Allergy and Hypersensitivity Flashcards

1
Q

With examples, give the different types of hypersensitivity reactions.

A
  • TYPE 1 - IgE mediated. EXAMPLE - ANAPHYLAXIS
  • TYPE II - Antibody dependant eg IgG or IgM. EXAMPLE - Haemolytic anaemia
  • TYPE III - Immune complex mediated. EXAMPLE - SLE
  • TYPE IV - T-Cell mediated. EXAMPLE - Rash
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2
Q

Describe what occurs in Type 1 hypersensitivity reactions. PART 1

A
  • CD4+ T helper cells activate B cells - produce IgE antibodies specific to antigen
  • Antibodies bind to Fc receptors on surface of mast cells and basophils
  • Cells become sensitised. Immediate response on re-exposure to same allergen.
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3
Q

Describe what occurs in Type 1 hypersensitivity reactions. PART 2

A
  • Allergen cross links bound IgE on sensitised cells - causes anaphylactic degranulation.
  • Chemical mediators e.g histamines and cytokines released
  • Vasodilation and smooth muscle contraction occurs
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4
Q

What mast cell mediators cause vasodilation and increased permeability, and smooth uscle spasms?

A
  • Histamines/PAF/ Prostaglandin D2/ Leukotriene C4/D4/E4
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5
Q

What causes leuocycte extravasation?

A
  • Cytokines
  • Chemotactic factors for neutrophils and eosinophils
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6
Q

Describe bronchial asthma

A
  • Chronic inflammation with intermittent/reversible airway obstruction
  • Dominated by presence of eosinophils, CD4+ cells and CD4+ NK cells expressing invariant TCR - recognises antigens
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7
Q

What causes the following and what are the responses?
- WHEAL AND FLARE
- ALLERGIC RHINITIS
- FOOD ALLERGY

A
  • WHEAL AND FLARE - Insect bites. Route of entry is subcutaenous and causes local increase in blood flow.
  • ALLERGIC RHINITIS - Caused by pollens when inhaled causing inflammation of nasal mucosa.
  • FOOD ALLERGY - Orally. Causes vomiting but progresses to anaphylaxis
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8
Q

What are some treatments for Type 1 hypersensitivity reactions?

A
  • IMMUNOTHERAPY - Allergy shots/ ANTIHISTIAMINES AND ANTI-INFLAMMATORIES
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9
Q

Describe anaphylaxis.

A
  • Severe reaction to allergens causing body wide degranulation of mast cells. Causes vasodilation and shock
  • Evoked by direct exposure or being in presence of allergen
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10
Q

What are some risk factors of anaphylaxis?

A
  • Age-related factors
  • Co-existing diseases
  • Concurrent medications
  • Emotional stress and acute infections
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11
Q

How can anaphylaxis be identified?

A
  • Sudden reductions in BP
  • Sudden skin, GI and respiratory symptoms
  • Itching, generalised hives and swollen tongue, lips etc.
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12
Q

How can anaphylaxis be treated? PART 1

A
  • Remove exposure to trigger
  • Assess airway, breathing and circulation
  • Call for help
  • Inject epinephrine intramuscularly into mid-anterolateral aspect of thigh
  • Place patient on back or position of comfort if respiratory distress and/or vomiting
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13
Q

How can anaphylaxis be treated? PART 2

A
  • Elevate lower extremities - can be fatal if patient sits/stands suddenly
  • When indicated, give high-flow supplemental oxygen by face mask
  • Establish IV access using needles and give 1-2 litres of saline rapidly
  • Perform CPR and continuously check patient vitals
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14
Q

Describe Type II hypersensitivity reactions.

A
  • IgG and IgM antibodies directed against antigens on host cells
  • Leads to cell lysis or tissue damage through complement (in)dependent mechanisms
  • Results in opsonisation, cell lysis by MAC and RBC agglutination
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15
Q

Describe complement dependent Type II hypersensitivity reactions.

A
  • Antibody targets antigens on host cells
  • Ab-Ag complexes activate complement causing cell lysis by MAC or opsonisation with C4 causing other immune cells to phagocytose opsonised material
  • Caused by incompatible blood transfusions, autoimmune haemolytic anaemia and Goodpasture’s syndrome
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16
Q

Describe antibody dependent cell mediated cytotoxicity in Type II hypersensitivity reactions.

A
  • Low concentrations of IgG coat target cells
  • Inflammatory cells e.g NK cells and granulocytes bind to IgG via Fc receptors and lyse target cells using perforins.
  • Occurs during transplant rejection, immune reactions against neoplasms/parasites
17
Q

Describe HDN.

A
  • Occurs when immune system develop antibodies against baby’s RBCs causing haemolysis
  • If mother is Rh- and carries Rh+ fetus, anti-Rh antibodies produced i.e IgG antibodies (anti-D antibodies)
  • Cross placenta into fetal circulation and lead to haemolysis
  • Treated with antibodies to the Rh antigen - no anti-D antibody production
18
Q

Describe Type III hypersensitivity reactions.

A
  • Generation of Ab-Ag immune complexes inducing inflammation
  • Antigens bind to antibodies and form immune complexes which deposit in tissues
  • Activates complement clasical pathway and recruits neutrophils and macrophages causing inflammation
  • Causes inflammation and tissue injury
19
Q

Describe serum sickness.

A
  • Occurs when patients administered serum from healthy people (containing antibodies beneficial to patients)
  • Antibodies produced against antigens in donor’s serum
  • Deposition of Ab-Ag complexes in kidneys and joints
  • Can cause glomerulonephritis and arthritis
20
Q

Describe the characteristics of Type IV hypersensitivity.

A
  • T-cell mediated NOT ANTIBODY MEDIATED
  • Reaction takes several days to develop
21
Q

What is the mechanism of Type IV hypersensitivity reactions?

A
  • CD4+ T helper cells recognise antigens in complex with MHC Class II on surface of APCs
  • CD4+ T cells secrete IL-2 inducing further cytokine release
  • Activated CD8+ T cells destroy target cells and activated macrophages produce hydrolytic enzymes.
  • Overreaction of cells and overproduction of cytokines causes inflammation and cell death.
22
Q

Describe the tuberculin skin test. PART 1

A
  • Determines if patient infected with Mycobacterium tuberculosis
  • Antigen injected subcutaenously and processed by APCs
  • Th1 cell recognises antigen and releases cytokines - act on vascular endothelium
23
Q

Describe the tuberculin skin test. PART 2

A
  • Recruitment of phagocytes and plasma to site of injection
  • Produces pale elevation of skin