Hyperparathyroidism NCLEX review notes for students who are prepping to take the NCLEX exam. The endocrine system is made-up of many disorders, such as hypoparathyroidism and hyperparathyroidism. As a student prepping for NCLEX, it is very important you know the differences between these two conditions.
As the nurse taking care of the patient with hyperparathyroidism it is important you understand the signs and symptoms, pathophysiology, causes, nursing interventions, and medical treatments.
Don’t forget to take the quiz on hypoparathyroidism vs hyperparathyroidism.
In this NCLEX review, you will learn the following:
- Pathophysiology of the parathyroid gland
Signs and symptoms of hyperparathyroidism
Causes of hyperparathyroidism
Medications for hyperparathyroidism
Lecture on Hyperparathyroidism
Normal calcium: 8.6 to 10.0 mg/dL (>10.0 is hypercalcemia)
Normal phosphate: 2.7 to 4.5 mg/dL (<2.7 hypophosphatemia)
Causes of Hyperparathyroidism
Primary Hyperparathyroidism: There is a problem with the parathyroid gland itself.
- Noncancerous growths: Adenoma (most common)
- Hyperplasia of the glands (enlargement)
- Cancerous growths
Secondary Hyperparathyroidism: A disease is causing the parathyroid gland to mess up.
- Hypocalcemia (very severe): causes the parathyroid to become overworked in trying to keep the calcium levels up.
- Vitamin D deficiency: low absorption of calcium (remember vitamin d helps with calcium absorption ) so the parathyroid gland overworks to produce PTH (with the intention of increasing calcium levels but can’t increase them).
- Chronic renal failure: kidneys aren’t able to activate the vitamin D so the small intestines can’t absorb calcium and the kidneys don’t absorb calcium (most common cause)
Signs and Symptoms of Hyperparathyroidism
Main reason for signs and symptoms is due to the high calcium levels: remember calcium plays an important role in bone health, muscle contraction, and nerve function….too much calcium causes the bones to become fragile (because calcium has left the bones), muscles and nerve function will slow down as well.
- Bones fractures (osteoporosis): PTH causing excessive stimulation of bone osteoclasts which causes major bone resorption where calcium leaks into the blood in excessive amounts and it causes the bones to become very fragile
- Calculi formation: increased calcium levels causes the kidneys to reabsorb calcium which can form stones (plus dehydration increases this risk).
- Constipation: high calcium levels slow down the GI system
- GI problems: nausea, vomiting, epigastric pain: (from calcium effects of causing increased GI acid)
- Frequent urination: high amounts of calcium cause the kidneys to work harder and put out more urine
- EKG changes: short QT interval
Nursing Interventions for Hyperparathyroidism
- Monitor vitals, EKG, renal stones (strain urine), calcium and phosphate levels
- Monitor intake and output and fluid status (encourage fluids….patients are risk for dehydration and kidney stone formation, however watch fluid status on patients with congestive heart failure and renal failure.
- Diet low is calcium and high in phosphate…watch phosphate in renal patients
Treatments and Medications (depend on the cause):
- Parathyroidectomy: main treatment for primary hyperparathyroidism
- Monitor respiratory status due to nature of surgery, Semi-Fowler’s position, trach kit, oxygen, and suction at bedside for emergency
- Watch for low calcium levels: tingling or numbness or excessive twitching in extremities or face, tetany, positive Trousseau’s or Chvostek’s Sign
- Monitor patient for laryngeal nerve damage: voice changes (hoarseness), problems swallowing or speaking
Medication Goals: to decrease parathyroid and calcium levels and keep patient hydrated
- IV fluids: normal saline for hydration
- Calcimimetics: “Senispar” decreases PTH, calcium, and phosphate levels (usually prescribed for patients with secondary hyperparathyroidism with CKD…patients with renal failure struggle with high phosphate levels so this medication helps with this as well)
- It mimics the role of calcium in the blood and deceives the parathyroid gland into thinking there is enough calcium in the blood so it will quit secreting PTH. Note: Take with food or right after meal….side effects: GI issues and hypocalcemia
- Calcitonin (injection or nasal sprays): naturally produced by the thyroid gland and helps lower calcium levels (suppresses osteoclast activity of the bones (helps protect bones) and increases the kidneys excretion of calcium).
- Loop diuretics “Lasix”: decreases calcium levels by inhibiting calcium reabsorption in the renal tubules (watch potassium levels)
- Bisphosphonates: “Pamidronate (Aredia) or Alendronate (Fosamax)” helps protect bones from losing calcium by slowing down osteoclasts (which break down bones) and allow osteoblasts to work (to help build bones)
- Patient education for Fosmax: take on empty stomach, by itself, with a full glass of water, and sit-up right for 30 minutes after taking (very hard on the esophagus and stomach and can cause ulcers)…wait 30 minutes before taking antacids, vitamins.
You may be interested in more NCLEX Reviews.
- Medication Guide Fosamax Tablets. 1st ed. Food and Drug Administration, 2013. Web. 26 July 2016.
- “Primary Hyperparathyroidism | NIDDK”. National Institute of Diabetes and Digestive and Kidney Diseases. N.p., 2012. Web. 26 July. 2016.