![Alternatively, they can be combined with a
longer acting antihistamine old generations
(e.g. chlorphenamine [chlorpheniramine]
maleate 12 mg sustained-release tablets
every 12 h)
so that peaks and troughs are blunted, and
histamine activity is blocked throughout the
night.](https://image.slidesharecdn.com/urticaria-230819143543-635c6222/85/urticaria-pptx-49-320.jpg)
urticaria .pptx
- 2. Erythemas The term erythema means blanchable redness (hyperemia) of the skin. A number of reactive skin conditions are referred to as erythemas. These include: A. Toxic erythemas related to viral and bacterial infections. B. Erythema muItiforme (EM). C. Erythema nodosum. .
- 3. URTICARIA DEFINITION Urticaria is a vascular reaction of the skin characterized by the appearance of wheals generally surrounded by a red halo or flare and associated with severe itching, stinging, or pricking sensations. These wheals are caused by localized edema. Clearing of the central region may occur and lesions may coalesce, producing an annular or polycyclic pattern.
- 4. Subcutaneous swellings (angioedema) may accompany the wheals. Angioedema may target the gastrointestinal and respiratory tracts, resulting in abdominal pain, coryza, asthma, and respiratory problems. Respiratory tract involvement can produce airway obstruction. Anaphylaxis and hypotension may also occur.
- 5. -The evolution of urticaria is a dynamic process. -New lesions evolve as old ones resolve. -Hives result from localized capillary vasodilation, followed by transudation of protein-rich fluid into the surrounding tissue; they resolve when the fluid is slowly reabsorbed. -The edema in urticaria is found in the superficial dermis.
- 6. Lesions of angioedema are less well demarcated. The edema in angioedema is found in the deep dermis or subcutaneous/submucosal locations.
- 7. Acute urticaria evolves over days to weeks, producing evanescent wheals that individually rarely last more than 12 h, with complete resolution of the urticaria within 6 weeks of onset. Daily episodes of urticaria and/ or angioedema lasting more than 6 weeks are designated chronic urticaria.
- 8. CLINICAL PRESENTATION. The sudden appearance of pink itchy wheals, which can come up anywhere on the skin surface . Lesions vary in size from the 2- to 4-mm edematous papules to giant hives, a single lesion of which may cover an extremity. They may be round or oval; when confluent, they become polycyclic. A portion of the border either may not form or may be reabsorbed, giving the appearance of incomplete rings
- 10. The most characteristic presentation is uniformly red edematous plaques surrounded by a faint white halo. .
- 11. Urticarial plaques in different stages of formation.
- 13. Superficial hives vary in color
- 14. Hives have become more extensive and confluent
- 15. Angioedema is a deeper, larger hive It is caused by transudation of fluid into the dermis and subcutaneous tissue. The lip is a common site.
- 16. PATHOPHYSIOLOGY Histamine is the most important mediator of urticaria. Histamine is produced and stored in mast cells. There are several mechanisms for histamine release via mast cell surface receptors. A variety of immunologic, nonimmunologic, physical, and chemical stimuli may be responsible for the degranulation of mast cell granules and the release of histamine into the surrounding tissue and circulation.
- 18. Histamine causes endothelial cell contraction, which allows vascular fluid to leak between the cells through the vessel wall, contributing to tissue edema and wheal formation.
- 19. When injected into skin, histamine produces the “triple response” of Lewis, the features of which are 1.local erythema (vasodilation), 2.the flare(axon reflex) with pruritus characterized by erythema beyond border of the local erythema, and a 3.wheal produced from leakage of fluid from the postcapillary venule.
- 20. Blood vessels contain two (and possibly more) receptors for histamine. H 1 receptors, when stimulated by histamine, cause an axon reflex, vasodilation, and pruritus. Acting through H 1 receptors, histamine causes Smooth muscle contraction in the respiratory and gastrointestinal tracts and pruritus and sneezing by sensory nerve stimulation.
- 21. H 1 receptors are blocked by antihistamines called H 1 antagonists (e.g., chlorpheniramine), which occupy the receptor site and prevent attachment of histamine. H 2 RECEPTORS: When H 2 receptors are stimulated, vasodilation occurs. H 2 receptors are also present on the mast cell membrane surface.
- 22. Activation of H 2 receptors alone increases gastric acid secretion. Cimetidine (Tagamet), ranitidine (Zantac), and famotidine (Pepcid) are H 2 blocking agents (antihistamines). Activation of both H 1and H 2receptors causes hypotension, tachycardia, flushing, and headache.
- 23. ETIOLOGY OF ACUTE URTICARIA Acute urticaria is IgE-mediated, complement- mediated, or nonimmune-mediated. 1.IgE-MEDIATED REACTIONS: Type I hypersensitivity reactions are probably responsible for most cases of acute urticaria. Circulating antigens such as foods, drugs, or inhalants interact with cell membrane–bound IgE to release histamine. Food allergies are the most common cause of anaphylaxis.
- 26. 2.IMMUNE-COMPLEX MEDIATED, ACUTE URTICARIA: Complement-mediated acute urticaria can be precipitated by administration of whole blood, plasma, immunoglobulins, and drugs or by insect stings. Type III hypersensitivity reactions (Arthus reactions) occur with deposition of insoluble immune complexes in vessel walls. The complexes are composed of IgG or IgM with an antigen such as a drug.
- 27. Urticaria occurs when the trapped complexes activate complement to produce anaphylotoxins C5a and C3a which are potent releasers of histamine from mast cells. Serum sickness (fevers , urticaria, lymphadenopathy, arthralgia , and myalgia), and systemic lupus erythematosus are diseases in which hives may occur as a result of immune complex deposition.
- 28. 3.NONIMMUNOLOGIC RELEASE OF HISTAMINE: Pharmacologic mediators, such as acetylcholine, opiates, polymyxin B, and strawberries, react directly with cell membrane–bound mediators to release histamine. Aspirin/NSAIDs cause a nonimmunologic release of histamine. The physical urticarias may be induced by both direct stimulation of cell membrane receptors and immunologic mechanisms.
- 29. The main types of urticaria. 1.Ordinary urticaria A. Acute ( up to 6 wks of continuous activity) B. Chronic (more than 6 wks of continuous activity) - Autoimmune chronic ordinary urticaria -Idiopathic chronic ordinary urticaria C. Episodic ( acute intermittent or recurrent activity) 2.Physical cold ,solar ,heat ,cholinergic dermographism (immediate pressure urticaria) delayed pressure 3.Hypersensitivity 4.Autoimmune 5.Pharmacological 6.Contact
- 30. Classification PHYSICAL URTICARIAS Physical urticarias are induced by physical and external stimuli, and they typically affect young adults.
- 31. Cold urticaria Patients develop wheals in areas exposed to cold (e.g. on the face when cycling in a cold wind). TREATMENT. a. Patients must learn to protect themselves from a sudden decrease in temperature. b. Cyproheptadine , loratadine, cetirizine, and other antihistamines may be effective.
- 32. Cold urticaria. The hive occurred within minutes of holding an ice cube against the skin.
- 33. Solar urticaria Hives that occur in sun-exposed areas minutes after exposure to the sun and disappear in less than 1 hour are called solar urticaria. This photoallergic disorder is caused by both sunlight and artificial light. Systemic reactions that include syncope can occur.
- 34. Heat urticaria Within 5 min of the skin being exposed to heat above 43°C, the exposed area begins to burn and sting, and becomes red, swollen, and indurated. This rare type of urticaria may also be generalized and is accompanied by cramps, weakness, flushing, salivation, and collapse.
- 35. Cholinergic urticaria Cholinergic urticaria, produced by the action of acetylcholine liberated from sympathetic nerves on the mast cell, is characterized by minute, highly pruritic, punctate wheals or papules 1-3 mm in diameter and surrounded by a distinct erythematous flare. These lesions occur primarily on the trunk and face. The condition spares the palms and soles. Lesions persist for 30-90 min and are followed by a refractory period of up to 24 h. Bronchospasm may occur.
- 36. The lesions may be induced in the susceptible patient by exercise, emotional stress, increased environmental temperature. Treatment with antihistamines is often effective . Antihistamines have been combined with other agents, such as montelukast and propranolol. Attenuated androgens, such as danazol, may be of benefit in refractory cases.
- 37. Round, red, papular wheals that occur in response to exercise, heat, or emotional stress.
- 38. Aquagenic urticaria This resembles cholinergic urticaria and is precipitated by contact with water, irrespective of its temperature. Dermographism (immediate pressure urticaria) This is the most common type of physical urticaria ,the skin mast cells releasing extra histamine after rubbing or scratching. The linear wheals are therefore an exaggerated triple response of Lewis.
- 39. They can readily be reproduced by rubbing the skin of the back lightly at different pressures, or by scratching the back with a fingernail or blunt object.
- 40. Hives are created by rubbing and linear lesions are produced by scratching
- 41. Delayed pressure urticaria Pressure urticaria is characterized by the development of swelling with pain that occurs 3-12h after sustained local pressure has been applied. It occurs most frequently on the feet after walking and on the buttocks after sitting. It is unique in that there may be a latent period of as much as 24 h before lesions develop. Kinins or prostaglandins rather than histamine probably mediate. Arthralgias, fever, chills, and leukocytosis can occur. The pain and swelling last for 8-24 h.
- 42. Hives form under the edge of the bra and waistband.
- 43. Course The course of an urticarial reaction depends on its cause. If the urticaria is allergic, it will continue until the allergen is removed, tolerated or metabolized. Most such patients clear up within a day or two, even if the allergen is not identified. Urticaria may recur if the allergen is met again. .
- 44. Complications Urticaria is normally uncomplicated, although its itch may be enough to interfere with sleep or daily activities and to lead to depression. In acute anaphylactic reactions, oedema of the larynx may lead to asphyxiation, and oedema of the tracheo- bronchial tree to asthma.
- 45. Some endogenous causes of urticaria. 1.Infection -Viral (e.g. hepatitis, infectious mononucleosis, HIV infection) -Bacterial -Mycoplasma -Intestinal parasites 2.Connective tissue disorders 3.Hyperthyroidism 4.Cancer -Lymphomas 5.Emotional stress Persons under severe emotional stress may have more marked urticaria, no matter what the primary cause is.
- 46. Some exogenous causes of urticaria. 1.Drugs, Penicillin, sulfonamide and related antibiotics are the most frequent offenders. Aspirin. (both topical and systemic) 2.Preservatives in lotions. 3.Foods and food additives : The most allergenic foods are chocolate, shellfish, nuts, peanuts, tomatoes, strawberries, melons, pork, cheese, garlic, onions, eggs, milk, and spices. 4.Bites. 5.Inhalants. 6.Pollens. 7.Insect venoms. 8.Animal dander. 9. Alcohol.
- 47. Treatment The ideal is to find a cause and then to eliminate it. In addition, aspirin – in any form – should be banned.
- 48. In general, antihistamines are the mainstays of symptomatic treatment. 1. New generations : Cetirizine 10 mg/ day and loratadine10mg/day, both with half-lives of around 12 h, are useful. If necessary, these can be supplemented with shorter acting antihistamines (e.g. hydroxyzine 10–25 mg up to every 6 h;, or acrivastine 8 mg three times daily).
- 49. Alternatively, they can be combined with a longer acting antihistamine old generations (e.g. chlorphenamine [chlorpheniramine] maleate 12 mg sustained-release tablets every 12 h) so that peaks and troughs are blunted, and histamine activity is blocked throughout the night.
- 50. If the eruption is not controlled, the dose of hydroxyzine can often be increased and still tolerated. H2-blocking antihistamines (e.g. cimetidine) may add a slight benefit if used in conjunction with an H1 histamine antagonist.
- 51. Chlorphenamine or diphenhydramine are often used during pregnancy because of their long record of safety, but cetirizine, loratadine and mizolastine should be avoided 2. Sympathomimetic agents can help urticaria, although the effects of adrenaline (epinephrine) are short lived. Pseudoephedrine (30 or 60 mg every 4 h) or terbutaline (2.5 mg every 8 h) can sometimes be useful adjuncts.
- 52. 3.A tapering course of systemic corticosteroids may be used, but only when the cause is known and there are no contraindications, and certainly not as a panacea to control chronic urticaria or urticaria of unknown cause. 4.Low doses of ciclosporin may be used for particularly severe cases
- 53. Anaphylaxis reaction Anaphylaxis is an acute and often life-threatening immunologic reaction, frequently heralded by scalp pruritus, diffuse erythema, urticaria, or angioedema. Bronchospasm, laryngeal edema, hyperperistalsis, hypotension, and cardiac arrhythmia may occur.
- 54. Antibiotics, especially penicillins, other drugs, and radiographic contrast agents are the most common causes of serious anaphylactic reactions. Hymenoptera stings are the next most frequent cause, followed by ingestion of crustaceans and other food allergens.
- 55. Causative agents can be identified in up to two- thirds of cases and recurrent attacks are the rule. Exercise-induced anaphylaxis is often dependent on priming by prior ingestion of a specific food, or food in general, and aspirin may be an additional exacerbating factor.
- 56. Treatment 1-For severe reactions, including anaphylaxis, respiratory and cardiovascular support is essential. 2-A 0.3 mL dose of a 1 :1000 dilution of epinephrine is administered every 10-20 min as needed. 3-In young children, a half-strength dilution is used.
- 57. 4-In rapidly progressive cases, intubation or tracheotomy may be required. 5-Adjunctive therapy includes intramuscular antihistamines (25-50 mg hydroxyzine or diphenhydramine every 6 h as needed) 6-and systemic corticosteroids(250mg hydrocortisone or 50 mg methylprednisolone intravenously every 6 h for 2-4 doses).
- 58. Erythema multiforme It is a skin condition of unknown cause, possibly mediated by deposition of immune complex (mostly IgM) in the superficial microvasculature of the skin and oral mucous membrane that usually follows an infection with herpes simplex or drug exposure.
- 59. Erythema multiforme: bullous and target lesions occurring in a favorite site
- 62. Some causes of erythema multiforme. -1.Viral infections, especially: herpes simplex, hepatitis A, B and C ,orf -2.mycoplasma -3.Bacterial infections -4.Fungal infections coccidioidomycosis -5.Parasitic infestations -6.Drugs -7.Pregnancy -8.Malignancy, or its treatment with radiotherapy -9.Idiopathic
- 63. Presentation EM minor is a self-limited, recurrent disease, usually of young adults, occurring seasonally in the spring and fall, with each episode lasting 1-4 weeks. -The symptoms of an upper respiratory tract infection may precede the eruption. -
- 64. Typically, annular non-scaling papules and plaques appear on the palms, soles, forearms and legs. -This lesion is the classic “target” or “iris” lesion with three zones: 1.central dusky purpura; 2.an elevated, edematous, pale ring; and 3.surrounding macular erythema -Lesions generally appear symmetrically and acrally . -Some lesions blister.
- 65. -The Stevens–Johnson syndrome is a severe variant of erythema multiforme associated with fever and mucous membrane lesions. The oral mucosa, lips and bulbar conjunctivae are most commonly affected, but the nares, penis, vagina, pharynx, larynx and tracheobronchial tree may also be involved. This merges with toxic epidermal necrolysis where the whole skin is affected more than 30% of the body surface area.
- 68. Stevens–Johnson type of erythema multiforme. The eyelids were also severely involved.
- 69. Course -Crops of new lesions appear for 1–2 weeks, or until the responsible drug or other factor has been eliminated. -Individual lesions last several days. -The site of resolved lesions is marked transiently by grey or brown patches, particularly in pigmented individuals.
- 70. Treatment: - The best treatment for erythema multiforme is to identify and remove its cause. -In mild cases, only symptomatic treatment is needed and this includes the use of antihistamines.
- 71. -Herpes simplex infections should be suspected in recurrent or continuous erythema multiforme of otherwise unknown cause. -Treatment with oral valaciclovir 500 mg once or twice daily or famciclovir 250 mg once or twice daily or acyclovir 10/kg/day may prevent attacks, both of herpes simplex for at least 6 months. and of the recurrent erythema multiforme that follows it.
- 72. In extensive cases of EM minor, systemic corticosteroids have been used, but because these theoretically may reactivate HSV, steroids are best given concurrently with an antiviral drug.
- 73. Erythema nodosum -Erythema nodosum is an inflammation of the subcutaneous fat (a panniculitis). It is type 4 hypersensitivity reaction an immunological reaction, elicited by various bacterial, -viral and fungal infections, -malignant disorders, -drugs -and by a variety of other causes
- 74. Erythema nodosum: large painful dusky plaques on the shins.
- 75. Some causes of erythema nodosum. 1.Infections Bacteria (e.g. streptococci, tuberculosis, brucellosis, leprosy, yersinia) Viruses Mycoplasma Rickettsia Chlamydia Fungi (especially coccidioidomycosis) 2.Drugs (e.g. sulphonamides , penicillin , oral contraceptive agents) 3.Systemic disease (e.g. sarcoidosis, ulcerative colitis, Crohn’s disease, Behçet’s disease) 4.Pregnancy
- 76. Presentation In most cases occurring in young adult women. The eruption consists of bilateral, symmetrical, deep, tender, bruise-like nodules, 1-10 cm in diameter, located pretibially. Initially, the skin over the nodules is red, smooth, slightly elevated, and shiny. The onset is generally acute, and frequently associated with fever , malaise, leg edema, and arthritis or arthralgia.
- 79. Over a few days, the lesions flatten, leaving a purple or blue-green color resembling a resolving bruise. The natural history is for the nodules to last a few days or weeks, appearing in crops, and then to involute slowly. EN is a reactive process. Lesions usually resolve in 6–8 weeks.
- 80. Investigations -Erythema nodosum demands a careful -history, -physical examination, -a chest X-ray, -throat culture for Streptococcus, -a Mantoux test -and an antistreptolysin-O (ASO) titre. - Serological testing for deep fungal infections.
- 81. Treatment 1 -The ideal treatment for erythema nodosum is to identify and eliminate its cause if possible. -For example, if culture or an ASO test confirms a streptococcal infection, a suitable antibiotic should be recommended. 2 -Bed rest and leg elevation are also an important part of treatment. 3 -NSAIDs such as aspirin, indomethacin or ibuprofen may be helpful.
- 82. 4. Systemic corticosteroids will result in rapid resolution of lesions, if not contraindicated by the underlying precipitating cause. 5. In acute lesions, colchicine is often rapidly effective at a dose of 0.6 mg twice daily.