passive cutaneous anaphylaxis

anaphylaxis

[an″ah-fi-lak´sis] an unusual or exaggerated reaction" >allergic reaction of an organism to foreign protein or other substances. Substances most likely to cause this include drugs such as antibiotics, local anesthetics, and codeine; drugs prepared from animals, such as insulin, adrenocorticotropic hormone, and enzymes; diagnostic agents, such as iodinated x-ray contrast media; biologicals used to provide immunity, such as vaccines, antitoxins, and gamma globulin; protein foods; the venom of bees, wasps, and hornets; and pollens, molds, and animal dander. The latex in gloves or Foley catheters may cause a reaction in sensitive individuals.Physiologic Basis. Anaphylaxis is an allergen-reagin reaction brought about by large quantities of IgE antibodies (immunoglobulins) that respond to the presence of foreign agents. Individuals who have an anaphylactoid type of immune response have a familial predisposition to overreact in the presence of an allergen because of their tendency to produce an overabundance of IgE antibodies. When an allergen enters the body reagins (IgE antibodies), which are attached to cells throughout the body, interact with the allergens. This interaction is destructive to some of the body's cells. If the interaction is severe, the outcome can be fatal.
During the interaction mast cells and eosinophils release histamine, slow-reacting substance of anaphylaxis (SRS-A), bradykinin, and enzymes. Histamine brings about bronchospasm, widespread peripheral vasodilation, and increased permeability of the capillaries. SRS-A causes increased constriction of the bronchioles and bronchi. Bradykinin has effects similar to those of histamine. Together they promote collapse of the vascular network by permitting the loss of fluid from the blood vessels into the interstitial fluid compartment.Clinical Manifestations. If the allergen comes into contact with cell-bound IgE in the respiratory tract, the tissues of the mucosa release chemical mediators that produce the symptoms of asthma and hay fever. An insect bite or sting can produce localized swelling, redness, and itching, or a more severe systemic reaction.
Local anaphylactic reactions usually produce mildly irritating symptoms, which should not be ignored because the reaction can rapidly escalate into a systemic response involving cells throughout the body. The patient may then experience generalized itching, swelling, and urticaria. As the process continues, respiration is impaired because of bronchospasm and laryngeal edema. If an airway is not maintained and supplemental oxygen provided, the person will die of respiratory failure.
Another life-threatening series of events is related to vascular collapse resulting from a shift in body fluid. The symptoms are hypotension, decreasing levels of consciousness, tachycardia, and diminished production of urine. Without effective treatment these symptoms progress to profound shock and death.Treatment and Patient Care. Mild anaphylaxis can be treated with antihistamines, local applications of cold to minimize swelling, and topical applications of medications to relieve itching and soothe the skin. All anaphylactic reactions require careful assessment and monitoring, and the patient should be instructed to seek additional help if he or she experiences dizziness, heart palpitations, or prolonged or spreading edema anywhere in the body. The drug of choice in the initial treatment of severe anaphylaxis is epinephrine, administered intravenously, subcutaneously, sublingually, or by intermittent positive pressure breathing. The mode of administration is governed by the urgency of the situation and the presenting symptoms. Epinephrine causes bronchodilation, reduces laryngeal spasm, and elevates the blood pressure.
Steroid therapy is initiated to counteract the effects of histamine by decreasing capillary permeability. Acting as antiinflammatory agents, steroids also stabilize mast cells and prevent further release of chemical mediators.
Supportive measures include administration of intravenous fluids and plasma to restore intravascular fluid volume. Pressor agents, such as dopamine, norepinephrine, and isoproterenol, are given to increase and maintain blood pressure.
The best way to control anaphylaxis is by preventing it from happening in the first place, but this is not always possible. A person engaging in normal activities outside the clinical setting can accidentally come in contact with an allergen. An allergic individual should be prepared for such an event by understanding his or her allergy and knowing what actions to take. Those with known atopic allergies should wear a medical identification necklace or bracelet, and those who undergo systemic reactions should carry with them at all times a kit containing diphenhydramine (Benadryl), a syringe and needle, and vials of epinephrine. These kits require a written prescription from a primary health care provider.
In the clinical setting, all health care personnel should be alert to the need for identifying patients with known allergies and communicating this information to their co-workers. Emergency equipment should be readily available in all places where drugs or diagnostic agents with a risk of provoking anaphylaxis are administered.active anaphylaxis that produced by injection of a foreign protein.antiserum anaphylaxis (passive anaphylaxis) that resulting from injection of serum of a sensitized person into a normal person.passive cutaneous anaphylaxis PCA; localized anaphylaxis passively transferred by intradermal injection of an antibody and, after a latent period (about 24 to 72 hours), intravenous injection of the homologous antigen and Evans blue dye; blueing of the skin at the site of the intradermal injection is evidence of the permeability reaction. Used in studies of antibodies causing immediate hypersensitivity reactions.reverse anaphylaxis that following injection of antigen, succeeded by injection of antiserum.

pas·sive cu·ta·ne·ous an·a·phy·lax·is (PCA),

a reaction that occurs in the guinea pig when antiserum is injected into the skin and, 6-24 hours later, specific antigen and a dye such as Pontamine blue or Evans blue are inoculated intravenously; the size of the blue areas at the sites of the antibody injections is a measure of the degree of altered permeability to dye-bound albumin.

passive cutaneous anaphylaxis

Abbreviation: PCA
A laboratory test of antibody levels in which serum from a sensitized person is injected into the skin. Intravenous injection of an antigen accompanied by Evan's blue dye at a later time reacts with the antibodies produced in response to the antigen, creating a wheal and blue spot at the site, indicating local anaphylaxis. See also: anaphylaxis

单词	passive cutaneous anaphylaxis
释义	DictionarySeeanaphylaxis passive cutaneous anaphylaxis passive cutaneous anaphylaxis [′pas·iv kyü′tā·nē·əs ‚an·ə·fə′lak·səs] (immunology) The vascular reaction at the site of intradermally injected antibody when, 3 hours later, the specific antigen, usually mixed with Evans blue dye, is injected intravenously. passive cutaneous anaphylaxis anaphylaxis [an″ah-fi-lak´sis] an unusual or exaggerated reaction" >allergic reaction of an organism to foreign protein or other substances. Substances most likely to cause this include drugs such as antibiotics, local anesthetics, and codeine; drugs prepared from animals, such as insulin, adrenocorticotropic hormone, and enzymes; diagnostic agents, such as iodinated x-ray contrast media; biologicals used to provide immunity, such as vaccines, antitoxins, and gamma globulin; protein foods; the venom of bees, wasps, and hornets; and pollens, molds, and animal dander. The latex in gloves or Foley catheters may cause a reaction in sensitive individuals.Physiologic Basis. Anaphylaxis is an allergen-reagin reaction brought about by large quantities of IgE antibodies (immunoglobulins) that respond to the presence of foreign agents. Individuals who have an anaphylactoid type of immune response have a familial predisposition to overreact in the presence of an allergen because of their tendency to produce an overabundance of IgE antibodies. When an allergen enters the body reagins (IgE antibodies), which are attached to cells throughout the body, interact with the allergens. This interaction is destructive to some of the body's cells. If the interaction is severe, the outcome can be fatal. During the interaction mast cells and eosinophils release histamine, slow-reacting substance of anaphylaxis (SRS-A), bradykinin, and enzymes. Histamine brings about bronchospasm, widespread peripheral vasodilation, and increased permeability of the capillaries. SRS-A causes increased constriction of the bronchioles and bronchi. Bradykinin has effects similar to those of histamine. Together they promote collapse of the vascular network by permitting the loss of fluid from the blood vessels into the interstitial fluid compartment.Clinical Manifestations. If the allergen comes into contact with cell-bound IgE in the respiratory tract, the tissues of the mucosa release chemical mediators that produce the symptoms of asthma and hay fever. An insect bite or sting can produce localized swelling, redness, and itching, or a more severe systemic reaction. Local anaphylactic reactions usually produce mildly irritating symptoms, which should not be ignored because the reaction can rapidly escalate into a systemic response involving cells throughout the body. The patient may then experience generalized itching, swelling, and urticaria. As the process continues, respiration is impaired because of bronchospasm and laryngeal edema. If an airway is not maintained and supplemental oxygen provided, the person will die of respiratory failure. Another life-threatening series of events is related to vascular collapse resulting from a shift in body fluid. The symptoms are hypotension, decreasing levels of consciousness, tachycardia, and diminished production of urine. Without effective treatment these symptoms progress to profound shock and death.Treatment and Patient Care. Mild anaphylaxis can be treated with antihistamines, local applications of cold to minimize swelling, and topical applications of medications to relieve itching and soothe the skin. All anaphylactic reactions require careful assessment and monitoring, and the patient should be instructed to seek additional help if he or she experiences dizziness, heart palpitations, or prolonged or spreading edema anywhere in the body. The drug of choice in the initial treatment of severe anaphylaxis is epinephrine, administered intravenously, subcutaneously, sublingually, or by intermittent positive pressure breathing. The mode of administration is governed by the urgency of the situation and the presenting symptoms. Epinephrine causes bronchodilation, reduces laryngeal spasm, and elevates the blood pressure. Steroid therapy is initiated to counteract the effects of histamine by decreasing capillary permeability. Acting as antiinflammatory agents, steroids also stabilize mast cells and prevent further release of chemical mediators. Supportive measures include administration of intravenous fluids and plasma to restore intravascular fluid volume. Pressor agents, such as dopamine, norepinephrine, and isoproterenol, are given to increase and maintain blood pressure. The best way to control anaphylaxis is by preventing it from happening in the first place, but this is not always possible. A person engaging in normal activities outside the clinical setting can accidentally come in contact with an allergen. An allergic individual should be prepared for such an event by understanding his or her allergy and knowing what actions to take. Those with known atopic allergies should wear a medical identification necklace or bracelet, and those who undergo systemic reactions should carry with them at all times a kit containing diphenhydramine (Benadryl), a syringe and needle, and vials of epinephrine. These kits require a written prescription from a primary health care provider. In the clinical setting, all health care personnel should be alert to the need for identifying patients with known allergies and communicating this information to their co-workers. Emergency equipment should be readily available in all places where drugs or diagnostic agents with a risk of provoking anaphylaxis are administered.active anaphylaxis that produced by injection of a foreign protein.antiserum anaphylaxis (passive anaphylaxis) that resulting from injection of serum of a sensitized person into a normal person.passive cutaneous anaphylaxis PCA; localized anaphylaxis passively transferred by intradermal injection of an antibody and, after a latent period (about 24 to 72 hours), intravenous injection of the homologous antigen and Evans blue dye; blueing of the skin at the site of the intradermal injection is evidence of the permeability reaction. Used in studies of antibodies causing immediate hypersensitivity reactions.reverse anaphylaxis that following injection of antigen, succeeded by injection of antiserum. pas·sive cu·ta·ne·ous an·a·phy·lax·is (PCA), a reaction that occurs in the guinea pig when antiserum is injected into the skin and, 6-24 hours later, specific antigen and a dye such as Pontamine blue or Evans blue are inoculated intravenously; the size of the blue areas at the sites of the antibody injections is a measure of the degree of altered permeability to dye-bound albumin. passive cutaneous anaphylaxis Abbreviation: PCA A laboratory test of antibody levels in which serum from a sensitized person is injected into the skin. Intravenous injection of an antigen accompanied by Evan's blue dye at a later time reacts with the antibodies produced in response to the antigen, creating a wheal and blue spot at the site, indicating local anaphylaxis. See also: anaphylaxis AcronymsSeePCA
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