Week 4 Flashcards
Mechanism of serum sickness
- mediated by Type III hypersenstivity rxn; involves formation of immune complexes
- complexes adhere to endothelium of vasculature causing inflammation and damage
- symptoms manifest 1-2 weeks following initial exposure to antigen
Type III hypersensitivity
-result from the deposition or formation of immune complexes in the tissues.
roles of complement and immunoglobulin in the development of serum sickness
- circulating immune complexes are trapped in vessel walls of various organs, where they activate complement
- A rise in the level of immune complexes is accompanied by a decrease in serum levels of C3 and C4 and an increase in the concentration of C3a/C3a desarginine, which induces mast cell degranulation to produce hives
labs with serum sickness
- Complete blood count and differential; thrombocytopenia is often present.
- Erythrocyte sedimentation rate and C-reactive protein; erythrocyte sedimentation rate is usually elevated.
- Urinalysis: mild proteinuria (50%), hemoglobinuria, and microscopic hematuria may be seen.
- Complement studies, including CH50, C3, and C4; serum complement levels (C3 and C4) are generally decreased and reach a nadir at about day 10. C3a anaphylatoxin may be increased
diagnosis of serum sickness
-diagnosis of serum sickness is made clinically based upon the characteristic pattern of acute or subacute onset of a rash, fever, and severe arthralgia and myalgia disproportionate to the degree of swelling, occurring after exposure to a potential culprit
small vessel vasculitis
- vasculitis predominantly affecting small vessels, defined as small intraparenchymal arteries, arterioles, capillaries, and venules. Medium arteries and veins may be affected.
- Deposition of circulating immune complexes(medium and small arteries only)results incontinuous inflammation of arterial wallsandthrombosis and obliteration of the arterial lumen, which eliminates blood flow to organs.
Treatment for serum sickness
• Discontinue the suspected causative drug. Most conditions are self-limited and resolve spontaneously after removal of the offending agent.
Consider topical or systemic corticosteroids, antihistamines (to relieve symptom of rash), or nonsteroidal anti-inflammatory drugs ( to relieve symptoms of arthralgias) for prolonged symptoms
signs and symptoms of Toxicodendron dermatitis
- Redness
- Itching
- Swelling
- Blisters
- Difficulty breathing, if you’ve inhaled the smoke from burning poison ivy
type IV hypersensitivity
- Delayed; T Cell-mediated
- Antigens cause activation of T lymphocytes, which release cytokines and recruit effector cells
- > 72 hours
mechanisms of type IV hypersensitivity reactions
-regulated by T cells and involve the action of effector cells. These types of hypersensitivities can be organized into three subcategories based on T-cell subtype, type of antigen, and the resulting effector mechanism.
first type IV subcategory
- CD4 TH1-mediated reactions are described as delayed-type hypersensitivities (DTH)
- introduction of antigen into the skin and phagocytosis by local antigen presenting cells (APCs). The APCs activate helper T cells, stimulating clonal proliferation and differentiation into memory TH1 cells. Upon subsequent exposure to the antigen, these sensitized memory TH1 cells release cytokines that activate macrophages, and activated macrophages are responsible for much of the tissue damage
second type IV subcategory
CD4 TH2-mediated reactions result in chronic asthma or chronic allergic rhinitis. In these cases, the soluble antigen is first inhaled, resulting in eosinophil recruitment and activation with the release of cytokines and inflammatory mediators.
third type IV subcategory
- CD8 cytotoxic T lymphocyte (CTL)-mediated reactions are associated with tissue transplant rejection and contact dermatitis
- APCs process and present the antigen with MHC I to naïve CD8 T cells. When these naïve CD8 T cells are activated, they proliferate and differentiate into CTLs. Activated TH1 cells can also enhance the activation of the CTLs. The activated CTLs then target and induce granzyme-mediated apoptosis in cells presenting the same antigen with MHC I.
Explain the delayed onset of symptoms following exposure to Toxicodendron species.
-due to sensitization of the antigen. After the T-cells are activated by the antigen presenting cell then the symptoms are noted
Describe how exposure to urushiol causes a type IV hypersensitivity reaction
- Toxicodendron species contain oleoresins known collectively as urushiol.
- Initially, these lesions tend to occur from the slow reaction to adsorbed urushiol; however, lesions that appear later are often secondary to contact with contaminated surfaces (eg, clothing, pet hair, gardening tools, camping equipment). Although a common misconception, fluid from the vesicles of a poison ivy rash does not contain urushiol and is not an irritant source for new lesions.
