Week 11: Chp 43: Hyperparathyroidism Flashcards
What accounts for primary hyperparathyroidism?
parathyroid adenomas
Secondary hyperparathyroidism occurs from what?
hyperplasia of the parathyroid glands
-most observed with patients with chronic renal failure or chronic malabsorption of calcium
Hyperparathyroidism causes what?
causes hypercalcemia secondary to its actions on bone, kidneys, and the bowel
-the action of PTH on bone leads to osteoclastic (breakdown of bone) activity and bone demineralization, which causes pathological fractures and bone lesions
The action of PTH on bone leads to what?
Osteoclastic (breakdown of bone) activity and bone demineralization, which causes pathological fractures and bone lesions
-osteoclastic activity increases release of calcium from the bone and leads to loss of bone density; increased renal absorption of calcium leads to elevated serum calcium levels
What are osteoclasts?
large cells that secrete enzymes and acids to dissolve microscopic bits of bone, and then the minerals and amino acids are reabsorbed (resorption)
What does osteoclastic activity do?
increases release of calcium from the bone and leads to loss of done density
-increased renal absorption of calcium leads to elevated serum calcium levels
What does increased calcium levels in the urine filtrate cause?
hypercalciuria that increases the potential for calcium containing renal stones
-reabsorption of calcium in the bowel is also increased in hyperparathyroidism
Patients with what condition may develop secondary hyperparathyroidism?
chronic renal failure
-decreased serum calcium and inactivated vitamin D develop early in renal failure, and PTH secretion increases the response to the hypocalcemia; over time, parathyroid gland hyperplasia develops because of low calcium levels; hyperparathyroidism can be differentiated from other causes of hypercalcemia, such as elevated calcium secondary to malignancy, through intact PTH assays
Clinical Manifestations
some may be asymptomatic but can present with
- polyuria, anorexia, and constipation associated with elevated serum calcium levels that impact the kidneys and GI tract
- cardiac changes associated with elevated calcium levels include; a prolonged PR interval and a shortened QT interval due to the shortening of the ST segment
- may also develop abdominal pain because hypercalcemia leads to increased secretion of gastrin in the stomach and associated peptic ulcer disease
- other: lethargy, confusion, muscle weakness, fatigue, and generalized bone pain (secondary to bone demineralization caused by osteoclastic activity)
Treatment goal for hyperparathyroidism
lowering serum calcium levels
Treatment plan
- increase fluid intake is indicated to minimize potential renal injury secondary to elevated serum calcium, and in patients with mild disease, increased oral fluid intake may treat the disorder
- more severe cases of hypercalcemia require IV infusions of normal saline to protect against renal calculi
- patients taught to decrease consumption of calcium containing antacids and vitamin D
- Thiazide diuretics are to be avoided because thy increase reabsorption of calcium in the kidney
The nurse prioritizes which nursing diagnosis in the patient after partial parathyroidectomy?
high risk for ineffective airway clearance linked to hypocalcemia
Clinical Manifestations are linked to?
elevated serum calcium
- elevated ionized and serum calcium levels
- decreased serum phosphorus levels
- muscle weakness and atrophy
- low back pain
- increased incidence of pathological fractures
- prolonged PR interval
- shortened QT interval
- constipation, anorexia, and nausea and vomiting
- renal stones
Nursing DIagnoses
- acute pain r/t pressure in renal tubules secondary to development of calcium-based renal calculi
- high risk for injury: falls r/t bone demineralization and calcium resorption
Nursing Assessments
- serum calcium levels
- serum phosphorus levels
- cardiac monitoring
- acid-base status