Hypersensitivity Reactions Flashcards

1
Q

Which of the hypersensitivity reactions is Antibody Independent?

A

Type 4 Reaction

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2
Q

What is the 1st exposure/priming of a Type 1 hypersensitivity reaction?

A

This is when a Dendritic Cell presents an allergen to a Th0 Cell–> Th2 CELL–> Activates B Cells–> Secrete Ig E

IgE will bind to the Mast cells through ERIIA receptors to release histamines during second response

**There are no free immune complexes present; IgE will be bound to the mast cell (mast cells are found in perivascular connective tissue)

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3
Q

What is the 2nd exposure of a Type 2 hypersensitivity reaction like?

A

Allergen binds mast cells by IgE antibody for the second time. This results in a cascade of events which causes the release of:

  • Neutrophil Chemotactic Factors
  • Eosinophil Chemotactic Factors
  • Proteases (to start complement cascade and results in tissue damage)
  • Histamines: Vasodilation, increased permeability, glandular secretions
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4
Q

How does asthma occur?

A

Type I hypersensitivity reaction that occurs from the activation of mast cells within the bronchioles

Results in:

  1. ) Increased glandular secretion–> increased luminal obstruction via mucus
  2. ) mucosal and submucosal swelling
  3. ) Bronchioconstriction
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5
Q

What are the strongest vasodilating signals in the Type I hypersensitivity reaction?

A

Leukotriene- C4, Leukotriene- D4, Leukotriene-E4

***STRONGEST VASODILATORS OF THE HUMAN BODY

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6
Q

What are the diseases associated with Type I hypersensitivity reactions?

A

Localized Type I Hypersensitivity Reactions:
Allergic Reactions, Rhinitis, Angioedema, Hay Fever

Granulized Type I Hypersensitivity Reactions:
Anaphylactic Shock

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7
Q

What is the key differentiating factor for Type 2 Hypersensitivity Reactions?

A

Antigen is always fixed and intrinsic to the tissue in which reaction occurs (IgG and IgM: “General Motors” Ab)

No free immune complexes

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8
Q

What are some of the common diseases associated with Type 2 Hypersensitivity reactions?

A

Acute Rheumatic Fever, Glomerulonephritis, Myasthenia Gravis, Hyperthyroidism (Grave’s Disease), Hemolytic Anemia

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9
Q

Mechanisms for these Type 2 Hypersensitivity Reactions?

A

Grave’s Disease/ Hyperthyroidism–> Ab binding to the TSH receptors will cause an increase in T3, T4 which will cause adaptive immune cells to attack and destroy these cells

Myasthenia Gravis–> attack of the immune cells by binding of Ab to the muscle receptors causing them to be the site of degradation!

Glomerulonephritis–> binding of complement antigens to the receptors of the glomerulus basement membrane makes these cells susceptible to cell-mediated attack.

Acute Rheumatic Fever–> streptococcus looks similar to certain protein on the heart which causes these receptors to start being degraded by immune cells as a response.

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10
Q

What are the 2 types of Type 3 Hypersensitivity reactions?

A

Immune Complex Formation: Generalized & Localized

Generalized (Serum Sickness)

Localized (Arthus Reactions)

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11
Q

What is the general process for Type 3 Hypersensitivity reactions?

A

It is dependent on the complement system:

Ab binds to Ab-antigen creating immuno-complex; this immunocomplex cannot be broken because macrophage activity is absent.

The Results:
The immune complex that is left behind will be activated by complement proteins which will settle in the walls of blood vessels.
- Formation of the Ag-Ab Complex
- Complement Activation
- Local necrotic Cells attack into the blood vessels

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12
Q

What is the localized arthrus reaction for Type 3 Hypersensitivity reactions?

A

Type 3 hypersensitivity reaction

-characterized by localized inflammation; fever, fatigability, general lymphadenopathy, raised under the skin

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13
Q

What are some other examples of Type 3 Hypersensitivity reactions?

A
Systemic Lupus Erythrematosus
Serum Sickness (General)
Arthus Reaction (Local)
PolyARTERITIS Nodosa
Post-Streptococcal Glomerulonephritis
Farmer's Lung
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14
Q

What are Type IV Hypersensitivity Reactions?

A

Delayed Type Hypersensitivity Reactions:

  • TH1 Cells are primarily activated
  • Tuberculoid Test (Tuberculosis)
  • Granuloma formation (inside epithelial cells + outside= macrophages)

Delayed Type Hypersensitivity Reactions:
Macrophage engulfment–> presentation to Th cell via IL-12–> Proliferation of many Th1 Cells (secretion of IL-2) –>clonal expansion–> Mature Th1 Cell secretion of TNF-GAMMA + IFN-GAMMA (Type 2 Interferon)

Mass migration of phagocytes to the site of infection*** to create granules around the epithelia

TNF–> increase the adhesion molecules for receptors
IFN-gamma–> recruitment of macrophages

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15
Q

What are examples of Type 4 Delayed Onset Hypersensitivity Reactions?

A
  • Urschiol Oil for Poison Ivy (Dermatitis)
  • TB Reaction
  • Multiple Sclerosis
  • Diabetes Mellitus I (TH1 cell mediated, Glutamic Acid Decarboxylase Enzyme Destruction on Insulin Receptors)
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