4.1, OVERVIEW OF NORMAL IMMUNE SYSTEM Itis the capacity of human body to resist all types of ‘microorganisms and their products (toxins) that tend to damage tissues or organs. Immunity is the collective efforts of cells, tissues ang various molecules of the immune system to recognize and defend against infectious diseases, Definition of Immunity: The ability of an organism to resist a particular infection or toxin by the action of specific antibodies or sensitized white blood cells. Function of Immune System: * To protect the human body against disease and foreign body. * Although it is usually beneficial to host, as it gives protection from diseases. Antigens: An antigen has been defined as any substance which, when introduced parenterally into the body, stimulates the production of an antibody with which it reacts specifically and inan observable manner. Antibodies: The humoral immune response is produced, when the body synthesizes specific immunoglobulin molecules called antibodies, which circulate in the body fluids (blood, tissue fluids and lymph). . Complications: Bone marrow, lymphocytes thymes, leukocytes etc. Types of Immunity: Immunity is divided into innate or acquired immunity. a ,( Types of Immunity ) 7 J | Innate immunity, Acquired immunity Passive ificlal -Individual Natural Artificial Natural Arti eg:After an eg: By inoculation —_—_eg, Mother to 9, By infecting aitack of of lve or killed foetus via placenta serum infections vaccine or toxoid or milk and diseases colustrum © Fig. 4.1 1. Innate or native immunit is the resistance to infections, which an individual possesses by virtue of his genetic and constitutional make up. It may be non-specific, when it indicates a degree of resistance to infections in general, or specific where resistance to a particular pathogen is concerned. 2. Acquired immunity: The resistance that an individual acquires during life is known as acquired immunity as distinct from inbom innate immunity. Active immunity refers to the resistance developed by an individual as a result of an antigenic stimulus. Active immunity may be natural, artificial. a. Natural Active Immunity: It results from either a clinical or an inapparent infection by a parasite. e.g. A person who has recovered from an attack of measles develops natural active immunity. 4. Artificial Active Immunity: It is the resistance induced by vaccines. Vaccines are Preparations of live or killed microorganisms or their products used for immunization. 8. BCG vaccines, oral polio, hepatitis-B etc. “e. Natural Passive Immunity: It is the resistance passively transferred from mother to baby. Inhuman infants, maternal antibodies are transmitted predominantly through the placenta. 4. Artificial Passive Immunit administration of antibodies. t is the resistance passively transferred to a recipient by the4.2. ASSESSMENT OF IMMUNE SYSTEM, DIAGNOSTIC EVALUATION are ee HISTORY COLLECTION Biographical and demographic data Gender: Age, sex and living environment has to be asked. Some auto immune diseases are more common in females as compared to males. Nutrition: Nurse should assess the nutritional pattern of patient. Inadequate intake of proteins, lipids impair immune function. Lipid deficiency also lead to deficiency of fat solution vitamins help in maturation of immune cells. Present Illness: Allergic reactions, altered immune system or disorders of lympathetic disorder produced clinical manifestations. Ask these manifestations; * Like rhinitis, sneezing, nasal stuffiness, wheezing, coughing, fatigue, vomiting, diarrhoea and pruritis has to be asked from patient. Patient may report lymph node swelling and edema of extremity. * Ask about severity and location of symptoms like severity of skin rash, location of swollen lymph nodes. * Ask about the treatment that decrease or stop the symptoms/disease ¢.g- Drugs, home remedies etc. Past Health History: * Childhood Disease: Ask about childhood disease or allergic manifestations. e.g. Sneezing, coughing and wheezing and treatment that relieved those illnesses. * Immunization: Ask about previous immunizations, any immunization taken against allergy. * * * * MEDICAL SURGICAL BYP" vious a ent about Prev" Allergies: Ask the client 20% relieve history of allergy and factors that particular allergy (food and drugs). Family health History? Ask ai a allergy and sensitivity, (4 Hay as it runs in families. Psychosocial history: Ask about like working in occupation (occupation cotton industries, dust exP0SU"®) ae of working (like in open field or near roadside), as it predispose the person for allergic reactions. Environment: Ask about home and outside environment like presence of pets, vegetation near house. Habits: Ask about habits of person like smoking, poor nutrition and alcohol intake and exercise. Review of Systems: All the body systems should be reviewed with regard to the following: associative problems. General Manifestations: Malaise, fatigue, unusual reaction to insect bite or medicines, including over the counter (OTCS) and fever. Integumentary system: Rashes, dermatitis, utricaria, pruritis, scratching dryness and scaling. Respiratory: Rhinitis, change in rate of respiration, dyspnea, frequent cough (dn or productive) bronchospasm, respirator distress and hyperventilation. Cardiovascular: Hypotension, tachycardia, vasculitis, anaemia and dysrhythmia. Gastro intestinal: Diarrhoea, vomiting cramping, food intolerances and colitis.(gare ereoutnrsrsinepenoN, # Genitourinary system: Hematuria, any discharge and increased frequency of urination and burning micturation. Musculoskeletal system: Joint mobility, edema and pain. Neuro sensory system: Hearing loss, visual changes, headache (migraine), ataxia, tetany and cognitive dysfunction. Apart from body systems, also assess organs to rule out presence of these symptoms: - Eyes: Excessive lacrimation, rubbing orblinking, conjunctivitis, dark circles around eyes. Ears: Pain in ear, feeling of fullness in ears and ruptured tympanic membranes. - Nose: Sneezing, rhinitis, nasal, polyps, nasal voice quality, nose rubbing and epistaxis. - Throat: Swollen lips or tongue, sore throat, itching of neck or throat, hoarseness of voice. PHYSICAL EXAMINATION Techniques used for assessment are inspection and palpation. * Inspection: Inspect the patient’s skin and mucus membrane for lesions, dermatitis, purpura, utricaria and inflammation. Also inspect for chills and sweating. Palpation: Axillary lymph nodes, anterior and posterior cervical nodes and inguinal lymph nodes are palpated for swelling, tenderness and warmth. Normally lymph nodes are small (1cm diameter or less than 1cm), round, soft, single, nontender particularly in cervical and inguinal areas. DIAGNOSTIC TEST Test of immunologic Status: * Complete blood counts. * CD, cell count in HIV patients depict depletion of T helper cells. * T and B lymphocyte assays. eg. Increased levels are present in chronic lymphocytic leukemia, multiple myeloma, digeorge syndrome and reduced levels are in acute lymphocytic leukemia and severe combined immunodeficiency disease. * Bone marrow biopsy done to rule out blood disorders. * Immunoglobulin assay: Test for humoral immunity. - Bcells quantification with monoclonal antibody. - Specific antibody response. - Total serum globulins and individual immunoglobulins by electrophoresis. Test for cellular immunity: * Total lymphocyte count. * Delayed hypersensitivity skin test. * Cytokine production. * Helper and suppressor T cell functions. * Phagocyte cell function test. * Acquired Immuno Deficiency Syndrome Test (AIDS) - Enzyme linked immunosorbent assay (ELISA) - done in HIV suspected patient. It has high sensitivity. - Western blot: More specific test for presence of HIV antibody.Radio immuno Precipitation assay (RIPA): Done in HIV Patients. It is More time consuming than western blot. Polymerase chain reaction, Hypersensitivity Test: Scratch test, Patch test, intradermal test and radio allergosorbent test (RAST) done to check hypersensitivity. Lymphangiography:Lymphan- giography allows direct visualization of the lympathetic system to assess the Presence of primary malignancy. Specific antigen antibody test: Complement fixation test, agglutination and immunofluorescence done to rule out specific antigen antibody reaction. Food allergy testing: Food allergy are tested by skin testing. 4.3. ALTERED IMMUNE RESPONSE 2 SSS Immune Response: “The specific reactivity induced in a host by an antigenic stimulus is known as the immune response.” Types: The immune response can be of two types: 1. The humoral (antibody mediated). 2. The cellular (cell mediated). _Mediated | Humoral Immunity (Antibody-Me | Immunity): | ided by the * Humoral immunity is provided PY activation of B Lymphocytes: * Tis also called B. Cell immunity. ioht against the invading * B. Lymphocytes fi tibodies into the organisms by secreting an blood and Lymph. * The blood and Lymph are body fluids (Humors) and the B Lympocytes provide immunity through ‘humors’. * Therefore, this type of immunity is called Humoral Immunity. It plays an important role in defense mechanism against the Bacterial and Viral infections. Cellular Immunity: * The cellular immunity is provided by the activation of T Lymphocytes. These cells encounter and destroy the organisms, which enter the body. Ttis also called cell mediated immunity or T cell immunity. Itis the major defense mechanism against infections by viruses, Fungi and few Bacteria like tubercle bacillus. Cellular immunity is also responsible for delayed allergic reactions and the Rejection of transplanted tissues. Altered immune response: Definition: A reaction or change of the immune system as a result of an allergic or irritant. Patients with Altered Immune Systems: Primarily an issue of lymphocyte response t0 conditions triggering the inflammatory response.p cule infections and inflammatory * onditions. ‘Anaphylat Exposure to new antigens and development of immunity. tic reactions, «Chronic inflammatory conditions, Long-term immunity. Chronic diseases such as asthma, COPD, chronic allergies (including latex, seasonal), autoimmune diseases such as lupus or secondary immunode- ficiency disorders. Altered immune response are listed below: 1. Hypersensitivity reaction. 2, Allergic disorders. 3, Immunodeficiency. 4, Autoimmune disorders. 4.3. HYPERSENSITIVITY aaa Immune Response is generally a protective process, which protects body against infectious agents and their toxins. But, immune response may sometimes be injurious to the host. An individual who has been sensitized by previous “posure to an antigen may respond to the same subsequent antigenic stimuli in an exaggerated eo leading to tissue damage, disease or ae death of the individual. Such a heightened ©xaggerated response is known as *Persensitivity, Bites. Definition: sensitivity Hypersensitivity (also called hypers' jesirable reaction or intolerance is a set of und reactions produced by the normal immune system, including allergics and auto immunity. When an antigen is environmental or exogenous and initiate immune response, it is called “allergy”. Antigen, which initiate immune response is called an “allergen”. Types: Atopic and non-atopic disorders. a. Atopic disorders: They have hereditary predisposition and production of local reaction to IgE antibodies. ¢.£- Allergic thinitis, asthma and atopic dermatitis/ eczema). b. Non-atopic dermatitis: It does not have genetic predisposition. e.g. Latex allergy. It can be type I and IV hypersensitivity reaction. Etiology and Risk Factors: 1. Host Defenses: Specific IgE formation can be influenced by vital infections, especially those caused by cytomegalovirus (CMV) and mononucleosis. Factors like air pollution, sex, age and secondhand smoke. . Nature of Allergen: Environmental allergens —air borne — Pollen, dust particles and animal dander. 3. Concentration of Allergen: Higher concentrations usually result in hyper- sensitivity responses of greater intensity. 4. Route of entrance into the body: Inhalation, Injection, Ingestion and Direct contact. 5. Exposure to the allergens: N * Exposure to allergens in early life. * Seasonal allergens—spring, fall.Pathophysiology: The key intermediate in allergic disease is the IgE antibody, There are two general categories of hypersensitivity reactions. a, Immediate (humoral or antigen — antibody): Immediate reaction occurs within minutes often exposure to the allergen. 4. Delayed (cell mediated): Delayed reaction is seen when there is a prolonged response to the initial allergen occurs for 2-8 hours approximately, Classification: Table: Classification of Immunologic Reactions (Gell and Coombs). Type Mediator Reaction I IgE Immediate. (Rarely IgG4) a IgG, IgM Cytotoxic. (Cell-Ag) MM | Ag-Ab Immune complexes complex. IV__|Tcells Cell-mediated. Note: This ‘classification is an oversimplication. i. Type I (Anaphylactic) Hypersensiti- vity: The anaphylactic response is a rapidly occurring reaction mediated by IgE antibodies. The allergen binds to IgE antibodies, which are attracted to the surface of mast cells and basophils, causing release of mediators. e.g. Allergic thinitis and Asthma. ED Table: Chemical Mediators of the aller, Reaction. "rele Mediator Action Histamine. Dilates blood vessels and increases vascular permeability. Platelet Dilates the blood activating factor. | vessels and constricts : the bronchial airways, Aids the secretion of platelets. Eosinophil Increase eosinophil chemotactic migration. factor of anaphylaxis (ECF-A). | Neutrophil Increase neutrophil chemotactic migration. | factor. Heparin. Anticoagulation. Bradykinin. Slows smooth muscle contraction. Increases mucous production. ii. Type II (cytolytic or cytotoxic) hypersensitivity: This type of reaction is initiated by IgG (or) IgM antibodies that react either with cell surface or tissue antigens. Cell or tissue damage occurs in the presence of complement or mononuclear cells. e.g. Hemolytic anaemia, Rh hemolytic disease in the newborn and autoimmune hyperthy- roidism. iii. Type IIT (immune complex) hyper- sensitivity: Immune complex reactions result when antigen bind to antibodies leading to tissue injury. The molecular size of the antigen antibody complexes is a" important feature in eliciting immune complex reactions.Of Rheumatoid arthritis and glomerulonephritis, ¢ IV (cell mediated or delayed) Hypersensitivity: In cell mediated nsitizedT cells respond to antigens by releasing lymphokines, some of which direct phagocytic cell activity. This reaction occurs 24-72 hrs after exposure to an allergen. Clinical Manifestations: During an allergic response, most cell activation and the release of chemical mediators result in: * * * * * * Increased vascular permeability. Edema. Dilatation of blood vessels. Smooth muscle contraction. Bronchospasm. Increased mucus secretion in the nose, lungs and GI tract. Diagnostic Evaluation: nes . History collection. Common allergy tests include: - Skin testing. - Radio allegro sorbent test (RAST). - Pulmonary function test (PFT). - Blood assays for IgE levels. Medical Management: 1. we + . Steroids Antihistamines. ¢.g. Diphenhydramine (Benadryl), Cetirizine (zyrtec), Fexofenadine (allegro) and Loratadine (Claritin). . Decongestants. e.g. Topical nasal sprays. e.g. Beclomethasone dipropionate, Triamcinolone (Nasacort) and Flunisolide (Nasarel). . Anticholinergics. e.g. Ipratropium for asthma. 5, Branchodilators. .Albuterol (ventolin) and Salmeterol (serevent). 6. Antileukotriencs —¢.g-Zafirlukast (accolate) and Zileuton (zyflo). | Nursing Management: * Assess the client’s history and current manifestation. Assess the types of allergens. e.g. House dust mites cockroach, animals are present in home, environmental factors such as smoke and chemicals. Identify allergen and avoid allergen. * Environmental control sometimes helps to eliminate airborne allergens. * Administer the medications as per doctor’s prescription. * fan inhaleris prescribed, the client must be taught how to use it correctly. 4.3B. ALLERGY a] Definitio1 ‘A damaging immune response by the body to a substance, especially a particular food, pollen, for dust to which it has become hypersensitivity. ALLERGY DISORDERS * Allergies are the result of immune system’s response to a substance. * Immune responses can be mild from coughing and a running nose, to a life threatening reaction known as anaphylaxis. * A person becomes allerge when their body develops antigens against a substance upon repeated exposure as the severity of the reaction may increase.y Anaphylayi : S 0 Serious, i ine allergic Teaction » life threatening e.g. Bee string to hypersensitive. It that is rapid in on: anaplylactic Teacti Stings, medication and the most common ‘ONS are to foods, insect’s and latex. An 7 9 1 acute allergic reaction to an antigen. which the body has become is a serious allergic reaction set and may cause death. Causes: Certain medications, such almor Common anaphylaxis triggers include: espeically penicillin, foods, as peanuts, tree nuts (walnuts, pecans, nds, cashew) wheat fish chelphin milk and €gg. Insect sting from bee, yellow jackets, wasps and fire ants. Symptoms: * Trouble breathing. * Skin rash or strange feeling. * Hives or swelling. * Tightness of the throat. Hoarse voice. * * Nausea. * Vomiting. * Abdominal pain. * Diarrhoea. * Dizziness. * Fainting. * Low blood pressure. * Rapid heart beat. Management and ‘An anaphyla immediately wit! jaline). Dos ee all times. Two inject control symptoms. reducing the risk * * Feeling of doom. Cardiac arrest. Treatment: i Id be treated ctic reaction shoul b it cr ves, available by prescription, doses tor that should be kept at tions may be NECeSSAry to Here are some tips for f anaphylaxis: ver: Very important to know Seed the reaction. Anallergis, wet eview your medical history and, if a conduct diagnostic tests. The most common triggers are: i its such d: Including peanuts, tree nu tens and pecans, fish, shellfish, cow’s milk and eggs. Latex: Found in disposable gloves, intravenous tubes, syringes, adhesive tapes and catheters. Health care workers, children with spina bifida and genitourinary abnormalities and people who work with natural latex are at higher- risk for latex-induced anaphylaxis. Medication: Including penicillin, aspirin and non-steroidal anti-inflammatory drugs such as Ibuprofen, and anesthesia. Insect sting: With bees, wasps, hornets, yellow jackets and fire ants being the most likely to trigger anaphylaxis. Avoid your trigger: Avoidance is the most effective way to prevent anaphylaxis. An allergist can work with development of specific avoidance measures tailored Specifically for age, activities, occupation, hobbies, hom? environment and access to medical catt —_ZALLERGIC RHINITIS Definition: “Allergic rhinitis isan inflammation of the nasal passages, usually associated with watery nasal discharge and itching of the nose a, Seasonal Allergic Rhinitis: Symptoms appear in around a particular season when the pollens of a particular plant, to which the patient is sensitive, are present in the air. b. Perennial Allergic Rhinitis: Symptoms are present throughout the year. Etiology: a. Seasonal Allergic Rhinitis: * Allergy to seasonal pollens and outdoor molds. * Seasonal pollen depends on wind for cross-pollination. b. Perennial Allergic Rhinitis: * Allergic with in the home such as: - Dust mites. - Cockroaches. - Molds and animal dander. - Animalallergens. Pathophysiology: Allergic Reaction + Exaggerated or Inappropriate Immune Reaction Damage to the host v ‘Type 1 hypersensitivity reaction IgE antibodies, mediated ¥ Mast cells and basophilis (Trigger) + Acute Rhinitis © Fig. 4.2 | Clinical Manifestations: a. Seasonal allergic rhinitis: * Paroxysmal sneezing. * 10-20 sneezes at a time. * Nasal obstruction. * Watery nasal discharge and itching in the nose. b. Perennial allergic Rhinitis: * Stuffy nose, loss of sense of smell due to mucosal oedema. * Postnasal drip, chronic cough and hearing impairment due to eustachian tube blockage. * Fluid in the middle ear. Diagnostic Evaluation: 1. Total and differential count: Peripheral eosinophilia may be seen, but this is an inconsistent finding. 2. Nasal smear: It shows large number of eosinophils in allergic rhinitis. 3. Skin tests: These tests help to identify specific allergen. They are prick, scratch and intradermal tests. * Skin prick test: A positive reaction is manifested by the formation of a central wheal and a surrounding zone of erythema (flare) within 10-15 min. Specific IgE measurements: It is an in vitro test to find the specific allergen. x , Radioallergosorbent test (RAST): It is an vitro test measures specific IgE antibody concentration in the patient’s serum. w }. Nasal provocation test: A crude method is to challenge the nasal mucosa with a small amount of allergen placed at the end of a toothpick and asking the patient to sniff into each nostril and to observe, if allergic symptoms are reproduced.Management: tvoidance of allergen. 2. Treatment with drugs. * Antihistaminies. ¢.¢. Azclastine (Astelin and Optivar). Oral Decongestants. e, Actifed. * Corticosteroids Nasal Sprays. ¢.g. Fluticasone and Mometasone. * Anti-drip Anticholinergic Nasal Sprays. e.g. Ipratropium, * Decongestant Nasal Sprays. e.g. Afrin and Nostrilla. * Anti-IgE. e.g. Omalizumab. 3. Saline Nasal Sprays: Use an over-the- counter nasal saline spray or home made salt water solution to flush the nose of irritants and help narrow the blood vessels, reducing congestion in the nose. 4. Immunotherapy. Immunotherapy suppresses the formation of IgE. It also taises the titre of specific IgG antibody. Immunotherapy has to be given for a year or so before significant improvement of symptoms can be noticed. * Intranasal cromolyn sodium, is recommeded for mild intermittent disease. * For allergic symptoms of moderate severity or for persistent disease intranasal corticosteroids can be used as monotherapy. * For severe symptoms, combination therapy with oral non-sedating antihistamines and intranasal steroids are : Sudafed and used. * Jfnasal obstruction persists a short course of intranasal decongestant can be used. Oral decongestant can be combined with antihistamines. fTIS, 3. DERMATITE Definition: ofthe dermic Dermatitis is an inflammati”., redness, of the skin, causing itchin&: Po and scaling, swelling and often oozing: 8°", 10 physical, Itis an inflammatory reaction 7s dermis is chemical or biologic®! oBeral and chemical damaged by repeated PhYSN onic. irritations. It may be acute or itis: = ieaeans Contact dermatitis is 1, Contact Derma’ paaee by direct contact in i tion. an a varticulat substance such as ee intravenously, jewellery eae sees he certain cleaning products, Per) cosmetics. The rash is very itchy, is Gane to a specific area, and often has clearly defined boundaries. Types of Contact Dermatitis: Substances can cause skin inflammation by one of two mechanisms - irritation (irritant contact dermatitis) or allergic reaction (allergic contact dermatitis). a. Irritant Contact Dermatitis: Chemical substance causes direct damage to the skin. Irritant contact dermatitis is more painful than itchy. b. Allergic Contact Dermatitis: It occus when a substance to which patient is sensitive (allergen) triggers an immune reaction in skin. Allergic contact dermatitis produces a red rash, bumps and sometimes blisters when severe. 2. Atopic Dermatitis: Atopic dermatitis is chronic, itchy inflammation of the upp¢t layers of the skin that often develops in peop!who have hay fever or asthma and in people who have family members with these conditions. It cannot be spread from person to person. 3. Seborrheic Dermatitis: Seborrheic Dermatitis (SD) a common, ‘chronic inflammatory skin disorder generally confined to areas of skin regions with a high density of sebaceous glands (e.g. Face, scalp, and upper trunk). 4, Exfoliative Dermatitis: Exfoliative dermatitis is severe inflammation that causes the entire skin surface to become red, cracked, and covered with scales. Stages of dermatit a. Acute stage of eczema: * Include inflammation, pain, heat, tendemess, swelling, and possible itching. characterised by extreme redness and drainage at the lesion site. * In acute eczema would experience vesicles, blisters, and intense redness of the skin. * The common examples for this stage of eczema would include acute nummular eczema, acute contact eczema, pompholyx eczema, and stasis eczema. 6. Sub-acute phase of eczema: * Includes symptoms associated with skin redness, inflammation and crusting; * There is no extreme swelling, redness, scaling of the skin, fissures, and a parched or scalded appearance to the skin. In the sub-acute phase, itching is more of concern than pain. One may experience some blistering or oozing of the skin. * ‘The common examples of the sub-acute phase include atopic eczema, contact allergy, stasis eczema, asteatotic eczema and nummular eczema. ‘» Chronic eczema: * Refers to eczema flares lasting three months or more. * The cycle of intense itching and subsequent urge to scratch tend to worsen and prolong the condition. * In the chronic stages of eczema the skin would show a thickened, leathery and /or fissuring appearance. * The skin may appear to be darker and rather dull in appearance. * Chronic eczema is more commonly seen with atopic eczema, fingertip eczema, hyperkeratosis eczema, and lichen simplex eczema. Etiology and Risk Factors: * Heredity. * Dryness of skin. * Interaction between a combination of immune system, physical environment and generic factors. Inritants and allergens like rubber, cosmetics and certain drugs. Family history of allergic conditions like food allergy, asthma etc. Varicose veins. Constant scratching. * Fungal infections. Exposure to environment allergens and irritants. * Nickle and Gold in Jewellery. Emotional stress.Pathophysiology: Immuno response of body activated ‘and It rolease hi ‘and other inflammatory mediators Immune response interacts with allergens Cause inflammatory condition Water binding capacity of skin reduced It leads to higher transepidermal water loss Drying and cracking of the skin Itching, rubbing and scratching of skin damages the skin further causing scales. © Fig. 4.3 Clinical Manifestations: * Red, oozing, crusted rashes on face that spread to scalp, diaper area, hands, arms, feet, or legs. * Dry skinall over body or areas of bumpy skin on the back of the arms and front of the thighs. * Ear discharge or bleeding. * Raw areas of the skin from scratching. Skin colouring changes, such as more or less colour than the normal skin tone. Diagnostic Evaluation: * History collection: To identify the cause, signs and symptoms. * Physical examination: To know the pattern and intensity of reaction. * Skin biop food allergi Patch tests: To detect the diagnosis of aljergic contact dermatitis. To detect misdiagnosis o¢ | Management: * Creams, shampoos or ointments, Prescription-strength hydrocortisone, Fluocinolone or Desonide are corticosteroids apply to the scalp or other affected area to control inflammation, * Antifungal shampoo alternated with q stronger medication: Ketoconazole shampoo may be effective, when alternated with a clobetasol scalp product (Temovate) twice weekly. * Antifungal medication: Doctor may recommend the antifungal medication terbinafine (Lamisil). This option is not often used, because it can have serious side effects, such as allergic reactions and liver problems. * Medications that affect immune system: Creams or lotions containing calcineurin inhibitors Tacrolimus (Protopic) and Pimecrolimus (Elidel) may be effective and have fewer side effects than corticosteroids do, Cream or gel that fights bacteria: Apply Metronidazole (Metrolotion, Metrogel) as a cream or gel once or twice daily until improvement. Light therapy with medication: This treatment combines Psoralen with light therapy (photochemotherapy). This therapy may not work for people with thick hair.Nursing Interventions: * Assess skin, noting colour, moisture, texture, temperature; note erythema, edema and tenderness. + Assess the skin systematically. Look for areas of irritant and allergic contact. + Assess skin for lesions, Note presence of excoriations, erosions, fissures, or thickening. * Bath or shower using lukewarm water and mild soap or nonsoap cleansers. * After bathing, allow skin to air dry or gently pat the skin dry. Avoid rubbing or brisk drying. * Apply topical lubricants immediately after bathing. * Apply topical steroid creams or ointmets to reduce inflammation and promote healing of skin. Encourage the patient to use appropriate hygiene methods. Keeping the skin clean, dry, and well lubricated reduces the skin trauma and risk of infection. 4.DRUG REACTIONS Defini “Any harmful or seriously unpleasant effects occurring at doses intended for therapeutic (including prophylactic/ diagnostic) effect and which requires reduction of dose or withdrawal of drug or forecasts hazard from future administration”. jon of ADRs: * TypeA : Augmented. * TypeB : Bizarre. e.g. Drug allergy and idiosyncrasy. * TypeC : Continuous : due to long term use. * ‘Type : Delayed: duration or critical time exposure. e.g. Teratogenesis. * TypeE : End of use. e.g. Acute adrenal insufficient due to abrupt steroid cessation. Causes: * Patient: Age, gender , genetic predisposition, allergic diathesis, disease and personality. * Drug: e.g. Anticancer drugs are Cytotoxic, Digoxin has steep DRC type rxn-a , AMAs -type rxn-b. * Prescriber: ADR may occur, if drug is used for inappropriately long time (Type C), at a critical phase in gestation (Type D) or is abrubtly d/c (Type E) or given with other drugs (Drug drug interactions). Risk factors: * Serious illness. * Renal insufficiency. * Liver disease. * Polypharmacy. * HIV infection. * Herpes infection. * Alcoholism Genetics(P” genetics). Allergy in response to drugs: a. Type III (immune complex): * Tissue deposition of drug antibody complexes with complement activation and inflammation. * Serum sickness, fever, rash, arthra- Igias, lymphadenopathy, urticaria, glomerulonephritis, vasculitis. * 1 to3 weeks after drug exposure.