Allergic rhinitis ,Atopic dermatitis, urticaris
- 1. ALLERGIC RHINITIS , URTICARIA, ANGIOEDEMA, ATOPIC DERMATITIS , BRONCHIAL ASTHMA
- 2. ALLERGIC RHINITIS • Definition: As per Allergic Rhinitis and its Impact on Asthma (ARIA), AR is defined as: -Type 1 hypersensitive inflammation of the nasal mucosa - Induced by exposure to allergic substance - With at least two of the four cardinal nasal symptoms, e.g. sneezing, rhinorrhea, nasal itching, and nasal block present for >1 hour/day on most/many days in a year • Prevalence: Affects 10-30% of adults and up to 40% of children globally
- 4. Causes and Triggers • Common Allergens: • Pollen (trees, grasses, weeds) • Dust mites • Pet dander • Mold spores • Other Triggers: • Smoke, strong odors, air pollution • Seasonal changes (spring, fall) • Drugs (Aspirin , NSAIDS)
- 5. DIAGNOSIS • The diagnosis of Allergic Rhinitis is based on a detailed history, characteristic signs and symptoms and the confirmed presence of allergen specific IgE. • Allergen specific IgE testing (either skin prick testing or In vitro specific IgE testing) have a supportive role in the diagnosis. It is very important that these tests should be guided by a careful history and local aerobiology. • Tests like total eosinophil count and total IgE lack specificity and sensitivity and is not recommended routinely.
- 6. MANAGEMENT 1. Allergen Avoidance • To avoid areas with high pollen, fungal, and dusty environment • Rigorous implementation of pest control measures • Control of house dust mites (most common, universal allergens) • 2. Pharmacological Treatment • Second-generation antihistamines are drugs of choice in mild intermittent AR for better safety efficacy ratio
- 7. For acute symptoms- Inhaled nasal steroids (INS) are the controller medications of choice
- 8. URTICARIA • Urticaria is a condition characterized by the development of wheals, angioedema, or both. • A wheal has three typical features: 1. Sharply circumscribed superficial central swelling almost invariably surrounded by reflex erythema 2. Itching or sometimes burning sensation 3. Resolves usually within 30 minutes to 24 hours. Angioedema is characterized by: 1.Sudden, erythematous, or skin-colored deep swelling in the lower dermis and subcutaneous plane or mucous membranes 2.Tingling, burning, tightness, and sometimes pain rather than itch 3.Resolution can take up to 72 hours (slower than that of wheals).
- 9. Types of urticaria 1.Acute urticaria(lasts for <6weeks)
- 10. Diagnosis and treatment of acute urticaria • Diagnosis is mainly clinical. Detailed history will help in identifying the inciting event or cause and will help in making a correct diagnosis. Keeping a food/event diary may help in identifying the allergen in patients with recurrent urticaria. Allergy skin testing is not usually indicated for patients with acute urticaria. •Treatment- • Anti histamines- Antihistamines are the first-line drugs used. Second-generation antihistamines(levocetirizine,fexofenadine), which are less sedating, are preferred in older school going children and adolescents. However, in infants and toddlers, first generation (chlorpheniramine,hydroxyzine) may be used to reduce irritability and improve sleep. • Adrenaline-It is used for extensive urticaria and angioedema. Dose—injection adrenaline 0.01 mL/kg of 1/1,000 adrenaline solution, subcutaneous or intramuscular. • Oral steroids- It is indicated only in severe urticaria or urticaria not responding to antihistamines. Tablet prednisolone 1–2 mg/kg/day for 3–5 days.
- 11. Chronic urticaria (lasts for >6 weeks) Chronic spontaneous urticaria- Chronic urticaria, which is not related to allergic reaction, may be associated with the presence of antithyroid antibodies, especially antithyroid peroxidase (TPO) antibodies. 35–40% may have a positive autologous serum skin test (pathergy test). Some patients may have anti-IgE or anti- IgE receptor antibodies.
- 13. Management of chronic urticaria-
- 14. ANGIOEDEMA • Angioedema or Quincke's edema is the rapid swelling (edema) of the dermis, subcutaneous tissue, mucosa and submucosal tissues. It is very similar to urticaria, but urticaria, commonly known as hives, occurs in the upper dermis.
- 15. TYPES OF ANGIOEDEMA 1. Acute or allergic angioedema – the swelling is caused by an allergic reaction, such as a reaction to peanuts. 2. idiopathic angioedema – there is no known cause for the symptoms of swelling . • 3. drug-induced angioedema – the swelling is a side effect of certain medications. • 4. hereditary angioedema – the swelling is caused by ‘faulty’ genes that are inherited from a person’s parents.
- 16. Acute or allergic angioedema • Almost always occurs with urticaria within 1-2 hours of exposure to the allergen • Nuts, shellfish, milk, eggs • Drugs, e.g. penicillin, NSAIDS, vaccines • Radiocontrast media • Natural rubber latex e.g. gloves, catheters • Reactions will recur with repetitive exposures or exposure to cross- reactive substances
- 17. Non-allergic drug reactions • Onset may be days to months after taking the medication • Commonly ACE inhibitors • Cascade of effects via kinin production and nitric oxide generation • Occurs without urticaria • ACE inhibitors increase bradykinin activity >>> Transient vasodilation >>> fluid in extracellular space • The incidence of angioedema from ACE inhibitors ranges in the literature from 0.1 to 2.2%
- 18. Idiopathic angioedema • Similar to acute allergic but angioedema keeps on recurring and often no known cause is found • Usually occurs with urticaria • 30-50% of this type of angioedema may be associated with some types of autoimmune disorders including SLE
- 19. Hereditary angioedema (HAE) • Inheritance- Autosomal Dominant • 3 types Type 1 and 2 mutation of C1NH gene on chromosome 11, (encoding C1 inhibitor protein) Type 3 mutation in F12 gene on chromosome 12, (encoding coagulation factor XII) • Type 1 results in low levels and function of circulating C1 inhibitor; • Type 2 has normal levels of C1 inhibitor protein but reduction in function • Decreased C1 inhibitor activity leads to excessive kallikrein, which in turn produces bradykinin, which we know is a potent vasodilator
- 20. Pathophysiology • Angioedema is swelling due to increased vascular permeability and extravasation of intravascular fluid. Known mediators of increased vascular permeability include the following: 1. Mast cell–derived mediators (e.g. histamine). 2. Bradykinin, a peptide containing nine amino acid residues produced from α2-globulin by the enzyme kallikrein. Bradykinin is a potent vasodilator which increases vascular permeability causing edema.
- 21. Signs and symptoms of angioedema Acute Angioedema: Large, thick, firm welts Swelling of the skin Pain or warmth in the affected areas Difficulty breathing or swallowing, in severe cases Hereditary Angioedema: • Sudden and severe swelling of the face, arms, legs, hands, feet, genitalia, digestive tract and airway • Abdominal cramping as a result of digestive tract swelling • Difficulty breathing due to swelling that obstructs the airway
- 22. Treatment IN ACUTE ANGIOEDEMA: • Initial stabilization (Airway, Breathing, Circulation) • Antihistamines e.g. IV chlorpheniramine, ranitidine • Anti-inflammatory medicines (corticosteroids) • Epinephrine shots (people with a history of severe symptoms can carry these with them) • Inhaler medicines that help open up the airways IN HEREDITARY ANGIOEDEMA: • Antihistamines and oral corticosteroid medications — although useful in treating hives and acute angioedema — are often ineffective in treating hereditary angioedema. • Medications used to treat hereditary angioedema on a long-term basis include certain androgens (male hormones), such as danazol, that help regulate levels of blood proteins.
- 24. ATOPIC DERMATITIS • Most common type of dermatitis • A chronic, pruritic, inflammatory skin disease with a wide range of severity • Non contagious • Primary symptom is pruritus (itch) • Hallmark of disease • Most debilitating symptom • AD is often called “the itch that rashes” • Scratching to relieve itch gives rise to the ‘itch-scratch’ cycle and can exacerbate the disease
- 25. • Usually develops in infancy or early childhood. • However can appear at any stage of life. • Patients experience periods of remission and exacerbation • Often for unexplained reasons. • Tooth erruptions, psychoemotional or stressful events are common known triggers • Often improves towards 5-6y of age
- 26. Pathophysiology
- 27. Clinical findings • Lesions typically begin as erythematous papules • Which then coalesce to form erythematous plaques • that may display weeping, crusting, or scaling • May often get infected causing pustules Atopic dermatitis Infantile phase Childhood phase Adult phase
- 28. Infantile phase • AD is usually noticed soon after birth • Usually sparing the diaper area and the nose. Key features • The earliest lesions affect the creases • Later localize to the cheeks, forehead, scalp and extensor surface of legs Area of distribution • ill-defined, erythematous, scaly, and crusted patches and plaques. Charecteristic skin lesion
- 29. Childhood phase • Xerosis is often generalized • Erythema and scaling arround the eyes can be seen • Dennie-Morgan folds (ie, increased folds below the eye)- often seen Key features • Flexural creases • The antecubital and popliteal fossae • Buttocks -thigh creases are often affected. Area of distribution • Lichenification is characteristic of childhood AD. • It signifies chronic scratching and is seen mostly over the folds, bony protuberances, and forehead. Characteristi c skin lesion
- 30. Adult phase • Xerosis is prominent Key features • Lesions become more diffuse • Cubital fossa and poplitial fossa and some times neck, face and hand Area of distribution • Lichenification may be present • A brown macular ring around the neck is typical but not always present Charecteristic skin lesion
- 31. Pearls of AD Treatment • The current therapeutic options for AD is not curative. • Approach should be • Individualized because of varied clinical presentations and disease burdens. • Dynamic to respond to changes over time. To manage flares Short term To control symptom between flares • Active lesion absent • But skin is dry and itchy Long term
- 33. THANK YOU.