The Parathyroid Glands 2 PDF

parathyroid glands DR. HAYAT MOHAMED  learning objectives 1. Anatomy and physiology of parathyroid glands 2. Disorders of the parathyroid glands 3. Causes of these Disorders 4. Multisystem effects of these disorders 5. Diagnostics OF these Disorders 6. Management OF these Disorders...

parathyroid glands DR. HAYAT MOHAMED  learning objectives 1. Anatomy and physiology of parathyroid glands 2. Disorders of the parathyroid glands 3. Causes of these Disorders 4. Multisystem effects of these disorders 5. Diagnostics OF these Disorders 6. Management OF these Disorders  Anatomy and physiology of parathyroid glands Functions of parathyroid glands  Its action of activating vitamin D in the kidneys.  It increases the resorption of calcium by the kidneys and the excretion of phosphate (more than is obtained from bones). Therefore, the overall effect of PTH is to raise the blood calcium level and lower the blood phosphate level.  Calcium ion delivery through the blood is essential for normal excitability of neurons and muscle cells and for the process of blood clotting.  The average PTH level is 8–51 pg/mL. Normal total plasma calcium level ranges from 8.5 to 10.2 mg/dL (2.12 mmol/L to 2.55 mmol/L).[  PTH/Calcium Homeostasis Low circulating serum calcium concentrations stimulate the parathyroid glands to secrete PTH, which mobilizes calcium from bones by osteoclastic stimulation. PTH also stimulates the kidneys to reabsorb calcium and to convert 25- hydroxyvitamin D3 (produced in the liver) to the active form, 1,25- Dihydroxyvitamin D3, which stimulates GI  Hyperparathyroidism Definition : Hyperparathyroidism is characterized by a greater-than-normal secretion of parathyroid hormone (PTH), one of the two major hormones that modulates calcium and phosphate homeostasis; the hormone Pathophysiology The following pathophysiological changes:  Increased resorption of calcium and activation of vitamin D and excretion of phosphate by the kidneys, which increase the risk of hypercalcaemia and hypophosphatemia.  Increased bicarbonate excretion and decreased acid excretion by the kidneys, which increases the risk of metabolic acidosis and hypokalaemia.  Increased release of calcium and phosphorus by bones, with resultant bone decalcification.  Increased deposits of calcium in soft tissues and the formation of renal calculi. Types of hyperparathyroidism: The three types of hyperparathyroidism are as follows:  In primary hyperparathyroidism, one or more of the parathyroid glands enlarges (usually because of an adenoma or gland hyperplasia), causing inappropriately high PTH secretion in relation to serum calcium concentration  In secondary hyperparathyroidism, the parathyroid gland responds appropriately to a reduced level of extracellular calcium; PTH concentrations rise and calcium is mobilized by increasing intestinal absorption  Tertiary hyperparathyroidism results from hyperplasia of the parathyroid glands and a loss of response to serum calcium levels. This disorder is most often seen in people with chronic renal failure. Etiology: Adenoma Chronic renal failure  Decreased intestinal absorption or insufficient consumption of vitamin D or calcium Genetic disorders Complications may include Osteoporosis, renal calculi development, cardiac arrhythmias, cholelithiasis, hypertension, and heart failure. Hypercalcemic crisis can occur can result in life- threatening neurological, cardiovascular, and renal complications Signs and symptoms Musculoskeletal system : bone pain (back, joints and shins) pathological fractures (women), muscle weakness and muscle atrophy Renal effects: renal calculi , Polyuria and Polydipsia Gastrointestinal system: abdominal pain, peptic ulcers, pancreatitis , nausea and constipation Cardiovascular system: arrhythmias, hypertension, Central nervous system: paraesthesias, depression and psychosis Metabolic effects: acidosis and weight loss Diagnosis Laboratory findings show that Elevated serum PTH and calcium levels Elevated urine calcium levels Serum phosphorus levels are decreased X-rays show Diffuse bone demineralization  Bone cysts Ultrasonography, CT scan, and MRI Help identify enlargement and abnormally functioning areas Needle biopsy : Evaluates the function of the parathyroids Treatment The recommended treatment for primary hyperthyroidism is the surgical removal of the abnormal parathyroid tissue For secondary disease, the goal is to correct the underlying cause of parathyroid hypertrophy Other treatments include hydration therapy and dialysis for renal failure Medications include bisphosphonates such as Alendronate to reduce bone turnover and maintain bone density Calcimimetics to decrease calcium and PTH levels. Diuretics to treat hypercalcemia in patients Nursing Process for the Patient with Hyperparathyroidism Data collection. assess the patient for symptoms related to hypercalcemia, including muscle weakness, lethargy, bone pain, anorexia, nausea, vomiting, behavioral changes, and renal insufficiency. Monitor serum calcium levels as ordered. Nursing diagnoses, planning, and implementation.  Risk for injury usually takes priority.  Risk for Injury (Fracture, Complications of Hypercalcemia) Related to Calcium Imbalance  Expected outcome: The patient will remain free from injury Nursing intervention.  Monitor patient for and report signs or symptoms of calcium imbalance.  Encourage oral fluids to prevent dehydration and kidney stones and help excrete calcium.  Encourage strengthening and weight-bearing exercises to help keep calcium in the bones.  Provide a safe environment for ambulation; assist the patient with ambulation if needed.  Encourage smoking cessation.  Teach patient symptoms to report and use of long-term medications  Evaluation. If the plan is effective, symptoms of hypercalcemia will be recognized and reported quickly, and complications and injury will be prevented. Nursing interventions  Teach the patient and family about the disease and its treatment; prepare the patient for surgery if indicated, and provide emotional support  Keep the patient hydrated as tolerated  Monitor the patient’s serum potassium, calcium, phosphate, and magnesium levels  Postoperatively, monitor the patient’s airway patency, and keep a tracheotomy tray at the patient’s bedside  Advance the patient’s activity level and diet as tolerated  Observe for signs of hypocalcemia (numbness and tingling around the mouth and in the extremities, and spasms) (after surgery)  Before discharge, teach the patient the signs and symptoms of complications and the importance of follow-up care– including laboratory testing–to evaluate the effectiveness of therapy.  Hypoparathyroidism Definition : Hypoparathyroidism occurs when the parathyroid glands don’t secrete enough PTH or when there’s decreased PTH action. It can be acute or chronic and is classified as idiopathic, acquired, or reversible Pathophysiology A decrease in PTH causes a decrease in bone resorption of calcium, a decrease in calcium absorption by the GI tract, and decreased resorption in the kidneys. This means that calcium stays in the bones instead of being moved into the blood, and more calcium is excreted from the body. The result is a decreased serum calcium level, called hypocalcemia. As calcium levels fall, phosphate levels rise. Etiology: Heredity The accidental removal of the parathyroid glands during thyroidectomy or other neck surgeries. Remove of the parathyroid glands for hyperparathyroidism or cancer. Hypomagnesemia , which impairs secretion of PTH. Hypomagnesemia can occur with chronic alcoholism or certain nutritional problems. Autoimmune disorders, radiation to the neck, neoplasms, and trauma. Atrophy of the parathyroid glands of unknown cause. Signs and symptoms  Musculoskeletal system muscle spasms, facial grimacing carpopedal spasms and tetany or convulsions  Integumentary system: brittle nails, hair loss and dry, scaly skin  Gastrointestinal system: abdominal cramps & malabsorption  Cardiovascular system: arrhythmias  Central nervous system: paraesthesias (lips, hands, feet) , mood disorders (irritability, depression, anxiety), hyperactive reflexes psychosis & increased intracranial pressure Signs and symptoms  Hypocalcemia causes irritability of the neuromuscular system and contributes to the chief symptom of hypoparathyroidism—tetany.  Tetany is a general muscle hypertonia, with tremor and spasmodic or uncoordinated contractions occurring with or without efforts to make voluntary movements. The signs Symptoms of latent tetany are:  Numbness, tingling, and cramps in the extremities  Stiffness in the hands and feet.  Bronchospasm, laryngeal spasm, carpopedal spasm  Dysphagia, photophobia, cardiac dysrhythmias  Anxiety, irritability, depression, and delirium.  ECG changes and hypotension also may occur.  Seizures. Diagnosis and treatment Laboratory studies show that a. Decreased serum calcium and PTH levels b. Increased serum phosphate.  An ECG is done to evaluate cardiac function. X- ray(radiographs) show bone changes. (bone density and bone malformation) Calcification is detected on x-rays of the subcutaneous or paraspinal basal ganglia of the brain. Therapeutic Measures Acute cases of hypoparathyroidism are treated with intravenous calcium gluconate. Long-term treatment includes a High-calcium diet ,with oral calcium and vitamin D supplements. Thiazide diuretics may also be used because they reduce the amount of calcium excreted in the urine. Magnesium is given if hypomagnesemia is present. Complications include : Heart failure, cataracts, tetany, bone deformities, laryngospasm, and vocal cord paralysis Nursing diagnoses, planning, and implementation  Risk for Injury Related to Hypocalcemia and Tetany  Expected outcome: The patient will remain free from injury; signs of tetany will be recognized and treated quickly. Nursing intervention : Monitor patient for signs of tetany, and report immediately to RN or physician so treatment can begin quickly. Make sure a tracheostomy set, endotracheal tube, and intravenous calcium are available for emergency use if laryngospasm occurs. Diet high in calcium and low in phosphorus is prescribed Teach the patient about the importance of follow-up laboratory testing. The patient needs to understand self-care for follow-up at home. Evaluation.  Injury is prevented through early recognition and reporting of signs and symptoms of tetany.  The patient should be able to describe correct treatment and self- care measures for home. Nursing interventions  Teach the patient and family about the disease and its treatment, and provide emotional support  Obtain specimens to test for serum electrolyte levels, especially serum calcium and phosphorus levels  Check the patient’s deep tendon reflexes  Keep calcium gluconate at the patient’s bedside, and prepare to administer in an emergency  If the patient underwent surgery, monitor his airway, and keep a tracheotomy tray at his bedside  Advance the patient’s activity and diet as tolerated; teach him and his family how to follow a high calcium, low- phosphate diet  Before discharge, teach the patient and his family the signs and symptoms of complications and the importance of follow-up care—including laboratory testing—to evaluate the effectiveness of therapy