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Hypersensitivities (Type 1 (Treatment
1) Antihistamines - Blocks the…
Hypersensitivities
Type 1
Treatment
1) Antihistamines - Blocks the effects of histamine
2) Beta-adrenergics (Epipens) - Decreases bronchoconstriction & bronchospasm
3) Corticosteroids - Decreases inflammation
4) Anticholinergics - Blocks the parasympathetic system
5) Anti-immunoglobulin E therapy - Asthma treatment
Prevention
-Avoidance of food containing allergens
-Limiting contact w/ dust, molds & fur during early infancy stages
-Desensitization therapy (Regular injection of the allergen over a long course of time w/ gradually increasing doses until tolerance to antigen can be achieved w/o causing a reaction)
Clinical Manifestations -Vary in severity & intensity -Mild reactions typically characterized by:
- Hives
- Allergic rhinitis
- Eczema
- Mild bronchoconstriction
-Severe reactions typically characterized by:
- Tightening of the throat
- Localized edema
- Wheezing
- Tachycardia
-Can be extremely severe & life-threatening (anaphylactic shock)
Etiology & Pathogenesis -Strongly influenced by genetic/hereditary linkage regarding IgE response to allergens-AKA "Immediate Hypersensitivity"-Principal antibody is IgE (produced by specialized plasma cells)-Principal cells are mast cells and basophils-Histamine is another important mediator, it causes:
- Increased permeability
- Vasodilation
- Utricaria formation
- Bronchoconstriction
- Increased mucous secretion
- Increased itching
Steps
- IgE binding to Mast Cells
- Antigen Cross-bridging
- Histamine Release (Mast Cell Degranulation)
Type 3
Etiology & Pathogenesis
-Results from failure of the immune & phagocytic systems to effectively remove antigen-antibody complexes and is not tissue specific
-Characterized by antigen-antibody complex deposition into tissues w/ subsequent activation of complement & subsequent self-sustaining inflammation
-Antigen & antibody must both either be soluble or insoluble to form a complex
-Mechanism is from activation of complement & other proinflammatory mediators in response to the antigen-antibody complex deposition
-Tend to be ongoing w/ variations in symptoms based on the fluctuation of antibody : antigen ratios
-Principal effector cells are neutrophils & mast cells
-
Causes
2. Extrinsic Environmental Antigen
-Can come from molds, plants, or animals and can be inhaled into the lungs
-Inhalation results in antigen-antibody complex formation in alveoli w/ immune complex deposition in the alveolar walls
3. Development of an Autoimmune Process
-Results in autoantibodies attacking self antigens
-The body forms both parts of the immune complex (antigen & antibody)
1. Recent History of Infection/Persistent Low-grade Infection
-Stimulates a weak antibody response
-Persistent/untreated infection provides a source of circulating antigen
-Antigen & antibody response leads to chronic immune complex production, which results in accumulation & deposition in tissues
Type 2
Examples
Myasthenia Gravis
-An autoimmune disease of the neuromuscular junction
-Antibodies are formed to act against the acetylcholine receptors on muscle membrane surfaces, primarily the motor end plate
-No effector cells involved
-The thymus is the principal organ believed to be the site of anti-ACh receptor antibody development
-Causes extreme muscular weakness, ptosis & diplopia
Grave Disease/Toxic Diffuse Goitre -Involves effector cells (neutrophils) binding to target cells & blocking the receptors from performing normal functions-Graves disease specifically involves autoantibodies attacking TSH receptors on normal, healthy cells; causing malfunction & excess production of T4 & T3-Results in hyperthyroidism; signs:
- Tachycardia
- Fatigue
- Weight loss
- Tremor
- Heat intolerance
- Diarrhea
- Emotional/mental changes
Hemolytic Disease
-Occurs during pregnancy when an Rh-negative mother is sensitized to the Rh-positive red cell group antigens of her fetus because of exposure during her current/previous pregnancy
-The exposure occurs when mixing of fetal & maternal blood takes place; can happen during an episode of antepartal bleeding/trauma to the placenta, during birth, or during miscarriage of an Rh-positive child
-The mother's Rh-positive IgG antibodies cross the placental barrier & attack the RBCs of the fetus
-The first Rh-positive child is usually unaffected unless placental tearing or leakage into the mother's circulation occurs during pregnancy
Graft Rejection -Involves both effector cells & the complement system-Affects transplanted tissues-Occurs when the transplanted donor tissue has an antigen to which the recipient has preformed antibodies-Onset begins immediately after revascularization of transplanted tissue; patient's antibodies attack the foreign protein antigens & form an antigen-antibody complex-Process usually finishes 48 hrs after transplantation w/ grafted tissue no longer being functional-Signs:
- Effector Cell Infiltration
- Complement-mediated Lysis of Donor Tissues
- Inflammation
- Vascular Thrombosis
- Hemorrhaging
Etiology & Pathogenesis
-AKA "Tissue-specific, Cytotoxic, or Cytolytic" Hypersensitivity
-Characterized by antibodies that attack antigens on the surface of specific cells/tissues (foreign)
-Involves direct cell death/malfunction from antigen-antibody reaction
-Reaction is often immediate, but can occur over time
-Mediated by the complement system & various effector cells
Type 4
Examples
Contact Dermatitis
-Most common type
-An immune/inflammatory response to various plant oils, chemicals, ointments, clothing, cosmetics dyes & adhesives
-Also an epidermal phenomenon
-Has a slow reaction (48-72 hours); due to skin-penetrating antigen (Hapten) being very small & incomplete
-Hapten is only completed when it combines with a normal body protein/carrier to become a hapten conjugate
-Dendritic cells process the complete antigen which causes a release of lymphokines, resulting in inflammation & attraction of other effector cells
Patch Testing Patch testing is used to diagnose for contact hypersensitivity; symptoms that persist despite avoidance of agent + appropriate topical therapy indicate contact dermatitis1+ Patch
- Involves erythema of entire area of exposure
- Patchy pustular responses are not positive and are irritant reactions
2+ Patch
- Involves erythema & vesicles
3+ Patch
- Involves erythema, vesicles & bullae
TB-Type Hypersensitivity
-Occurs when someone who has been previously infected by TB is exposed to TB antigen in a TB test
-A dermal phenomenon that peaks in 48-72 hrs
-Person experiences erythema, induration & inflammation at the site of intradermal injection
-Amount is very small & reaction disappears when antigen has degraded
-People w/ severe reactions may experience tissue necrosis at site
Etiology & Pathogenesis
-AKA "Delayed Hypersensitivity"
-Characterized by tissue damage resulting from a delayed cellular reaction to an antigen
-Primary antibody involvement is absent
-Principal mediators are lymphocytes (Helper Ts and/or Killer Ts)
-Principal effectors are lymphocytes & macrophages involved in early phases
-Has a slow onset w/ a series of events that occur gradually
-Mast cells regulate leuokocyte migration in microvasculature
-Suppressor Ts inhibit other T-Cell actions