Hypersensitivites Flashcards

1
Q

Hypersensitivity

A

Excessive adaptive immune response due to innocuous antigens (allergens)

Symptoms are due to response NOT allergens

4 types

1) immediate hypersensitivity
- mast cells and IgE are responsible

2) antibody mediated
- IgM and IgG antibodies are responsible

3) immune simplex-mediated
- antigen-antibody complexes are responsible

4) T-cell mediated (delayed)
- CD4/* T cells are responsible

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2
Q

Sensitization phase vs effector phase

A

Sensitization phase
- initial exposure w/ NO tissue pathology or clinical signs

Effector phase
- clinical signs as a response to subsequent exposures after initial exposure

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3
Q

Type 1 hypersensativites

A

Immediate hypersensitivity
- Most COMMON form

Mast cells bind allergen antigens via Fc receptors
- eventually cross link w/ IgE and cause degranulation of histamine and allergy mediate cytokines

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4
Q

Specific steps in the sensitization phase

A

1) dendritic cells migrate to lymph nodes w/ allergen antigen to prime T-cells for future exposure
2) differentiation into TH2 and class switching to IgE occurs in lymph nodes

3) antigen-specific IgE binds to high affinity IgE Fc receptors on mast cells
* waits for subsequent exposure*

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5
Q

Mast cell degranulation

A

Requires at least 2 molecules of IgE must bind to an allergen

When degranulation occurs, the following are released

  • histamine and enzymes (causes vascular permeability)
  • cytokines (IL3/4 and TNF-a)
  • chemokines (CCL3)
  • lipid mediators (prostaglandins and leukotrienes)
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6
Q

IL-3, IL-4, TNF-a, prostaglandins and leukotrienes specific effects

A

IL-3: works to promotes eosinophil production and activation

IL-4: stimulates and amplifies TH2 cell response

TNF-a: promotes inflammation and stimulates stroking production

Prostaglandins and leukotrienes: smooth muscle contraction, chemotaxis of eosinophils and increases vascular permeability
- also bronchoconstriction

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7
Q

What is the primary mover in type 1 hypersensitivity?

A

Histamine

  • is stored in mast cells
  • binds to H2 receptors and causes the following

1) vasodialation and increased vascular permeability
2) smooth muscle contraction
3) increased mucus production

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8
Q

What is the secondary mediator in type 1 hypersensitivity?

A

Prostaglandins and leukotrienes
- not stored and is produced de novo from histamine reactions

  • Prostaglandin effects:
  • vasodilation
  • bronchoconstriction
  • chemotaxis for neutrophils and eosinophils

Leukotrienes

  • vasodilation
  • increases vascular permeability
  • smooth muscle contraction
  • increases mucus production

act as positive feedback loops

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9
Q

What molecules dominate the early and late phase reactions?

A

Early phase (IgE mediated activation of mast cells):

  • histamine
  • neutrophils

Late phase (Accumulation of inflammatory cells):

  • neutrophils
  • ICAM-1
  • eosinophils

long term exposure causes mediated chronic allergic inflammation

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10
Q

Exposure an doseage of allergen with respect to the symptoms

A

Intravenous high dosage = systemic/anaphylaxis shock

Subcutaneous low dosage = wheel and flare symptoms

Inhalation low dosage = asthma and rhinitis

Ingestion = diarrhea and vomiting w/ hives
this can lead to blood borne as secondary

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11
Q

Inhaled allergens and how it causes localized anaphylaxis in upper respiratory responses

A

Mast cells in nasal mucosa and conjunctiva react
- usually seasonal and year-round

Symptoms

  • inflammation of nasal airway causes stuffy nose and rhinitis
  • increased mucus production
  • itchy eyes
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12
Q

Inhaled allergens and how it causes localized anaphylaxis in lower respiratory responses

A

Causes allergic asthm a
- mast cells in lower airways are reactive

Treated w/ SABA

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13
Q

Skin allergies

A

Mast cells in dermis are activated
- also is associated with filaggrin protein defects (causes itching) which allows the allergen to penetrate easier

Extreme cases lead to hives

  • subcutaneous mast cell degranulation
  • leads to vasodilation and edema
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14
Q

Intradermal skin tests

A

Used to determine if someone is allergic to allot he most common allergens
- patient is monitored for immediate reaction and 8-48hrs after for delayed reaction

has a rare chance of causing new sensitization and late-phase reactions to an allergen

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15
Q

Systemic anaphylaxis

A

Occurs when allergens enter the blood

  • causes mass degranulation of mast cells
  • causes immediate vomiting, malaise, systemic edema and vasodilation

Treatment = Epi pen and corticosteroids (if needed)

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16
Q

Molecular mimicry in prolonged strep throat

A

Untreated and prolonged strep throat causes antibodies to be created that attack both strep throat and cardiac tissues

  • results in rheumatic fever
  • is a type 2 hypersensitivity
17
Q

Drug induced hemolytic anemia

A

type 2 hypersensativity reaction that is caused when drugs (usually penicillin allergeries) act as happens for antibodies to attack blood cells