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Immunology - First Aid > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

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
Q

When does an acute hemolytic transfusion reaction take place?

Why?

A

During transfusion
or within 24 hr

(due to preformed antibodies)

26
Q

What is clinical presentation of acute hemolytic transfusion reaction?

A
  • Fever
  • hypotension
  • tachypnea
  • tachycardia
  • flank pain
  • hemoglobinuria (intravascular)
  • jaundice (extravascular)
27
Q

What is pathogenesis of febrile nonhemolytic transfusion reaction
?

A

Cytokines created by donor WBCs accumulate during storage of blood products
Reactions prevented by leukoreduction of blood products

28
Q

When does a febrile nonhemolytic transfusion reaction take place?

Why?

A

Within 1-6 hr

due to preformed cytokines

29
Q

Transfusion related acute lung injury mechanism?

Timing?

Symptoms?

A

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
Q

Delayed hemolytic transfusion reaction mechanism?

Timing?
Why does it have this timing?

Symptoms?

A

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
Q

A person with respiratory distress & noncardiogenic pulmonary edema is having which type of reaction?

A

Transfusion related acute lung injury

32
Q

A patient presenting with fever, shivering and headache 3 hours after receiving blood transfusion is having which type of reaction?

A

Febrile nonhemolytic transfusion reaction

Immunology - First Aid (15 decks)

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