Module 3- Child Urticaria/anaphylaxis/adverse reactions/allergies Flashcards
Urticaria
arbitrarily designated as acute, lasting less than 6 weeks, or chronic, lasting more than 6 weeks. It is also classified by trigger: allergic, physical/inducible, infectious, autoimmune, or spontaneous/idiopathic
Viral infections are identified as the cause of acute urticaria
chronic urticaria, infections are considered an exacerbating factor
urticaria or angioedema pathogenesis
Mast cells release of a variety of vasoactive mediators triggered by different stimuli, including cross-linking of Fc receptor–bound IgE by allergens or anti-FcεRI antibodies
Inducible (physical) urticarias
heterogeneous group of disorders in which urticaria or angioedema is triggered by physical stimuli, including pressure, cold, heat, water, or vibrations
Dermographism
most common form of physical urticaria, occurring at skin sites subjected to mechanical stimuli
S & S- Urticaria
wheals with reflex erythema that are pruritic and transient, resolve w/out any changes to the skin
Systemic features include headache, wheezing, and syncope
S&S of angioedema
rapid erythematous or skin-colored swelling that is associated with burning or pain more than pruritus
Lab findings for Urticaria and angioedema
Testing for specific IgE antibody to food or inhalant allergens or infections may be helpful,
Treatment- General measures Urticaria and angioedema
effective treatment is identification and avoidance of the triggering agent, Underlying infection should be treated appropriately,
Antihistamines
H1 antihistamines given orally or systemically are the mainstay of therapy, second-generation H1 antihistamines are first-line tx, if urticaria is refractory then increase dose by 4folds
Other Pharmacologic Agents for Urticaria and angioedema
Third-line treatment for chronic spontaneous urticaria is the addition of a leukotriene-receptor antagonist, cyclosporine A, or omalizumab,
Treatment of chronic urticaria with hydroxychloroquine, azathioprine, sulfasalazine, dapsone, colchicine, and intravenous immune globulin
Anaphylaxis
cute life-threatening clinical syndrome that occurs when large quantities of inflammatory mediators are rapidly released from mast cells and basophils after exposure to an allergen in a previously sensitized patient
Anaphylactoid
mimic anaphylaxis but are not mediated by IgE antibodies. They may be mediated by anaphylatoxins such as C3a or C5a or through nonimmune mast cell degranulating agents
S&S of Anaphylaxis
history is the most important tool
*Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both with either resp compromise or decreased blood pressure
*Two or more of the following that occur rapidly after exposure to a likely allergen for that patient- skin mucosal tissue involvement, respiratory compromise, reduced blood pressure, gastrointestinal symptoms
*Reduced blood pressure after exposure to a known allergen for that patient
Lab findings in anaphylaxis
absence does not rule out, tryptase released by mast cells can be measured within 3 hours of onset but can be normal
Electrocardiographic abnormalities may include ST-wave depression, bundle branch block, and various arrhythmias. Arterial blood gases may show hypoxemia, hypercapnia, and acidosis. The chest radiograph may show hyperinflation.
Prevention of anaphylaxis
Strict avoidance of the causative agent is extremely important, and effort to determine its cause should be made, beginning with a thorough history
carry epinephrine for self-administration
carry an oral antihistamine such as diphenhydramine or cetirizine, preferably in liquid or chewable preparation to hasten absorption
Treatment of anaphylaxis
antihistamines- diphenhydramine or cetirizine for younger patient along with ranitidine- h2 blocker
Fluids- persistent hypotension
Bronchodilators
Corticosteroids
Vasopressors
Observations
Can be fatal
Adverse Reactions to drugs
undesirable and unintended response elicited by a drug
Allergic or hypersensitivity drug reactions are adverse reactions involving immune mechanisms
Antibiotic drug reactions
Amoxicillin, trimethoprim–sulfamethoxazole, and ampicillin are the most common causes of cutaneous drug reactions
Penicillin and other b-lactam antibiotics
share a common β-lactam ring structure and a marked propensity to couple to carrier proteins, the R-side chains of the penicillins and cephalosporins have been implicated in most allergic reactions to these medications
Sulfonamide reactions
reactive metabolite (hydroxylamine) produced by cytochrome P-450 oxidative metabolism
Type of reactions
type I (IgE-mediated) reactions,
type II (cytotoxic) reactions such as drug-induced hemolytic anemia or thrombocytopenia,
type III (immune complex) reactions such as serum sickness,
type IV (T-cell–mediated) reactions such as allergic contact dermatitis
