Pedia Seminar SGD.pptx Diphu medical college and hospital,Assam

Concise approach

1. Allergic rhinitis Presented by – Kalpana Kakati

2. Acknowledgement We would like to convey our heartfelt appreciation and gratitude to the respected Department of paediatrics for providing us with the chance to work on this wonderful, highly informative topic “Allergic rhinitis, Atopic dermatitis and Urticaria Angioedema ” and helping us to make it a success, which has aided us in conducting effective studies and gaining in-depth knowledge on it. Secondly, we would like to thank all our friends for guiding us all through. Lastly, we would like to thank Diphu Medical College and Hospital for providing us with the platform to present ourselves. Thank you everyone who helped!!

3. Introduction The condition is due to an IgE -mediated reaction to specific allergens,commonly inhaled house dust mite,pollen and spores. Most common atopic allergic reaction. Affects 10 to 25% of population Most commonly seen in young Children.

4. Clinical feature and diagnosis Presentation is with sneezing, itching, nasal obstruction and clear rhinorrhea that are seasonal or perennial with exacerbation. Anosmia Headache Fatigue Drowsiness

5. Precipitating factor Allergens present in the environment. House dust and dust mites Feathers Tobacco smoke Industrial chemicals Animal dander

6. Predisposing factor Genetic— 1.Multiple gene interaction are responsible for allergic phenotype. 2.Chromosomes 5,6,11,12& 14 control inflammatory process in atopic. 3. 50 % of allergic rhinitis patients have a positive family history of allergic rhinitis .

7. Common allergens Pollens Molds Insects Animals Dust mites Ingestants

8. Pathophysiology Immunoglobulin (Ig) E mediated type 1 hypersensitivity response to an antigen in a genetically susceptible person. Type 1 hypersensitivity causes local vasodilation and increased capillary permeability.

9. Diagnosis 1. Diagnosis is clinical 2. Examination shows pale nasal mucosa ,hypertrophied nasal turbinate and thin mucoid rhinorrhoea with or without conjunctival itching and redness. 3. Supportive test such as eosinophilia on nasal smear . 4. Skin test for common allergens and increased serum total or allergen specific IgE are not essential. 5. Skin test may be negative vin children during the first 1-2 years of illness while the sensitization is confined to nose and sinuses.

10. Differential diagnosis Food allergy (egg protein, cow milk,sea food) Foreign body in the nose Atopic dermatitis Medication induced rhinitis Non-allergic rhinitis Infectious causes

11. Treatment Avoidance of allergens causing rhinitis Topical corticosteroid spray provide symptomatic relief. Long term topical decongestant are discouraged due to the risk of rebound congestion and rhinitis medicamentosa.

12. ATOPIC DERMATITIS Presented by – Raju Pratim Baishya

13. Atopic dermatitis is an acute, subacute or chronic relapsing, endogenous eczema, characterized by dry skin and pruritic, recurrent, symmetric dermatitic lesions. The etiology is unclear. Genetic predisposition is an important factor but the inheritance pattern has not been ascertained. Immunological changes include elevated IgE levels, increased levels of allergen specific IgE and abnormalities of lymphocytes.

14. Clinical Features and Diagnosis In children, two distinct patterns of AD are seen. Infantile pattern Atopic dermatitis may have onset in infancy, after 3 months of age. The chief features are itchy, erythematous papulovesicles , seen on the face (Fig. 25.27), but may become generalized. The lesions clear by 18 months of age in 40% and evolves into the childhood pattern in the rest. Childhood pattern The childhood pattern is characterized by dry lichenified and crusted plaques, seen mainly on antecubital (Fig. 25.28) and popliteal fossa, the neck and face. Most (70%) clear by 10 yr of age. Common complications include the occurrence of superimposed bacteria or viral (herpes simplex, molluscum contagiosum) and fungal infections.

15. The diagnosis of atopic dermatitis is facilitated by diagnostic criteria (Table 25.9).

16. TREATMENT Parents and the child should be educated about the disease and its chronic course. There is limited role for dietary restriction. Breastfeeding decreases the chance of developing atopic dermatitis. Patients are educated to avoid scratching, avoid contact with irritants, like woolens and chemicals. Mild soaps and cleansing lotions are used.

17. Measures to reduce exposure to house dust mite, e.g. using barriers on pillows and mattresses, regular vacuuming of rooms may help. There is no contraindication to vaccination except in children specifically allergic to eggs, in whom influenza and yellow fever vaccines are avoided.

18. Acute eczema is treated with wet dressing; topical steroids and topical and oral antibiotics, are used when indicated. The role of oral anti histaminics is controversial. Chronic eczema is managed by hydration followed by application of emollients like petrolatum. Topical steroids are sometimes combined with keratolytic agents like salicylic acid (in lichenified lesions). It is preferred to use the least potent steroid, which reduces symptoms. Potent steroids should be avoided on face and genitalia. Topical immunomodulators like tacrolimus and pimecrolimus are useful because of their steroid sparing action and rapid reduction in itching. Oral antihistaminics might be used to break the itch-scratch cycle. Narrow band UVB, psoralens with UV A (PUV A) and oral cyclosporine are useful in resistant cases.

19. Urticaria Presented by – Saharul Alom

20. Defintion Urticaria is a vascular reaction of the skin characterized by appearance of itchy wheals, which are elevated (edematous) pale, erythematous, transient and evanescent plaque lesions which last for 24 to 72 hours.

21. Etiology 1. Allergic ( IgE -mediated): Foods (nuts, shellfish, eggs, milk) Drugs (penicillin, aspirin, NSAIDs) Insect bites/stings 2. Non-allergic (Non- IgE ): Physical factors (cold, heat, pressure, sunlight, exercise) Infections (viral hepatitis, helminthiasis, URTI) Autoimmune diseases (SLE, thyroid disorders) Idiopathic (most common in chronic urticaria)

22. Pathophysiology Mast cell degranulation → release of histamine, prostaglandins, leukotrienes → ↑ vascular permeability → edema in dermis → formation of wheals (hives) .

23. Clinical Features Skin lesion : Wheals: Raised, red or pale, edematous lesions with itching. Angioedema: Deeper swelling (lips, eyelids, tongue). Lesions are transient, usually lasting < 24 hours. In severe cases: Dyspnea, wheezing, abdominal pain, hypotension → Anaphylaxis.

24. Fig : Urticaria

25. Classification Acute urticaria — lasts < 6 weeks (often allergic). Chronic urticaria — lasts > 6 weeks (often idiopathic or autoimmune). Physical urticaria — triggered by physical stimuli (pressure, cold, etc.). Cholinergic urticaria — due to heat, exercise, stress.

26. Investigations Usually clinical diagnosis. For chronic/recurrent cases: CBC with eosinophil count ESR Thyroid function tests (T3, T4, TSH, anti-TPO) Allergy testing (skin prick test) Stool exam (for parasites) ANA (if autoimmune suspected)

27. Management Identify and remove cause (if known). Symptomatic treatment: Antihistamines: Non-sedating: Cetirizine, Loratadine, Fexofenadine Sedating (at night): Hydroxyzine, Chlorpheniramine Systemic corticosteroids: Short course in severe cases. Adrenaline (IM): For anaphylaxis.

28. Management Avoid triggers: Heat, alcohol, tight clothes, certain foods. Chronic/refractory cases: Montelukast (Leukotriene antagonist) Omalizumab (Anti- IgE monoclonal antibody) Cyclosporine (in resistant autoimmune urticaria)

29. Complications Anaphylaxis (life-threatening emergency). Angioedema causing airway obstruction. Sleep disturbance and reduced quality of life (chronic cases)

30. Prognosis Acute: Usually self-limiting. Chronic: May persist for months to years but often remits spontaneously.

31. Type Trigger Duration Example Acute urticaria Food, drugs, infection <6 weeks Food allergy Chronic urticaria Idiopathic, autoimmune >6 weeks Autoimmune thyroiditis Physical urticaria Cold, heat, pressure Variable Cold urticaria Angioedema Deep dermal/submucosal swelling Variable ACE inhibitor–induced Summary table:

32. Angioedema Presented by – Md Fuzal Ahmod

33. Definition Angioedema is a localized, non-pitting, transient swelling of the deeper layers of the skin and submucosa, resulting from increased vascular permeability due to release of vasoactive mediators like histamine or bradykinin . It often occurs with urticaria but can also occur independently.

34. Sites Commonly Involved Face (especially lips, eyelids, tongue) Oral cavity Larynx (may cause airway obstruction) Hands, feet, genitalia Gastrointestinal tract (causing abdominal pain, vomiting)

35. Fig : Angioedema

36. Etiopathogenesis Angioedema results from increased vascular permeability due to mediator release by mast cells or due to defective regulation of the complement system .

37. Type Mechanism Example / Cause Mediator Allergic (IgE-mediated) Type I hypersensitivity reaction Foods, drugs, insect stings Histamine Non-allergic (pseudoallergic) Direct mast cell activation NSAIDs, opiates, contrast agents Histamine ACE inhibitor–induced Inhibition of bradykinin breakdown ACE inhibitors (captopril, enalapril) Bradykinin Hereditary angioedema (HAE) Autosomal dominant deficiency or dysfunction of C1 esterase inhibitor (C1-INH) Family history present Bradykinin Acquired angioedema (AAE) Acquired C1-INH deficiency (autoimmune, lymphoproliferative disorders) Older adults Bradykinin Idiopathic Unknown cause – Histamine/bradykinin Types and Mechanisms

38. Investigations Skin prick test / RAST Serum C4 , C1-INH level , and C1-INH function . C1q level History of ACE inhibitor / NSAID use CBC, ESR, LFT .

39. Management A. General Measures Identify and remove precipitating cause (e.g. discontinue ACE inhibitors, stop triggering food or drugs). Airway protection is priority — intubate if laryngeal edema suspected. Avoid alcohol, stress, and trauma (may precipitate hereditary angioedema attacks).

40. Type Treatment Remarks Allergic / Histaminergic angioedema - Antihistamines (cetirizine, diphenhydramine) - Systemic corticosteroids (prednisolone 40–60 mg/day) - Adrenaline (IM 0.3–0.5 mg of 1:1000) in severe cases Rapid response; same as urticaria Bradykinin-mediated (HAE, ACE inhibitor–induced) - C1-INH concentrate (plasma-derived or recombinant) - Fresh frozen plasma (FFP) if C1-INH not available - Icatibant (bradykinin receptor antagonist) - Ecallantide (kallikrein inhibitor) Antihistamines and steroids are ineffective Long-term prophylaxis (HAE) - Androgens: Danazol, Stanozolol (↑ C1-INH synthesis) - Tranexamic acid (antifibrinolytic) Used for recurrent attacks Pharmacological management:

41. Complications Airway obstruction (laryngeal edema → respiratory failure) Anaphylactic shock Abdominal complications (mimicking acute abdomen) Psychological stress due to recurrent episodes

42. Prognosis Allergic angioedema: Excellent prognosis; resolves with treatment. Hereditary angioedema: Lifelong tendency, but manageable with prophylaxis. ACE inhibitor–induced: Resolves after drug withdrawal.

43. Feature Urticaria Angioedema Depth of edema Superficial (dermis) Deep (subcutaneous/submucosal) Itching Prominent Usually absent Duration < 24 hrs 24–72 hrs Site Any part of skin Face, lips, tongue, larynx, gut Mediator Histamine Histamine / Bradykinin Danger Mild discomfort May cause airway obstruction Difference between Urticaria & Angioedema