Module-3-IMMUNOLOGY PART 1 PDF

 Course Content 1. Infectious and Inflammatory Disorders A. Infectious Disorders of Adults ▪ Pneumonia 2. Immunologic Disorders ▪ Tuberculosis A. Multiple Sclerosis ▪ Ebola...

 Course Content 1. Infectious and Inflammatory Disorders A. Infectious Disorders of Adults ▪ Pneumonia 2. Immunologic Disorders ▪ Tuberculosis A. Multiple Sclerosis ▪ Ebola ▪ MERS CoV B. Ulcerative Colitis ▪ H1N1 C. Acute Glomerulonephritis ▪ Covid 19 ▪ Hepatitis D. Allergy (Hypersensitivity) ▪ Guillain- Barre Syndrome E. Lupus Erythematous ▪ Sexually Transmitted Disease (STD’s) F. Rheumatoid Arthritis B. Inflammatory Disorders (All body systems) G.Type 1 DM 1. Gastro-intestinal System a. Inflammatory Bowel Disease, 3. Transplant Rejection b. Crohn’s and Ulcerative Colitis c. Appendicitis, Peritonitis d. Pancreatitis e. Cholecystitis 2. Urinary System a. Cystitis b. Urolithiasis (Stones) 3. Reproductive System a. Pelvic Inflammatory Disease b. Benign Hypostatic Hypertrophy 4. Skin a. System Lupus Erythematosus Immunology The study of the immune system Evolving science dealing with body’s ability to distinguish self from non-self Distinction is made through a complex network of highly specialized cells or tissues - Collectively called the “Immune System” - Also known as “Defense Host System” - Critical to one’s survival  Immunity Immunity: is the ability of the body to defend itself against infectious agents. Immunity is essential for survival: a. Defends us from bacteria, virus, and other pathogens b. Detects abnormal cells that periodically develop in life and destroy them (e.g., cancer cells, tumor cells etc) c. Ability to recognize non-self substances from self one’s Types of Immunity i. Nonspecific Immunity (innate immunity) ii. Specific Immunity(Acquired or Adaptive Immunity) Innate (Nonspecific) Immunity ✔Non-specific is the 1st line of defense. ✔ It distinguishes self antigen from non-self, but does not distinguish one type of pathogen from another. ✔It can kill all types of pathogens. ✔Defense is inborn or natural, thus it does not need to be exposed to the invader ✔Both external and internal defense EXTERNAL INNATE DEFENSE ❖Skin Physical barrier to penetration by pathogens; secretions contain lysozyme (enzyme that destroys bacteria) ❖ Digestive tract High acidity of stomach protection by normal bacterial population of colon EXTERNAL INNATE DEFENSE ❖Respiratory tract Secretion of mucus Movement of mucus by cilia Alveolar macrophages ❖Genitourinary tract Acidity of urine Vaginal lactic acid INTERNAL INNATE DEFENSE ❖Phagocytic cells Ingest and destroy bacteria, cellular debris, denatured proteins, and toxins ❖Interferons Inhibit replication of viruses ❖Complement proteins promote destruction of bacteria enhance inflammatory response INTERNAL INNATE DEFENSE ❖Endogenous pyrogen Secreted by leukocytes and other cells; produces fever ❖Natural killer (NK) cells Destroy cells infected with viruses, tumor cells, and mismatched transplanted tissue cells ❖Mast cells Release histamine and cytokines that promote adaptive immunity Acquired Immunity Acquired immunity involves destruction of foreign invading organisms by specifically producing sensitized lymphocytes or antibodies ❖Lymphocytes are key players in acquired immunity. Types of Acquired Immunity 1. Cell mediated immunity 2. Humoral (antibody mediated immunity) - Both types of acquired immunity are initiated by ANTIGENS - Immunization induces acquired immunity Antigens - are chemical substances (proteins, lipoproteins, polysaccharides) - located on the surfaces of foreign bodies - are capable of inducing antibody production or sensitized lymphocytes in the host body. E.g. Antigens can be bacteria, virus, protozoan's, parasites, insect venoms, pollen, transplanted organ Lymphocytes Lymphocytes in acquired immunity i. T-lymphocytes(helper T-cells, cytotoxicT-cells, suppressor T- cells) ✔ is responsible for “cell-mediated” immunity ii. B-lymphocytes ✔is responsible for forming antibodies that provide “humoral” immunity. Types of T cells and their function 1. Helper T cells, 2. Cytotoxic T cells 3. Suppressor T cells 1. Helper T-cell(CD4+) Helper T-cell(CD4+) most numerous of the T cells(3/4th) serve as the major regulator of virtually all immune functions - When activated by antigens helper T-cells produces protein mediators, called lymphokines, that act on other cells of the immune system - In the absence of the lymphokines from the helper T cells, the remainder of the immune system is almost paralyzed. 2. Cytotoxic T(CD8+) Cells is a direct-attack cell capable of killing micro-organisms also called killer cells. it kill invaders by direct attack through the following methods: 1. They bore a hole through the membrane, so that electrolytes and fluid enters and burst the microbes 2. They release toxic substances and kill invaders  The cytotoxic cells also play an important role in destroying ✔Cancer cells, ✔Heart transplant cells ✔Viral infected cells ✔Other types of cells that are foreign to the person’s own body. 3. Suppressor T cells Prevent the cytotoxic cells from causing excessive immune reactions that might be damaging to the body’s own tissues(immune tolerance) General Management 1. History Taking The history should note the patient’s age along with information about past and present conditions and events that may provide clues to the status of the patient’s immune system. BE ALERT for the following signs and symptoms: Respiratory System - Changes in respiratory rate - Cough (dry or productive) - Abnormal lung sounds (wheezing, crackles, rhonchi) - Rhinitis - Hyperventilation - Bronchospasm BE ALERT for the following signs and symptoms: Cardiovascular System - Hypotension - Gastrointestinal System - Tachycardia - Hepatosplenomegaly - Dysrhythmia - Colitis - Vasculitis - Vomiting - Anemia - Diarrhea BE ALERT for the following signs and symptoms: Genitourinary System - Frequency and burning on urination - Hematuria - Discharge Musculoskeletal System - Joint mobility, edema, and pain BE ALERT for the following signs and symptoms: Neurosensory System - Cognitive dysfunction - Hearing loss - Visual changes - Headaches and migraines - Ataxia - Tetany General Management 2. Physical Assessment - On physical examination the skin and mucous membranes are assessed for lesions, dermatitis, purpura (subcutaneous bleeding), urticaria, inflammation, orany discharge. - Any signs of infection are noted. - The patient’s temperature is recorded, and the patient is observed for chills and sweating. - The anterior and posterior cervical, axillary, and inguinal lymph nodes are palpated for enlargement; if palpable nodes are detected, their location, size, consistency, and reports of tenderness on palpation are noted. - Joints are assessed for tenderness, swelling, increased warmth, and limited range of motion. - The patient’s respiratory, cardiovascular, genitourinary, gastrointestinal, and neurosensory systems are evaluated for signs and symptoms indicative of immune dysfunction. - Any functional limitations or disabilities the patient may have are also assessed.  Diagnostic Evaluation ⮚A series of blood tests and skin tests and a bone marrow biopsy may be performed to evaluate the patient’s immune competence. ⮚Various laboratory tests may be performed to assess immune system activity or dysfunction. ⮚The studies assess leukocytes and lymphocytes, humoral immunity, cellular immunity, phagocytic cell function, complement activity, hypersensitivity reactions, specific antigen–antibodies, or human immunodeficiency virus (HIV) infection. Humoral (Antibody-mediated) Immunity Tests ⮚ B-cell quantification with monoclonal antibody ⮚ In vivo immunoglobulin synthesis with T-cell subsets ⮚ Specific antibody response ⮚ Total serum globulins and individual immunoglobulins (electrophoresis, immunoelectrophoresis, single radial immuneodiffusion, nephelometry, and isohemagglutinin techniques).  Cellular (Cell-mediated) Immunity Tests ⮚ Total lymphocyte count ⮚T-cell and T-cell-subset quantification with monoclonal antibody ⮚Delayed hypersensitivity skin test ⮚ Cytokine production ⮚ Lymphocyte response to mitogens, antigens, and allogenic cells 1. Multiple Sclerosis Multiple sclerosis (MS) is a chronic demyelinating disease that affects the myelin sheath of neurons in the CNS.  INCIDENCE Onset occurs between 20-40 years of age. Women are more affected than men. (AANN,2011). Whites are more affected than Hispanics , blacks , or Asians. Most prevalent in colder climates of North America & Europe. Migration. ETIOLOGY & RISK FACTORS Exact cause is not known yet. Most theories suggest that MS is an immunogenetic viral disease (with Epstein Barr virus). Risk factors are: – Age ( most of the time between 20-40 yrs). – Sex (women have more chance). – Family history (genetic susceptibility). – Certain infections ( like Epsteinbarr virus). Continued risk factors… – Climate (more in cold climate areas). – Certain auto-immune diseases (higher risks with thyroid disease, type-1 DM or IBD). – Smoking. – Stress, fatigue. – Physical injury. – Pregnancy (may relating to stress to labour, or puerperium). PATHOPHYSIOLOGY Due to etiological factors Activated T-cells (which recognise self Ag) expressed in CNS, & Macrophages (B-cells) enters the brain from peripherral circulation Production of inflammatory cytokines & reactive O2 species Inflammation Then activated T-cells & B-cells cause demyelination and destruction of oligodendrocytes Formation of plaque Causes scarring & destruction of sheath Compensatory system starts causing subsidation of edema & inflammation After that some remyelination process occurs which is often incomplete Multiple sclerosis. CLINICAL MANIFESTATIONS The course of illness varies from person to person. The 4 clinical patterns (types) have been identified:- 1. Relapsing – remitting MS (most common initial pattern): Episodes of acute worsening with recovery and a stable course between relapses. 2. Primary progressive MS: Gradual, nearly continuous neurologic deterioration from onset of manifestations. 3. Secondary progressive MS: Gradual neurologic deterioration with or without superimposed acute relapses in a client who previously had relapsing remiting MS. 4. Progressive relapsing MS: Gradual neurologic deterioration from the onset of manifestations but with sub-sequent superimposed relapses.  The other symptoms are:- ⮚ Cerebellar sign: ⮚ Sensory: – Numbness , tingling and other – Nystagmus parasthesias – Ataxia – Patchy blindness (scotomas) – Dysarthria – Blurred vision – dysphagia – Vertigo, tinnitus,decreased hearing, chronic neuropathic pain ⮚ Motor: – Radicular (nerve root) pain in – weakness or paralysis of limbs , trunk lower thoracic abdominal region. or head – Lhermitte’ s sign is a transient – Diplopia sensory symptom described as an electric shock radiating down the – Scanning speech spine or into limbs with flexion of – Spasticity of muscles that are neck. chronically affected. DIAGNOSTIC EVALUATION There is no definitive test for MS. Detailed history of episodes of neurologic dysfunction Physical examination Other tests include: – CSF evaluation (for presence of IgG antibody or oligoclonal bonding) – Evoked potentials of optic pathways & auditory system to assess presence of slowed nerve conduction. – MRI of brain and spinal cord (to determine the presence of MS plaques) – CT scan ( to detect areas of demyelination , but with less detail as by MRI). MEDICAL MANAGEMENT No exact cure. Aim is to prevent or postpone the long term disability (often evolves slowly over many years). The treatment falls into 3 categories:- 1. Treatment of acute relapses. 2. Treatment aimed at disease management. 3. Symptomatic treatment. 1. Treatment of acute relapse:- 2. Treat exacerbations: (treatment aimed at disease ⮚ Corticosteroid therapy management) ( anti-inflammatory & immunosupressive ⮚ Interferon-Beta 1b property ) - Betaseron, given subcutaneously. (antiviral & immuno-regulatory) For example: (for ambulatory clients with relapsing – ✔ Methyl-prednisolone , (given I.V. remitting). or orally) ⮚ Interferon Beta 1a ✔ Azathioprine & - Avonex, cyclophosphamide (in severe (for treating replasing form of MS). cases) ⮚ Glatiramer acetate - Copaxane , (for relapsing re-emitting MS). 3. Symptomatic treatment: ⮚For Tremor : ⮚ For bladder dysfunction: - propanolol, phenobarbital, - oxybutynin, propantheline. clonazepam. ⮚ For constipation: ⮚For dysesthesias & trigeminal neurolgia: - psyllium hydrophilic mucilloid, - carbamazepine, phenytoin, suppositories. amitriptyline. ⮚ For fatigue: ⮚For dysesthesias: - amantadine, modafinil. - Transcutaneous electrical ⮚ For spasticity: nerve stimulation (TENS) is also helpful. - baclofen, diazefen, dantrolone. 4. Nutritional therapy:- - megavitamin therapy (cobalamin/vit. B12 and vit. C ) - low fat diet. - high roughage diet (to relieve constipation) 5. Other therapies:- (to improve neurological functioning) ✔Physical and speech therapies. ✔Exercise. ✔Water exercise. SURGICAL MANAGEMENT Deep brain stimulation: if other options have failed then a device is implanted that stimulates an area of brain. (in case of severe tremor in limbs). Implantation of a drug catheter or pump: a catheter is placed in lower spinal area to deliver a constant flow of drug like baclofen. (in case of severe pain or spasticity).  NURSING MANAGEMENT 1. Nursing diagnosis: 2. Nursing diagnosis: Impaired urinary elimination pattern related to Impaired elimination pattern related to bladder dysfunction as evidenced by low output immobility & demyelination as and acute pain. evidenced by disturbed bowel Intervention: movement. Assess the skin for incontinance associated dermatitis with each voiding. Intervention: Maintain fluid intake of 2000ml /day. Assess for normal bowel movement. Toilet every 2 hour. Administer suppository as adviced by Scan bladder for post void residual volume. physician. If PVR is more than 100ml , then catheterize. Teach client to consume high fibre diet and 2000 ml of fluid. 3. Nursing diagnosis: 4. Nursing diagnosis: Fatigue related to increased energy Impaired physical mobility related to needs as evidenced by facial weakness, contractures, spasticity and expression of client. ataxia as evidenced by pain in muscles and verbal experience. Intervention: Intervention: Keep the environment cool. Provide mental support. Assess the degree of muscle spasticity. Plan for rest periods during the day. Stretch muscles & perform ROM Facilitate sleep by reducing night exercise. time interruption, noise, and light. Administer anti-spasmotics as ordered. Position in neutral alignment. Consult with doctor for splints. 2. Acute Glomerulonephritis 🞂 Acute glomerulonephritis is a common disease in children and it is one of the diseases that are presented commonly with hematuria which means red urine (blood in urine). Acute Glomerulo Nephritis in all probabilities results secondary to a proceeding streptococcal (beta-hemolyticus type 12) infection of throat or skin. A history of upper respiratory infection. 🞂 Acute Nephritis or glomerulonephritis is an infective renal disease characterized by sudden onset of hematuria, oliguria, edema and hypertension. 🞂 Acute glomerulonephritis is an immune – mediated inflammatory disease of the capillary loops in the renal glomeruli. 🞂 The antigen – antibody complex deposition within the glomeruli results in glomerular injury which is manifested aforementioned symptoms Pathophysiology INCIDENCE 🞂 More common in male than females. 🞂 Most common in preschool and early school age children with a peak age of onset of 6-7 years. 🞂 Rare in children under two years of age. 🞂 On average responsible for 2 to 4% of pediatric admissions 🞂 Accounts for about 90% of renal diseases in childhood 🞂 Varies with the prevalence of nephritogenic strains of streptococci and the likelihood of cross – infection. ETIOLOGY: 1.Presumed cause – antigen – 🞂 Most cases are post infectious antibody reaction secondary to and have been associated with an infection in the body. -Pneumococcal 2.Initial infection: -Viral infection 🞂 Usually either an upper respiratory infection or a skin -Acute post streptococcal infection, usually one to 3 weeks glomerulonephritis is the most before the onset of symptoms common of the post infectious 🞂 Most frequent causative agent – renal disease in childhood. nephritogenic strains of group - -Streptococcal pharyngitis is A beta – haemolytic more common in the winter. streptococcus (type 12), acute post – streptococcal glomerulonephritis (APSGN) is the most common. CLINICAL MANIFESTATION: Urinary symptoms: Hypertension: 🞂 Present in over 50 per cent of patients. 🞂 Decreased urine output 🞂 Usually mild. 🞂 Bloody or brown – coloured urine. 🞂 Rise in blood pressure may be sudden. 🞂 Usually appears during the first four to Edema: five days of the illness. 🞂 Present in most patients Malaise Usually mild. Mild headache 🞂 Often manifested by Periorbital 🞂 Gastrointestinal disturbances, oedema in the morning especially anorexia and vomiting, often 🞂 May appear only as rapid weight with abdominal and long pain. gain. 🞂 Pallor 🞂 May be generalized and influenced 🞂 Irritability by posture. 🞂 Lethargy 🞂 Dysuria 🞂 Fever Management 🞂 History of illness and physical examination help in clinical diagnosis. 🞂 The confirmation of diagnosis is done by the following: Urine examination: It shows increased specific gravity, smoke dirty brown colour urine with reduced total amount in 24 hrs. Mild to moderate or severe albuminuria is detected. Microscopic examination reveals presence of red cells, WBCs, pus cells, epithelial cells and granular cast. Proteinuria (3+ to 4+) Blood examination: 🞂 Blood examination demonstrates increased level of urea, creatine, ESR, ASO titer and anti – DNAase ‘B’. There is decreased level of Hb%, serum complement and albumin in blood. Hyponatremia and hyperkalemia may occur in persistent oliguria. Throat swab culture: 🞂 Throat swab culture may show presence of beta – hemolyticus streptococcus in some children. Chest X-ray: 🞂 It may show pulmonary congestion THERAPEUTIC MANAGEMENT AGN with impaired renal function as severe oliguria and azotemia needs hospitalization for special attention. Mild oliguria patients with normal blood pressure can be managed at home with OPD – based treatment. Treatment is essentially symptomatic Monitoring: 🞂 The patient should be monitored closely for the presence of hematuria, decreased urinary output, and signs of volume overload like edema, hypertension and congestive heart failure. 🞂 Daily record the general condition, edema, Diet: consciousness level, weight, heart rate, 🞂 Diet should be arranged with respiratory rate, blood pressure, fluid intake and urinary output. restriction of protein, salt and fluid 🞂 The kidney function tests must be monitored at intake, till oliguria and increased regular intervals. blood urea level persist. 🞂 Carbohydrate containing food to be Bed rest: allowed freely. 🞂 The diet of the patient need not be 🞂 It is rarely indicated except during the acute restricted routinely. phase when complications of acute renal failure may be present. 🞂 Fluid intake should be allowed in a 🞂 Protect the child from fatigue and contact with calculated amount (i.e., total amount other respiratory infections. of previous day urine output in 24 hrs plus insensible losses to be allowed to 🞂 Position: drink on that day). 🞂 In congestive heart failure or hypertension, make 🞂 Daily weight recording is important the patient lie in a propped up position and provide oxygen. to assess the increase and decrease of edema. Fluid balance: 🞂 Diuretics are of limited value 🞂 Regular measurement of vital signs, when severe renal failure is not body weight and intake and output is essential to monitor the disease’s severe, diuretic therapy (usually progress and detect complications furosemide {lasix} is helpful if that may appear at any time during the course of the disease. significant edema and fluid overload are present. 🞂 A record of daily weight is the most useful means to assess fluid balance 🞂 Rarely, children with AGN and should be kept for children develop ARF with oliguria that treated at home and for those who are hospitalized. significantly alters the fluid and 🞂 Sodium and water restriction is useful electrolyte balance. when the output is significantly reduced (< 2 to 3 dl/24hr.) 🞂 Fluid restriction is needed in 🞂 In these children the water allowed is case of acute renal failure when equivalent to the calculated urine output is diminished. insensible loss plus the volume of urine excreted. Hypertension: 🞂 Acute hypertension must be anticipated and identified early. 🞂 Blood pressure measurements are taken every 4 to 6 hrs. 🞂 Significant but not severe hypertension is controlled with loop diuretics. 🞂 Other antihypertensive drugs, such as calcium channel blockers, beta blockers, or angiotensin – converting enzyme inhibitors, may be needed in severe cases. Dialysis: 🞂 May be required in patient with severe and prolonged oliguria or anuria,and renal failure. Penicillin: 🞂 Administered of antibiotic (preferably Penicillin) is needed for 7 to 10 days to eradicate streptococci in the throat or skin. 🞂 Anti hypertensive (nifedipine, atenolol) and diuretics are used to control hypertension and its consequences. 🞂 Magnesium sulphate may be prescribed in the encephalopathy to reduce cerebral edema. 🞂 Sedatives (diazepam) may be required in restless patients. 🞂 Management of complication like CCF, hypertensive encephalopathy, etc should be done promptly to prevent life threatening outcome. Dopamine infusion, steroid therapy and respiratory support may require for some patients. NURSING DIAGNOSIS: 🞂 Impaired urinary elimination related to glomerular dysfunction. 🞂 Infection related to group A beta- haemolytic streptococcus pharyngitis, upper respiratory infection. 🞂 Fluid volume excess related to altered renal function (or) diminished glomerular filtration increased Na+ retention. 🞂 Activity intolerance related to edema. 🞂 Altered skin integrity related to edema 🞂 Altered nutritional, less than body requirement, related to albuminuria and GI disturbances. 🞂 Fear and anxiety related to disease processes. 🞂 High risk for seizure activity related to hypertensive encephalopathy. 🞂 Knowledge deficit regarding care of the child with renal disease and continuation of care at home. COMPLICATION 1.Hypertensive encephalopathy: CHD Manifestation: Manifestations: 🞂 Dyspnea 🞂 Restlessness 🞂 Tachycardia 🞂 Convulsions 🞂 Liver engorgement. 🞂 Vomiting Duration: 🞂 Severe headache 🞂 Visual disturbance 🞂 Variable 🞂 Cause – probably ischemia secondary to vasospasm. 🞂 Usually subsides rapidly with the Duration: onset the fall in blood pressure. 🞂 Usually one to two days. 3.Uremia (rare): 🞂 Ends spontaneously with decreased blood pressure. Manifestation: 🞂 Evidence of acidosis 2.Congestive heart failure: 🞂 Drowsiness 🞂 Cardiac failure may occur due to persistent hypertension, hypervolemia and peripheral 🞂 Coma vasoconstriction. 🞂 Muscular twitching 🞂 Convulsions. 4.Anaemia: usually caused by hyperyolaemia rather than a loss of red blood cells in the urine. 5.Renal failure may occur with severe oliguria or anuria or increased B.P 🞂 It may occur in two phases:- 🞂 First phase: this stage of edema with oliguria may last for 5 – 10 days. 🞂 Second phase: this stage of dieresis starts with the increased of urine and decreased edema.  3. Allergy (Hypersensitivity) Allergy is an immune response to harmless antigens. Mechanism: IgE bind FCE receptors on mast cells and basophils, and causes release of granules with inflammatory agents. The immune system reacts to a usually harmless substance in the environment. This substance can be pollen, mold, dust, animal dander, certain foods, insect stings, etc. and is referred to as an allergen. Immune Hypersensitivity Hypersensitivity is an improperly strong response. Immediate hypersensitivity: Mediated by antibodies. Types: ⮚allergy - up to anaphylactic shock. ⮚Induction of antibody-mediated cytotoxicity. ⮚Sickness due to accumulation of immune complexes.  Delayed hypersensitivity: Mediated by T cells. Hyper-activity of CTLs and macrophages. Contact sensitivity. Types of Allergies http://photos.gograph.com/thumbs/CSP/CSP956/k9565679.jpg ⮚Food Allergy ⮚Skin Allergy ⮚Dust Allergy ⮚Insect Sting Allergy ⮚Pet Allergies ⮚Eye Allergy ⮚Drug Allergies ⮚Allergic Rhinitis ⮚Latex Allergy ⮚Mold Allergy ⮚Cockroach Allergy Food Allergies Food allergies are estimated to affect 4%-6% of children, and 4% of adults. It is most common in babies and children, but can appear at any age. The most common type of food allergens include: http://lamamd.com/blog/wp-content/uploads/2012/04/food-allergies.jpg ⮚Eggs ⮚Milk ⮚Peanuts ⮚Tree nuts ⮚Fish ⮚Shellfish ⮚Wheat ⮚Soy What Is An Allergic Reaction? A person is exposed to an allergen by inhaling it, swallowing it, or getting in on their skin. After a person is exposed, there is a sequence of events that create an allergic reaction: ⮚The body produces an antibody, IgE, to bind the allergen ⮚These antibodies attach to a mast cell, which can be found in the airways, intestines, and elsewhere ⮚Allergens bind to the IgE, which is attached to the mast cell, which causes the mast cells to release a variety of chemicals into the blood such as histmamine. Histamine causes most of the symptoms of an allergic reaction What Are Symptoms of an Allergic Reaction? Common symptoms of Food allergies can cause: an allergic reaction to ⮚Stomach cramps inhaled or skin allergens include: ⮚Vomiting ⮚Diarrhea ⮚Itchy, watery eyes ⮚Sneezing Insect sting allergies can ⮚Itchy, runny nose cause: ⮚Rashes ⮚Swelling ⮚Feeling tired or ill ⮚Redness ⮚Hives ⮚Pain Allergy Diagnosis If you or someone you know has allergy symptoms, an allergist or immunologist can help with a diagnosis. You must first find out what you are allergic to in order to have effective treatment. Allergy testing can identify the specific allergens that trigger your reactions. There is skin testing, as well as allergy blood tests. Skin tests give fast results and usually cost less than blood tests. Blood tests are helpful because it only involves a single needle prick, however it costs more. All test results must be interpreted with the medical history. Allergy Treatment There are two types of allergy treatment: 1. Medication – Decongestants and antihistamines http://images.clipartpanda.com/fault-clipart-medicine-jar-clip-art.jpg are the most common. They help to reduce a stuffy nose, runny nose, sneezing or itching. Corticosteroids treat inflammation in the nose. 1. Immunotherapy – A preventive treatment for allergic reactions that involves giving gradual http://clipartzebraz.com/cliparts/syringe-clip-art/cliparti1_syringe-clip-art_07.jpg increase doses of the allergen. The slow increase of the allergen allows the immune system to become less sensitive to the allergen. What is Anaphylaxis? Anaphylaxis is a serious, life-threatening allergic reaction. The most common anaphylactic reactions are to food, insect stings, medications, and latex. Anaphylaxis requires immediate medical treatment, including an injection of epinephrine along with a trip to an emergency room. If not http://ecx.images-amazon.com/images/I/61nBKqSEzwL._UX500_.jpg treated properly, anaphylaxis can be fatal. Anaphylaxis Symptoms Symptoms of anaphylaxis typically start within 5-30 minutes of coming into contact with the allergen. Warning signs may include: http://images.clipartpanda.com/choke-clipart-1046007-Royalty-Free-RF-Clip-Art-Illustration-Of-A-Cartoon-Choking-Businessmanb.jpg ⮚ Red rash, with hives/welts, usually itchy ⮚ Swollen throat or areas of the body ⮚ Wheezing ⮚ Passing out ⮚ Chest tightness ⮚ Trouble breathing ⮚ Hoarse voice ⮚ Vomiting ⮚ Diarrhea ⮚ Stomach Cramping ⮚ Pale or red color to the face or body ⮚ Trouble swallowing Anaphylaxis Treatment The best way to manage anaphylaxis is: ⮚Avoid allergens ⮚Be prepared for an emergency If you are at risk for anaphylaxis, carry auto-injectable epinephrine (often referred to as an epi-pen). http://lessonpix.com/drawings/73267/100x100/Epinephrine+Autoinjector.png 4. Systemic Lupus Erythematosus Systemic lupus erythematosus is a chronic, multisystem, inflammatory, autoimmune disorder characterized by formation of autoantibodies directed against self-antigens and immune-complex formation resulting in damage to essentially any organ. Although SLE affects primarily women of childbearing age, approximately 5% of cases present in childhood, mainly around puberty. SLE is rare in children younger than 9 years of age. Although there is a female predominance of this disease in adolescence and adulthood, there is an equal gender distribution in children. The overall prevalence of SLE in the pediatric population is 10 to 25 cases per 100,000 children. A LITTLE BIT OF HISTORY Lupus is the Latin word for wolf. Erythematosus means red rashes. In 1851, Dr. Cazenave discovered red rashes on a patient’s face that looked like wolf bites. He named the rash Discoid Lupus Erythematosus (DLE). In 1885, Sir William Osler recognized that many people with lupus had a disease involving not only the skin but many other organs or systems. He named the disease Systemic Lupus Erythematosus (SLE). TYPES OF LUPUS 1. Systemic Lupus Erythematosus (SLE) One that most people refer to when they say “lupus”. The symptoms of SLE may be mild or serious. Although SLE usually first affects people between the ages of 15 and 45, it can occur in childhood or later in life as well. 2. Discoid Lupus Erythematosus (DLE) A chronic skin disorder in which a red, raised rash appears on the face, scalp, or elsewhere. The raised areas may become thick and scaly and may cause scarring. The rash may last for days or years and may recur. A small percentage of people with discoid lupus have or develop SLE later. 3. Neonatal Lupus A rare disorder that can occur in newborn babies. Scientists suspect that neonatal lupus is caused by auto-antibodies in the mother’s blood called anti- Ro (SSA) and anti-La (SSB). Auto-antibodies (“auto” means “self”) are blood proteins that act against the body’s own parts. At birth, the babies have a skin rash, liver problems, and low blood counts. These symptoms gradually go away over several months, although in rare cases, babies with neonatal lupus may have a heart problem that slows down the natural rhythm of the heart. Some drugs may cause SLE-like features and hence this condition is called “drug-induced lupus”. The features typically go away completely when the drug is stopped. The kidneys and brain are rarely involved.  CLINICAL FEATURES CARDIAC ▪ Endocarditis ▪ Myocarditis ▪ Pericarditis CONSTITUTIONAL ▪ Fatigue ▪ Fever ▪ Weight loss GASTROINTESTINAL ▪ Abdominal pain ▪ Nausea & vomiting DERMATOLOGICAL ▪ Alopecia ▪ Butterfly rash ▪ Mucous membrane lesion ▪ Photosensitivity ▪ Purpura ▪ Raynaud’s phenomenon ▪ Urticaria ▪ Vasculitis HEMATOLOGIC ▪ Anemia ▪ Leukopenia ▪ Thrombocytopenia MUSCULOSKELETAL ▪ Arthralgia ▪ Arthritis ▪ Myositis PULM ONARY ▪ Pleurisy ▪ Pulmonary hypertension ▪ Pulmonary parenchyma NEUROPSYCHIATRIC ▪ Cranial neuropathies ▪ Organic brain syndrome ▪ Peripheral neuropathies ▪ Psychosis ▪ Seizures ▪ Transverse myelitis RENAL ▪ Casts ▪ Hematuria ▪ Nephrotic syndrome ▪ Proteinuria RETICULOENDOTHELIAL ▪ Hepatomegaly ▪ Lymphadenopathy ▪ Splenomegaly Clinical presentation varies in different patients & the disease activity varies over time in a single patient 1. Majority of patients have arthralgia of the hand 2. Most frequent manifestations in children include fever, rash, alopecia, arthritis & renal involvement 3. Compared with adults, children have a higher incidence of malar rash, anemia, leukopenia, neurologic & renal involvement WHAT CAUSES SLE? WHAT CAUSES SLE? SLE is an autoimmune disorder that develops when the body’s immune system begins to attack its own tissues. Its cause is unknown, but it is likely that a combination of genetic, environmental, and, possibly, hormonal factors work together to cause SLE. This occurs through the production of “auto-antibodies” that attack a person’s own cells thus contributing to the inflammation of various parts of the body, and may cause damage to organs and tissues. The most common type of auto-antibody that develops in people with SLE is called an antinuclear antibody (ANA) because it reacts with parts of the cell’s nucleus (command centre). WHAT CAUSES SLE? The fact that SLE can run in families indicates that its development has a genetic basis; however, no specific “lupus gene” has been identified yet. Studies suggest that several different genes may be involved in determining a person’s likelihood of developing the disorder, which tissues and organs are affected, and the severity of disease. However, it is believed that genes alone do not determine who gets SLE and that other factors also play a role. Some of the other factors scientists are studying include sunlight, stress, certain drugs, and agents such as viruses. DIAGNOSIS Diagnosis of systemic lupus erythematosus (SLE) is based on clinical symptoms & lab findings Diagnosis based on the American College of Rheumatology criteria for the diagnosis of definite lupus in children ▪ ≥4 criteria on the list either at the present time or at some time in the past, there is a strong chance that you have lupus. ▪ 11 common criteria, or measures that was developed by the American College of Rheumatology (ACR): 1. Malar rash – a rash over the cheeks & nose, often in the shape of a butterfly 2. Discoid rash – a rash that appears red, raised, disk-shaped patches 3. Photosensitivity – a reaction to sun or light that causes a skin rash to appear or get worse 4. Oral Ulcers – sores appearing in the mouth 5. Arthritis – joint pain & swelling of 2 or more joints in which the bones around the joints do not become destroyed 6. Serositis – inflammation of the lining around the lungs (pleuritis) or inflammation of the lining around the heart that causes chest pain which is worse with deep breathing (pericarditis) 6. Kidney disorder – persistent protein or cellular casts in the urine. 7. Neurological disorder – seizures or psychosis 8. Blood disorder – anemia, leukopenia, lymphopenia, or thrombocytopenia 9. Immunologic disorder – anti-DNA or anti-Sm or positive antiphospholipid antibodies 10. Abnormal antinuclear antibody (ANA) Diagnosis of systemic lupus erythematosus (SLE) is based on clinical symptoms & lab findings Diagnosis based on the Systemic Lupus International Collaborating Clinics (SLICC) classification criteria for systemic lupus erythematosus (SLE) ▪ ≥4 criteria (at least 1 clinical & 1 immunologic criteria) or Biopsy-proven lupus nephritis with positive antinuclear antibody (ANA) or Anti-double stranded deoxyribonucleic acid (dsDNA) ▪ Symptom/finding need not be present all at the same time C L I N I C A L C R I T E R I A: Chronic cutaneous lupus, including: Acute cutaneous lupus, including: ▪ Classic discoid rash: localized (above the neck) or generalized (above & ▪ Lupus malar rash (do not count if malar below the neck) discoid) ▪ Hypertrophic (verrucous) lupus ▪ Bullous lupus ▪ Lupus panniculitis (profundus) ▪ Toxic epidermal necrolysis variant of systemic lupus erythematosus (SLE) ▪ Mucosal lupus ▪ Lupus erythematosus tumidus ▪ Maculopapular lupus rash ▪ Chilblains lupus ▪ Photosensitive lupus rash (In the absence of ▪ Discoid lupus/lichen planus overlap dermatomyositis) or ▪ Subacute cutaneous lupus (nonindurated Oral Ulcers or Nasal Ulcers psoriaform &/or annular polycyclic lesions that ▪ Oral: palate, buccal, tongue resolve w/out scarring, although occasionally w/ post-inflammatory dyspigmentation or ▪ In the absence of other causes, such as vasculitis, Behcet’s disease, infection telangiectasias) (herpesvirus), inflammatory bowel disease, reactive arthritis, & acidic foods C L I N I C A L C R I T E R I A: Serositis Nonscarring alopecia ▪ Typical pleurisy for >1 day or ▪ Diffuse thinning or hair fragility w/ visible broken hairs pleural effusions or pleural rub ▪ In the absence of other causes such as ▪ Typical pericardial pain (pain w/ alopecia areata, drugs, iron deficiency, & recumbency improved by sitting androgenic alopecia forward) for >1 day or pericardial effusion or pericardial rub Synovitis involving ≥2 joints or pericarditis by ▪ Characterized by swelling or effusion electrocardiography ▪ Or tenderness in ≥2 joints & at least 30 ▪ In the absence of other causes, minutes of morning stiffness such as infection, uremia, & Dressler’s pericarditis Renal ▪ Urine protein–to-creatinine ratio (or 24-hour urine protein) representing 500 mg protein/24 hours or red blood cell casts C L I N I C A L C R I T E R I A: Neurologic ▪ Seizures ▪ Psychosis ▪ Mononeuritis multiplex (in the absence of other known causes such as primary vasculitis) ▪ Myelitis ▪ Peripheral or cranial neuropathy (in the absence of other known causes such as primary vasculitis, infection, & diabetes mellitus) ▪ Acute confusional state (in the absence of other causes, including toxic/metabolic, uremia, drugs) C L I N I C A L C R I T E R I A: Hemolytic anemia Leukopenia (