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Osteitis fibrosis cystica, abbreviated OFC, also known as osteitis fibrosaosteodystrophia fibrosaand von Recklinghausen’s disease of bone not to be confused with von Recklinghausen’s disease, neurofibromatosis type Iis caused by hyperparathyroidismwhich is a surplus of parathyroid hormone from over-active parathyroid glands.
This surplus stimulates the activity of osteoclastscells that break down bone, in a process known as osteoclastic bone resorption. The gliter can be triggered by a parathyroid adenomahereditary factors, parathyroid carcinomaor renal osteodystrophy. Osteoclastic bone resorption releases minerals, including calciumfrom the bone into the bloodstream, causing both elevated blood calcium levels, and the structural changes which weaken ogiter bone. The symptoms of the disease are the consequences of both the general softening of the bones and the excess calcium in the blood, and include bone fractureskidney stonesnauseamoth-eaten appearance in the bones, appetite loss, and weight loss.
Osteitis fibrosa cystica – Wikipedia
First described in the nineteenth century, OFC is currently detected through a combination of blood testingX-raysand tissue sampling. Beforearound half of those diagnosed with hyperparathyroidism in the United States saw it progress to OFC, but with early identification techniques and improved treatment methods, instances of OFC in developed countries are increasingly rare.
Where treatment is required, it normally involves addressing the underlying hyperparathyroidism before commencing long-term treatment for OFC—depending on its cause and severity, this can range from hydration and exercise to surgical intervention.
Osteitis fibrosa cystica is defined as the classic skeletal manifestation of advanced hyperparathyroidism. The major symptoms of OFC are bone pain or tenderness, bone fracturesand skeletal deformities such as bowing of the bones.
The underlying hyperparathyroidism may cause kidney stonesnauseaconstipationfatigue and weakness. X-rays may indicate thin bones, fractures, bowing, and cysts.
Fractures are most commonly localized in the arms, legs, or spine. The addition of weight loss, appetite lossvomiting, polyuriaand polydipsia to the aforementioned symptoms may indicate that OFC is the result of parathyroid carcinoma.
Symptoms are also often more severe. Osteitis fibrosa cystica is the result of unchecked hyperparathyroidism, or the overactivity of the parathyroid glandswhich results in an overproduction of parathyroid hormone PTH.
PTH causes the release of calcium from the bones into the blood, and the reabsorption of calcium in the kidney. Thus, excess PTH in hyperparathyroidism causes elevated blood calcium levels, or hypercalcemia.
The vast majority of cases of hyperparathyroidism are the result of the random formation of benign, but metabolically active, parathyroid adenoma swellings. Approximately 1 in 10 documented cases of hyperparathyroidism are a result of hereditary factors. Disorders such as familial hyperparathyroidism, multiple endocrine neoplasia type 1 MEN Type 1 and hyperparathyroidism-jaw tumor syndrome can, if left unchecked, result in OFC. Major mutations which can lead to hyperparathyroidism generally involve the parathyroid hormone receptor, G proteinsor adenylate cyclase.
Parathyroid carcinoma cancer of the parathyroid gland is the rarest cause of OFC, accounting for about 0. OFC onset by parathyroid carcinoma is difficult to diagnose. OFC is a common presentation of renal osteodystrophywhich is a term used to refer to the skeletal complications of end stage renal disease ESRD. When calcitriol levels decrease, parathyroid hormone levels increase, halting the storage of calcium, and instead triggering its removal from the bones.
The effects of OFC on bone are largely dependent on the duration of the disease and the level of parathyroid hormone PTH produced. It activates the parathyroid-hormone related protein receptor located on osteoblasts and osteocytesboth of which are responsible for the building and calcification of bone.
Abnormalities affecting the parathyroid glands cause a surplus of PTH, which, in turn, increases the activity and frequency of osteoblasts and osteocytes. Generally, the first bones to be affected are the fingers, facial bones, ribs, and pelvis. OFC may be diagnosed using a variety of techniques. Muscles in patients afflicted with OFC can either appear unaffected or “bulked up.
Blood tests on patients with OFC generally show high levels of calcium normal levels are considered to range between 8. X-rays may also be used to diagnose the disease.
Usually, these X-rays will show extremely thin bones, which are often bowed or fractured. However, such symptoms are also associated with other bone diseases, such as osteopenia or osteoporosis.
Cysts may be lined by osteoclasts and sometimes blood pigments, which lend to the notion of “brown tumors. Fine needle aspiration FNA can be goifer to biopsy bone lesionsonce found on an X-ray or other scan. Such tests can be vital in diagnosis and can also prevent unnecessary treatment and invasive surgery. The brown tumors commonly associated with OFC display many of the same characteristics of osteoclasts.
Osteitis fibrosa cystica
Nucleoli also tend to be smaller than average. Medical management of OFC consists of Vitamin D treatment, generally alfacalcidol or calcitrioldelivered intravenously. Studies have shown that in giter of OFC caused by either end-stage goiyer disease or primary hyperparathyoidism, this method is successful not only in treating underlying hyperparathyoidism, but also in causing the regression of brown tumors and other symptoms of OFC. In especially severe cases of OFC, parathyroidectomy, or the full removal of the parathyroid glands, is the chosen route of treatment.
Parathyroidectomy has been shown to result askel the reversal of bone resorption and the complete regression of brown tumors. Bone transplants have proven successful in filling the lesions caused by OFC. A report showed that in 8 out of 11 instances where cavities caused by OFC were filled with transplanted bone, the lesion healed and the transplanted bone blended rapidly and seamlessly with the original asoep.
Almost all who undergo parathyroidectomy experience increased bone density and repair of the skeleton within goiteer.
Additionally, patients with OFC who have undergone parathyroidectomy begin to show regression of brown tumors within six months. This results from a combination of suppressed parathyroid glands due to prolonged hypercalcaemiaas well as the need for calcium and phosphate in the mineralization of new bone. Thirty percent of patients with OFC-like tumors caused by metastatic parathyroid carcinoma who undergo surgery see a local recurrence of symptoms.
The post-surgical survival rate hovers around seven years, while patients who do not undergo surgery have a survival rate of around five years. Osteitis fibrosa cystica has long been a rare disease. The hospitalization rate for hyperparathyroidism goitet the United States in was 8.
Rates of OFC increase alongside cases of unchecked primary hyperparathyroidism. In developing countries, such as India, rates of disease as well as case reports often mirror those published in past decades in the developed world.
This mutation also tends to affect younger individuals. The condition was first described by Gerhard Engel in and Friedrich Daniel von Recklinghausen inthough William Hunterwho died inis credited with finding the first example of axkep disease.
The discovery and subsequent description of the parathyroid glands is credited to Ivar Sandstrom, though his publication, On a New Gland in Man and Several Mammals-Glandulae Parathyroideaereceived little attention.
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Gustaf Retzius and Eugene Gley compounded his research, the latter credited with the discovery of the function of the parathyroid glands. The patient’s symptoms disappeared, only to return in approximately six years as a result of renal stones that were diagnosed only after the patient had died. Inblood tests on a female patient suffering from renal stone-based OFC revealed extremely high blood calcium levels. Fuller Albright diagnosed and treated the woman, who suffered from a large tumor of the neck as well as renal stones.
The first published literature to describe a brown tumor which was linked to OFC was published inthough clinical reports from before do draw a correlation between the disease and tumors previous to the publication. The advent of the multichannel autoanalyzer in the s and 70s led to an increase in early diagnosis of primary hyperparathyroidism.
This increase led to a sharp decline in the prolonged manifestation of the disease, leading to a drop in the number of cases of OFC due to the early detection of hyperparathyroidism. From Wikipedia, the free encyclopedia. Osteitis fibrosa cystica Osteitis fibrosa cystica of the tibia. Arrows point to the brown tumors which are typically present in bones of people with OFC. Endocrine, nutritional, and metabolic diseases”. Archived from the original on National Library of Medicine.
Journal of the Royal Society of Axkep. German National Goiterr Institute. Proceedings of the National Academy of Sciences. University of Pittsburgh School of Medicine. National Institute of Health.
Department of Health and Human Services. Archived PDF from the original on A Complication of Parathyroid Carcinoma”. The Western Journal of Medicine. Journal of Clinical Pathology.
Clinical Orthopaedics and Related Research. New England Journal of Medicine. Journal of Bone and Mineral Research. British Journal of Surgery.
Canadian Medical Association Journal. An early historical survey”. Annals of the Royal College of Surgeons of England. A case report and review of the literature”. Gotier of Medical Case Reports. Diseases of the asiep system E00—E35— Hypoglycemia beta cell Hyperinsulinism G cell Zollinger—Ellison syndrome. Iodine deficiency Cretinism Congenital hypothyroidism Myxedema Myxedema coma Euthyroid sick syndrome.
Hyperthyroxinemia Thyroid hormone resistance Familial dysalbuminemic hyperthyroxinemia Hashitoxicosis Thyrotoxicosis factitia Graves’ disease Thyroid storm. Endemic goitre Toxic nodular goitre Toxic multinodular goiter Thyroid nodule.
Primary Secondary Tertiary Osteitis fibrosa cystica. Cushing’s syndrome Pseudo-Cushing’s syndrome sex hormones: Polycystic ovary syndrome Premature ovarian failure testicular: