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Allergic Disorders In Children

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Allergic Disorders In Children

  1. 1. Allergic Disorders in Children
  2. 2. Allergy  It represents the clinical expression of IgE-mediated allergic diseases that have a familial predisposition and that manifest as hyper- responsiveness in the target organs. Atopy It refers to the genetic tendency to develop allergic diseases
  3. 3. Why Allergy Is Important?  Allergy affects approximately 15-30% of the general population around the world, most of which are children.  Most allergies interfere with sleep, intellectual functioning and recreational activities, whereas food allergy leads to considerable anxieties and fear of accidentally ingesting some notorious allergen. • Allergies are chronic conditions and fighting them may need a change of lifestyle, or even profession, adhering to a diet and to maintain allergen avoidance.
  4. 4. Types of Allergen • There are 2 types of Allergens (a) Allergens from the natural environment: - high molecular weight compounds(> 10 kDa). - most of these allergens have an enzymatic function examples are: pollen, fungi , spores, house dust mites, epidermis of house pets, insect venom, some food proteins, etc. (b) Allergens from a chemically contaminated environment: - usually low-molecular chemical compounds(<10kDa). - need to bind to a carbohydrate to attach to IgE. examples are: metals, drugs, additives to food products, latex.
  5. 5. Cells Involved In Allergic Reactions • CD4+ T cells play the central role in allergic inflammation. • Types of CD4+:  T helper 1 (TH1) - Secretes IL-2, TNF-b, and interferon-g (IFN-g). - Antagonize the allergic response.  T helper 2 (TH2): - Produces IL-4, IL-5, IL-6,IL-9,IL-10, and IL-13. IL-4 and IL-13 play the main role in allergic response.  T-regulatory (Treg) cells - critical role in expression of allergic and autoimmune diseases. - These cells have the ability to suppress effector T cells of either the Th1 or Th2 phenotypes
  6. 6. Mechanism of action of allergens • Generally allergic reactions takes place in following steps: 1) Primary Exposure 2) Secondary Exposure & Release of mediators
  7. 7. Allergic Cascade
  8. 8. Types of allergic reactions
  9. 9. Allergies to be covered....  Allergic rhinitis  Atopic dermatitis  Urticaria and Angioedema  Insect bites  Food allergy  Anaphylaxis
  10. 10. Allergic Rhinitis  Inflammatory disorder of the nasal mucosa marked by nasal congestion, rhinorrhea, and itching, often accompanied by sneezing and conjunctival inflammation.
  11. 11. Common allergens  Pollen  House dust  Mite  Animal dander  Smoke
  12. 12. Symptoms of Allergic Rhinitis • Recurrent episodes of sneezing • Pruritus, rhinorrhea • Nasal congestion and lacrimation • Snorting throat clearing • Postnasal drip. • Nasal obstruction unilateral or bilateral
  13. 13. Related Anatomic Structures Compromised by Allergic Rhinitis
  14. 14. Sequelae Of Allergic Rhinitis • Elongated facies – Allergic shiners, allergic salute • Nose – Septal deviation, polyps, drainage, turbinate hypertrophy, hyponasality • Mouth – Cobblestoning of oropharynx •Chest – wheezing • Skin
  15. 15. Classification Of Allergic Rhinitis •Intermittent allergic rhinitis : Symptoms present for less than 4 days a week , or for less than 4 consecutive weeks. • Persistent allergic rhinitis : Symptoms present for more than 4 days a week and for more than 4 consecutive weeks
  16. 16. Severity Of Allergic rhinitis
  17. 17. Allergic Rhinitis And Quality Of Life • Sleep loss or disturbance • Increased daytime sleepiness • Learning problems • Reduction in work productivity
  18. 18. Diagnosis  The 3 most common tests used to confirm the diagnosis 1)Skin testing 2)Nasal smear 3) In vitro testing for serum levels of specific IgE antibodies.
  19. 19. Prevention : Avoidance Of Allergens • Removing a pet from the house • Covering pillows and mattresses • Washing bedding with hot water • Vacuuming mattresses and pillows. No dry dusting
  20. 20. Pharmacotherapy Drug type Itch / sneezing Discharge Blockag e Impaire d smell Preparation Antihistamin es +++ ++ + - Fexofenadin e Cetrizine Anticholinergic s - +++ - - Ipratropium Decongesta nts - +++ ++ - Xylometazoli ne Oxymetazoli ne Mast Cell Stabilizers + + - - Sodium cromoglycat e
  21. 21. Atopic Dermatitis  Chronic Relapsing Skin Disease  Most commonly during early infancy and childhood  AD remains a clinical diagnosis  Pruritus is a consistent feature Family history of atopic disease (asthma, allergic rhinitis, atopic dermatitis)
  22. 22. Etiology  Complex integration of environmental and genetic factors  Wool, harsh detergents are particularly irritating  Emotional stress can lead to flares  Exclusive breast feeding for first 3 months of life is associated with lower incidence rates of atopic dermatitis during childhood in children with a family history of atopy
  23. 23.  In healthy people, the skin acts as a protective barrier against external irritants, moisture loss, and infection.  Proper function of the skin depends on adequate moisture and lipid content, functional immune responses, and structural integrity.  Severely dry skin is a hallmark of AD.  This results from compromise of the epidermal barrier, which leads to excess transepidermal water loss, allergen penetration, and microbial colonization.
  24. 24. Filaggrin  Structural protein in the epidermis  It is critical to skin barrier function.  Genetic mutations in the filaggrin gene family have been identified in up to 50% of patients with severe AD.
  25. 25. Clinical features  Vary with the age  Infancy:  Ill-defined scaling, erythematous patches and confluent, edematous papules and vesicles are typical.  Scalp and face are most often involved  When crawling : extensor surfaces especially knees are involved
  26. 26. Childhood  Lesions are drier, less eczematous, involve flexural areas & neck  Scaling, fissured & crusted hands become troublesome  Infraorbital folds (Morgan lines)
  27. 27. Chronic or chronically relapsing Pruritic, erythematous papulovesicular eruptions that progress to scaling lichenified dermatitis is common.
  28. 28. Diagnosis  Radioallergosorbent tests (RASTs) or skin tests may suggest dust mite allergy.  Eosinophilia and increased serum IgE levels may be present but are nonspecific.
  29. 29. Treatment  Reduction of trigger factors  Bland emollients, mild non alkali soaps  Scented soaps and oil can be irritating  Cotton clothing is preferable to wool and synthetics  Topical steroids  Systemic steroids for severe, acute flares  Calcineurin inhibitors: tacrolimus, pimecrolimus: no skin atrophy, therefore, useful on face and neck  Antihistamines helpful in breaking itch-scratch cycle
  30. 30. Urticaria and Angioedema  Urticaria (hives) is a vascular reaction of the skin characterized by wheals surrounded by a red halo or erythema.  Cardinal symptom is PRURITUS  Caused by swelling of the upper dermis  Up to 20% of the population experience urticaria at some point in their lives
  31. 31. Rash in urticaria
  32. 32.  Angioedema can be caused by the same pathogenic mechanisms as urticaria, but the pathology is in the deep dermis and subcutaneous tissue.  Swelling is the major manifestation  Commonly affects the face or a portion of an extremity  May be painful or burning, but not pruritic  May last several days
  33. 33. Angioedema
  34. 34. COMMON CAUSES OF ACUTE URTICARIA  Idiopathic  Upper respiratory streptococcal infections, helminthes  Food reactions  Shellfish, nuts etc.  Drug reactions  IV administration Blood products, contrast agents
  35. 35. ETIOLOGY OF CHRONIC URTICARIA  Idiopathic: over 50% of chronic urticaria  Physical urticarias: many patients with chronic urticaria have physical factors that contribute to their urticaria  These factors include pressure, cold, heat, water (aquagenic), sunlight (solar), vibration, and exercise  Cholinergic urticaria is triggered by heat and emotion
  36. 36. DERMATOGRAPHISM  Most common form of physical urticaria  Sharply localized edema or wheal within seconds to minutes after the skin has been rubbed  Affects 2-5% of the population
  37. 37. PATHOPHYSIOLOGY  The mast cell is the major effector cell in urticaria  Immunologic Urticaria: antigen binds to IgE on the mast cell surface causing degranulation, which results in release of histamine  Histamine binds to H1 and H2 receptors to cause arteriolar dilatation, venous constriction and increased capillary permeability.
  38. 38.  Non-Immunologic Urticaria: not dependent on the binding of IgE receptors  For example, aspirin may induce histamine release through a pharmacologic mechanism where its effect on arachidonic acid metabolism causes a release of histamine from mast cells. • Physical stimuli may induce histamine release through direct mast cell degranulation
  39. 39. CLINICAL FINDINGS  Lesions typically appear over the course of minutes, enlarge, and then disappear within hours  Individual wheals rarely last >12hrs  Erythema blanches with pressure  Urticaria may be acute or chronic  Acute = new onset urticaria < 6 weeks  Chronic = recurrent urticaria (most days) > 6 weeks  Most urticaria is acute and resolves
  40. 40. Diagnosis  Urticaria is a clinical diagnosis  A detailed history and physical examination  If a physical urticaria is suspected, a challenge test with the respective trigger may be performed  IgE-mediated food allergy is far more likely to present with acute urticaria  A detailed food diary or dietary modification may reveal foods (or additives) that cause fluctuations in symptoms of chronic urticaria  Allergy testing is not routinely performed in patients with
  41. 41. Treatment The following are examples of H1 antihistamines: • 1st Generation - Diphenhydramine - Hydroxyzine - Chlorpheniramine • 2nd Generation - Cetirizine - Loratadine - Fexofenadine
  42. 42.  Epinephrine 1 : 1,000, 0.01 mL/kg intramuscularly – rarely needed  Cyclosporine 4-6 mg/kg/day has been effective in some adults with chronic urticaria but its use is limited by hypertension and/or nephrotoxicity .
  43. 43. Insect bites  Allergic responses to stinging : 1. Localized cutaneous reactions 2. Systemic anaphylaxis  Allergic reactions that are caused by inhalation of airborne particles of insect origin result in: 1. Acute or 2.Chronic respiratory symptoms seasonal or perennial: i. Rhinitis ii. Conjunctivitis iii. Asthma
  44. 44.  Most reactions to biting and stinging insects are limited to a primary lesion isolated to the area of the bite and do not represent an allergic response.  Occasionally, insect bites or stings induce pronounced localized reactions or systemic reactions that may be based on: 1. Immediate or 2. Delayed hypersensitivity reactions.
  45. 45.  Members of the order Hymenoptera include: i. Apids: * Honeybee * Bumblebee ii. Vespids * Yellow jacket * Wasp * Hornet iii. Formicids * Fire ants * Harvester ants
  46. 46. Clinical features  Insect bites are usually urticarial but may be papular 1.Simple local reactions i. Involve limited swelling ii. Pain iii. Generally last <24 hr. 2.Large local reactions i. Develop over hours and days ii. involve swelling of extensive areas (>10 cm) iii. May last for days
  47. 47. 3.Generalized cutaneous reactions Typically progress within minutes and include cutaneous symptoms of : i. Urticaria ii. Angioedema iii. Pruritus beyond the site of the sting 4.Systemic reactions are identical to anaphylaxis from other triggers and may includes symptoms of: i. Generalized urticaria ii .Laryngeal edema iii. Bronchospasm iv. Hypotension
  48. 48. 5. Toxic reactions Stings from a large number of insects at once may result in toxic reactions of : i. Fever ii. Malaise iii. Emesis iv. Nausea 6.Delayed/Late reactions i. Serum sickness ii. Nephrotic syndrome iii. Vasculitis iv. Neuritis v. Encephalopathy
  49. 49. Diagnosis Generally evident from: i. History of exposure ii. Typical symptoms iii. Physical findings
  50. 50.  The primary reasons to pursue skin prick testing are to confirm reactivity when: i. Venom immunotherapy (VIT) is being considered ii. It is clinically necessary to confirm venom hypersensitivity as a cause of a reaction
  51. 51. Treatment At local site: i. Cold compresses ii. Topical medications to relieve itching iii. oral antihistaminics, analgesic  Anaphylactic reactions after a sting are treated exactly like anaphylaxis from any cause  Stingers should be removed promptly by scraping, with caution not to squeeze the venom sac because doing so could inject more venom  Sting sites rarely become infected, possibly owing to the antibacterial actions of venom constituents
  52. 52. Venom Immunotherapy(VIT)  Hymenoptera VIT is highly effective (95-97%) in decreasing the risk for severe anaphylaxis.  Immunotherapy against Hymenoptera is indicated in those ≥17 yr of age who have specific IgE to venom allergens and a history of generalized urticaria or a systemic reaction
  53. 53. Prevention  Avoidance of stings and bites is essential to reduce the risk of stings, sensitized individuals should: 1. Avoid attractants – perfumes, bright-colored clothing outdoors 2. Wear gloves when gardening 3. Wear long pants and shoes with socks when walking in the grass or through fields
  54. 54. Drug allergy  Drug allergy is an abnormal response to the medicine or metabolites through immunological reactions are known as hypersensitivity reaction that occurs during or after use of the drug.
  55. 55. Classification of ADR • Type A (pharmacological 85-90%) – PREDICTABLE – Side effects – Drug interactions – Drug toxicity • Type B (Hypersensitivity) – UNPREDICTABLE – Hypersensitivity – Idiosyncratic reactions – Pseudoallergy
  56. 56. CLINICAL FEATURES  Severe skin reactions, often on the palms and soles.  Fever, sometimes as high as 104 degrees F, is always present and usually appears before the skin rash.  Joint pain (50%) - usually seen in the larger joints, but occasionally the finger and toe joints may also be involved.  Swelling of lymph nodes, particularly around the site of the injection, is seen in 10-20% of cases.  Urine analysis may show traces of blood and protein in the urine.  Other symptoms may include changes in vision, and
  57. 57. Erythema multiforme and Steven Johnson Syndrome: Cotrimoxazole Penicillin Tetracyclines NSAIDs Anticonvulsant
  58. 58. Toxic epidermal necrolysis  Aspirin  Penicillin  Phenytoin  Sulfasalazine
  59. 59. Acneform eruptions :  Corticosteroids  Iodides  Isoniazid
  60. 60. Fixed Drug Eruption  Patients may complain of burning in the affected area before the appearance of lesions but systemic symptoms are usually absent.  The period required for sensitization ranges from weeks to years and the time between drug administration & eruption can be anything from a day or two to a few weeks.  It is so named because the site of the eruption is FIXED  It occurs in exactly the same place when the same drug is again encountered
  61. 61. Treatment  Discontinuation of the drug.  When the drug is considered to be very important and cannot be replaced, can continue to be provided with the approval of the family, and by way of desensitization.  Mild clinical manifestations – no treatment needed.  For pruritus, urticaria or edema -antihistamines  When very severe clinical symptoms - supportive treatment with corticosteroids and maintain fluid and electrolyte needs, transfusion, antibiotic
  62. 62. Food allergy Adverse reactions to foods consist of any untoward reaction following the ingestion of a food or food additive and are classically divided into  food intolerances which are adverse physiologic responses  food allergies which are adverse immunologic responses  When allergens are encountered in the GI system, they activate an immune response. The allergic cascade is activated and response is
  63. 63. Common food allergens  Peanuts  Sea food  Cow’s milk  Egg  Wheat  Soy products  Fruits
  64. 64. Clinical features  Gastrointestinal : 1) Food protein–induced enterocolitis syndrome (FPIES) typically manifests in the first several months of life as irritability, intermittent vomiting and protracted diarrhoea 2) Food protein-induced proctocolitis presents in the first few mo of life as blood-streaked stools in otherwise healthy infants
  65. 65. 3) Food protein–induced enteropathy often manifests in the first several months of life as diarrhea, often with steatorrhea and poor weight gain 4) Eosinophilic gastroenteropathies may appear from infancy through adolescence, more frequently in boys manifests as chronic gastroesophageal reflux, intermittent emesis, food refusal, abdominal pain, dysphagia, irritability, sleep disturbance, and failure to respond to conventional reflux medications
  66. 66.  Oral allergy syndrome  Skin Manifestations Atopic dermatitis , Acute urticaria and angioedema  Perioral dermatitis & perioral flushing  Respiratory manifestations : Food induced rhinoconjunctivitis  Anaphylaxis
  67. 67. Treatment  Appropriate identification and elimination of foods responsible for food hypersensitivity reactions are the only validated treatments for food allergies.
  68. 68. Anaphylaxis  Anaphylaxis is defined as a serious allergic reaction that is rapid in onset and may cause death.  Anaphylaxis in children, particularly infants, is underdiagnosed.  Anaphylaxis occurs when there is a sudden release of potent biologically active mediators from mast cells and basophils leading to symptoms
  69. 69. Diagnosis of Anaphylaxis  Anaphylaxis is highly likely when any 1 of the following 3 criteria is fulfilled: 1. Acute onset of an illness (minutes to several hours) with involvement of the skin and/or mucosal tissue AND AT LEAST 1 OF THE FOLLOWING: a. Respiratory compromise b. Reduced BP or associated symptoms of end-organ dysfunction 2. Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours): a. Involvement of the skin/mucosal tissue b. Respiratory compromise c. Reduced BP or associated symptoms d. Persistent gastrointestinal symptoms 3. Reduced BP following exposure to known allergen for that
  70. 70. Thank you

Hinweis der Redaktion

  • Patients with mutations in the human FOXP3 gene lack Treg cells and develop severe immune dysregulation, with
    polyendocrinopathy, food allergy, and high serum IgE levels
  • When the body is first subjected to the allergen (antigen), the condition is referred to
    as primary exposure. Because no antibodies has been formed previously, no symptoms of the allergy are produced during the primary
    exposure. However during the subsequent exposure, the allergen contacts the antigen-antibody reactions.
    During secondary expose the antibody become attach to the mast cells-white blood cells (basophils), and form a complex and as a result basophils burst due to antigen-antibody reaction causes a liberation of histamine, bradykinin and other mediators of allergic symptoms.
  • Drugs causing thrombocytopenia : sufonamides, penicillin, quinine , linezolid, nsaids
    Causes of serum sickness : penicillin,sulfonamides,quinine,ibuprofen,quinidine
  • Allergic shiners : blackish discolouration and puffiness under eyes
    Allergic salute : habitual upward stroking of the nose to relieve itching and wipe off secretions
    Hyponasility : rhinolalia clausa
    Cobblestoning of naopharynx : due to lymphoid aggregates, inflammation
  • Nasal smear in allergic rhinitis shows presence of eosinophils
  • The consequence of epidermal barrier dysfunction and an altered stratum corneum leading to increased transepidermal water loss
  • Erythema Multiforme
    • A self-limiting cutaneous hypersensitivity reaction to infection (mostly) or drugs
  • Egg – ovalbumin,ovomucoid
    Milk -

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