Quiz 10/25
Signs and symptoms + Assessment of myasthenia gravis
**Motor Manifestations • Progressive (proximal) muscle weakness that worsens with repetitive use and usually improves with rest • Poor posture • Ocular palsies • Ptosis; incomplete eyelid closure • Diplopia • Respiratory compromise • Loss of bowel and bladder control • Fatigue **Sensory Manifestations • Muscle achiness • Paresthesias • Decreased sense of smell and taste -Ask about specific muscle weakness. Although the onset of MG is usually insidious (slow), some instances of fairly rapid development have been caused by infection, pregnancy, or anesthesia. A temporary increase in weakness may be noted after vaccination, menstruation, and exposure to extremes in environmental temperature. - Patients with MG are typically hospitalized for diagnostic evaluation, myasthenic/cholinergic crisis resulting in respiratory failure, or periods of exacerbation when gas exchange is threatened. - Additional areas of inquiry include any history of ptosis (drooping eyelids), diplopia (double vision), or dysphagia (difficulty chewing or swallowing) and the type of diet best tolerated. Assess history of respiratory difficulty, choking, or voice weakness. Other areas of assessment include asking about any difficulty holding up the head, brushing teeth, combing hair, or shaving. Assess for the presence of paresthesias or aching in weakened muscles. Finally, ask about a history of thymus gland tumor. The most common symptoms of MG are related to involvement of the levator palpebrae or extraocular muscles. Pupillary responses to light and accommodation are usually normal. - For most patients, the muscles of facial expression, chewing, and speech are affected (bulbar involvement). Note the patient's smile, which may be transformed into a snarl. The jaw may hang so that the patient must prop it up with the hand. Chewing and swallowing difficulties, choking, and regurgitation of fluids through the nose may lead to considerable weight loss. - Ask about the patient's nutritional intake and any recent weight loss. He or she may have more difficulty eating after talking. After extended conversations, the voice may be weaker or exhibit a nasal twang. In some patients, the tongue has fissures (ulcers). - Because limb weakness is more often proximal (closer to the body), the patient may have difficulty climbing stairs, lifting heavy objects, or raising the arms overhead. Neck weakness may be mild or severe enough to cause difficulty in holding the head erect. -In the most advanced cases of MG, all muscles are weakened, including those associated with respiratory function and the control of bladder and bowel. In these severe cases, ask about bowel and bladder function. Assess respiratory rate, depth, pattern, and Spo2 frequently to ensure adequate gas exchange. Muscle atrophy, although rarely severe, occurs in a small percentage of patients with MG. The tendon reflexes should be assessed, but they are not often affected. Assess for pain, although this is seldom a major concern. Some patients report that their weakened muscles ache. If present, paresthesias (painful tingling sensations) affecting the muscles of the face, hands, and thighs are not associated with any loss of sensation. Lost or decreased sensations of smell and taste have been reported. Consciousness is not altered. - In Eaton-Lambert syndrome, a form of myasthenia often seen with small cell carcinoma of the lung, the muscles of the trunk and the pelvic and shoulder girdles are most commonly affected. Although weakness increases after exertion, muscle strength may temporarily increase during the first few contractions, followed by rapid decline. Diagnosis is confirmed by electromyography (EMG). Management differs somewhat from that of other types of MG. Treatment includes removing the tumor, managing the cancer, and administering drug therapy to release acetylcholine (ACh)
Diagnostic testing for myasthenia gravis
-A standard series of laboratory studies is usually performed for patients with known or suspected MG. Thyroid function should be tested because thyrotoxicosis (excessive thyroid hormone) is present in a small number of myasthenic patients. -Serum protein electrophoresis evaluates the patient for immunologic disorders. Immunologic-based diseases, such as rheumatoid arthritis, systemic lupus erythematous, and polymyositis, may be associated with the disease -Several types of antibodies are found in the majority of patients with MG and include forms directed against the acetylcholine receptor (AChR) and the enzyme muscle-specific receptor tyrosine kinase (MuSK). However, whereas a positive antibody test confirms diagnosis, a negative finding does not rule out the disease. -Some patients with MG have a thymoma, and therefore patients are assessed for this condition. The thymus, an H-shaped gland located in the upper mediastinum beneath the sternum, is where B- and T-cells interact, refining self-recognition of these white blood cells. It is hypothesized that thymic abnormalities cause the breakdown in tolerance that causes the immune-mediated attack on AChR in myasthenia gravis. A thymoma is seen on a chest x-ray or a CT scan. - Most common electrodiagnostic test performed to detect MG is repetitive nerve stimulation (RNS) of proximal nerves. diagnoses most cases of generalized MG but far fewer cases of ocular MG. Each nerve studied is electrically stimulated 6 to 10 times at 2 or 3 Hertz. The compound muscle action potential (CMAP) is recorded with surface electrodes over muscle. In MG, there is a progressive decline in CMAP amplitude (force, or strength) with the first 4 or 5 stimuli. During electromyography (EMG) to diagnose MG, a recording electrode is placed into skeletal muscle and the electrical activity of skeletal muscle can be monitored in a way similar to electrocardiography (ECG). A progressive decrease in the amplitude of the electrical waveform is a classic sign of MG. -Single-fiber EMG (SFEMG) is a newer and most sensitive form of electromyography in detecting defects of neuromuscular transmission. This test compares the stability of the firing of one muscle fiber with that of another fiber innervated by the same motor neuron. The time interval between the two firings normally shows a minor degree of variability, called jitter. Defective transmission increases jitter or actually blocks successive discharges. This test can diagnose almost all cases of generalized and ocular MG. -Pharmacologic tests with the cholinesterase inhibitors edrophonium chloride (Tensilon) and neostigmine bromide (Prostigmin) may be performed. This older test is often referred to as a Tensilon challenge test. Tensilon is used most often for testing because of its rapid onset and brief duration of action. This drug inhibits the breakdown of ACh at the postsynaptic membrane, which increases the availability of ACh for excitation of postsynaptic receptors. Tensilon testing may be used also to help determine whether increasing weakness in the previously diagnosed myasthenic patient is due to a cholinergic crisis (too much cholinesterase inhibitor drugs) or a myasthenic crisis (too little cholinesterase inhibitor drugs). In a cholinergic crisis, muscle tone does not improve after giving Tensilon. Instead, weakness may actually increase, and fasciculations (muscle twitching) may be seen around the eye and face. **The Tensilon test can cause cardiac dysrhythmias and cardiac arrest, but these reactions rarely occur. Be sure that atropine sulfate, the antidote for Tensilon, is available in case these complications occur.
Clinical manifestations of Rheumatoid Arthritis
Clinical manifestations of RA vary, usually reflecting the stage and severity of the disease. •Joint pain. One of the classic signs, joints that are painful are not easily moved. •Swelling. Limitation in function occurs as a result of swollen joints. •Warmth. There is warmth in the affected joint and upon palpation, the joints are spongy or boggy. •Erythema. Redness of the affected area is a sign of inflammation. •Lack of function. Because of the pain, mobilizing the affected area has limitations. •Deformities. Deformities of the hands and feet may be caused by misalignment resulting in swelling. •Rheumatoid nodules. Rheumatoid nodules may be noted in patients with more advanced RA, and they are nontender and movable in the subcutaneous tissue.
Pathophysiology of Rheumatoid Arthritis
In RA, transformed autoantibodies (rheumatoid factors [RFs]) are formed that attack healthy tissue, especially synovium, causing inflammation. The disease then begins to involve the articular cartilage, joint capsule, and surrounding ligaments and tendons. immunity and inflammation factors cause cartilage damage in patients with RA. The synovium then thickens and becomes hyperemic, fluid accumulates in the joint space, and a pannus forms. The pannus is vascular granulation tissue composed of inflammatory cells; it erodes articular cartilage and eventually destroys bone. As a result, in late disease, fibrous adhesions, bony ankylosis, and calcifications occur; bone loses density, and secondary osteoporosis occurs •Autoimmune reaction. In RA, the autoimmune reaction primarily occurs in the synovial tissue. •Phagocytosis. Phagocytosis produces enzymes within the joint. •Collagen breakdown. The enzymes break down collagen, causing edema, proliferation of the synovial membrane, and ultimately pannus formation. •Damage. Pannus destroys cartilage and erodes the bone. •Consequences. The consequences are loss of articular surfaces and joint motion. •Degenerative changes. Muscle fibers undergo degenerative changes, tendon and ligament elasticity and contractile power are lost.
Joint involvement and systemic complications
Joint deformity occurs as a late, articular manifestation, and secondary osteoporosis can cause bone fractures. Observe common deformities, especially in the hands and feet. Extensive wrist involvement can result in carpal tunnel syndrome Gently palpate the tissues around the joints to elicit pain or tenderness associated with other rheumatoid complications, unless the patient is having severe joint pain. For example, Baker's cysts (enlarged popliteal bursae behind the knee) may occur and cause tissue compression and pain. Tendon rupture is also possible, particularly rupture of the Achilles tendon ◾In addition to increased joint swelling and tenderness, moderate to severe weight loss, fever, and extreme fatigue are common in late disease exacerbations, often called "flare-ups." Some patients have the characteristic round, movable, nontender subcutaneous nodules, which usually appear on the ulnar surface of the arm, on the fingers, or along the Achilles tendon. These nodules can disappear and reappear at any time and are associated with severe, destructive disease. Rheumatoid nodules usually are not a problem themselves; however, they occasionally open and become infected and may interfere with ADLs. ◾Inflammation of the blood vessels results in vasculitis, particularly of small to medium-size vessels. When arterial involvement occurs, major organs can become ischemic and malfunction. Increased lesions indicate increased vasculitis, and a decreased number indicates decreased vasculitis. These lesions can lead to ulcerations, which heal slowly as a result of decreased circulation. Peripheral neuropathy associated with decreased circulation can cause footdrop and paresthesias (burning and tingling sensations), usually in older adults. ◾Respiratory complications may manifest as pleurisy, pneumonitis, diffuse interstitial fibrosis, and pulmonary hypertension. ◾Cardiac complications include pericarditis and myocarditis. ◾Assess for eye involvement, which typically manifests as iritis and scleritis. If either of these complications is present, the sclera of one or both eyes is reddened and the pupils have an irregular shape. Visual disturbances may occur. ◾Several syndromes are seen in patients with advanced RA. The most common is Sjögren's syndrome, which includes a triad of: • Dry eyes (keratoconjunctivitis sicca [KCS], or the sicca syndrome) • Dry mouth (xerostomia) • Dry vagina (in some cases) ◾Less commonly observed is Felty's syndrome, which is characterized by RA, hepatosplenomegaly (enlarged liver and spleen), and leukopenia. ◾Caplan's syndrome is characterized by the presence of rheumatoid nodules in the lungs
Mangement of myasthenia gravis
MG is one of the most treatable neurologic disorders. The classic presentation of MG is muscle weakness that increases when the patient is fatigued and limits his or her mobility and ability to participate in activities. Management for this disease falls into two categories: • Treatment that affects the symptoms of MG without influencing the actual course of the disease (anticholinesterases or cholinergic drugs) • Therapeutic efforts for inducing remission, such as the administration of immunosuppressive drugs or corticosteroids, plasmapheresis, and thymectomy (removal of the thymus gland) -Both myasthenic crisis and cholinergic crisis increase muscle weakness and the patient's risk for respiratory compromise. The diaphragm and intercostal muscles may be affected, which inhibits the patient's ability to maintain adequate gas exchange, breathe deeply, and cough effectively. In addition, dysphagia may result in the aspiration of foods, liquids. Because of their respiratory muscle involvement, many pt have an increased risk for lung infections. The patient who cannot cough effectively may require oropharyngeal or nasopharyngeal suctioning. -Collaborate with the respiratory therapist (RT) to provide chest physiotherapy consisting of postural drainage, percussion, and vibration to mobilize secretions and improve gas exchange. -Because breathing difficulty or the inability to breathe easily is frightening, be aware of the patient's mental and emotional status during periods of respiratory compromise. Monitor his or her response to drug therapy for muscle weakness. Monitor for pulmonary congestion that can lead to respiratory complications like pneumonia and atelectasis. -Noninvasive mechanical ventilation (NIMV) can be used to support patients with acute respiratory failure from MG crisis while awaiting improvement from IV immunoglobulin (IVIG) therapy or plasma exchange. -Assess the patient's muscle strength before and after periods of activity. Provide assistance as necessary to prevent the patient from becoming fatigued. Schedule him or her for tests, treatments, and other activities early in the day or during the energy peaks after giving -Keep a bag-valve-mask setup (e.g., Ambu), equipment for oxygen administration, and suction equipment at the bedside of the patient with myasthenia gravis in case of respiratory distress. the prescribed drugs.
Emergency care: Myasthenic Crisis
Myasthenic crisis is often caused by some type of infection. For other patients, increasing muscle weakness leads to an overdose of anticholinesterase drugs. As a result, the patient may experience a mixed crisis. The Tensilon test, although not always conclusive, is important procedure for differentiation. Tensilon produces a temporary improvement in myasthenic crisis but worsening or no improvement of symptoms in cholinergic crisis. -The priority for nursing management of the patient in myasthenic crisis is maintaining adequate respiratory function to promote gas exchange. The acutely ill patient may need intensive nursing care for monitoring. He or she may require mechanical ventilation or other technologic support. -Cholinesterase-inhibiting drugs are withheld because they increase respiratory secretions and are usually ineffective for the first few days after the crisis begins. Drug therapy is restarted gradually and at lower dosages.
What is rheumatoid arthritis
Rheumatoid arthritis (RA) is a chronic, progressive, systemic inflammatory autoimmune disease process that affects primarily the synovial joints. Systemic means this disease affects the body system, affecting many joints and other tissues. It is a diffuse connective tissue disease and is chronic in nature. It is characterized by diffuse inflammation and degeneration in the connective tissues. Early and aggressive treatment to suppress synovitis may lead to a remission. RA is a disease characterized by natural remissions and exacerbations. Because rheumatoid arthritis is a systemic disease, areas of the body besides the synovial joints can be affected. Inflammatory responses similar to those occurring in synovial tissue may occur in any organ or body system in which connective tissue is prevalent. If blood vessel involvement (vasculitis) occurs, the organ supplied by that vessel can be affected, leading to eventual failure of the organ or system in late disease
Self-management for Myasthenia Gravis
Stress the importance of lifestyle adaptations such as avoiding heat (e.g., sauna, hot tubs, sunbathing), crowds, overeating, erratic changes in sleep habits, or emotional extremes. Teach the signs of exacerbation, such as increased weakness, increased diplopia, ptosis, and problems with chewing or swallowing. Remind the patient to plan activities to allow for rest periods and to conserve energy. Provide the drug regimen in a written format that includes the names, purposes, dosages, scheduled dosage times, and side effects of the drugs. Explain that the drugs are normally taken before activities such as eating, participating in sports, or working. Stress the importance of maintaining therapeutic blood levels by taking the medications on time and as prescribed and not missing or postponing doses. In addition, inform the patient of the side effects of anticholinesterase drugs and drugs that can worsen symptoms, such as corticosteroids, narcotics, antidysrhythmics, and antimalarials. Check with the pharmacist before starting or stopping drugs. In preparing the patient for discharge, explain the signs and symptoms of myasthenic and cholinergic crises and the need to contact the health care provider whenever either type of crisis is suspected.
Causes of Rheumatoid Arthritis
The onset of rheumatoid arthritis (RA) may be acute and severe or slow and progressive; patients may have vague symptoms that last for several months before diagnosis. The onset of the disease is more common in the winter months than in the warmer months. The manifestations of RA can be categorized as early or late disease and as articular (joint) or extra-articular. Diffuse connective tissue diseases have unknown causes, but they are also thought to be the result of immunologic abnormalities. •Genetics. Researchers have shown that people with a specific gene marker called the HLA shared epitope have a fivefold greater chance of developing rheumatoid arthritis than do people without the marker. •Infectious agents. Infectious agents such as bacteria and viruses may trigger the development of the disease in a person whose genes make them more likely to get it. •Female hormones. 70% of people with RA are women, and this occur because of the fluctuations of the female hormones. •Environmental factors. Environmental factors such as exposure to cigarette smoke, air pollution, and insecticides. •Occupational exposures. Substances such as silica and mineral oil may harm the worker and result in contact dermatitis.
Drug therapy for myasthenia gravis
Two groups of drugs are typically prescribed for the treatment of myasthenia gravis (MG): anticholinesterases and immunosuppressants. Be sure to give these drugs on time to maintain blood levels and thus improve muscle strength. Monitor and document the patient's response to drug therapy. Provide information for the patient and the family about the indications for, effectiveness of, and side effects of the drugs used in the treatment of MG ◾Cholinesterase (ChE) inhibitor drugs are the first-line management of MG. These drugs are also referred to as anticholinesterase drugs or antimyasthenics. They enhance neuromuscular impulse transmission by preventing the decrease of ACh by the enzyme ChE. This increases the response of the muscles to nerve impulses and improves muscle strength. The ChE inhibitor drug of choice is pyridostigmine (Mestinon, Regonol). -Expect a day-to-day variation in dosage depending on the patient's changing symptoms. -Administer ChE inhibitors with a small amount of food to alleviate GI **Instruct the patient to eat meals 45 minutes to 1 hour AFTER taking ChE inhibitors to avoid aspiration. This is especially important if the patient has bulbar involvement. -Drugs containing magnesium, morphine or its derivatives, curare, quinine, quinidine, procainamide, or hypnotics or sedatives should be avoided because they may increase the patient's weakness. Antibiotics such as neomycin and certain tetracyclines impair transmitter release and also increase myasthenic symptoms **A potential adverse effect of ChE inhibitors is cholinergic crisis.Sudden increases in weakness accompanied by hypersalivation, sweating, and increased bronchial secretions help identify this as a cholinergic crisis rather than a myasthenic crisis. -A cholinergic crisis is more likely to be associated with nausea, vomiting, and diarrhea. Teach the patient and family to monitor for these two types of crises: 1. Myasthenic crisis—an exacerbation (flare-up or worsening) of the myasthenic symptoms caused by not enough anticholinesterase drugs 2. Cholinergic crisis— acute exacerbation of muscle weakness caused by too many anticholinesterase drugs
Classes of Myasthenia gravis
• Class I: Any ocular muscle weakness; may have weakness of eye closure; all other muscle strength is normal • Class II: Mild weakness affecting other than ocular muscles; may also have ocular muscle weakness of any severity: • Class IIa: Predominantly affecting limb, axial muscles, or both; may also have lesser involvement of oropharyngeal muscles • Class IIb: Predominantly affecting oropharyngeal, respiratory muscles, or both; may also have lesser or equal involvement of limb, axial muscles, or both • Class III: Moderate weakness affecting other than ocular muscles; may also have ocular weakness of any severity: • Class IIIb: Predominantly affecting oropharyngeal, respiratory muscles, or both; may also have lesser or equal involvement of limb, axial muscles, or both; • Class IV: Severe weakness affecting other than ocular muscles; may also have ocular muscle weakness of any severity: • Class IVa: Predominantly affecting limb, axial muscles, or both; may also have lesser involvement of oropharyngeal muscles • Class IVb: Predominantly affecting oropharyngeal, respiratory muscles, or both; may also have lesser or equal involvement of limb, axial muscles, or both; use of a feeding tube to avoid aspiration and maintain nutrition • Class V: Defined by the need for intubation, with or without mechanical ventilation, except when used during routine postoperative management
Assessment and Diagnostic testing for Rheumatoid Arthritis
•Antinuclear antibody (ANA) titer: Screening test for rheumatic disorders, elevated in 25%-30% of RA patients. Follow-up tests are needed for the specific rheumatic disorders, e.g., anti-RNP is used for differential diagnosis of systemic rheumatic disease. Measures the titer of a group of antibodies that destroy the nuclei of cells and cause tissue death in pt with autoimmune disease ◾Rheumatoid factor (RF): Positive in more than 80% of cases (Rose-Waaler test). Measures the presence of unusual antibodies of the immunoglobulins G (IgG) and M (IgM) types that develop in a number of connective tissue diseases. ◾Latex fixation: Positive in 75% of typical cases. ◾Agglutination reactions: Positive in more than 50% of typical cases. ◾Serum complement: C3 and C4 increased in acute onset (inflammatory response). Immune disorder/exhaustion results in depressed total complement levels. ◾Erythrocyte sedimentation rate (ESR): Usually greatly increased (80-100 mm/hr). May return to normal as symptoms improve. The high-sensitivity C-reactive protein, or hsCRP, is another useful test to measure inflammation and may be done with or instead of the ESR. As the name implies, it is more sensitive to inflammatory changes than the ESR. It is also very useful for detecting infection anywhere in the body. ◾CBC: Usually reveals moderate anemia. WBC is elevated when inflammatory processes are present. monitor the pt's complete blood count (CBC) for a low hemoglobin, hematocrit, and red blood cell (RBC) count. An increase in white blood cell (WBC) count is consistent with an inflammatory response. A decrease in the WBC count may indicate Felty's syndrome, a complication associated with late RA. Thrombocytosis (increased platelets) can also occur in patients with late RA ◾Immunoglobulin (Ig) (IgM and IgG): Elevation strongly suggests autoimmune process as cause for RA. ◾X-rays of involved joints: Reveals soft-tissue swelling, erosion of joints, and osteoporosis of adjacent bone (early changes) progressing to bone-cyst formation, narrowing of joint space, and subluxation. Concurrent osteoarthritic changes may be noted. ◾Radionuclide scans: Identify inflamed synovium. ◾Direct arthroscopy: Visualization of area reveals bone irregularities/degeneration of joint. ◾Synovial/fluid aspirate(arthrocentesis): May reveal volume greater than normal; opaque, cloudy, yellow appearance (inflammatory response, bleeding, degenerative waste products); elevated levels of WBCs and leukocytes; decreased viscosity and complement (C3 and C4). Teach the patient to use ice and rest the affected joint for 24 hours after arthrocentesis, monitor the insertion site for bleeding or leakage of synovial fluid. Notify the health care provider if either of these problems occurs. ◾Synovial membrane biopsy: Reveals inflammatory changes and development of pannus (inflamed synovial granulation tissue). pain.
Surgical management for Rheumatoid Arthritis
•Reconstructive surgery. Reconstructive surgery is indicated when pain cannot be relieved by conservative measures and the threat of loss of independence is eminent. •Synovectomy. Synovectomy is the excision of the synovial membrane to remove inflamed synovium, may be needed for joints like the knee or elbow •Tenorrhaphy. Tenorrhaphy is the suturing of a tendon. •Arthrodesis. Arthrodesis is the surgical fusion of the joint. •Arthroplasty. Arthroplasty is the surgical repair and replacement of the joint. Total joint arthroplasty (TJA) may be indicated when other measures fail to relieve.
Non pharmacological treatment for rheumatoid arthritis
◾Adequate rest, proper positioning, and ice and heat applications are important in pain management. If acute inflammation is present, ice packs may be applied to "hot" joints for pain relief until the inflammation lessens. The ice pack should not be too heavy. ◾Heated paraffin (wax) dips may help increase comfort of arthritic hands. Finger and hand exercises are often done more easily after paraffin treatment. ◾To relieve morning stiffness or the pain of late-stage disease, recommend a hot shower rather than a sponge bath or a tub bath. It is often difficult for the patient with RA to get into and out of a bathtub, although special hydraulic lifts and tub chairs are available to allow the patient to bathe. Safety (grab) bars and nonskid tread in the tub or shower floor are important safety features to discuss with all patients. Some older adults prefer using shower chairs and a walk-in shower that does not have a ledge that could cause falls. ◾Hot packs applied directly to involved joints may be beneficial. Teach patients to use the microwave or stovetop heating instructions to warm heat packs at home. Remind them to follow the instructions given with each heating device used. ◾Plasmapheresis (sometimes called plasma exchange) is an in-hospital procedure prescribed by a health care provider in which the patient's plasma is treated to remove the antibodies causing the disease. This procedure may be combined with steroid pulse therapy for patients with severe, life-threatening disease.
Assessment + Diagnostic testing for hypoparathyroidism
◾Ask about any head or neck surgery or radiation therapy because these treatments may damage the parathyroid glands and cause hypoparathyroidism. Also ask whether the neck has ever sustained a serious injury in a car crash or by strangulation. ◾Assess whether the patient has any manifestations of hypoparathyroidism, which may range from mild tingling and numbness to muscle tetany. Tingling and numbness around the mouth or in the hands and feet reflect mild to moderate hypocalcemia. Severe muscle cramps, spasms of the hands and feet, and seizures (with no loss of consciousness or incontinence) reflect a more severe hypocalcemia. The patient or family may notice mental changes ranging from irritability to psychosis. ◾The physical assessment may show excessive or inappropriate muscle contractions that cause finger, hand, and elbow flexion. This can signal an impending attack of tetany. Check for Chvostek's sign and Trousseau's sign; positive responses indicate potential tetany ◾Bands or pits may encircle the crowns of the teeth, which indicate a loss of calcium from the teeth with enamel loss. ◾Diagnostic tests for hypoparathyroidism include electroencephalography (EEG), blood tests, and CT scans. EEG changes revert to normal with correction of hypocalcemia. Serum calcium, phosphorus, magnesium, vitamin D, and urine cyclic adenosine monophosphate (cAMP) levels may be used in the diagnostic workup for hypoparathyroidism. The CT scan can show brain calcifications, which indicate chronic hypocalcemia.
Persistent, Erosive Rheumatoid Arthritis Advanced, Unremitting Rheumatoid Arthritis
◾Corticosteroids. Systemic corticosteroids are used when the patient has unremitting inflammation and pain or needs a "bridging" medication while waiting for slower DMARDs to begin taking effect. ◾Glucocorticoids (steroids):usually prednisone (Deltasone)—are given for their fast-acting anti-inflammatory and immunosuppressive effects. Prednisone may be given in high dose for short duration (pulse therapy) or as a low chronic dose. Moderate-dose short-term tapering bridge therapy may be used when inflammation is symptomatic and other RA medications are insufficient or have not yet had an effect. Chronic steroid therapy can result in numerous complications, such as: • Diabetes mellitus • infection • Fluid and electrolyte imbalances • Hypertension • Osteoporosis • Glaucoma ◾Instruct patients taking chronic steroids to take calcium 1200 to 1500 mg daily plus vitamin D 400 mg daily to help prevent osteoporosis. Bisphosphonate drugs may also be prescribed. Bone density measurements (DEXA [dual-energy x-ray absorptiometry] scans) are done every 2 to 3 years to monitor for bone loss. -Steroids can cause a moonfaced appearance, acne, striae, "buffalo humps," and weight gain ---------------------------------------------------- ◾Immunosuppressants. Immunosuppressive agents are prescribed because of their ability to affect the production of antibodies at the cellular level. -Cortisone injections in single joints may be used to relieve local pain and inflammation. Have the patient ice and rest the joint for 24 hours after the procedure. Oral analgesics also are sometimes needed during that time. Other immunosuppressive agents that may be used as a last resort are azathioprine (Imuran) and cyclophosphamide (Cytoxan). -Cyclophosphamide is sometimes given specifically to control RA vasculitis. Such immunosuppressive drugs may cause bone marrow suppression and occasionally leukemia or lymphoma. White blood cell counts are expected to decrease 7 to 14 days after the administration of IV cyclophosphamide; therefore monitor laboratory results closely to ensure safe limits. Hemorrhagic cystitis is a concern more with oral cyclophosphamide. Instruct the patient to drink water and void frequently (about every 2 hours while awake), which dilutes the urine and empties the bladder, thus decreasing opportunity for bladder irritation from residual drug. Hair thinning or loss can be seen with immunosuppressive medications. Cyclophosphamide may also cause sterility; strict birth control is recommended. ◾Antidepressants. For most patients with RA, depression and sleep deprivation may require the short-term use of low-dose antidepressants such as amitriptyline, paroxetine, or sertraline, to reestablish an adequate sleep pattern and to manage chronic pain.
Drug Therapy for Moderate, Erosive Rheumatoid Arthritis
◾Cyclosporine. Neoral, an immunosuppressant is added to enhance the disease modifying effect of methotrexate.
Non-surgical management for hyperparathyroidism
◾Diuretic and hydration therapies are used for reducing serum calcium levels in patients who have milder disease. Usually furosemide (Lasix, Uritol ), a diuretic that increases kidney excretion of calcium, is used together with IV saline in large volumes to promote calcium excretion. ◾Drug therapy for patients who have more severe manifestations of primary or secondary hyperparathyroidism or who have hypercalcemia related to parathyroid cancer involves the use of cinacalcet (Sensipar). This drug is the first in a new class of drugs known as calcimimetics. When taken orally, the drug binds to calcium-sensitive receptors on parathyroid tissue. This binding reduces PTH production and release. The result is decreased serum calcium levels, stabilization of other minerals, and decreased progression of PTH-induced bone complications. The initial dose is low (30 mg orally twice daily) and is gradually increased to the maximum maintenance dose of 90 mg three times daily. The patient's serum calcium must be monitored for hypocalcemia on a regular basis for the duration of therapy. ◾For patients who do not respond to cinacalcet, oral phosphates are used to inhibit bone resorption and interfere with calcium absorption. IV phosphates are used only when serum calcium levels must be lowered rapidly. Calcitonin decreases the release of skeletal calcium and increases the kidney excretion of calcium. It is not effective when used alone because of its short duration of action. The therapeutic effects are greatly enhanced if calcitonin is given along with glucocorticoids. ◾Monitor cardiac function and intake and output every 2 hours during hydration therapy. Continuous cardiac monitoring may be needed. Compare recent ECG tracings with the patient's baseline tracings. Especially look for changes in the T waves and the QT interval, as well as changes in rate and rhythm. Monitor serum calcium levels, and immediately report any sudden drop to the health care provider. ◾Sudden drops in calcium levels may cause tingling and numbness in the muscles. Preventing injury is important because the patient with chronic hyperparathyroidism often has significant bone density loss and is at risk for pathologic fractures. Teach unlicensed assistive personnel (UAP) to handle the patient carefully. Use a lift sheet to reposition the patient rather than pulling him or her.
Early and late Manifestations of Rheumatoid Arthritis
◾Early Disease Manifestations. The patient with RA typically reports joint signs and symptoms of joint inflammation,generalized weakness, and fatigue. Anorexia and a weight loss of about 2 to 3 pounds (1 kg) usually occur early in the disease process. Persistent low-grade fever may accompany these manifestations. In patients with early disease, the upper-extremity joints are involved initially—often the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints of the hands. These joints may be slightly reddened, warm, stiff, swollen, and tender or painful, particularly on palpation (caused by synovitis). The typical pattern of joint involvement in RA is bilateral and symmetric (e.g., both wrists). The number of joints involved usually increases as the disease progresses. In early disease, the patient may report migrating symptoms known as migratory arthritis. The presence of only one hot, swollen, painful joint (out of proportion to the other joints) may mean the joint is infected. Refer the patient to the health care provider (generally the rheumatologist) immediately if this is the case. Single hot, swollen joints are considered infected until proven otherwise and require immediate long-term antibiotic treatment. ◾Late Disease Manifestations. As the disease worsens, the joints become progressively inflamed and very painful. The patient usually has frequent morning stiffness (also called the gel phenomenon), which lasts for 45 minutes to several hours after awakening. On palpation, the joints feel soft and look puffy because of synovitis and effusions (joint swelling with fluid, especially the knees). The fingers often appear spindle-like. Note any muscle atrophy (which can result from disuse secondary to joint pain) and a decreased range of motion in the affected joints. Most or all synovial joints are eventually affected. The temporomandibular joint (TMJ) may be involved in severe disease, but such involvement is uncommon. When the TMJ is affected, the patient may have pain when chewing or opening the mouth. When the spinal column is involved, the cervical joints are most likely to be affected. During clinical examination, gently palpate the posterior cervical spine and identify it as cervical pain, tenderness, or loss of motion.
Nonsurgical management of hypoparathyroidism
◾Focuses on correcting hypocalcemia, vitamin D deficiency, and hypomagnesemia. For patients with acute and severe hypocalcemia, IV calcium is given as a 10% solution of calcium chloride or calcium gluconate over 10 to 15 minutes. ◾Acute vitamin D deficiency is treated with oral calcitriol (Rocaltrol), 0.5 to 2 mg daily. Long-term therapy for vitamin D deficiency is 50,000 to 400,000 units of oral ergocalciferol daily. The dosage is adjusted to keep the patient's calcium level in the low-normal range (slightly hypocalcemic), enough to prevent symptoms of hypocalcemia. It must also be low enough to prevent increased urine calcium levels, which can lead to stone formation. ◾Acute hypomagnesemia is corrected with 50% magnesium sulfate 2-mL doses (up to 4 g daily)IV. ◾Long-term oral therapy for hypocalcemia involves the intake of calcium, 0.5 to 2 g daily, in divided doses. Teach the patient to eat foods high in calcium but low in phosphorus. Milk, yogurt, and processed cheeses are avoided because of their high phosphorus content. Stress that therapy for hypocalcemia is lifelong. Advise the patient to wear a medical alert bracelet. With adherence to the prescribed drug and diet regimen, the calcium level usually remains high enough to prevent a hypocalcemic crisis.
Surgical Management for Myasthenia Gravis
◾For patients with MG, thymectomy (removal of the thymus gland) is usually performed early in the disease. The procedure is not always immediately effective. Those who have surgery within 2 years of the onset of myasthenic symptoms show the most improvement, but many patients do not experience a change in status despite thymectomy. Because there is no way to predict whether remission or improvement will occur, it is important to avoid making promises but be optimistic. ◾Immediately before surgery, pyridostigmine (Mestinon) may be given with a small amount of water to keep the patient stable during and after surgery. If steroids have been used, they are also given before surgery and are tapered during the postoperative period. Antibiotics are administered immediately before or during the surgery. Plasmapheresis may be used before and after surgery to decrease circulating antibodies. ◾One of two surgical approaches may be used: the transcervical incision (minimal access technique) or the sternal split. -The transcervical approach is becoming more popular because it allows more rapid recovery with less discomfort after surgery, especially if done using the video-assisted thoracoscopic surgery (VATS) technique. However, this procedure is used only for patients who do not have a thymoma. Only a small dressing and an IV line are needed after surgery. -The older sternal split procedure is preferred when patients have a thymoma. It allows the surgeon to directly see the mediastinum and areas around the thymus. When thymoma is present, all surrounding involved structures (i.e., the pericardium, the innominate vein, a portion of the superior vena cava, and a portion of the lung) are removed. A single chest tube is placed in the anterior mediastinum. The patient is usually admitted to the critical care unit after surgery. Thymoma should be considered as a potentially malignant tumor requiring prolonged follow-up. ◾The presence of myasthenic weakness can still complicate its management. Although patients with adequate respiratory effort and gas exchange may be extubated immediately after surgery, most require a gradual weaning from the ventilator. Prolonged ventilatory assistance is rare. After the patient is extubated, pay special attention to respiratory status and maintaining a patent airway. Encourage the patient to turn, breathe deeply 3 to 6 times every 15 to 30 minutes in the hours after extubation, and use incentive spirometry.
thymectomy nursing care
◾For the patient having a thymectomy, monitor respiratory effort and promote effective gas exchange. Observe for signs of pneumothorax or hemothorax, including: • Chest pain • Sudden shortness of breath • Diminished or delayed chest wall expansion • Diminished or absent breath sounds • Restlessness or a change in vital signs (decreasing blood pressure or a weak, rapid pulse) If respiratory distress or symptoms of ineffective gas exchange occur, provide oxygen to the patient and raise the head of the bed to at least 45 degrees. Then report any of these signs and symptoms to the surgeon or Rapid Response Team immediately!
What is Hypoparathyroidism?
◾Hypoparathyroidism is a rare endocrine disorder in which parathyroid function is decreased. Problems are directly related to a lack of parathyroid hormone (PTH) secretion or to decreased effectiveness of PTH on target tissue. Whether the problem is a lack of PTH secretion or an ineffectiveness of PTH on tissues, the result is the same: hypocalcemia. ◾Iatrogenic hypoparathyroidism, the most common form, is caused by the removal of all parathyroid tissue during total thyroidectomy or by surgical removal of the parathyroid glands. ◾Idiopathic hypoparathyroidism can occur spontaneously. The exact cause is unknown, but an autoimmune basis is suspected. It may occur with other autoimmune disorders such as adrenal insufficiency, hypothyroidism, diabetes mellitus, pernicious anemia, and vitiligo. ◾Hypomagnesemia (decreased serum magnesium levels) may also cause hypoparathyroidism. Hypomagnesemia is seen in patients with malabsorption syndromes, chronic kidney disease, and malnutrition. It causes impairment of PTH secretion and may interfere with the effects of PTH on the bones, kidneys, and calcium regulation.
Emergency care: cholinergic Crisis ------------------------------------ Emergency care: Myasthenic Crisis
◾In cholinergic crisis, do not give anticholinesterase drugs while the patient is maintained with mechanical ventilation. Atropine 1 mg IV may be given and repeated, if necessary. When atropine is prescribed, observe the patient carefully. Secretions can be thickened by the drug, which causes more difficulty with airway clearance and possibly the development of mucus plugs. Unless complications such as pneumonia or aspiration develop, the patient in crisis improves rapidly after theappropriate drugs have been given. Continue to provide assistance as necessary because he or she tires easily after minimal exertion ---------------------------------------------------- ◾Myasthenic crisis is often caused by some type of infection. For other patients, increasing muscle weakness leads to an overdose of anticholinesterase drugs. As a result, the patient may experience a mixed crisis. The Tensilon test, although not always conclusive, is important procedure for differentiation. Tensilon produces a temporary improvement in myasthenic crisis but worsening or no improvement of symptoms in cholinergic crisis. -The priority for nursing management of the patient in myasthenic crisis is maintaining adequate respiratory function to promote gas exchange. The acutely ill patient may need intensive nursing care for monitoring. He or she may require mechanical ventilation or other technologic support. -Cholinesterase-inhibiting drugs are withheld because they increase respiratory secretions and are usually ineffective for the first few days after the crisis begins. Drug therapy is restarted gradually and at lower dosages.
Assessment for hyperparathyroidism
◾Manifestations of hyperparathyroidism may be related either to the effects of excessive PTH or to the effects of the accompanying hypercalcemia. ◾Ask about any bone fractures, recent weight loss, arthritis, or psychological stress. Ask whether the patient has received radiation treatment to the head or neck. The patient with chronic disease may have a waxy pallor of the skin and bone deformities in the extremities and back. ◾High levels of PTH cause kidney stones,deposits of calcium in the soft tissue of the kidney. ◾Bone lesions are due to an increased rate of bone destruction and may result in pathologic fractures, bone cysts, and osteoporosis. ◾GI problems (e.g., anorexia, nausea, vomiting, epigastric pain, constipation, weight loss) are common when serum calcium levels are high. Elevated serum gastrin levels are caused by hypercalcemia and lead to peptic ulcer disease. ◾Fatigue and lethargy may be present and worsen as the serum calcium levels increase. When serum calcium levels are greater than 12 mg/dL, the patient may have psychosis with mental confusion, which leads to coma and death if left untreated.
First-Line Disease-Modifying Antirheumatic Drugs.
◾Methotrexate (MTX) (Rheumatrex), an immunosuppressive medication, in a low, once-a-week dose (generally 25 mg or less per week orally) is the mainstay of therapy for RA because it is effective and relatively inexpensive ◾Leflunomide (Arava), is a slowacting immune-modulating medication that helps diminish inflammatory symptoms of joint swelling and stiffness and improves mobility. The drug is generally prescribed as a loading dose of 100 mg orally daily for 3 days followed by 20 mg orally daily thereafter. Inform the patient that Arava takes 4 to 6 weeks and sometimes up to 3 months before maximum benefit is realized. -Arava is a potent medication that is generally tolerated, but side effects of hair loss, diarrhea, decreased WBCs and platelets, or increased liver enzymes have been reported. Teach pt to report changes. Remind them to avoid alcohol. -Arava can cause birth defects, and therefore recommend strict birth control to women of childbearing age. Tell patients to contact the health care provider immediately if pregnancy occurs while taking the drug. Cholestyramine (Questran) is available to help block the drug's action. ◾hydroxychloroquine (Plaquenil). This drug slows the progression of mild rheumatoid disease before it worsens. It is an antimalarial drug that helps decrease joint and muscle pain. Patients generally tolerate Plaquenil quite well. In a few cases, mild stomach discomfort, light-headedness, or headache has been reported. The most serious adverse effect of Plaquenil is retinal damage. Teach patients to report blurred vision or headache. Eye examination done before taking the drug and every 6 months to detect changes in the cornea, lens, or retina. If this rare complication occurs, the health care provider discontinues the drug
What is Myasthenia gravis (MG)?
◾Myasthenia gravis (MG) is an acquired autoimmune disease characterized by muscle weakness. There are two types of MG: ocular andgeneralized. About two thirds of patients initially present with reports about vision that arise from disturbances of the ocular muscles. MG may take many forms—from mild disturbances of the cranial and peripheral motor neurons to a rapidly developing, generalized weakness that may lead to death from respiratory failure. MG can present at any age, and the incidence is slightly higher among men. It is a progressive disease. ◾MG is caused by distorted acetylcholine receptors (AChRs) in the muscle motor end plate membranes. Antibodies are attached to the AChRs. As a result, nerve impulses are reduced at the neuromuscular junction; nerve impulses do not result in muscle contraction.
Pharmacological Therapy for Early Rheumatoid Arthritis
◾NSAIDs. COX-2 medications block the enzyme involved in inflammation while leaving intact the enzyme involved in protecting the stomach lining. It was once thought that celecoxib (Celebrex), a COX-2 inhibiting NSAID, should be given rather than the older NSAIDs like ibuprofen. However, all COX-2 inhibiting drugs have recently been associated with cardiovascular disease, such as myocardial infarction, and some have been taken off the market. The risk for GI bleeding is also high in patients taking Celebrex, and the drug cannot be given to those who have had recent open heart surgery. To decrease GI problems, the NSAID may be given with an H2-blocking agent, such as ranitidine (Zantac) or misoprostol (Cytotec). ◾Methotrexate. Methotrexate is currently the standard treatment of RA because of its success in preventing both joint destruction and long-term disability.Methotrexate (MTX) (Rheumatrex), an immunosuppressive medication, in a low, once-a-week dose (generally 25 mg or less per week orally) is the mainstay of therapy for RA because it is effective and relatively inexpensive. It is a slow-acting drug, taking 4 to 6 weeks to begin to control joint inflammation. Methotrexate is often given in combination with biologic therapies because the combination may be more effective than either drug alone. Monitor patients for potential adverse effects, such as decreasing WBCs and platelets (as a result of bone marrow suppression) or elevations in liver enzymes or serum creatinine. Patients taking MTX are at risk for infection. Remind patients to avoid alcoholic beverages while taking MTX to prevent liver toxicity. Teach to observe for toxic effects, which include mouth sores and acute dyspnea from pneumonitis. Rarely, lymph node tumor (lymphoma) has been associated in those who have RA and are taking MTX. Folic acid, one of the B vitamins, is often given to those who are taking MTX to help decrease some of the drug's side effects. Pregnancy is not recommended while taking methotrexate because birth defects are possible. Strict birth control is recommended for childbearing women who are in need of MTX to control their RA ◾Analgesics. Additional analgesia may be prescribed for periods of extreme pain.
Biological Response Modifiers for Rheumatoid Arthritis
◾Newest classes of DMARDs. ◾Most BRMs neutralize the biologic activity of tumor necrosis factor-alpha (TNFA) by inhibiting its binding with TNF receptors. All these drugs are extremely expensive at this time, and insurance companies may not completely pay for their use. ◾Teach patients receiving any one of the BRMs that they are at a high risk for developing infection. Remind patients with multiple sclerosis (MS), tuberculosis (TB), or a positive TB test that they should not receive TNF inhibitors because they make patients susceptible to flare-ups of these diseases. ◾Etanercept (Enbrel) is given subcutaneously as 25 mg twice weekly for most patients. Immunosuppression with medications such as methotrexate is generally tried before using Enbrel or other biological response modifiers. Most patients tolerate Enbrel or Enbrel and methotrexate together; however, laboratory monitoring is important. Combination therapy requires CBC, serum creatinine, and a liver panel to be drawn regularly, generally every 4 to 8 weeks. Teach the patient or family member how to self-administer Enbrel injections. -Injection site reaction and systemic infection (especially respiratory) are possible adverse effects. Ice and hydrocortisone 1% cream can be used if a red, itchy rash at the injection site develops. ◾Infliximab (Remicade), first approved to treat Crohn's disease, is given in a single IV infusion over several hours. The initial dose generally used for RA is 3 mg/kg of body weight. The drug dosage is repeated at weeks 2 and 6. After these first three infusions, a maintenance dose of 3 mg/kg of body weight is given every 8 weeks, depending on the response of the patient. For patients who do not respond to the first three infusions, the drug dosage may be increased up to 10 mg/kg of body weight given at 4- week intervals. -Patients typically take methotrexate before starting Remicade and continue on combination therapy. Teach the patient to report and observe for symptoms of Remicade infusion reaction: chest discomfort, tachycardia, shortness of breath, or light-headedness. If any of these symptoms are reported, decrease the IV rate or discontinue it! Acetaminophen and Benadryl are medications often given before the start of Remicade and are often used at the time of reported infusion reaction. Those who experience serious adverse effects, such as hypertension or anaphylaxis, require permanent discontinuation of the drug. ◾Adalimumab (Humira) is the first fully human TNFA inhibitor and is given by subcutaneous injection. Symptoms of inflammatory arthritis tend to decrease with the use of Humira, including less joint swelling, less stiffness, and better mobility. Injection site reactions and adverse effects similar to the other TNFA inhibitors have been reported. Careful monitoring, especially with combination therapy of Humira and methotrexate or other drug that affects the body's immunity, is important and similar to combination therapy with other BRMs. ◾Anakinra (Kineret) is another biological response modifier. Instead of affecting tumor necrosis factor-alpha (TNFA), however, it works to inhibit a different protein signal of the immune system called interleukin-1 (IL-1). IL-1 is also a pro-inflammatory protein that signals the immune system to increase inflammation. It is thought that IL-1 is a weaker protein than TNF, but having an alternative drug that targets a different receptor site is helpful when a patient cannot take other biologics. Those who have multiple sclerosis or tuberculosis cannot take TNF inhibitors, but Kineret can be used with this population. Injection site reactions occur more often with Kineret compared with other BRMs. Ice and hydrocortisone 1% cream are recommended. Remind patients to rotate injection sites. Kineret is administered with a simple jet for self-administration. ◾Abatacept (Orencia) and rituximab (Rituxan, MabThera) require IV infusions every 2 weeks to start and then may be more spread out, depending on the drug. Like the results of the other BRMs, patients usually report feeling a benefit from these drugs in 2 weeks, but it may take months for the maximum benefit to be seen. ◾Golimumab (Simponi) is the first biologic that is administered only once each month for both RA and psoriatic arthritis. Teach patients that this drug has a black box warning for serious infections that may lead to hospitalization or death from opportunistic pathogens ◾Tocilizumab (Actemra) is given when the patient cannot tolerate other drugs. Tocilizumab is different from other biologics because it is the first humanized interleukin-6 (IL-6) receptor-inhibiting monoclonal antibody that is available for patients with RA. It can be used alone or in combination with other DMARDs. Teach patients about adverse drug effects, including hypertension, GI distress, infection, and an increase in low-density lipoproteins (LDLs) and liver enzymes. Like for other biologics, teach the patient about the high risk of infection (e.g., tuberculosis) when taking Actemra. ◾One of the newest biologics is tofacitinib (Xeljanz), which has been approved for moderate to severe RA as monotherapy or in combination with methotrexate. This drug is a tyrosine kinase inhibitor (TKI). Tyrosine kinases usually facilitate cytokine-mediated (e.g., interleukin) signals that promote the inflammatory process. Teach patients that tofacitinib carries a black box warning alerting patients about its potential for serious opportunistic infections, tuberculosis, lymphoma, and other cancers.
Collaborative Care for myasthenia gravis
◾Occupational and physical therapists evaluate patients for assistive-adaptive devices. In collaboration with the nurse, they also teach the patient and family energy conservation techniques and ideas for making work and self-management easier after discharge from the hospital. Weakness of the speech and facial muscles often results in dysarthric (slurred) and nasal speech. In collaboration with the speech-language pathologist (SLP), determine the patient's ability to communicate. Instruct the patient to speak slowly while attempting to lip-read. Repeat what the patient says to check that it is correct. Questions that can be answered with "yes" or "no" or by gestures may be used along with other communication systems such as eye blinking, notebook and pencil, computer, handheld mobile devices, and picture, letter, or word boards. ◾The patient with myasthenia gravis (MG) may have difficulty maintaining an adequate intake of food and fluid because the muscles needed for chewing and swallowing become weakened and tire easily. In collaboration with the dietitian, occupational therapist, and speech language pathologist, evaluate the patient's nutritional status and his or her ability to receive adequate oral nutrition. High-calorie snacks are often well tolerated. Monitor the effectiveness of the nutrition program by recording the patient's calorie counts, intake and output, serum prealbumin levels, and daily weights If cannot swallow, a feeding tube may be used. ◾The patient's inability to completely close the eyes may lead to corneal abrasions and further decrease vision and comfort. During the day, apply artificial tears to keep the corneas moist and free from abrasion. A lubricant gel and shield may be applied to the eyes at bedtime to provide more extensive coverage. To help relieve diplopia, cover the eyes with a patch for 2 to 3 hours at a time, one eye at a time. At times, patients tape their eyes shut at night.
What is Plasmapheresis?
◾Plasmapheresis is a method by which antibodies are removed from the plasma to decrease symptoms. This is used as short-term management of an exacerbation of MG. Six exchanges occur over a 2-week period with follow-up exchanges weekly or monthly as needed, usually as an ambulatory care patient.
Diagnostic Testing for Hyperparathyroidism
◾Serum PTH, calcium, and phosphorus levels and urine cyclic adenosine monophosphate (cAMP) levels are the laboratory tests used to detect hyperparathyroidism. X-rays may show kidney stones, calcium deposits, and bone lesions. Loss of bone density occurs in the patient with chronic hyperparathyroidism. Other diagnostic tests include arteriography, CT scans, venous sampling of the thyroid for blood PTH levels, and ultrasonography. Explain the procedures and care for the patient undergoing diagnostic tests.
Complementary and alternative medicine (CAM) therapies for rheumatoid arthritis
◾Some patients may have pain relief from hypnosis, acupuncture, imagery, music therapy, or other technique. Stress management is also popular as a pain relief intervention. ◾Adequate nutrition is an important part of the management of RA. Obesity should be avoided or treated if present. The inflammatory state may place a greater burden on the metabolism of some essential nutrients. This catabolic state may be related to increased cytokine production, specifically tumor necrosis factor. According to the National Center for Complementary and Alternative Medicine, some supplements have been found to help decrease inflammation and include: • Cold water fish or fish oil capsules containing omega-3 fatty acids at 2.5 to 5 g daily (should not be taken if the patient is taking anticoagulant therapy) • Gamma-linolenic acid (GLA), an omega-6 fatty acid found in the oils of certain plant seeds, such as primrose and black currant ◾Other complementary and alternative medicine (CAM) therapies are safe and have been scientifically proven to be effective to help control RA pain for most people. Examples include mind-body therapies, such as relaxation techniques, imagery, and spiritual practices
Surgical Management for hyperparathyrodism
◾Surgical management is the treatment of choice for patients with hyperparathyroidism. For those who are not candidates for surgery, medication can help control the problems. Priority nursing interventions focus on monitoring and preventing injury. ◾Surgical management of hyperparathyroidism is a parathyroidectomy. Before surgery the patient is stabilized and calcium levels are decreased to near normal. The operative procedure can be performed as minimally invasive surgery, mini-incision surgery, or with a traditional transverse incision in the lower neck. All four parathyroid glands are examined for enlargement. If a tumor is present on one side but the other side is normal, the surgeon removes the glands containing tumor and leaves the remaining glands on the opposite side intact. If all four glands are diseased, they are all removed. Nursing care before and after surgical removal of the parathyroid glands is the same as that for thyroidectomy. The remaining glands, which may have atrophied as a result of PTH overproduction, require several days to several weeks to return to normal function. A hypocalcemic crisis can occur during this critical period, and the serum calcium level is assessed frequently after surgery. Check serum alcium levels whenever they are drawn until calcium levels stabilize. Monitor for manifestations of hypocalcemia, such as tingling and twitching in the extremities and face. Check for Trousseau's and Chvostek's signs, either of which indicates potential tetany. The recurrent laryngeal nerve can be damaged. Assess the patient for changes in voice patterns and hoarseness. When hyperparathyroidism is due to hyperplasia (tissue overgrowth), three glands plus half of the fourth gland are usually removed. If all four glands are removed, a small portion of a gland may be implanted in the forearm, where it produces PTH and maintains calcium homeostasis. If all these maneuvers fail, the patient will need lifelong treatment with calcium and vitamin D because the resulting hypoparathyroidism is permanent.
What is hyperparathyroidism?
◾The parathyroid glands maintain calcium and phosphate balance. Serum calcium level is normally maintained within a narrow range. Increased levels of parathyroid hormone (PTH) act directly on the kidney, causing increased kidney reabsorption of calcium and increased phosphorus excretion. ◾In hyperparathyroidism, these processes cause hypercalcemia (excessive calcium) and hypophosphatemia (inadequate blood phosphorus level). In bone, excessive PTH levels increase bone resorption (bone loss of calcium) by decreasing osteoblastic (bone production) activity and increasing osteoclastic (bone destruction) activity. This process releases calcium and phosphorus into the blood and reduces bone density. With chronic calcium excess and hypercalcemia, calcium is deposited in soft tissues. Exact triggering mechanisms are unknown, primary hyperparathyroidism results when one or more parathyroid glands do not respond to the normal feedback of serum calcium levels. The most common cause is a benign tumor in one parathyroid gland. Others include Vit D deficiency, Chronic kidney disease with hypocalcemia, neck tumor or radiation