Showing posts with label allergic disorders. Show all posts
Showing posts with label allergic disorders. Show all posts

Friday, April 10, 2009

drug reactions

Prompt recognition of these reactions, drug withdrawl, and appropriate therapeutic interventions can minimize toxicity. Sulfonamide antibiotics, allupurinol, amine antiepileptic drugs (phenytoin and carbamazepine), lamotrigine, and the oxicam are associated with the highest risk of these reactions.
Pathogenesis of drug reactions
Cutaneus responses to drugs can arise as a result of immunologic or nonimmunologic mechanisms.
Immunologic :
Drug frequently elicit an immune response , but small number of individuals experience clinical hypersensitivity reactions . IgE dependent drug reactions are usually manifest in the skin and gastrointestinal, respiratory and cardiovascular systems. Primary symptoms and signs include pruritus, urticaria, nausea, vomiting, cramps, bronchospasm and laryngeal edema and occasion anaphylatic shock with hypotension and death.
Immune complex dependent reactions is characterized by fever, arthritis, arthritis, neuritis, edema, and an urticaria, popular, or purpuric rash. In classic serum sickness , symptoms develop 6 days or more after exposure to a drug, the latent period representing the time needed to synthesize antibody. The antibodies responsible are largely of the igG or igM class.
Cytotoxicity and delayed hypersensitivity may be important in the etiology of morbilliform exanthema, hypersensitivity syndrome , SJS , or TEN, but this is not proven.
Nonimmunologic drug reactions :
The mechanisms may be due to activation of effect pathways, overdosage , cumulative toxicity , side effects, ecologic disturbance , interactions between drugs, metabolic alterations , exaggeration of preexisting dermatologic conditions , or inherited protein or enzyme deficiencies.

allergic rhinoconjunctivitis

after exposure to allergen:
-sneezing
-itching of nose and eyes
-clear rhinorrhea or nasal congestion
It is the most common allergic disease and significantly affects quality of live as well as school performance and attendance. It frequently coexist with asthma. Prevalence is at 15% in the postadolescent years.
The pathologic changes in allergic rhinoconjunctivitis are chiefly hyperemia, edema, and increased serous and mucoid secretions caused by mediator release, all of which lead to variable degrees of nasal obstruction, pruritus, and rhinorrhea.
Laboratory:
Eosinophilia often can be demonstrated on smears of nasal secretions or blood.
Skin testing to identify allergen-specific IgE is the most sensitive and specific test for inhalant allergies, alternatively, radioallergosorbent assay test (RAST), immuno CAP, or other in vitro tests can be done for suspected allergens.
Treatment
* identification and avoidance of causative allergens cannot be overstated.
* antihistamines-to control itching, sneezing, and rhinorrhea. Sedating antihistamines: diphenhydramine, chlorpheniramine, hydroxyzine, clemastine.
* decongestan-phenilephrine and oxymetazoline should not be used for more than 4 days. Pseudoephedrine and phenylpropanolamine are often combined with antihistamines or expectorants.
* corticosteroids- mometasone nasal spray has been approved for use in children.
* other pharmacologic agents- montelukast is approved for perennial allergic rhinitis in children 6 months and older. Intranasal ipratropium can be used as adjunctive therapy for rhinorrhea.
* surgical therapy- turbinectomy and functional sinus surgery

pruritus

Typical features
-pruritus
-facial and extensor involvement in infants and young children
- flexural lichenification in older children and adolescents
- chronic or relapsing dermatitis
-personal or family history of Atopic disease
Clinical :
Erythematous papules associated with excoriations, vesiculation, and serous exudate, thickened skin with accentuated markings /lichenification and fibrotic papules. It may be secondarily infected with candida.
Treatment:
-avoidance of irritants such as detergents, chemicals, and abrasive materials as well as extremes of temperature and humidity is important in managing this disease.
-avoidance of food allergens: eggs, milk, peanuts, soy, wheat, and fish, etc.
- patients with Atopic dermatitis have evaporative losses due to a defective skin barrier. Appliying a wet facecloth or towel to the involved area for 15-20 minutes
-an effective emollient combined with hydration therapy will help skin healing and can reduce the need for topical corticosteroids. Petroleum jelly / vaseline is effective. Moisturizers often need to be applied several times daily .
-corticosteroids can decrease s aureus colonization. discontinued when inflammation resolves.
-calcineurin inhibitors: its immunomodulatory agents that inhibit the transcription of proinflammatory cytokines as well as other allergic mediators and target key cells in allergic inflammation.
-anti-infective therapy : mupirocin, cephalosporin.
-antipruritic agents: antihistamines, anxiolytics.

urticaria and angioedema

Urticaria: Erythematous, blanchable, circumscribed, pruritic, edematous papules ranging from 1-2mm to several centimeters in diameter and involving the superficial dermis. Individual lesions can coalesce.
Angioedema : edema extending into the deep dermis or subcutaneous tissues.
Both resolve without sequelae-urticaria usually within hours , angioedema within 72 hours.
Mast cell degranulation, dilated venules, and dermal edema are present in most forms of urticaria or angioedema.
Physical stimuli including pressure, cold, heat, water, or vibrations.
Clinical:
The immediate form is known as familial cold urticaria, in which Erythematous macules appear rather than wheals, along with fever, arthralgias, and leukocytosis.
The delayed form consists of Erythematous, deep swellings that develop 9-18 hours after local cold challenge without immediate lesions.
Solar urticaria , which occurs within minutes after exposure to light of appropriate wavelength , pruritus is followed by morbilliform Erythema and urticaria.
Laboratory:
Specific tests for physical urticarias such as an ice cube test or a pressure test.
Treatment:
- Avoidance of the triggering agents.
- epinephrine, especially when laryngeal edema complicates an attack.
- H1 antihistamines, cyproheptadine-cold urticaria. Diphenhydramine - dermographism. hydroxyzine- cholinergi urticaria.
- corticosteroids - usually not indicated in the treatment of acute or chronic urticaria.
- tricyclic antidepressant doxepin blocks both H1 and H2 histamine receptors.

Food allergy

* temporal relation between ingestion of a suspected food and onset of allergic symptoms.
* positive prick skin test or in vitro test to a suspected food allergen confirmed by a double-blind, placebo-controlled food challenge.
the highest prevalence of food allergy is found in children with moderate to severe Atopic dermatitis. Children with asthma have been found to have food-induced wheezing in some studies.
Clinical:
-most reactions to foods occur minutes to 2 hours after ingestion.
- hives, flushing, facial angioedema , and mouth or throat itching are common.
- anaphylatoid reactions can occurs after ingestion of foods such as certain fish containing high amounts of histamine.
Treatment:
- eliminating and avoiding foods