PN 2 EXAM 3

PN 2 EXAM 3 N2 Exam 3 Type 1 Diabetes – an autoimmune dysfunction involving the destruction of beta cells, which produce insulin in the islets of Langerhans of the pancreas. Type 1 is an absolute lack of insulin secretion o Absence of insulin production; patient is dependent on insulin to prevent ketoacidosis and maintain life o Onset is frequently in childhood; usually ages 10-15 o This is forever o First sign is often Diabetic Ketoacidosis Type 2 is a combination of insulin resistance and inadequate insulin secretion to compensate o Often linked to obesity, sedentary lifestyle, and heredity o Onset is predominately in adulthood, generally after the age of 35 o Usually controlled with diet, exercise and oral hypoglycemics o Usually found by accident; the patient keeps coming back for a wound that won’t heal or repeated vaginal infections Signs and Symptoms: o Both Type 1 and Type 2: 3 Ps: polyuria, polydipsia, and polyphagia o Fatigue o Increased frequency of infections Type 1: o Weight loss o Bed-wetting, blurred vision o Enuresis (involuntary urination, especially in children at night) in children, nocturia in adults o Abdominal pain o Rapid onset Type 2: o Weight gain, visual disturbances o Slow onset; usually around 40 years old o Fatigue and malaise o Recurrent vaginal yeast Diagnostics: o The criteria for diagnosis must include two findings on separate days – must also be the test plus a random glucose greater than 200 mg/dL o Fasting blood glucose level above 126 mg/dL o Oral glucose tolerance test: 2- hour glucose values greater than 200 mg/dL o Glycosylated hemoglobin (A1C) greater than 6.5% Medications: Insulin: o Rapid-acting insulin: lispro, aspart, glulisine ▪ Given before meals ▪ Onset: 5-15 minutes ▪ Peak: 30-90 minutes ▪ Duration: les than 5 hours ▪ Given subcutaneously ▪ Given in conjunction with intermediate- or long-acting insulin to provide control between meals and at night ▪ Because of quick onset, patient must eat immediately o Short-Acting Insulin: regular ▪ Given approximately 30-60 minutes before meals ▪ Onset: 30 minutes – 1 hour ▪ Peak: 2-3 hours ▪ Duration: 5-8 hours ▪ This is our clear insulin ▪ Given alone or in combination with longer-acting insulin ▪ Given for sliding scale coverage ▪ Can be given subcutaneously, IV, or IM ***only insulin that can be given IV • U-500 is for patient who is insulin resistant, never given IV • U-100 is for most patients and can be given IV o Intermediate-Acting insulin: NPH, Novolin N ▪ Hypoglycemia tends to occur in mid to late afternoon ▪ Onset: 2-4 hours ▪ Peak: 4-10 hours ▪ Duration: 10-16 hours ▪ This is our cloudy insulin ▪ Given for control between meals and at night ▪ Contains protamine (a protein), which causes a delay in the insulin absorption or onset and extends the duration of action of the insulin ▪ Give NPH insulin subQ only – can be mixed with short-acting or rapid-acting o Long-Acting Insulin: glargine (Lantus), detemir (Levemir) ▪ CANNOT be diluted or mixed with any other insulin ▪ Usually given at bedtime ▪ Onset: 2-4 hours ▪ No peak ▪ Duration: 24 hours ▪ Detemir may be given twice a day, dependent on dose ▪ Only given subQ Insulin starting dose is 0.4 – 1 unit/kg/day, the dose is adjusted until the blood sugar is normal and there is no glucose or ketones in the urine Basal/bolus dosing is the most common method of daily dosing; it is a combination of long-acting insulin and rapid-acting insulin Insulin pumps are an alternative to daily insulin injections o Pump is programmed to deliver insulin through a needle in the subQ tissue. The needle needs to be changed at least every 2-3 days to prevent infection o Only rapid-acting insulin is used in infusion pump o Complications: accidental cessation of insulin administration, obstruction of the tubing/needle, pump failure, and infection Insulin Pens are prefilled with 150-300 units of insulin o Convenient for travel o Used for patients who have vision impairment or problems with dexterity Insulin sites should be rotated to prevent lipodystrophy or lipohypertrophy – lumps under the skin from an accumulation of extra fat at the site of many subQ injections Oral Medications: Sulfonylureas – glipizide, glimepiride, glyburide o Stimulates insulin release from the pancreas causing a decrease in blood sugar levels and increases tissue sensitivity to insulin o Monitor for hypoglycemia - biggest side effect of this medication o Given 30 mutes before meals o Avoid alcohol due to disulfiram effect Thiazolinediones – avandia (Rosiglitazone), and actos (Pioglitazone) o Reduces the production of glucose by the liver (gluconeogenesis) o Increases tissue sensitivity to insulin – does not increase insulin production o Reverse insulin resistance by acting on muscle, fat, and to a lesser extent the liver to increase glucose utilization and diminish glucose production o Monitor for fluid retention, especially in clients who have a history of HF o Monitor for elevation of ALT, LDH, and triglyceride levels o Patient should report rapid weight gain, shortness of breath or decreased exercise tolerance o Use additional birth control because this medication increases pregnancy risk Biguanides – metformin o Decreases sugar production by the liver (gluconeogensis) and helps the muscles use insulin to break down sugar o Increases tissue sensitivity to insulin o Slows carbohydrate absorption in the intestines o Monitor for lactic acidosis – especially in patients who have kidney disorders or liver dysfunction o STOP for 48 hours before any type of elective radiographic test with iodine contrast dye and restart 48 hours after test o Take with food – causes GI discomfort (diarrhea), this does stop o This medication lowers lipids and triglycerides Treatment is insulin for Type 1 diabetes Treatment for Type 2 diabetes – first diet and exercise, then oral hypoglycemics, then insulin Diet: calories should be complex carbohydrates, then fats, and lastly protein ***protein should be limited 10-20% because most diabetics have renal disease o Patient should get a high fiber diet because fiber slows the glucose absorption in the intestines Exercise should not be started until after the blood sugar normalizes o Should be done at the same time every day; when the blood sugar is highest; and the patient should eat before exercising Hypoglycemia – a condition characterized by a decrease in serum glucose level (less than 70 mg/dL), which results in decreased cerebral function o Signs and Symptoms: ▪ Drowsiness ▪ Cool and clammy skin ▪ Shaky ▪ Tachycardia ▪ Shallow respirations ▪ Nausea ▪ Headache ▪ Slurred speech ▪ ***Can mimic stroke but should check BS first and/or treat for hypoglycemia and assess patient ▪ Rapid onset – seen in Type 1 and Type 2 diabetes o Treatment: ▪ 15-20 grams of glucose or simple carbs ▪ 4-6 oz of juice or soda (not diet) ▪ 2 tablespoons of raisins ▪ 1 tablespoon of sugar, honey, or corn syrup ▪ 8 oz of nonfat or 1% milk o ***Glucose absorption is delayed in foods with a lot of fat so NO cake, cookies, or candy bars ▪ Can give glucagon IV or IM for a patient that cannot swallow or has altered LOC ▪ D50 o Once the blood sugar is up, the patient should eat complex carbs and protein o To prevent hypoglycemia the patient should eat, take their insulin, check blood sugar regularly, and know signs and symptoms of hypoglycemia Diabetic Ketoacidosis (DKA) – an extreme increase in the hyperglycemic state; anything that increases blood sugar can throw a client in to DKA (illness, infection, skipping insulin) o ***DKA may be the first sign of Type 1 diabetes o Signs and Symptoms: ▪ Abdominal pain, anorexia, nausea, vomiting, diarrhea ▪ Confusion increasing to coma ▪ Warm, dry, flushed skin ▪ Tachycardia with a weak pulse ▪ Kussmaul’s respirations – trying to blow off CO2 to compensate for the metabolic acidosis ▪ Fruity, acetone breath ▪ Polyuria, Polydipsia, and Polyphagia ▪ Glucose will be greater than 300 mg/dL ▪ pH is low (less than 7.3), CO2 is normal, and HCO3 is low – metabolic acidosis ▪ Ketones are high ▪ Hematocrit is high due to dehydration ▪ Hyperkalemia – potassium follows sugar o The onset for this is rapid – think type 1 diabetes Hyperosmolar Hyperglycemia Nonketosis (HHNK) or Hyperglycemia Hyperosmolar State (HHS) – these people are making just enough insulin so that they are not breaking down fats – no fat breakdown=no ketones=NO acidosis o ***Think type 2 diabetes o Signs and Symptoms: ▪ More severe altered LOC ▪ Warm, dry, flushed skin ▪ Tachycardia ▪ Tachypnea ▪ Polyuria ▪ Greater than 600 mg/dL blood sugar ▪ NO acidosis ▪ Hematocrit is high due to dehydration o The onset is slow – think type 2 diabetes o Treatment for HHNK and DKA: ▪ Treat the underlying cause (infection) ▪ Regular insulin administered IV ▪ Kayexalate for hyperkalemia ▪ Sodium Bicarb for severe acidosis ▪ Once glucose gets closer to 250 mg/dL add glucose to the IV fluids to prevent cerebral edema and hypoglycemia Diabetic Retinopathy – impaired vision and blindness o Encourage yearly eye exams Diabetic Neuropathy – caused from damage to sensory nerve fibers resulting in numbness and pain; leads to ischemia and infection o Patient may have sexual dysfunction o Neurogenic bladder – can have incontinence or retention (either pee or don’t) o Gastroparesis – delayed gastric emptying that causes regurgitation – patient is at risk for aspiration o Provide foot care o Encourage annual exams by a podiatrist Diabetic Nephropathy – damage to the kidneys from prolonged elevated blood glucose levels and dehydration o Monitor hydration and kidney function (serum creatinine) o Report an hourly output of urine less than 30 mL/hour o Monitor blood pressure o Encourage yearly urine analysis, BUN, microalbumin, and serum creatinine o Don’t shoot heroin and avoid boner pills o Encourage water Geriatric Patients with Diabetes: o Issues to consider: ▪ Balance and gait ▪ Nutritional status ▪ Visual changes ▪ Cognitive level ▪ Functional capacity o Elderly patients should avoid high-intensity exercise that can increase the risk of myocardial ischemia, which can be asymptomatic in diabetes – strength training is best Immunity and Inflammation Immunodeficiency is the inability to produce a normal complement of antibodies or immunologically sensitized T cells (cell-mediated immunity), especially in response to specific antigens Immunodeficiency disorders are due to dysfunction or impairment of one or more of the immune response mechanisms. The mechanisms include phagocytosis, humoral response, B cell- and T cell-mediated response or combination, the complement system, and a combined cell and humoral response. Primary Immune Response – occurs when an antigen is initially introduced into the system; it involves both mast cell degranulation and activation of the plasma proteins o Disorder: HIV Secondary or specific immune antibody response – includes the activation of B cells and the memory cells (IgG, IgM, IgA, and IgE); and activation of T cells, cytotoxic (killer) cells, lymphokine-producing cells, helper cells, and suppressor cells (humoral immunity) to a specific antigen o Disorders: Myasthenia gravis, Fibromyalgia, Rheumatoid arthritis (classified as a connective tissue disorder), Systemic Lupus Erythematosus (vascular and connective tissue disorder) HIV – a retrovirus that is transmitted through blood and body fluids; HIV targets CD4+ lymphocytes (T-cells or T-lymphocytes); both are part of specific acquired (adaptive) immunity Normally, CD4+ T cells orchestrate the immune system process in responding to foreign antigens. HIV is found in feces, urine, tears, saliva, cerebrospinal fluid, cervical cells, lymph nodes, corneal tissue, and brain tissue Progression of HIV infection: o Manifestations occur within 2-4 weeks of infection o Symptoms are similar to those of influenza (Flu-like symptoms) and can include a rash and a sore throat o This stage is marked by a rapid rise in the HIV viral load, decreased CD4+ cells, and increased CD8 cells o Lymphadenopathy persists throughout the entire disease process o Chronic asymptomatic infection: ▪ This stage may be prolonged and clinically silent (asymptomatic) ▪ The patient may remain asymptomatic for 10 years or more ▪ Anti-HIV antibodies are produced (HIV positive) ▪ CD4+ cells are destroyed (these cells keep us immune) ▪ Dramatic loss of immunity begins o 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 Risk factors for HIV: o Unsafe sexual practices o Rape o Prostitution o Multiple sexual partners o Exposure to contaminated blood and contaminated needles o Occupational Assessment: o Subjective Data (mostly stage 1 and 2): ▪ Chills ▪ Rash ▪ Anorexia, nausea, and weight loss ▪ Weakness and fatigue ▪ Headache and sore throat ▪ Night sweats o Objective Date: Less than 200 is full diagnosis of AIDs Signs and Symptoms: o Kaposi’s Sarcoma – caused by an interaction between HIV, a weakened immune system, and the human herpesvirus-8 (HHV-8) – linked to the spread of HIV and HHV-8 through sexual activity ▪ This is a vascular malignancy first noticed on the skin or mucous membranes – can also invade the lungs Diagnosis: o 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 test or indirect immunofluorescence assay test) ▪ ELISA detects HIV antibodies ▪ Western blot detects antibodies to specific viral proteins – this test is expensive and is used as confirmation of positive ELISA test o Positive result or report of a detectable quantity from any of the following HIV virologic (viral load) testing: ▪ RNA quantification (HIV viral load test) – determines viral load before beginning treatment; this test can be repeated to monitor disease progression, identify compliance, and determine medication resistance Nursing Care: o Assess risk factors – sexual practices, IV drug use o Monitor fluid intake and urinary output o Obtain daily weights to monitor weight loss o Monitor nutritional intake o Monitor electrolytes o Assess skin integrity – rashes, open areas, bruising o Assess the client’s pain status o Monitor vital signs – especially temperature o Assess lung sounds/ respiratory status – diminished lung sounds o Assess neurological status – confusion, dementia, visual changes Medications: o Highly active antiretroviral therapy (HAART) involves using 3 or 4 medications in combination to reduce medication resistance, adverse effects, and dosages o Fusion inhibitors: Enfuvirtide (Fuzeon)– blocks the fusion of HIV with the host cell o Entry inhibitors: Maraviroc (Selzentry) o Nucleoside reverse transcriptase inhibitors: Zidovudine (Retrovir) – interferes with the virus’s ability to convert RNA into DNA o Non-nucleoside reverse transcriptase inhibitors: Delavirdine (Rescriptor) and efavirenz (Sustiva) – inhibit viral replication in cells o Protease inhibitors: Raltegravir (Isentress) o Antineoplastic medication: Interleukin (Interferon) – immunostimulant that enhances the immune response and reduces the production of cancer cells (commonly used in Kaposi’s sarcoma) o Long-term effects of HAART therapy are hypertension, diabetes, osteopenia, and hyperlipidemia Patient Education: o Frequent hand hygiene to reduce the risk of infection o Avoid crowded areas or traveling to countries with poor sanitation o Avoid raw foods (fruits and vegetables) and undercooked meats, fish, or eggs o ***Avoid cleaning the pet litter boxes to reduce risk of toxoplasmosis Opportunistic infections: o Bacterial diseases: tuberculosis, bacterial pneumonia, and septicemia (blood poisoning) o HIV-associated malignancies: Kaposi’s sarcoma, lymphoma, and squamous cell carcinoma o Viral diseases: cytomegalovirus, herpes simplex, and herpes zoster virus o Fungal diseases: pneumocystitis jirovecil pneumonia (PCP – do drugs), candidiasis, crytospoidiosis, and pencilliosis o Protozoal diseases: such as PCP, toxoplasmosis, microsporidiosis, crytospoidiosis, isosporiasis, and leishmaniasis Wasting syndrome: o Maintain nutrition orally or by TPN if indicated o Monitor weight, calorie counts, and I&O o Provide between-meal supplements/snacks o Decrease fat content of foods to prevent complications of fat intolerance o Six small feedings, high in protein Seizures (HIV encephalopathy): o Maintain safety o Implement seizure precautions Systemic Lupus Erythematosus (SLE) SLE is an autoimmune disorder that affects multiple organs – it is characterized by a diffuse production of autoantibodies that attack and cause damage to body organs and tissue In autoimmune disorders, small antigens may bond with healthy tissue. The body then produces antibodies that attack the healthy tissue. This may be triggered by toxins, medications, bacteria, and/or viruses Risk Factors for SLE: o Females between 20 and 40 o Familial tendencies o More prevalent in Africa Americans, Asians, and Native Americans o The incidence of lupus declines in women following menopause but remains steady in men. o Diagnosis of lupus can be delayed in older adult clients because many of the manifestations mimic other disorders or can be associated with reports common to the normal aging process. o Joint pain and swelling can significantly limit ADLs in older adult clients who have comorbidities. ▪ Older adult clients are at an increased risk for fractures if corticosteroid therapy is used. Signs and Symptoms: Subjective Data o Fatigue/malaise (initial – early) o Alopecia o Blurred vision o Malaise o Pleuritic pain o Anorexia/weight loss o Depression o Joint pain, swelling, tenderness Objective Data o Physical Assessment Findings o Fever (also a major symptom of exacerbation) o Anemia o Lymphadenopathy o Pericarditis (presence of a cardiac friction rub or pleural friction rub) o Raynaud’s phenomenon (arteriolar vasospasm in response to cold/stress) o Findings consistent with organ involvement (kidney, heart, lungs, and vasculature) o Butterfly rash on face Clinical manifestations termed CREST: o Calcinosis: The development of small white calcium deposits under the skin. A chalky fluid drains when the lumps break open. o Raynaud’s syndrome is prevalent in most patients with scleroderma. Spasms of arteries and arterioles occur spontaneously, usually due to exposure to cold or emotional stress. o Esophageal movement is decreased because of deposits of collagen and muscle atrophy. o Sclerodactyly of the fingers and toes. o Telangiectasia: A permanent dilation of the capillaries, arterioles, and venules. Diagnostics: o Antinuclear antibodies (ANA): antibodies produced against one’s own DNA; positive titers in 95% of patients who have lupus o Erythrocyte sedimentation rate (ESR): elevated due to systemic inflammation o BUN and serum creatinine: Increased with kidney involvement o BUN = 5-20 o Creatinine = 0.4-1.5 Medications: o NSAIDs ▪ Used to reduce inflammation and arthritic pain. ▪ NSAIDs are contraindicated for clients who have renal compromise. ▪ Monitor for NSAID-induced hepatitis. ▪ ***Liver enzymes o Corticosteroids (prednisone [Deltasone]) ▪ Used for immunosuppression and to reduce inflammation. ▪ Monitor for fluid retention, hypertension, and renal dysfunction. ▪ Do not stop taking steroids or decrease the dose abruptly. ▪ ***Cushing’s o Immunosuppressant agents – methotrexate and azathioprine (Imuran) ▪ Used to suppress the immune response. ▪ Nursing Considerations – Monitor for toxic effects (bone marrow suppression, increased liver enzymes). o Antimalarial – hydroxychloroquine (Plaquenil) ▪ Used for suppression of synovitis, fever, and fatigue. ▪ Nursing Considerations – Encourage frequent eye examinations. Meds can damage eyes Complications: o Lupus nephritis (renal failure/glomerulonephritis) ▪ Clients whose SLE is unable to be managed with immunosuppressants and corticosteroids may experience renal failure secondary to glomerulonephritis. This is a major cause of death, and a renal transplant may be necessary. ▪ Nursing Actions – Monitor for periorbital and lower extremity swelling and hypertension. Monitor the client’s renal status (creatinine, BUN). ▪ Client Education • Teach the client the importance of taking immunosuppressants and corticosteroids as prescribed. • Teach the client the importance of avoiding stress and illness. o Pericarditis and myocarditis (instruct the client to report chest pain) - Inflammation of the heart, its vessels, and the surrounding sac can occur secondary to SLE. ▪ Nursing Actions – Monitor for chest pain, fatigue, arrhythmias, and fever. ▪ Client Education • Take immunosuppressants and corticosteroids as prescribed. • Avoid stress and illness. • Report chest pain to the provider. Rheumatoid Arthritis Rheumatoid arthritis (RA) is a chronic, progressive inflammatory disease that can affect tissues and organs but principally attacks the joints producing an inflammatory synovitis. It involves joints bilaterally and symmetrically, and it typically affects several joints at one time. RA typically affects upper joints first. RA is an autoimmune disease that is precipitated by WBCs attacking synovial tissue. The WBCs cause the synovial tissue to become inflamed and thickened. The inflammation can extend to the cartilage, bone, tendons, and ligaments that surround the joint. Joint deformity and bone erosion may result from these changes, decreasing the joint’s range of motion and function. RA is also a systemic disease that can affect any connective tissue in the body. Common structures that are affected are the blood vessels, pleura surrounding the lungs, and pericardium. Iritis and scleritis can also develop in the eyes. Rheumatoid arthritis is most often seen in older adults and usually progresses to systemic stages involving the heart, lungs, and other vital organs. Comorbid diseases complicate symptom management. Older adults often hesitate to exert themselves and frequently delay seeking help because they believe that nothing can be done for them. Fear and anxiety of the possible flare-up episodes and eventual disability outcomes are contributing factors to depression. Risk Factors o Female gender (3:1) o Age 20 to 50 years o Genetic predisposition o Epstein-Barr virus o Stress o Environmental factors Signs and Symptoms: o Subjective Data ▪ Pain at rest and with movement ▪ Morning stiffness ▪ Pleuritic pain (pain upon inspiration) ▪ Xerostomia (dry mouth) ▪ Anorexia/weight loss ▪ Fatigue ▪ Paresthesias ▪ Recent illness/stressor ▪ Joint pain ▪ Lack of function Common early clinical manifestations include diffuse musculoskeletal pain, low-grade fever, possible anorexia, and loss of weight. Later, articular (within the joint) manifestations include synovitis, which is inflammation of the synovial capsule that causes escape of synovial fluid into the synovial capsule. Subsequent hypertrophy and symmetrical joint deformity (particularly wrists, hands, or knees) occur. Pain; muscle spasm; and weakness, because of contractures of muscles, tendons, and ligaments; and muscle and soft tissue damage greatly impact the person’s daily activities. o Objective Data ▪ Clinical findings depend on the area affected by the disease process ▪ Joint swelling and deformity, warmth, and erythema. ▪ Finger, hands, wrists, knees, and foot joints are generally affected. ▪ Finger joints affected are the proximal interphalangeal and metacarpophalangeal joints. ▪ Joints may become deformed merely by completing ADLs. ▪ Ulnar deviation, swan neck, and boutonniere deformities are common in the fingers. o Subcutaneous nodules ▪ Fever (generally low grade) ▪ Muscle weakness/atrophy ▪ Reddened sclera and/or abnormal shape of pupils ▪ Lymph node enlargement Diagnostics: o Morning stiffness lasting more than one hour o Arthritis of three or more joint areas o Arthritis of hand joints o Symmetrical arthritis o Rheumatoid nodules over extensor surfaces or bony prominences o Serum rheumatoid factors o Radiographic changes o Anti-CCP antibodies – Positive ▪ This test detects antibodies to cyclic citrullinated peptide (anti- CCP). The result is positive in most people who have rheumatoid arthritis, even years before symptoms develop. ▪ The test is more sensitive for RA than rheumatoid factor (RF) antibodies. o RF antibody ▪ Diagnostic level for rheumatoid arthritis is 1:40 to 1:60 (expected reference range 1:20 or less). ▪ High titers correlate with severe disease. ▪ Other autoimmune diseases also can increase RF antibody. o Erythrocyte sedimentation rate (ESR) – Elevated ▪ The increase is associated with the inflammation or infection in the body. ▪ 20 to 40 mm/hr is mild inflammation. ▪ 40 to 70 mm/hr is moderate inflammation. ▪ 70 to 150 mm/hr is severe inflammation. ▪ Other autoimmune diseases also can increase ESR antibody. o C-reactive protein (may be done in place of ESR) – Positive ▪ This test is useful for diagnosing disease or monitoring disease activity, and for monitoring the response to anti-inflammatory therapy. o Antinuclear antibody (ANA) titer (antibody produced against one’s own DNA) ▪ A positive ANA titer is associated with RA (it is normally negative at 1:20 dilution). ▪ Other autoimmune diseases also can increase ANA. o Elevated WBCs ▪ WBC count may be elevated during an exacerbation secondary to the inflammatory response. Decreased RBCs due to anemia. Nursing Care: o Apply heat or cold to the affected areas as indicated based on client response. o Morning stiffness (hot shower) o Pain in hands/fingers (heated paraffin) o Edema (cold therapy) o Assist with and encourage physical activity to maintain joint mobility (within the capabilities of the client). o Monitor the client for indications of fatigue. Medications: o NSAIDs (Treatment begins with NSAIDs.) ▪ NSAIDs provide analgesic, antipyretic, and anti-inflammatory effects. NSAIDs can cause considerable gastrointestinal (GI) distress. ▪ Nursing Considerations: • Request a concurrent prescription for a GI-acid lowering agent (histamine2-receptor antagonist, proton pump inhibitor) if GI distress is reported. • Monitor for fluid retention, hypertension, and renal dysfunction. ▪ Client Education: ▪ Instruct the client to take the medication with food or with a full glass of water or milk. If taking routinely, o H2-receptor antagonist may also be prescribed. ▪ Observe for GI bleeding (coffee ground emesis; dark, tarry stools). ▪ Avoid alcohol, which can increase the risk of GI complications. ▪ ***Check BUN and Creat! o Corticosteroids ▪ Corticosteroids (prednisone) are strong anti-inflammatory medications that may be given for acute exacerbations or advanced forms of the disease. They are not given for long-term therapy due to significant adverse effects (osteoporosis, hyperglycemia, immunosuppression, cataracts). ▪ Nursing Considerations: • Observe for Cushingoid changes. • Monitor weight and blood pressure. ▪ Client Education: • Instruct the client to observe for changes in vision, blood glucose, and impaired healing. • Instruct the client to avoid crowds. • Instruct the client to follow the provider’s prescription, such as alternate day dosing, tapering, and discontinuing medication. o Disease modifying anti-rheumatic drugs (DMARDs) ▪ DMARDs work in a variety of ways to slow the progression of RA and suppress the immune system’s reaction to RA that causes pain and inflammation. Relief of symptoms may not occur for several weeks. o Antimalarial agent – hydroxychloroquine (Plaquenil) o Antibiotic – minocycline (Minocin) o Sulfonamide – sulfasalazine (Azulfidine) o Biologic response modifiers – etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira), and chelator penicillamine (Cuprimine) o Cytotoxic medications – methotrexate (Rheumatrex), leflunomide (Arava), cyclophosphamide (Cytoxan), and azathioprine (Imuran). These medications can cause severe adverse effects. Complications o Sjogren’s syndrome (triad of symptoms – dry eyes, dry mouth, and dry vagina) o Sjögren’s syndrome is a chronic inflammatory disorder involving the eyes that can be a primary problem or secondary to RA. There is a decrease in lacrimation and salivation due to obstruction of the secretory ducts by the immune complexes. Dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) are hallmarks of the disorder. o Manifestations include swelling of the lacrimal ducts and parotid glands and fatigue. o Nursing Actions: ▪ Provide the client with eye drops and artificial saliva, and recommend vaginal lubricants as needed. ▪ Provide fluids with meals. Types of hypersensitive Reactions Contact Dermatitis o Allergic contact dermatitis (ACD) is an inflammation of the skin caused by direct contact with an allergen. o It is a type 4 allergic reaction, or delayed hypersensitivity reaction. o The skin inflammation varies from mild irritation and redness to open sores, depending on the type of irritant, the body part affected, and the sensitivity of the individual. o Irritants include water, soaps, detergents, solvents, acids, and alkalis. o The rash is generally confined to the site of contact but may be transmitted by the fingers to other sites o Medications: ▪ Topical steroids - Triamcininolone (Aristocort): Ointment used on dry or cracked skin, creams used on inflamed skin or weeping lesions ▪ Systemic steroids - Prednisone (Deltasone): Severe cases involving more than 20% of total body surface area (TBSA) ▪ Antihistamines - Diphenhydramine (Benadryl) Hydroxyzine HCL (Atarax, Vistaril): Used to relieve pruritus associated with contact dermatitis