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72 Cards in this Set

  • Front
  • Back
What is our first line of defense against microbial invaders?
epithelial cells that coat the skin and make up the lining of the respiratoty, GI, and GU tract
How do antibodies react with antigens?
1. coat the antigen's surface
2. neutralize antigens if they are toxins
3. precipitate the antigens out of the solution if they are dissolved
*prepare antigens so that phagocyctic cells of the blood and tissue can dispose them
What is an allergic or hypersensitivity disorder?
inappropriate or exaggerated responses to specific antigen initiated by IgE antibodies
Define atony?
allergic reactions that are characterized by action of the IgE antibodies and genetic predisposition to allergic reaction
What happens during an allergic reaction?
lymphocytes respond to an antigen and antibodies are produced aggresively to a substance that is normally harmless. Chemical mediators are then produced ranging from mild to deadly
What are immunoglobulins?
antibodies (serum proteins)formed by lymphocytes and plasma cells in response to immunogenic stimulus
What the 5 immunoglobulins and where are they found?
IgE, IgD, IgG, IgM, IgA
found in the lymph nodes, tonsils, appendix, peyers patches of intestinal tract and blood and lymph
How do the Ig's differ?
each reacts with a specific effector cell and molecule to protect the body
What do IgG, IgM, IgA specifically do?
protective functions, neutralize toxins, viruses, precipitation, aggulation, and lysis of bacteria and other foreign material
What does IgE specifically do?
involved in allergic disorders and parasitic infections
located in resp and intestinal tract
How do the IgE work?
two more more IgE molecules bind to an allergen and trigger mast cells/basophils, which release chemical mediators (histamines, serotinin, kinins, anaphylaxis, neutrophil factor)
What do chemical mediators produce?
alleric reactions such as skin reactions, asthmas, hay fever
How do antibodies combine with antigens?
lock and key, only certain antigens fit certain antibodies, must have affinity
What is an epitope?
an immunologically active site on an antigen
Why is it important that antibodies are bivalent?
they have two combining sites, so antibody becomes crosslinked between two antigens causing them to clump (aggluatination) and cleared from the bloodstream easier
What is the role of the B cells
they are programmed to produce one specific antibody, to destroy and remove that antigen
What is the role of the T cells?
secrete lymphokines that encourage cell growth, promote cell activation, destroy targets cells and stimulate macrophages
They assist in digestion and removal of antigen
Where are mast cells located and what do they do?
located in skin and mucous membranes
when stimulated by antigens release chemical mediators
where are the IgE located?
occupy certain receptors on mast cells and bind antigens
Summarize allergen response
allergen triggers B cell to make IgE antibody, IgE antibody attaches to mast cell, when antigen reappears it binds to IgE and triggers mast cell to release chemical mediators
Describe histamine: where are they released from, how fast do they have an effect, their s/s
released from mast cells granules within 15 mins of exposure, causes localized edema, pruritis, bronchio spasm, dilation of small vessels and constriction of large vessels, incr GI secretions
What is the difference betwen histamine 1 and 2?
1 are found in bronchiolar and vascular smooth muscle (benadryl)
2 are found in GI (zantac)
Describe eosinophil chemotactic factor of anaphylaxis
performed in mast cells and effect movement of eosinophils at site of allergen, released from disrupted mast cells
Describe platelet-activating factor
responsible for platelet aggregation and leukocyte infiltration, causes bronchoconstriction and inc vascular permeability
Describe prostaglandins
produce smooth muscle contraction, vasodilation, incr capillary permeability, fever and pain
What are primary mediators?
found in mast cells or basophils, first effect on blood vessesl, smooth muscles, glandular secretions, second effect on cellular infiltration
histamine, eosinophil chemotactic factor, platelet-activiating factor, prostagladins
What are secondary mediators?
inactive precursors that are formed or released in response to primary mediators
leukotrienes, bradykinin, serotonin
What do leukotrienes do?
initiate inflammatory response, cause smooth muscle contraction, bronchial contraction, mucus secretion, wheal-and-flare rx of skin
BRONCHOSPASM- asthma
What does bradykinin do?
incr vascular permeability, vasodilation, hypotension, smooth muscle contraction (bronchi), nerve cell fibers causing pain
What does serotonin do?
vasoconstrictor and contraction of bronchial smooth muscle
What is hypersensitivity?
excessive or aberrant immune response, usually following re-exposure, initated by buildup of antibodies
Describe Type I hypersensitivity?
ANAPHYLACTIC-occurs within minutes of exposure, mediated by IgE, causes release of vasoactive amines and other mediators
-vasodilation, inc capillary permeability, smooth muscle contraction, eosinophilia, laryngeal stridor, angioedema, hypotension, bronchial, GI, uterine spasm, hives, asthma, ALLERGIC RHINITIS,
Describe Type II hypersensitivity
, thrombocytopenia
Describe Type III hypersensitivity
Immune complex, injury from vasoactive amines deposited, acute inflammation often in joints and kidneys, SLE, nephritis, RA
s/s-urticaria, joint pain, fever, rash, adenopathy, bacterial endocarditis
Describe Type IV hypersensitivity
delayed-type/cellular hypersensitivity (24-72 hours), tissue damage from lymphokines, macrophages, lysozymes
s/s-CONTACT DERMATITIS, PPD, hashimotos, itching, erythema, raised lesions
Assessment/tests of allergic disease
health history, OLDCART, WBC eosinphil level (15-40%), smear blood samples of eosinophils, Total serum immunoglobulin E levels,skin tests, provocative test (direct adm), radioimmunoassay that measures specific IgE
What are atopic disorders?
hereditary predisposition and local rx to IgE antibodies
allergic rhinitis, asthma, dermatitis/eczema
What are nonatopic diseases?
lack the genetic component and organ specificity
latex allergy, contact dermatitis
Describe anaphylaxis
antigen binds with IgE on mast cells and peripheral blood basophils, chemical mediators are released causing vascular permeability changes (dec BP), flushing, urticaria, angioedema, hypotension, bronchconstriction, mucosal edmea and inflamm, right away
What are common causes of anaphylaxis
foods, meds (antibiotics,IV anesthetics, asprin, NSAIDS, opiods), insects, latex, radiocontrast agents
What are mild clinical manifestations of anaphylaxis
peripheral tingling, warmth sensation, fullness in mouth and throat, nasal congestion, periorbital swelling, pruritis, sneezing, tearing within the first 2 hours of exposure
What are moderate clinical manifestations of anaphylaxis
flushing, warmth, anxiety, itching, bronchospasm, edema of airway, dyspnea, cough, wheezing
What are severe clinical manifestations of anaphylaxis
abrubt onset, bronchospasm, laryngeal edema, severe dyspnea, cyanosis, HYPOTENSION, dysphagia,abdominal cramping, V/D, SZ, cardiac arrest, coma
How can one prevent anaphylaxis
strict avoidance of allergen, screening, wearing identification, immunotherapy, desensitization
What is the medical management for anaphylaxis?
oxygen, epinephrine (1:1000 dilute), antihistamine, corticosteroids, IV fluids, vasopressor, glucagon,
Describe allergic rhinitis
(hay fever, seasonal allergic rhinitis), most common form of respiratory allergy mediated by Type I hypersensitivity, IgE response, 10-25% of population
Describe what happens with allergic rhinitis
exposure of antigen builds antibodies, re-exposure histamine is released causing tissue edema from vasodilation and inc capillary permeability
What are the s/s of allergic rhinitis?
sneezing, nasal congestion, clear, watery nasal discharge and itching, itching of throat, dry cough, headache, pain over sinuses, epistaxis (nose bleed0, fatigue, loss of sleep, poor concentration
How is allergic rhinitis diagnosed?
history, physical exam, relationship between seasons/stress, nasal smear, peripheral blood count, total serum IgE, epicutaneous and intradermal testing, RAST, food elimination/challenge, nasal provocation tests
How is allergic rhinitis treated?
avoidance, pharmacotherapy, immunotherapy
How do antihistamines work?
What are they typically used for?
What are their side effects?
selectively bind to H1 receptors, preventing the action of histamines
used for allergic rhinitis
side effects-nervousness, tremors, dizziness, dry mouth, palpitations, anorexia, nausea, vomiting
How to adrenergic agents work?
What are their side effects?
activate alpha-adrenergic receptor sites on smooth muscle of mucosal vessels reducing local blood flow, fluid exudation and mucosal edema
usually topical, can not be used long term--rebound effect
side effects-HYN, dysrhythmias, palpitations, CNS stimulation, irritability, tremor, tachyphylaxis
When are corticosteroids used? what are their side effects?
severe cases, metered spray, topical, oral, parenteral
suppress hosts immune system, must not stop suddenly, weight gain, fluid retention, gastric irriation, glucose intolerance, adrenal suppression
Describe immunotherapy
injection of allergen extracts, gradually increasing quantities to reduce IgE circulating, increasing blocking antibody IgG and reducing mediator cell sensitivity
What are some nursing considerations for immunotherapy
should only be done in office with epinephrine is available, patient should wait 30 mins before allowed to leave
What type of hypersensivity is contact dermatitis?
What causes it?
Type IV- delayed
direct skin contact with chemicals or allergens
Describe the 4 types of contact dermatitus
1. allergic-contact to skin (avoidance, corticosteroids, compress, antihistamines
2. irritant-contact that causes damage (removal, hydrophilic cream, antibodics)
3. phototoxic- allergic reaction that requires sun
4. photoallergic- allergic reaction tha requires light
S/S of contact dermatitus
itching, burning, erythema, skin lesions, edema, weeping, crusting, dry and peeling skin, hemorrhagic bullae
Describe atopic dermatitus
type I immediate hypersensitivity, elevated IgE and peripheral eosinophilia, pruritus, hyperirritability, excess dryness, lesions, redness
may lead to asthma and allergic rhinitis
How is atopic dermatitus managed?
antihistamines, avoidance, skin moisturizing, topical corticosteroids, antibodies, immunosuppressive agents, decrease itching
What is dermatitis medicamentosa?
type I, skin rash associated with medications
What is urticaria?
hives, type I, effects skin, mucous membranes, larynx, GI tract
if last >6 weeks chronic
What is angioneurotic edema?
live hives yet effects deeper layers of skin that has diffuse swelling
effects lips, eyelids, cheeks, hands, feet, genitalia, tongue, bronchi, GI
Swelling usually appears in one place at a time
What is hereditary angioedema?
edema of skin, resp tract, digestive tract
precipated by trauma but genetic
can last 1-4 days, can cause resp obstruction
epinephrine, antihistamines, corticosteroids
What type of hypersensitivity are food allergies?
What are the s/s of food allergies?
IgE mediated type I
urticaria, dermatitis, wheezing, coughing, laryngeal edema, angioedema, itching, swelling, abd pain, N/V/D
What are common food allergy foods?
What causes the most severe reactions?
seafood, legumes, seeds, tree nuts, berries, egg whites, buckwheat, milk, chocolate
PEANUT and TREE NUTS
What is the medical management of food allergies?
avoidance, H1 blockers, antihistamines, adrenergic agents, corticosteroids, cromolyn sodium, early recognition of reaction
What is serum sickness?
Type III, IgE & IgG, use to be found in animal sources of vaccinations
What are the s/s of serum sickness and how is it treated?
inflammtion, lymphadenopathy, fever, urticarial, purpuric, tender and swollen joints, cardiac involvement, Guillain-Barre
antihistamines, corticosteroids, ventilator support
What routes of exposure can occur to latex allergies?
cutaneous, mucosal, parenteral, aerosol
-condoms, catheters, airways, nipples, IV lines, medical devices
What are the two types of latex allergy?
Type IV- delayed hypersensitivity, most common
TypeI immediate hypersensitivity
What are s/s of Type IV and Type II?
Type IV- pruritus, edema, erythema, crusting of skin
Type I- rhinitis, conjuctivitis, asthma, anaphylaxis, urticaria, wheezing, dyspnea, laryngeal edema, bronchospasm, tachycardia, angioedema, hypotension, cardiac arrest