Immune System Notes PDF

ALTERATIONS IN INFLAMMATORY AND IMMUNOLOGIC RESPONSE (ACUTE AND CHRONIC) Anatomy and physiology of the immune system NORMAL IMMUNE RESPONSE Immunity: Body’s ability to resist disease. Functions of immune response DEFENSE Body protects against invasions by microorganisms...

ALTERATIONS IN INFLAMMATORY AND IMMUNOLOGIC RESPONSE (ACUTE AND CHRONIC) Anatomy and physiology of the immune system NORMAL IMMUNE RESPONSE Immunity: Body’s ability to resist disease. Functions of immune response DEFENSE Body protects against invasions by microorganisms Prevents the development of infection by attacking foreign antigens and pathogens. HOMEOSTATIS Damaged cellular substances are digested and removed. Through this mechanism, the body’s different cell types remain uniform and unchanged. SURVEILLANCE Mutations continually arise in the body but are normally recognized as foreign cells and destroyed. Antigen vs antibody Antigen substance that elicits an immune response. Antibody Substances in the body that kills and destroys antigen. Types of immunity INNATE IMMUNITY Present at birth, and its primary role is first-line defense against pathogens. Involves a nonspecific response, and neutrophils and monocytes are the primary white blood cells (WBCs) involved. Not antigen specific so it can respond within minutes to an invading microorganism without prior exposure to that organism. ACQUIRED IMMUNITY Development of immunity, either actively or passively.  I. ACTIVE (what you make) a. Natural - Infection b. Artificial - Vaccination II. PASSIVE (receive the antibodies) a. Natural - Breastmilk b. Artificial - Blood plasma/blood serum - Post prophylactic IMMUNOGLOBULINS CLASSES : GAMED OR MGAED IgM – found in the lymph fluid and blood to immediately respond to infection - first immunoglobulin that b cell can produce IgG – only type of antibody that crosses the placenta -provides passive immunity - most abundant IgA – type of antibody found in the nose and other breathing passages or airway - the alimentary tract, saliva, vagina IgE – least abundant antibody in the plasma -activate eosinophils to kill helminth worms -an elevated number or IgE is found in patients with allergies; binds to mast cells IgD – least of all antibodies, exists in small amounts LYMPHOID SYSTEM Central (or primary) and peripheral lymphoid organs. Central LYMPHOID SYSTEM 1. Thymus gland - Differentiation and maturation of T lymphocytes essential for a cell mediated immune response. Antigens are carried by the bloodstream or lymph channels to regional lymph nodes after introduction. Antigens interact with B and T lymphocytes and macrophages in the lymph nodes. 2. Bone marrow – site for lymphocyte production PERIPHERAL LYMPHOID SYSTEM The lymph nodes Tonsils; - Stop germs entering the body through the mouth or the nose. Contain a lot of white blood cells, which are responsible for killing germs. Spleen; - Peripheral lymph organ, Important as the primary site for filtering foreign antigens from the blood. Consists of two kinds of tissue: White pulp containing B and T lymphocytes Red pulp containing erythrocytes. NOTE: Macrophages line the pulp and sinuses of the spleen. Gut-, genital-, Bladder epithelial cells Alert the immune system during infection Directly mediate bacterial clearance by: Secreting antimicrobial compounds into the urine Expelling invading bacteria back into the bladder lumen to reduce intracellular load. Vagina: Lined with stratified squamous epithelia with mucus and unique flora. Vaginal epithelial cells and innate leukocytes provide the first line of cellular defense. Local antibodies and T cells provide long-term protection in the vagina.  Bronchial-, Lymphoid tissue is found in the submucosa of the gastrointestinal (GI) (gut- associated), genitourinary (genital-associated), and respiratory (bronchial-associated) tracts protects the body surface from external microorganisms. Skin-associated lymphoid tissues - Skin-associated lymph tissue primarily Consists of lymphocytes and Langerhans’ cells (a type of dendritic cell) found in the epidermis of skin. When Langerhans’ cells are depleted, the skin can neither initiate an immune response nor support a skin-localized delayed hypersensitivity reaction. Lymph nodes Filter substances that travel through the lymphatic fluid Contain lymphocytes (white blood cells) that help the body fight infection and disease. Cells Involved in Immune Response Mononuclear Phagocytes Lymphocytes Natural Killer Cells Dendritic Cells Cytokines Mononuclear Phagocytes Includes monocytes in the blood and macrophages in the body. Responsible for capturing, processing, and presenting the antigen to the lymphocytes. Stimulates a humoral or cell-mediated immune response. Capturing is accomplished through phagocytosis. Macrophage bound antigen, which is highly immunogenic, is presented to circulating T or B lymphocytes and thus triggers an immune response Lymphocytes Produced in the Bone Marrow. B and T Lymphocytes  B lymphocytes (bursa-equivalent lymphocytes) in birds, it was discovered that they mature under the influence of the bursa of Fabricius, hence the name B cells. However, this lymphoid organ does not exist in humans. Bursa- equivalent tissue in humans is the bone marrow. B cells differentiate into plasma cells when activated. Plasma cells produce antibodies (immunoglobulins) T Lymphocytes Cells that migrate from the bone marrow to the thymus differentiate into T lymphocytes (thymus-dependent cells). Thymus secretes hormones (thymosin) that stimulate the maturation and differentiation of T lymphocytes. 70% to 80% of the circulating lymphocytes Primarily responsible for immunity to: Intracellular viruses Tumor cells Fungi. Categories of t lymphocytes T Cytotoxic Cells Attacking antigens on the cell membrane of foreign pathogens and releasing cytolytic substances that destroy the pathogen. Have antigen specificity and are sensitized by exposure to the antigen. T Helper Cells Involved in the regulation of cell-mediated immunity and the humoral antibody response. Subsets are called TH1 cells and TH2 cells. Natural Killer Cells o involved in cell-mediated immunity. o large lymphocytes with numerous granules in the cytoplasm. o recognition and killing of virus-infected cells, tumor cells, and transplanted grafts. o significant role in immune surveillance for malignant cell changes. Dendritic Cells o a system of cells that are important to the immune system, especially the cell mediated immune response. o Found in skin, the lining of the nose, the lungs, the stomach, and the intestine. Cytokines o soluble factors secreted by WBCs and a variety of other cells in the body. o act as messengers between the cell types. o instruct cells to alter their proliferation, differentiation, secretion, or activity. Immunologic Disorders / Reactions Hypersensitivity reactions Type I: allergic rhinitis; anaphylaxis Type II: Early transplant rejections, Grave’s disease, Good pasture’s Syndrome, Myasthenia Gravis Type III: AGN SLE Type IV: contact dermatitis Other Auto immune disorders Hypersensitivity Reactions Immune system is overreactive against foreign antigens or reacts against its own tissue, resulting in tissue damage. Autoimmune diseases Body fails to recognize self-proteins and reacts against self-antigens. IMPORTANT TERMS IN HYPERSENSITIVITY REACTIONS Atopic reactions 20% of the population is atopic, having an inherited tendency to become sensitive to environmental allergens.  Result are allergic rhinitis, asthma, atopic dermatitis, urticaria, and angioedema. Atopic dermatitis a chronic, inherited skin disorder characterized by exacerbations and remissions. Caused: several environmental allergens. Although patients have elevated IgE levels and positive skin tests, the histopathologic features do not represent the typical, localized wheal-and-flare type I reactions. Skin lesions are more generalized and involve vasodilation of blood vessels, resulting in interstitial edema with vesicle formation. Urticaria AKA: Hives Cutaneous reaction against systemic allergens occurring in atopic people. Characteristics: Transient wheals that vary in size and shape and may occur all over the body. Develops rapidly after exposure to an allergen and may last minutes or hours. Histamine causes localized vasodilation (erythema), transudation of fluid (wheal), and flaring. Flaring - dilated blood vessels on the edge of the wheal. Histamine is responsible for the pruritus associated with the lesions. Angioedema a localized cutaneous lesion similar to urticaria but involving deeper layers of the skin and the submucosa. Occurs in the eyelids, lips, tongue, larynx, hands, feet, GI tract, and genitalia. Dilation and engorgement of the capillaries secondary to the release of histamine cause the diffuse swelling. Lesions may burn, sting, or itch, and can cause acute abdominal pain if in the GI tract. Swelling may occur suddenly or over several hours and usually lasts for 24 hours. TYPE I HYPERSENSITIVITY REACTIONS: ANAPHYLAXIS AND ALLERGIC RHINITIS Anaphylaxis Clinical response to an immediate (Type I hypersensitivity) immunologic reaction between a specific antigen and an antibody. When mediators are released systemically (e.g., after injection of a drug, after an insect sting) Occurs within minutes and can be life threatening due to bronchial constriction and subsequent airway obstruction and vascular collapse. Initial symptoms: Edema and itching at the site. Shock: rapid, weak pulse; hypotension; dilated pupils; dyspnea; and possibly cyanosis. Bronchial edema and angioedema – DEATH Common Causes of Anaphylaxis Foods Peanuts Tree nuts (e.g., walnuts, pecans, cashews, almonds) Shellfish (e.g., shrimp, lobster, crab), fish, milk, eggs, soy, wheat Medications Antibiotics Allopurinol Radiocontrast agents Anesthetic agents Vaccines, hormones (insulin, vasopressin, adrenocorticotropic hormone), aspirin, nonsteroidal anti-inflammatory drugs  Animal serums (tetanus antitoxin, snake venom antitoxin, rabies antitoxin), antigens used in skin testing Insects Bees, Wasps, Hornets, Yellow jackets, Ants (including fire ants) Latex Medical and nonmedical products containing latex Clinical Manifestations Severe systemic reactions Abrupt onset with the same signs and symptoms described previously. Symptoms progress rapidly to bronchospasm, laryngeal edema, severe dyspnea, cyanosis, and hypotension. Dysphagia (difficulty swallowing), abdominal cramping, vomiting, diarrhea, and seizures can also occur. Cardiac arrest and coma may follow. Moderate systemic reactions Flushing, warmth, anxiety, and itching in addition to any of the milder symptoms. Bronchospasm and edema of the airways or larynx with dyspnea, cough, and wheezing. Onset of symptoms is the same as for a mild reaction. Mild systemic reactions Peripheral tingling and a sensation of warmth, possibly accompanied by a sensation of fullness in the mouth and throat. Nasal congestion, Periorbital swelling, pruritus, sneezing, and tearing of the eyes can also be expected. Onset of symptoms begins within the first 2 hours after exposure. Preventive measures Strict avoidance of potential allergens. Medical Management Management depends on the severity of the reaction. Initially, respiratory and cardiovascular functions are evaluated. In cardiac arrest, cardiopulmonary resuscitation (CPR). Supplemental oxygen is provided during CPR or if the patient is cyanotic, dyspneic, or wheezing. Antihistamines and corticosteroids may also be administered to prevent recurrences of the reaction and to treat urticaria and angioedema. Intravenous fluids, volume expanders, and vasopressor agents are administered to maintain blood pressure and normal hemodynamic status. Aminophylline and corticosteroids may also be administered to improve airway patency and function If with episodes of bronchospasm or a history of bronchial asthma or chronic obstructive pulmonary disease Monitoring because of the risk for a “rebound” or delayed reaction 4 to 10 hours after the initial allergic reaction. Patients with severe reactions are monitored closely for 12 to 14 hours in a facility that can provide emergency care, if needed. Nursing Management Assess the patient for signs and symptoms of anaphylaxis (airway, breathing pattern, and vital signs). Observed for signs of increasing edema and respiratory distress. Rapid initiation of emergency measures (intubation, administration of emergency medications, insertion of intravenous lines, fluid administration, and oxygen administration) are important to reduce the severity of the reaction and to restore cardiovascular function. Patient must be instructed about antigens that should be avoided and about other strategies to prevent recurrence of anaphylaxis. All patients who have experienced an anaphylactic reaction should receive a prescription for preloaded syringes of epinephrine. The nurse instructs the patient and family in their use and has the patient and family demonstrate correct administration. ALLERGIC RHINITIS Clinical Manifestations Sneezing and nasal congestion; clear, watery nasal discharge; and nasal itching. Itching of the throat and soft palate is common. Drainage of nasal mucus into the pharynx results in multiple attempts to clear the throat and results in a dry cough or hoarseness. Headache, pain over the paranasal sinuses, and epistaxis can accompany allergic rhinitis. Allergic rhinitis can affect quality of life by also producing fatigue, loss of sleep, and poor concentration. Assessment and Diagnostic Findings Nasal smears, peripheral blood counts, total serum IgE, epicutaneous and intradermal testing, RAST, food elimination and challenge, and nasal provocation tests. Results indicative of allergy as the cause of rhinitis include increased IgE and eosinophil levels and positive reactions on allergen testing. False-positive and false-negative responses to these tests, particularly skin testing and provocation tests, may occur. Medical Management Goal of therapy: To provide relief from symptoms. Avoidance therapy Pharmacologic therapy, Immunotherapy. Avoidance Therapy - Remove the allergens that act as precipitating factors. Simple measures and environmental controls are often effective in decreasing symptoms. Examples: use of air conditioners, air cleaners, humidifiers, and dehumidifiers; removal of dust-catching furnishings, carpets, and window coverings; removal of pets from the home or bedroom; the use of pillow and mattress covers that are impermeable to dust mites; and a smoke-free environment. Pharmacologic Therapy Antihistamines Second generation or non-sedating H1 receptor antagonist Adrenergic Agents  Mast cell stabilizers Corticosteroids Leukotriene modifiers, block the synthesis or action of leukotrienes and prevent the signs and symptoms associated with asthma TYPE II HYPERSENSITIVITY REACTIONS: Cytotoxic and Cytolytic Reactions Cytotoxic and cytolytic reactions Involving the direct binding of IgG or IgM antibodies to an antigen on the cell surface. Antigen-antibody complexes activate the complement system, which mediates the reaction. Cellular tissue is destroyed in one of two ways: activation of the complement system resulting in cytolysis or enhanced phagocytosis. Target cells that destroyed in type ii reactions Erythrocytes, Platelets, Leukocytes. Antigens in type ii reactions ABO blood group Rh factor Drugs. Disorders characterize by type ii reactions ABO incompatibility transfusion reaction, Rh incompatibility transfusion reaction, Autoimmune and drug-related hemolytic anemias, Leukopenias, Thrombocytopenias, Grave’s Disease Goodpasture syndrome. Hemolytic Transfusion Reactions A classic type II reaction occurs when a recipient receives ABO-incompatible blood from a donor. Naturally acquired antibodies to antigens of the ABO blood group are in the recipient’s serum but are not present on the erythrocyte membranes, Good pasture syndrome Disorder involving the lungs and kidneys. An antibody- mediated autoimmune reaction occurs involving the glomerular and alveolar basement membranes. Circulating antibodies combine with tissue antigen to activate the complement system, which causes deposits of IgG to form along the basement membranes of the lungs or kidneys. Reaction may result in pulmonary hemorrhage and glomerulonephritis. Assessment Clinical manifestations indicating pulmonary and renal involvement Shortness of breath Hemoptysis Decreased urine output Edema and weight gain  Hypertension and tachycardia Medical management Corticosteroids, immunosuppressive drugs (e.g., cyclophosphamide [Cytoxan], azathioprine [Imuran]), plasmapheresis, and dialysis. Plasmapheresis removes the circulating anti–glomerular basement membrane (GBM) antibodies, and immunosuppressive therapy inhibits further antibody production. Renal transplantation can be attempted after the circulating anti-GBM antibody titer decreases. Appropriate for a critically ill patient who is experiencing acute kidney injury and respiratory distress is instituted. Focus on suppressing the autoimmune response with medications; corticosteroids, plasmapheresis Supportive therapy for pulmonary and renal involvement GRAVES DISEASE An autoimmune disease of unknown etiology characterized by diffuse thyroid enlargement and excessive thyroid hormone secretion. (80% Hyperthyroidism) Characterized by remissions and exacerbations, with or without treatment. More common in women. Precipitating factors Insufficient iodine supply, Infection, and stressful life events may interact with genetic factors. Cigarette smoking increases the risk of Graves’ disease and the development of eye problems associated with the disease. Pathophysiology In Graves’ disease the patient develops antibodies to the TSH receptor. Antibodies attach to the receptors and stimulate the thyroid gland to release T3, T4, or both. Excessive release of thyroid hormones leads to the clinical manifestations associated with thyrotoxicosis. Clinical Manifestations Increases metabolism and tissue sensitivity to stimulation by the sympathetic nervous system. Goiter Auscultation of the thyroid gland may reveal bruits, a reflection of increased blood supply. Exophthalmos Eyelids do not close completely, Exposed corneal surfaces become dry and irritated. corneal ulcers and eventual loss of vision. Changes in the ocular muscles result in muscle weakness - diplopia. Early stages: may exhibit only weight loss and increased nervousness. Acropachy (clubbing of the digits) may occur with advanced disease Older patients: confusion and agitation, dementia may be suspected and delay the diagnosis. Complications Thyrotoxicosis AKA: thyrotoxic crisis or thyroid storm An acute, severe, and rare condition that occurs when excessive amounts of thyroid hormones are released into the circulation. Diagnostic Studies Two primary laboratory findings: CONFIRM Decreased TSH levels Elevated free thyroxine (free T4) levels. Total T3 and T4 levels may also be assessed, but they are not as definitive. RAIU test: Differentiate Graves’ disease from other forms of thyroiditis.  with Graves’ disease shows a diffuse, homogeneous uptake of 35% to 95%, whereas with thyroiditis shows an uptake of less than 2%. MEDICAL INTERVENTION Drug Therapy. Radioactive Iodine Therapy. Surgical Therapy. Nutritional Therapy. Drug Therapy Antithyroid Drugs First-line antithyroid: Propylthiouracil (PTU) and methimazole (Tapazole) Inhibit the synthesis of thyroid hormones. INDICATION: Young patient, hyperthyroidism during pregnancy, and the need to achieve a euthyroid state before surgery or radiation therapy. Effects on 1-2 weeks or 4-8 weeks. IODINE used with other antithyroid drugs to prepare the patient for thyroidectomy or for treatment of thyrotoxicosis. Administration of iodine in large doses rapidly inhibits synthesis of T3 and T4 and blocks the release of these hormones into circulation. Decreases the vascularity of the thyroid gland, making surgery safer and easier. Effects in 1 -2 weeks. β-Adrenergic Blockers. Used for symptomatic relief of thyrotoxicosis. Block the effects of sympathetic nervous stimulation, thereby decreasing tachycardia, nervousness, irritability, and tremors. Propranolol: administered with other antithyroid agents. Atenolol: Use in the hyperthyroid patient with asthma or heart disease. Radioactive Iodine Therapy Treatment of choice for most nonpregnant adults. Damages or destroys thyroid tissue, thus limiting thyroid hormone secretion.  Effect may not be seen for up to 3 months. Although RAI is usually effective, it has a high incidence of posttreatment hypothyroidism (80% of adequately treated persons), resulting in the need for lifelong thyroid hormone therapy. Surgical Therapy Thyroidectomy: A large goiter causing tracheal compression, Been unresponsive to antithyroid therapy Thyroid cancer. Additionally, surgery may be done when an individual is not a candidate for RAI. One advantage that thyroidectomy has over RAI is a more rapid reduction in T3 and T4 levels. Subtotal thyroidectomy Often the preferred surgical procedure and involves the removal of a significant portion(90%) of the thyroid gland. Endoscopic thyroidectomy Minimally invasive procedure. Several small incisions are made, and a scope is inserted. Instruments are passed through the scope to remove thyroid tissue or nodules. Appropriate procedure for patients with small nodules (less than 3 cm) and no evidence of malignancy. Advantages: less scarring, less pain faster return to normal activity. Nutritional Therapy High-calorie diet (4000 to 5000 cal/day) may be ordered to satisfy hunger, prevent tissue breakdown, and decrease weight loss. Avoid caffeine-containing liquids to decrease the restlessness and sleep disturbances associated with these fluids. Refer to a dietitian for help in meeting individual nutritional needs. NURSING INTERVENTION Acute Thyrotoxicosis Administer medications: Monitor: Cardiac dysrhythmias and decompensation, ensuring adequate oxygenation, and administering IV fluids to replace fluid and electrolyte losses. Ensuring adequate rest may be a challenge because of the patient’s irritability and restlessness Provide a calm, quiet room and cool environment. Using light bed coverings and changing the linen frequently if the patient is diaphoretic; Establish a supportive, trusting relationship to facilitate coping by a patient who is irritable, restless, and anxious. Exophthalmos applying artificial tears to soothe and moisten conjunctival membranes. Salt restriction may help reduce periorbital edema. Elevate the patient’s Dark glasses reduce glare and prevent irritation If the eyelids cannot be closed, lightly tape them shut for sleep. Teach to exercise the intraocular muscles several times a day by turning the eyes in the complete range of motion. Good grooming can help reduce the loss of self-esteem from an altered body image. For severe exopthalmos, treatment options include corticosteroids, radiation of retroorbital tissues, orbital decompression, or corrective lid or muscle surgery. Thyroid Surgery: Subtotal thyroidectomy Before surgery, antithyroid drugs, iodine, and β- adrenergic blockers may be administered to achieve a euthyroid state. Iodine reduces vascularization of the thyroid gland, reducing the risk of hemorrhage.  Iodine is mixed with water or juice, sipped through a straw, and administered after meals. Assess for signs of iodine toxicity: swelling of the buccal mucosa, excessive salivation, nausea and vomiting, and skin reactions. If toxicity occurs, discontinue iodine administration and notify the health care provider. Post op Assess the patient every 2 hours for 24 hours for signs of hemorrhage or tracheal compression: Irregular breathing, neck swelling, frequent swallowing, sensations of fullness at the incision site, choking, and blood on the anterior or posterior dressings. Place in a semi-Fowler’s position and support the patient’s head with pillows. Avoid flexion of the neck and any tension on the suture lines Monitor vital signs and calcium levels. Complete the initial assessment by checking for signs of tetany secondary to hypoparathyroidism (e.g., tingling in toes, fingers, around the mouth; muscular twitching; apprehension) and by evaluating difficulty in speaking and hoarseness. Monitor Trousseau’s sign and Chvostek’s Expect some hoarseness for 3 or 4 days after surgery because of edema. Control postoperative pain by giving medication. If postoperative recovery is uneventful, the patient ambulates within hours after surgery, is permitted to take fluid as soon as tolerated, and eats a soft diet the day after surgery. The appearance of the incision may be distressing to the patient. Reassure the patient that the scar will fade in color and eventually look like a normal neck wrinkle. A scarf, jewelry, a high collar, or other covering can effectively camouflage the scar. HEMOLYTIC ANEMIA Condition caused by the destruction or hemolysis of RBCs at a rate that exceeds production. ETIOLOGIC CAUSE inheriting genetic conditions that cause anemia, certain infections certain medications Types of haemolytic anemia Inherited anemia Acquired anemia Inherited Hemolytic Anemias One or more of the genes that control red blood cell production are faulty. Can lead to problems with the hemoglobin, cell membrane, or enzymes that maintain healthy red blood cells. Examples: Sickle Cell Anemia, Thalasemia, GGlucose-6-Phosphate Dehydrogenase (G6PD) Deficiency Thalasemia Inherited blood disorders in which the body doesn't make enough of certain types of hemoglobin. Causes the body to make fewer healthy red blood cells than normal. Common in Southeast Asian, Indian, Chinese, Filipino, Mediterranean, or African origin or descent. Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency Red blood cells are missing an important enzyme called G6PD. G6PD is part of the normal chemistry inside red blood cells. In G6PD deficiency, if red blood cells come into contact with certain substances in the bloodstream, the missing enzyme causes the cells to rupture (burst) and die. Factors can trigger the breakdown of the red blood cells. taking sulfa or antimalarial medicines; being exposed to naphthalene, eating fava beans; having an infection. Mostly affects males of African or Mediterranean descent.  Sickle Cell Anemia a serious, inherited disease. body makes abnormal hemoglobin causes the red blood cells to have a sickle, or crescent, shape. Sickle cells don't last as long as healthy red blood cells. They usually die after only about 10 to 20 days. The bone marrow can't make new red blood cells fast enough to replace the dying ones. Acquired Hemolytic Anemias Immune Hemolytic Anemia Immune system destroys your red blood cells. Three main types: autoimmune, Alloimmune drug-induced. Autoimmune hemolytic anemia (AIHA). Immune system makes antibodies (proteins) that attack your red blood cells. AIHA accounts for half of all cases of hemolytic anemia. ETIOLOGIC FACTORS: Chronic lymphocytic leukemia Non-Hodgkin's lymphoma and other blood cancers Epstein-Barr virus Cytomegalovirus Mycoplasma pneumonia Hepatitis and HIV After you have a blood and marrow stem cell transplant. Autoimmune hemolytic anemia (AIHA). The antibodies made by the body are called warm antibodies. This means they're active (that is, they destroy red blood cells) at warm temperatures, such as body temperature. Other types of AIHA, the body makes cold-reactive antibodies. These antibodies are active at cold temperatures.  Cold-reactive antibodies can become active when parts of the body, such as the hands or feet, are exposed to temperatures lower than 32 to 50 degrees Fahrenheit (0 to 10 degrees Celsius). Warm antibody AIHA is more common than cold antibody AIHA. Alloimmune hemolytic anemia. Occurs if your body makes antibodies against red blood cells that you get from a blood transfusion. Happens if the transfused blood is a different blood type than your blood. Can occur during pregnancy if a woman has Rh-negative blood and her baby has Rh- positive blood. "Rh-negative" and "Rh-positive" refer to whether your blood has Rh factor. Rh factor is a protein on red blood cells. Drug-induced hemolytic anemia Certain medicines can cause a reaction that develops into hemolytic anemia such as penicillin, bind to red blood cell surfaces and can cause antibodies to develop. Other medicines cause hemolytic anemia in other ways. Examples: chemotherapy, acetaminophen, quinine and antimalarial medicines, anti-inflammatory medicines, and levodopa. Physical damage to red blood cell membranes can cause them to break down faster than normal due to: Changes in the small blood vessels. An artificial heart valve or other device used in blood vessels. Hemodialysis Heart-lung bypass machine, which may be used during open-heart surgery. Preeclampsia or eclampsia. Preeclampsia is high blood pressure during pregnancy. Eclampsia, which follows preeclampsia, is a serious condition that causes seizures in pregnant women. Malignant hypertension. This is a condition in which your blood pressure suddenly and rapidly rises. Thrombotic thrombocytopenic purpura. This rare blood disorder causes blood clots to form in small blood vessels throughout the body. Blood cell damage also may occur in the limbs as a result of doing strenuous activities, such as taking part in marathons. Paroxysmal Nocturnal Hemoglobinuria A disorder in which the red blood cells are faulty due to a lack of certain proteins. The body destroys these cells more quickly than normal. People who have PNH are at increased risk for blood clots in the veins and low levels of white blood cells and platelets. Systemic Lupus Erythematosus CONCEPTS Chronic, progressive, systemic inflammatory disease that can cause major organs and systems to fail. Connective tissue and fibrin deposits collect in blood vessels on collagen fibers and on organs. deposits lead to necrosis and inflammation in blood vessels, lymph nodes, gastrointestinal tract, and pleura. No cure for the disease is known but remissions are frequently experienced by clients who manage their care well. ETIOLOGY IDIOPATIC: but is believed to be a defect in immunological mechanisms, with a genetic origin. Precipitating factors: include medications, stress, genetic factors, sunlight or ultraviolet light, and pregnancy. THREE TYPES OF LUPUS Discoid type limited to the skin and only rarely involves other organs. Systemic lupus more common and usually more severe than discoid; it can affect any organ system in the body. With systemic lupus, there may be periods of remission and flares. The third type of lupus is drug induced. Drug induced: drugs most commonly implicated in precipitating this condition are hydralazine (Apresoline), procainamide (Pronestyl), isoniazid (INH), chlorpromazine (Thorazine), d-penicillamine, and some anti-seizure medications. Symptoms usually do not present until after months or years of continued administration. The symptoms are usually abolished when the drugs are discontinued. Clinical manifestations Erythema of the face (malar rash; also called a butterfly rash) Dry, scaly, maculopapular rash on the face or upper body Fever Weakness, malaise, and fatigue Anorexia Weight loss Photosensitivity Joint pain Erythema of the palms Anemia Positive ANA test and lupus erythematosus preparation Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein level Medical-Nursing Interventions Provide a high-vitamin and high-iron diet. Provide a high-protein diet if there is no evidence of kidney disease. Assess the impact of pain or stiffness on the client’s ability to perform interpersonally, socially, and professionally. SLE-related arthritis usually does not result in deformity as in rheumatoid arthritis, but physical activity may still be severely limited at times. Strategies may have to be developed so that the client is able to maintain a maximum level of function in each of these areas. Monitor skin integrity and provide frequent oral care. Instruct the client to avoid spicy or citrusy foods. Rinse mouth with Hydrogen peroxide that helps keep oral ulcers clean. Instruct the client to clean the skin with a mild soap, avoiding harsh and perfumed substances. Assist with the use of ointments and creams for the rash as prescribed. Identify factors contributing to fatigue. Administer iron, folic acid, or vitamin supplements as prescribed if anemia occurs. Assess for the signs of joint inflammation (warmth, redness, swelling) or decreased motion. Usual signs of inflammation may not be present with this disease. Instruct in measures to conserve energy, such as pacing activities and balancing rest with exercise. Administer topical or systemic corticosteroids, salicylates, and nonsteroidal anti- inflammatory drugs as prescribed for pain and inflammation. Administer medications to decrease the inflammatory response as prescribed.  Monitor intake and output, as well as daily weight for signs of fluid overload if corticosteroids are used. Instruct the client to avoid exposure to sunlight and ultraviolet light. Instruct the client that scalp hair loss may be caused by high-dose corticosteroids (prednisone) and immunosuppressant drugs. Monitor for proteinuria and red cell casts in the urine (for renal impairment). Monitor for bruising, bleeding, and injury. Assist with plasmapheresis as prescribed to remove autoantibodies and immune complexes from the blood before organ damage occurs. Glomerulonephritis Glomerulonephritis refers to a group of kidney disorders characterized by inflammatory injury in the glomerulus, most of which are caused by an immunological reaction. The disorder results in proliferative and inflammatory changes within the glomerular structure. Destruction, inflammation, and sclerosis of the glomeruli of the kidneys occur. Inflammation of the glomeruli results from an antigen-antibody reaction produced by an infection elsewhere in the body. Loss of kidney function develops. Etiology Immunological diseases Autoimmune diseases Antecedent group A β-hemolytic streptococcal infection of the pharynx or skin History of pharyngitis or tonsillitis 2 to 3 weeks before symptoms Types of glomerulonephritis Acute: Occurs 2 to 3 weeks after a streptococcal infection Chronic: May occur after the acute phase or slowly over time Complications Kidney failure Hypertensive encephalopathy  Pulmonary edema Heart failure Clinical manifestation Periorbital and facial edema that is more prominent in the morning Anorexia Decreased urinary output Cloudy, smoky, brown-colored urine (hematuria) Pallor, irritability, lethargy In an older child: Headaches, abdominal or flank pain, dysuria Hypertension Proteinuria that produces a persistent and excessive foam in the urine Azotemia Increased blood urea nitrogen and creatinine levels Increased anti–streptolysin O titer (used to diagnose disorders caused by streptococcal infections) Medical-Nursing Interventions Monitor vital signs, intake and output, and characteristics of urine. Measure daily weights at the same time of day, using the same scale, and wearing the same clothing. Limit activity; provide safety measures. Diet restrictions of sodium depend on the stage and severity of the disease, especially the extent of the edema; in addition, potassium may be restricted during periods of oliguria. Monitor for complications (e.g., kidney failure, hypertensive encephalopathy, seizures, pulmonary edema, heart failure). Administer diuretics (if significant edema and fluid overload are present), antihypertensives (for hypertension), and antibiotics (to a child with evidence of persistent streptococcal infections) as prescribed. Initiate seizure precautions and administer anticonvulsants as prescribed for seizures associated with hypertensive encephalopathy. Instruct parents to report signs of bloody urine, headache, or edema. Instruct parents that the child needs to obtain appropriate treatment for infections, specifically for sore throats, upper respiratory infections, and skin infections. NEUROLOGIC DISORDER MYASTHENIA GRAVIS Marked weakness and fatigue of voluntary muscles Decrease acetylcholine or – communication of nerve cells Increase acetylcholinesterase – inactive form Decrease sensitivity to acetylcholine by the receptor site Defect in transmission of nerve impulse at the myoneural junction Etiology Unknown Autoimmune (post viral infection) Diagnostic Test Tensilon Test (Edrophonium) Short acting cholinergic is administered Increased muscle strength is observed (+Tensilon) EMG Manifestations Ptosis, diplopia and eye squint (early sign) May start from ocular to oropharyngeal, facial and to respiratory muscle paralysis Muscle weakness more pronounce in the evening 3 D’s dysphagia, dysphonia, dysarthria Drooping faces Respiratory paralysis (cause of death) Nursing Interventions Supportive Assess gag reflex before feeding Administer meds 20-30 mins. Before meals to prevent aspiration Administer meds at precise time to prevent respiratory distress which may cause death Protect from falls due to weakness Start meal with cold beverages to improve ability to swallow  Avoid exposure to infection Adequate rest and activity Medical management Plasmapheresis - involves removal of antibodies from the plasma to inhibit immune response Myasthenic crisis – caused by undermedication Cholinergic crisis – caused by overmedication Medications Neostigmine Pyridostegmine Contraindicated medications MEDICATIONS TO AVOID (increases muscle weakness) Muscle relaxant Barbiturates Morphine sulfate Tranquilizers Neomycin Rheumatoid arthritis Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disease that primarily attacks peripheral joints and surrounding muscles, tendons, ligaments, and blood vessels. Spontaneous remissions and unpredictable exacerbations mark the course of the disease. Potentially crippling, RA usually requires lifelong treatment and sometimes surgery. What causes it? RA is currently believed to have an autoimmune basis, although the cause remains unknown. Pathophysiology Cartilage damage resulting from inflammation triggers further immune responses, including complement activation. Complement, in turn, attracts polymorphonuclear leukocytes and stimulates the release of inflammatory mediators, which exacerbates joint destruction. What to look for? Initial symptoms may include fatigue, malaise, anorexia, persistent low-grade fever, weight loss, and lymphadenopathy. The patient may also experience vague articular symptoms. What tests tell you In early stages, X-rays show bone demineralization and soft-tissue swelling. Later, they help determine the extent of cartilage and bone destruction, erosion, subluxations, and deformities and show the characteristic pattern of these abnormalities. Other tests and findings include: Positive RF test occurs in 75% to 80% of patients (as indicated by a titer of 1:160 or higher). Synovial fluid analysis usually shows increased volume and turbidity but decreased viscosity and complement (C3 and C4) levels, with WBC count possibly exceeding 10,000/l. Serum globulins are elevated. ESR is elevated. Complete blood count shows moderate anemia and slight leukocytosis How it’s treated? Salicylates, particularly aspirin, provide the mainstay of RA therapy because they decrease inflammation and relieve joint pain. Other useful medications include: NSAIDs, such as indomethacin, ketorolac, and ibuprofen antimalarials, such as chloroquine and hydroxychloroquine (Plaquenil) tumor necrosis factor inhibitors, such as etanercept (Embrel) penicillamine (Depen) corticosteroids, such as prednisone immunosuppressants, such as methotrexate (Trexall), cyclophosphamide (Cytoxan), and azathioprine (Imuran). What to do? Assess all joints carefully. Look for deformities, contractures, immobility, and inability to perform ADLs. Monitor vital signs and note weight changes, sensory disturbances, and level of pain. Administer analgesics as ordered and watch for adverse effects. Supportive measures include 8 to 10 hours of sleep every night, adequate nutrition, frequent rest periods between daily activities, and splinting to rest inflamed joints. A physical therapy program, including ROM exercises and carefully individualized therapeutic exercises, forestalls loss of joint function. Application of heat relaxes muscles and relieves pain. Moist heat, such as hot soaks, paraffin baths, and whirlpools, usually works best for patients with chronic disease. Ice packs are effective during acute episodes. Advanced disease may require synovectomy, joint reconstruction, or total joint arthroplasty. Diabetes mellitus Diabetes mellitus is characterized by disturbances in carbohydrate, protein, and fat metabolism. Diabetes is a major risk factor for myocardial infarction (MI), stroke, renal failure, and peripheral vascular disease. It’s also the leading cause of blindness in adults. Two forms exist: type 1 and the more prevalent type 2 diabetes mellitus. Type 1 diabetes usually occurs before age 30 (although it may occur at any age); the patient is usually thin and will require exogenous insulin and dietary management to achieve control. Type 1 is an autoimmune disease strongly associated with human leukocyte antigens DR 3 and 4. It may also be associated with certain viral infections. Pathophysiology The effects of diabetes mellitus result from insulin deficiency or resistance to endogenous insulin. Normally, insulin allows glucose transport into the cells for use as energy or storage as glycogen.Insulin also stimulates protein synthesis and free fatty acid storage in adipose tissue. Insulin deficiency compromises the body tissues’ access to essential nutrients for fuel and storage. Signs and Symptoms Fatigue polyuria related to hyperglycemia polydipsia nocturia dry mucous membranes poor skin turgor weight loss blurred vision polyphagia Patients with type 1 diabetes must take insulin daily because of their absolute insulin deficiency. Patients with type 2 diabetes may require insulin to control blood glucose levels unresponsive to diet and oral antidiabetic agents, or during periods of acute stress. Patients with other types of diabetes commonly require daily insulin therapy to achieve blood glucose control. What to do? Emphasize that adherence to the treatment plan is essential. It’s crucial to bring the patient’s blood glucose level within an acceptable range (usually less than 120 mg/dl before a meal and 180 mg/dl between meals) and alleviate or prevent diabetic ketoacidosis (DKA) or hypoglycemia. For the patient with unstable diabetes who isn’t experiencing DKA or HHNS, monitor blood glucose levels several times per day as prescribed until they stabilize. Administer insulin as prescribed, and keep the practitioner informed until blood glucose levels are under control. Then expect to begin the patient on an insulin regimen. Preserving potassium Monitor an elderly patient closely for evidence of fluid overload. Monitor the patient’s electrolyte levels closely and administer potassium replacement therapy as ordered. Patients with an extremely low pH level may require bicarbonate therapy to treat acidosis, but fluid and insulin replacement alone usually correct metabolic acidosis. The meal plan is the cornerstone of diabetes care because it directly controls the body’s major glucose source. Your patient can prevent widely fluctuating blood glucose levels by controlling his food intake. If he takes insulin or sulfonylureas, he’ll need to adhere to his meal plan even more carefully to avoid hypoglycemia. Monitor the patient for complications related to insulin therapy, which include hypoglycemia, the dawn phenomenon (early morning rise in blood glucose), insulin lipodystrophy (usually caused by continually using the same injection site), insulin allergy, and insulin resistance. Administer oral antidiabetics as prescribed. Check the patient’s history for conditions — such as pregnancy, breast-feeding, stressful situations, or illnesses — that increase insulin requirements, as well as for known allergies to sulfa agents. Monitor the patient for adverse reactions. AIDS/HIV Human immunodeficiency virus (HIV) is a retrovirus that is transmitted through blood and body fluids (semen, vaginal secretions). HIV targets CD4+ lymphocytes, also known as T-cells or T-lymphocytes. ◯ T-cells work in concert with B-lymphocytes. Both are part of specific acquired (adaptive) immunity. ◯ HIV integrates its RNA into host cell DNA through reverse transcriptase, reshaping the host’s immune system.  HIV is found in feces, urine, tears, saliva, cerebrospinal fluid, cervical cells, lymph nodes, corneal tissue, and brain tissue, but epidemiologic studies indicate that these are unlikely sources of infection. All women who are pregnant should be screened for HIV. HIV infection is one continuous disease process with three stages. ◯ Progression of HIV infection Manifestations occur within 2 to 4 weeks of infection. Symptoms are similar to those of influenza and can include a rash and a sore throat. This stage is marked by a rapid rise in the HIV viral load, decreased CD4+ cells, and increased CD8 cells. The resolution of clinical manifestations coincides with the decline in viral HIV copies. Lymphadenopathy persists throughout the disease process. ◯ Chronic asymptomatic infection This stage may be prolonged and clinically silent (asymptomatic). The client may remain asymptomatic for 10 years or more. Anti-HIV antibodies are produced (HIV positive). Over time, the virus begins active replication using the host’s genetic machinery. ☐ CD4+ cells are destroyed. ☐ The viral load increases. ☐ Dramatic loss of immunity begins. ◯ AIDS This stage is characterized by life-threatening opportunistic infections. This is the end stage of HIV infection. Without treatment, death occurs within 5 years. All people with AIDS have HIV, but not all people with HIV have AIDS. Health Promotion and Disease Prevention Teach the client how the virus is transmitted and ways to prevent infection, such as the use of condoms, abstinence, and avoiding sharing needles. Encourage the client to maintain up-to-date immunizations, including yearly seasonal influenza and pneumococcal polysaccharide vaccine (PPSV). Health care providers should use standard precautions when caring for the client. Assessment Risk Factors ◯ Unprotected sex (vaginal, anal, oral) ◯ Multiple sex partners ◯ Occupational exposure (health care workers) ◯ Perinatal exposure ◯ Blood transfusions (not a significant source of infection in the U.S.) ◯ Intravenous drug use with a contaminated needle ◯ HIV infection may go undiagnosed in older adult clients due to the similarity of its manifestations to other illnesses that are common in this age group. ◯ Older adults are more susceptible to fluid and electrolyte imbalances, malnutrition, skin alterations, and wasting syndrome than younger adults. ◯ Older women experience vaginal dryness and thinning of the vaginal wall, increasing their susceptibility to HIV infection. Subjective Data ◯ Chills ◯ Rash ◯ Anorexia, nausea, weight loss ◯ Weakness and fatigue ◯ Headache and sore throat ◯ Night sweats Objective Data ◯ Physical Assessment Findings and Laboratory Data A confirmed case classification meets the laboratory criteria for a diagnosis of HIV infection and one of the four HIV infection stages. ☐ Stage 4 has no data available concerning CD4+ T-cell counts and percentages, and no information on the AIDS-defining illness of the client. Diagnostic Procedures HIV determination ☐ Positive result from an HIV antibody screening test (enzyme-linked immunosorbent assay [ELISA]) confirmed by a positive result from a supplemental HIV antibody test (Western blot or indirect immunofluorescence assay test) ☐ Positive result or report of a detectable quantity from any of the following HIV virologic (viral load) testing: HIV nucleic acid (DNA or RNA) detection test (reverse transcriptase [RT-PCR]) Branched DNA (bDNA) method Nucleic acid sequenced-based assay (NASBA) Liver profile, biopsies, and testing of stool for parasites ☐ Nursing Actions Prepare the client for the test. ☐ Client Education Inform the client about the details of the test, such as length and what to expect. Brain or lung MRI or CT scan ☐ Detailed image of the brain or lung to detect abnormalities ☐ Nursing Actions Prepare the client for the procedure. ☐ Client Education Inform the client about the length of time the test takes (sometimes up to 1 hr). Patient-Centered Care Nursing Care ◯ Assess risk factors (sexual practices, IV drug use). ◯ Monitor fluid intake/urinary output. ◯ Obtain daily weights to monitor weight loss. ◯ Monitor nutritional intake. ◯ Monitor electrolytes. ◯ Assess skin integrity (rashes, open areas, bruising). ◯ Assess the client’s pain status. ◯ Monitor vital signs (especially temperature). ◯ Assess lung sounds/respiratory status (diminished lung sounds). ◯ Assess neurological status (confusion, dementia, visual changes). ◯ Encourage activity alternated with rest periods. ◯ Administer supplemental oxygen as needed. ◯ Provide analgesia as needed. ◯ Provide skin care as needed. Medications ◯ Highly active antiretroviral therapy (HAART) involves using three to four HIV medications in combination with other antiretroviral medications to reduce medication resistance, adverse effects, and dosages. Infusion inhibitors – enfuvirtide (Fuzeon) ☐ Blocks the fusion of HIV with the host cell Entry inhibitors – maraviroc (Selzentry) Nucleoside reverse transcriptase inhibitors (NRTIs) – zidovudine (Retrovir) ☐ Interfere with the virus’s ability to convert RNA into DNA Non-nucleoside reverse transcriptase inhibitors (NNRTIs) – delavirdine (Rescriptor) and efavirenz (Sustiva) ☐ Inhibit viral replication in cells Protease inhibitors – atazanavir (Reyataz), nelfinavir (Viracept), saquinavir (Invirase), and indinavir (Crixivan) ☐ Inhibit an enzyme needed for the virus to replicate Integrase inhibitors – raltegravir (Isentress) Antineoplastic medication – interleukin (Interferon) ☐ Immunostimulant that enhances the immune response and reduces the production of cancer cells (used commonly with Kaposi’s sarcoma) ◯ Nursing Considerations  Monitor laboratory results (CBC, WBC, liver function tests). Antiretroviral medications may increase alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin, mean corpuscular volume (MCV), high-density lipoproteins (HDLs), total cholesterol, and triglycerides. ◯ Client Education Educate the client about the side effects of the medications and ways to decrease the severity of the side effects. Educate the client about the need to take medications on a regular schedule and to not miss doses. Missed medication doses can cause drug resistance. Teamwork and Collaboration ◯ Infectious disease services may be consulted to manage HIV. ◯ Respiratory services may be consulted to improve respiratory status. ◯ Nutritional services may be consulted for dietary supplementation. ◯ Rehabilitation services may be consulted for strengthening and improving the client’s level of energy. Alternative Therapy ◯ Vitamins, herbal products, and shark cartilage may help alleviate the symptoms of HIV. Ask the client if she is taking herbal products. These can alter the effects of the prescribed medications. Care After Discharge ◯ Refer the client to local AIDS support groups as appropriate. ◯ Home health service may be indicated for clients who need help with strengthening and assistance regarding ADLs. ◯ Home health services may also provide assistance with IVs, dressing changes, and total parenteral nutrition (TPN). ◯ Respiratory services may be consulted for providing portable oxygen. ◯ Long-term care facilities may be indicated for clients with chronic HIV. ◯ Hospice services may be indicated for clients who have a late stage of HIV. ◯ Food services may be indicated for clients who are homebound and need meals prepared. ◯ Client Education Instruct the client to practice good hygiene and frequent hand hygiene to reduce the risk of infection. Instruct the client to avoid crowded areas or traveling to countries with poor sanitation. Encourage the client to avoid raw foods, such as vegetables and meats. Instruct the client to avoid cleaning pet litter boxes to reduce the risk of toxoplasmosis. Encourage the client to keep the home environment clean and to avoid being exposed to family and friends who have colds or flu viruses. Provide client teaching. ☐ Transmission, infection control measures, and safe sex practices ☐ The importance of maintaining a well-balanced diet ☐ Self-administration of prescribed medications and potential side effects ☐ Signs/symptoms that need to be reported immediately (infection) Instruct the client to adhere to the antiretroviral dosing schedules. Instruct the client about the need for frequent follow-up monitoring of CD4+ and viral load counts. Encourage the use of constructive coping mechanisms. Assist the client with identifying primary support systems. Teach the client to report signs of infection immediately to the health care provider. Complications Opportunistic Infections ◯ Bacterial diseases, such as tuberculosis, bacterial pneumonia, and septicemia (blood poisoning) ◯ HIV-associated malignancies, such as Kaposi’s sarcoma, lymphoma, and squamous cell carcinoma ◯ Viral diseases, such as those caused by cytomegalovirus, herpes simplex, and herpes zoster virus ◯ Fungal diseases, such as PCP, candidiasis, cryptococcosis, and penicilliosis ◯ Protozoal diseases, such as pneumocystis jiroveci pneumonia (PCP), toxoplasmosis, microsporidiosis, cryptosporidiosis, isosporiasis, and leishmaniasis ◯ Nursing Actions Implement and maintain antiretroviral medication therapy as prescribed. Administer antineoplastics, antibiotics, analgesics, antifungals, and antidiarrheals as prescribed. Administer appetite stimulants (to enhance nutrition). Monitor for skin breakdown. Maintain fluid intake. Maintain nutrition. ◯ Client Education Teach the client to report signs of infection immediately to the health care provider. Wasting Syndrome ◯ Nursing Actions Maintain nutrition orally or by TPN if indicated. Provide between-meal supplements/snacks. Serve at least six small feedings with high protein value. Fluid/Electrolyte Imbalance ◯ Nursing Actions Monitor fluid/electrolyte status. Report abnormal laboratory data promptly. Maintain IV fluid replacement. Make dietary adjustments to reduce diarrhea. Seizures (HIV encephalopathy) ◯ Nursing Actions Maintain client safety. Implement seizure precautions. HEPATITIS B Viral hepatitis is the most common type of hepatitis. Toxic and drug-induced hepatitis occurs secondary to an exposure to a chemical or medication agent such as alcohol, industrial toxins, ephedra, or acetaminophen. Hepatitis can occur in conjunction with other viruses such as varicella-zoster, cytomegalovirus, or herpes simplex. There are five major categories of viral hepatitis. ◯ Hepatitis A virus (HAV) ◯ Hepatitis B virus (HBV) ◯ Hepatitis C virus (HCV) ◯ Hepatitis D virus (HDV) ◯ Hepatitis E virus (HEV) After exposure to a virus or toxin, the liver becomes enlarged from the inflammatory process. As the disease progresses, there is an increase in inflammation and necrosis, interfering with blood flow to the liver. Individuals can be infected with hepatitis and remain symptom-free, and therefore are unaware that they could be contagious. ASSESSMENT Type Route of Transmission Risk Factors Hepatitis A (HAV) › Fecal-oral route › Ingestion of contaminated food or water › Close personal contact with an infected individual Hepatitis B (HBV) › Blood › Unprotected sex with infected individual › Infants born to infected mothers › Contact with infected blood › Injection drug users Hepatitis C (HCV) › Blood › Drug abuse › Sexual contact Hepatitis D (HDV) › Coinfection with HBV › Injection drug users › Unprotected sex with infected individual Hepatitis E (HEV) › Fecal-oral route › Ingestion of contaminated food or water HEPATITIS B ☐ Elevated alanine aminotransferase (ALT): Expected reference range 3 to 35 IU/L or 8 to 20 units/L. ☐ Elevated aspartate aminotransferase (AST): Expected reference range 5 to 40 units/L. ☐ Normal or elevated alkaline phosphatase (ALP): Expected reference range 30 to 120 units/L. ☐ Elevated total bilirubin level: Expected reference range 0.1 to 1.0 mg/dL. ☐ Presence of hepatitis B surface antigen (HBsAg) indicates that the individual is infectious. ☐ Presence of hepatitis B surface antibody (anti-HBs) indicates recovery and immunity from HBV infection. ☐ Presence of hepatitis B core antibody (anti-HBc) indicates previous or ongoing infection. ☐ Presence of IgM antibody to hepatitis B core antigen (IgM anti-HBc) indicates acute infection. ☐ Presence of hepatitis B e antigen (HBeAg) indicates that the virus is replicating. ☐ Presence of hepatitis B e antibody (anti-HBe) is a predictor of long-term clearance of the virus. ◯ Diagnostic Procedures Liver biopsy: This is the most definitive diagnostic approach, and it is used to identify the intensity of the infection, and the degree of liver damage. ☐ Nursing Actions Before the procedure: Explain the procedure. Witness informed consent. Ensure the client fasts for at least 2 hr. Administer preprocedural medications as prescribed. During the procedure: Assist the client into the supine position with the upper right quadrant of the abdomen exposed. Assist client with relaxation techniques. Instruct client to exhale breath and hold for at least 10 seconds while the needle is inserted. Instruct client to resume breathing once the needle is withdrawn. Apply pressure to the puncture site. After the procedure Assist client to a right side-lying position and maintain for several hours. Monitor the client’s vital signs. Assess for abdominal pain. Assess for bleeding from puncture site. PATIENT CENTERED CARE Nursing Care ◯ Most clients will be cared for in the home unless they are acutely ill. ◯ Enforce contact precautions if indicated. ◯ Limit the client’s activity in order to promote hepatic healing. ◯ Provide a high-carbohydrate, high-calorie, low- to moderate-fat, and low- to moderate-protein diet, and small, frequent meals to promote nutrition and healing. ◯ To promote hepatic rest and the regeneration of tissue, administer only necessary medications. ◯ Educate the client and family regarding measures to prevent the transmission of the disease with others at home (avoid sexual intercourse until hepatitis antibody testing is negative, avoid alcohol, avoid over-the-counter medications or herbal medications, use proper hand hygiene). ◯ Provide culturally sensitive care.  MEDICATIONS : ◯ Hepatitis B Acute infection ☐ No medications, supportive care. Chronic infection ☐ Antiviral medications: adefovir dipivoxil (Hepsera), interferon alfa-2b (Intron A), peginterferon alfa-2a (Pegasys), lamivudine (Epivir-HBV), entecavir (Baraclude), and telbivudine (Tyzeka). COMPLICATIONS : Chronic hepatitis ◯ Ongoing inflammation of the liver cells. ◯ Results from hepatitis B, C, or D. ◯ Increases the client’s risk for liver cancer. Fulminating hepatitis ◯ Extremely progressive form of viral hepatitis. ◯ Clients develop symptoms of viral hepatitis, then within hours or days develop severe liver failure. ◯ Prevention of viral hepatitis. ◯ No medications, supportive care. Cirrhosis of the liver ◯ Permanent scarring of the liver that is usually caused by chronic inflammation. Liver cancer Liver failure ◯ Irreversible damage to liver cells, with decreased ability to function adequately to meet the body’s needs. DENGUE Causative agent Dengue fever is a mosquito-borne infection caused by dengue virus. It is found in tropical and sub- tropical climates around the world. The disease is endemic in more than 100 countries, including countries in South East Asia. Dengue virus encompasses four different serotypes, each of which can lead to dengue fever and severe dengue (also known as 'dengue haemorrhagic fever'). Clinical features Dengue fever is clinically characterised by high fever, severe headache, pain behind the eyes, muscle and joint pain, nausea, vomiting, swollen lymph nodes and rash. Some infected people may not develop apparent symptoms, while some may only have mild and non-specific symptoms such as fever and rash. The symptoms of first infection are usually mild. Once recovered, lifelong immunity to that serotype of dengue virus will develop. However, cross-immunity to the other three serotypes after recovery is only partial and temporary. Subsequent infections with other serotypes of dengue virus are more likely to result in severe dengue. Severe dengue is a severe and potentially fatal complication of dengue fever. Initially, the features are similar to dengue fever such as high fever. When the fever begins to subside (usually 2 – 7 days after symptom onset), warning signs of severe dengue may start to develop, which include severe abdominal pain, persistent vomiting, rapid breathing, fatigue, restlessness and manifestations of bleeding tendency such as nose or gum bleeding, and possibly blood in vomit or stool. In severe cases, it may progress to circulatory failure, shock and death. Mode of transmission Dengue fever is transmitted to humans through the bites of infective female Aedes mosquitoes. After feeding on a dengue-infected person, the mosquito becomes infected and may spread the disease by biting other people. The disease cannot be spread directly from human to human, but there is evidence of low possibility of maternal transmission from a pregnant mother to her baby. In Hong Kong, the principal vector Aedes aegypti is not found, but Aedes albopictus, which can also spread the disease, is a mosquito commonly found in the locality. Incubation period The incubation period is usually 4 – 7 days (may range from 3 to 14 days). Management There is no specific treatment for dengue fever and severe dengue. Dengue fever is mostly self- limiting and most people will recover after a week. Symptomatic treatment is given to relieve discomfort. For patients with severe dengue, hospitalization with supportive management is often needed. Prevention The best preventive measure is to avoid mosquito bites. Prevention of mosquito bites 1. Wear loose, light-coloured, long-sleeved tops and trousers. 2. Use DEET-containing insect repellent on exposed parts of the body and clothing. Pregnant women and children of 6 months or older can use DEET-containing insect repellent. In general, use DEET of up to 30% for pregnant women and up to 10% for children 3. Take additional preventive measures when engaging in outdoor activities: Avoid using fragrant cosmetics or skin care products Re-apply insect repellents according to instructions If both insect repellents and sunscreen are used, apply insect repellents after sunscreen Prevention of mosquito proliferation 1. Prevent accumulation of stagnant water Change the water in vases once a week Avoid using saucers underneath flower pots Cover water containers tightly Ensure air-conditioner drip trays are free of stagnant water Put all used cans and bottles into covered dustbins 2. Control vectors and reservoir of the diseases Store food and dispose of garbage properly LEPTOSPIROSIS Leptospirosis is a bacterial disease that affects humans and animals. It is caused by the bacteria of the genus Leptospira. The disease occurs all over the world, but is most common in warm climates. Leptospirosis can infect cattle, pigs, horses, dogs, and wild animals such as rodents (rats, mice), mongoose, and sea mammals. Signs and Symptoms Leptospirosis can cause flu-like symptoms and can be mistaken for other diseases. In some persons, the infection can be mild and without obvious symptoms. The symptoms include fever, chills, muscle aches, rash, jaundice (yellowing skin and eyes), headache, red eyes, abdominal pain, vomiting, and diarrhea. A person can be come ill 2 days to 4 four weeks after being exposed. The symptoms may last from a few days to several weeks. Without treatment, recovery may take several Transmission You can get Leptospirosis by swimming or wading in freshwater puddles, ponds, or streams contaminated with animal urine, or by encountering wet soil or plants contaminated with animal urine. The bacterium enters the body through broken skin or through the soft tissues on the insides of the mouth, nose, or eyes. You can also get it by direct contact to urine, blood, or tissues from an infected animal. Leptospirosis is rarely spread from person to person. Treatment A doctor can prescribe medicines to treat leptospirosis. Leptospirosis is treated with antibiotics, such as doxycycline or penicillin. If not treated, the patient can develop meningitis, respiratory distress, kidney damage, or liver damage. In rare cases, even death may occur. COVID Coronaviruses are a family of viruses that can cause illnesses such as the common cold, severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). In 2019, a new coronavirus was identified as the cause of a disease outbreak that originated in China. The virus is known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The disease it causes is called coronavirus disease 2019 (COVID-19). SYMPTOMS Symptoms of coronavirus disease 2019 (COVID-19) may appear 2 to 14 days after exposure. This time after exposure and before having symptoms is called the incubation period. You can still spread COVID-19 before you have symptoms. This is called pre symptomatic transmission. Common symptoms can include: Fever. Cough. Tiredness. Early symptoms of COVID-19 may include a loss of taste or smell. Other symptoms may include:  Shortness of breath or difficulty breathing. Muscle aches. Chills. Sore throat. Runny nose. Headache. Chest pain. Pink eye (conjunctivitis). Nausea. Vomiting. Diarrhea. Rash. If you have emergency COVID-19 symptoms, seek care immediately. Emergency symptoms can include: Trouble breathing. Constant chest pain or pressure. Trouble staying awake. New confusion. Pale, gray or blue-colored skin, lips or nail beds — depending on skin tone. COVID-19 Prevention Actions There are many ways your actions can help protect you, your household, and your community from severe illness from COVID-19. Protect yourself and those around you: Get vaccinated as soon as it’s your turn and follow local guidance on vaccination. Keep physical distance of at least 1 meter from others, even if they don’t appear to be sick. Avoid crowds and close contact. Wear a properly fitted mask when physical distancing is not possible and in poorly ventilated settings. Clean your hands frequently with alcohol-based hand rub or soap and water. Cover your mouth and nose with a bent elbow or tissue when you cough or sneeze. Dispose of used tissues immediately and clean hands regularly. If you develop symptoms or test positive for COVID-19, self-isolate until you recover.