Flashcards in Hypersensitivity Deck (32)
What are mediators of allergic reactions (Type I IgE-mediated) and what do they do?
--complement: more inflammatory cells and cytokines
--acetylcholine: bronchiole smooth muscle contraction
--leukotrienes: delayed and more prolonged, similar to histamine
--kinins: vasodilate, smooth muscle contraction
--eosinophils: show up in allergic rxn, attract more leukocytes and eosinophils
What is atopy and what can cause it?
genetic predisposition to the development of immediate, type I IgE mediated hypersensitivity reactions upon exposures to common environmental antigen such as pollens, food, or animal dander
How to atopic reactions typically manifest?
What are the two defined phases of type I hypersensitivity reactions? What occurs in each phase and when does each occur?
1. primary/initial: vasodilation, vascular leakage, smooth muscle contraction
occurs 5-30 min after exposure, subsides w/in 60 min
2. secondary/late-phase: more intense infiltration of tissues with eosinophils and other acute and chronic inflammatory cells as well as tissue destruction in the form of epithelial cell damage
occurs: 2-8 hours after initial phase, can last several days
What does histamine do in the type I hypersensitivity inflammatory response? Is it released in the primary or secondary phase?
-potent vasoactive amine
-increases nitric oxide production
-relaxes vascular smooth muscle
-increases permeability of capillaries and venules
-causes smooth muscle contraction
What does acetylcholine do in type I IgE inflammatory response? Is it released in the primary or secondary phase?
-bronchial smooth muscle contraction
-dilation of small blood vessels via parasympathetic nervous system
-mimics many actions of histamine
What do kinins do in type I IgE inflammatory response? Is it released in the primary or secondary phase?
-potent inflammatory peptides
-smooth muscle contraction
What chemicals are released in the second, or late phase of a type I hypersensitivity reaction?
leukotrienes and prostaglandins
provide similar effects as histamine, but longer lasting and delayed
What do you consider investigating if a pt presents with chronic urticaria? (if patients h and p suggests associated disease)
Anaphylaxis could include local responses and?
-life threatening reaction from release of histamine into systemic circulation that produces massive vasodilation, hypertension, arterial hypoxia, and airway edema
When does the late-stage response from anaphylaxis occur?
sometimes occurs and onset is several hours after exposure
What meds do the late-stage anaphylactic response best respond to?
steroids, but also give H1 and H2 inhibitors
Anaphylaxis: What are the sx a pt will present with?
--generalized pruiritis, flushing and sense of impending doom
--urticaria and angioedema
-resp tract involvement (wheezing, SOB, laryngeal edema) 50% result in resp failure
-anaphylactic shock occurs in 30% of cases
Anaphylactic shock occurs in 30% of cases. What happens in this stage?
--cardiovascular collapse from hypovolemia
--alterations in peripheral vascular resistance
How does cardiovascular collapse result from hypovolemia?
--due to increased vascular permeability and loss of up to 50% of blood volume
What is management of anaphylaxis?
--Depends on severity--
-stabilization (may include: intubation, IV's w/fluid)
-**epinephrine (drug of choice b/c reverse hypotension and bronchospasm)
-antihistamines H1 and H2
-corticosteroids (helps w/ late phase rxn)
Why do you give steroids to anaphylaxis patients?
Why do you give Benadryl?
Will volume hurt the patient?
Steroids = delayed rxn
Benadryl = histamine blocker
volume will not hurt pt b/c pt is not a heart failure pt
What are the common drug allergies?
Beta-lactam abx (penicillins, cephalosporins)
-sulfonamides (trimethoprim/sulfamethoxazole [bactrim/septra])
-NSAIDs (Ibuprofen, Aleve)
What is drug is most commonly known for causing stevens-johnsons syndrome?
sulfonamides (trimethoprim/sulfamethoxazole [bactrim/septra])
What are the classic drug reaction patterns?
More serious manifestations:
-drug-induced exanthems (rash)
How long will it take to manifest sx in a patient that takes a drug they are allergic to?
--Depends on whether they have been previously sensitized--
--previously sensitized = rapid development sx
--no previously sensitized =may takes days to develop or may not appear until next exposure
What is the fundamental question to ask anytime someone presents with an allergic reaction?
Are there systemic symptoms, especially shortness of breath? (losing air? swelling in face?)
What should anaphylactic patients always have?
What is the treatment of choice in Type I hypersensitivity reactions--allergic rhinitis? (not including significant breathing problems)
What are the two most important mediators to think about when it comes to mediator specific medications with type 1 hypersensitivity?
histamines and leukotrienes
What works well for allergic rhinitis? When should the pt start taking it?
-nasal steroids (REMEMBER THESE DONT BLOCK HISTAMINE, but work well to decrease inflammation)
-need to take before allergies start
What are symptoms of allergic rhinitis?
-rhinorrhea (runny nose)
-watery eyes (conjunctivitis)
People with allergic rhinitis frequently present with other forms of atopy including?
Severe AR attacks may be accompanied by systemic:
malaise, fatigue, headache, and muscle soreness from sneezing