanism of type IV hypersensitivity?

A

Two mechanisms, each involving T cells
(cell-mediated):

  1. Direct cell cytotoxicity: CD8+ cytotoxic T cells kill targeted cells
  2. Inflammatory reaction: effector CD4+ T cells recognize antigen and release inflammation-inducing cytokines

Response does not involve antibodies (vs types I,
II, and III).

17
Q

Which hypersensitivity reaction is cell-mediated?

A

Type IV hypersensitivity

18
Q

Which hypersensitivity response does not involve antibodies?

A

Type IV hypersensitivity

19
Q

Examples of Type IV hypersensitivity?

A

4T’s: T cells, Transplant rejections, TB skin
tests, Touching (contact dermatitis)

  • Contact dermatitis (eg, poison ivy, nickel allergy)
  • Graft-versus-host disease
  • Tests:
    >PPD for TB infection
    >patch test for contact dermatitis
    >Candida skin test for T cell immune function
20
Q

What are the types of blood transfusion reactions?

A

Allergic/ anaphylactic reaction

Acute hemolytic transfusion reaction

Febrile nonhemolytic transfusion reaction

Transfusion related acute lung injury

Delayed hemolytic transfusion reaction

21
Q

What is pathogenesis of allergic/ anaphylactic reaction?

A

Type I hypersensitivity reaction against plasma proteins in transfused blood

IgA-deficient individuals should receive blood products without IgA

22
Q

Which type of blood transfusion reaction occurs within minutes?

Why?

A

Allergic/ anaphylactic reaction

Within minutes to 2-3 hr

(due to release of preformed inflammatory mediators in degranulating mast cells)

23
Q

What is clinical presentation of allergic/ anaphylactic reaction?

A

Allergies:

  • urticaria
  • pruritus

Anaphylaxis:

  • wheezing
  • hypotension
  • respiratory arrest
  • shock
24
Q

What is pathogenesis of acute hemolytic transfusion reaction?

A

Type II hypersensitivity reaction

Typically causes intravascular hemolysis (ABO blood group incompatibility)

25
When does an acute hemolytic transfusion reaction take place? Why?
During transfusion or within 24 hr (due to preformed antibodies)
26
What is clinical presentation of acute hemolytic transfusion reaction?
- Fever - hypotension - tachypnea - tachycardia - flank pain - hemoglobinuria (intravascular) - jaundice (extravascular)
27
What is pathogenesis of febrile nonhemolytic transfusion reaction ?
Cytokines created by donor WBCs accumulate during storage of blood products Reactions prevented by leukoreduction of blood products
28
When does a febrile nonhemolytic transfusion reaction take place? Why?
Within 1-6 hr | due to preformed cytokines
29
Transfusion related acute lung injury mechanism? Timing? Symptoms?
Two-hit mechanism: - Neutrophils are sequestered and primed in pulmonary vasculature due to recipient risk factors - Neutrophils are activated by a product (eg, antileukocyte antibodies) in the transfused blood and release inflammatory mediators → ↑ capillary permeability → pulmonary edema Within minutes to 6 hrs - Respiratory distress - noncardiogenic pulmonary edema
30
Delayed hemolytic transfusion reaction mechanism? Timing? Why does it have this timing? Symptoms?
Anamnestic response to a foreign antigen on donor RBCs (Rh [D] or other minor blood group antigens) previously encountered by recipient Typically causes extravascular hemolysis Onset over 24 hr Usually presents within 1-2 wk (due to slow destruction by reticuloendothelial system) Generally self limited and clinically silent - Mild fever - hyperbilirubinemia
31
A person with respiratory distress & noncardiogenic pulmonary edema is having which type of reaction?
Transfusion related acute lung injury
32
A patient presenting with fever, shivering and headache 3 hours after receiving blood transfusion is having which type of reaction?
Febrile nonhemolytic transfusion reaction