Critical Care: Exam 2- PTH

What is parathyroid hormone (PTH)?

Parathyroid hormone is a hormone secreted by the parathyroid glands that primarily maintains normal serum calcium (Ca²⁺) levels.

What is the primary function of parathyroid hormone (PTH)?

To maintain normal serum calcium levels by increasing calcium in the bloodstream when calcium levels are too low.

How does parathyroid hormone (PTH) increase serum calcium levels?

PTH increases serum calcium by stimulating calcium release from bones, increasing calcium reabsorption in the kidneys, and activating vitamin D to increase calcium absorption from the gastrointestinal tract.

How does parathyroid hormone (PTH) affect calcium in the bones?

PTH stimulates bone resorption, which releases calcium from the bones into the bloodstream and increases serum calcium levels.

How does parathyroid hormone (PTH) affect calcium reabsorption in the kidneys?

PTH increases calcium reabsorption in the kidneys, allowing more calcium to return to the bloodstream instead of being excreted in the urine.

How does parathyroid hormone (PTH) affect phosphorus excretion in the kidneys?

PTH increases phosphorus excretion through the kidneys, causing more phosphorus to leave the body in the urine and generally decreasing serum phosphorus levels.

How does parathyroid hormone (PTH) affect vitamin D activation?

PTH stimulates the kidneys to activate vitamin D, which helps increase calcium absorption from the gastrointestinal tract.

How does activated vitamin D affect calcium levels?

Activated vitamin D increases calcium absorption from the gastrointestinal tract into the bloodstream.

How does PTH indirectly increase calcium absorption in the gastrointestinal tract?

PTH stimulates vitamin D activation in the kidneys, and activated vitamin D increases calcium absorption from the intestines into the bloodstream.

What is the overall effect of PTH on serum calcium and phosphorus levels?

PTH increases serum calcium and generally decreases serum phosphorus by increasing phosphorus excretion through the kidneys.

What is the difference between the effects of calcitonin and PTH on serum calcium?

Calcitonin lowers serum calcium, while PTH raises serum calcium.

What is the role of vitamin D in calcium regulation?

Activated vitamin D increases calcium absorption from the gastrointestinal tract into the bloodstream.

Which hormone raises serum calcium levels, calcitonin or PTH?

PTH raises serum calcium levels.

Which hormone lowers serum calcium levels, calcitonin or PTH?

Calcitonin lowers serum calcium levels.

Which substance increases calcium absorption from the gastrointestinal tract?

Activated vitamin D.

What is hyperparathyroidism?

Hyperparathyroidism occurs when the parathyroid glands produce excessive amounts of PTH, affecting calcium and phosphorus regulation.

What are the three types of hyperparathyroidism?

Primary hyperparathyroidism, secondary hyperparathyroidism, and tertiary hyperparathyroidism.

What is the main difference between primary, secondary, and tertiary hyperparathyroidism?

Primary hyperparathyroidism originates from a problem within the parathyroid glands. Secondary hyperparathyroidism is a compensatory response to another condition affecting calcium balance. Tertiary hyperparathyroidism develops after long-standing secondary hyperparathyroidism, when the glands continue releasing excessive PTH despite normal or high calcium levels.

Can a patient with hyperparathyroidism be asymptomatic?

Yes. Some patients have no obvious symptoms, and hyperparathyroidism may be discovered through abnormal laboratory results.

What are the classic symptoms associated with hyperparathyroidism?

"Bones, Stones, Abdominal Groans, Psychic Moans," referring to bone pain and fractures, kidney stones, abdominal symptoms, and mental or emotional changes.

What does "Bones, Stones, Abdominal Groans, Psychic Moans" mean?

Bones refers to bone pain, osteoporosis, and fractures. Stones refers to kidney stones. Abdominal groans refers to abdominal pain, decreased appetite, and constipation. Psychic moans refers to lethargy, emotional distress, confusion, or psychosis.

## Primary Hyperparathyroidism

What is primary hyperparathyroidism?

Primary hyperparathyroidism occurs when the parathyroid glands directly secrete excessive amounts of PTH, usually resulting in elevated serum calcium levels.

What is the most common cause of primary hyperparathyroidism?

A benign parathyroid adenoma, which is a noncancerous growth in a parathyroid gland that produces excessive PTH.

What other condition can cause primary hyperparathyroidism besides a parathyroid adenoma?

Parathyroid carcinoma, which is a cancerous growth of the parathyroid gland.

What are the typical laboratory findings in primary hyperparathyroidism?

PTH is elevated, serum calcium is elevated, and serum phosphorus is typically low or may be normal. Vitamin D levels may be low or normal.

Why is serum calcium elevated in primary hyperparathyroidism?

Excessive PTH increases calcium release from bones, calcium reabsorption by the kidneys, and calcium absorption through activated vitamin D.

Why is serum phosphorus usually low in primary hyperparathyroidism?

Excessive PTH increases phosphorus excretion by the kidneys, which generally lowers serum phosphorus levels.

What are the clinical manifestations of primary hyperparathyroidism?

Patients may be asymptomatic or experience decreased appetite, abdominal pain, lethargy, emotional distress, confusion or psychosis, poor coordination, paresthesias, polyuria, hypercalciuria, kidney stones, gallstones, bone pain, osteoporosis, fractures, muscle weakness, fatigue, hyporeflexia, and constipation.

How does hypercalcemia affect neuromuscular function in primary hyperparathyroidism?

Hypercalcemia decreases neuromuscular excitability, which can cause muscle weakness, fatigue, decreased reflexes, and constipation.

How can primary hyperparathyroidism affect the kidneys?

Increased calcium levels can cause hypercalciuria, polyuria, dehydration, and kidney stone formation.

How can primary hyperparathyroidism affect the bones?

Excessive PTH can increase bone resorption, contributing to bone pain, decreased bone density, osteoporosis, and fractures.

How can primary hyperparathyroidism affect mental status?

Hypercalcemia can cause lethargy, emotional distress, confusion, and in severe cases, psychosis.

What is the primary treatment for primary hyperparathyroidism when surgery is indicated?

Parathyroidectomy, which involves surgically removing the abnormal parathyroid gland or glands.

How is hypercalcemia managed in primary hyperparathyroidism?

Treatment may include IV isotonic fluids, loop diuretics after adequate fluid replacement when indicated, and medications that lower serum calcium.

Why are IV isotonic fluids used to manage hypercalcemia?

IV isotonic fluids restore circulating volume and help the kidneys excrete excess calcium through the urine.

When may loop diuretics be used to treat hypercalcemia?

They may be used after adequate fluid replacement when clinically indicated, because they increase calcium excretion in the urine. They are not routinely used before correcting dehydration.

What is alendronate (Fosamax) used for in hyperparathyroidism?

Alendronate is a bisphosphonate that decreases bone resorption and may help improve or preserve bone density.

What are IV bisphosphonates used for in hypercalcemia?

IV bisphosphonates inhibit bone resorption and help lower serum calcium levels.

What are calcimimetic agents used for in hyperparathyroidism?

Calcimimetic agents, such as cinacalcet, make the calcium-sensing receptors more sensitive to calcium, reducing PTH secretion and helping lower serum calcium.

What is secondary hyperparathyroidism?

Secondary hyperparathyroidism occurs when the parathyroid glands increase PTH secretion as a compensatory response to conditions that cause low calcium or disrupt calcium and phosphorus balance.

What is the purpose of increased PTH secretion in secondary hyperparathyroidism?

The body increases PTH secretion to compensate for low calcium levels or other problems that interfere with normal calcium regulation.

What are the common causes of secondary hyperparathyroidism?

Chronic kidney disease (CKD), vitamin D deficiency, malabsorption disorders, hyperphosphatemia, renal failure, and poor calcium absorption.

How can chronic kidney disease cause secondary hyperparathyroidism?

CKD reduces phosphorus excretion and vitamin D activation, disrupting calcium balance and stimulating the parathyroid glands to release more PTH.

How can vitamin D deficiency cause secondary hyperparathyroidism?

Vitamin D deficiency reduces calcium absorption from the gastrointestinal tract, which can lower serum calcium and stimulate increased PTH secretion.

How can malabsorption disorders cause secondary hyperparathyroidism?

Malabsorption disorders can reduce the absorption of calcium and vitamin D from the gastrointestinal tract, triggering increased PTH secretion.

How can hyperphosphatemia contribute to secondary hyperparathyroidism?

Excess phosphorus can bind calcium and contribute to decreased free serum calcium, stimulating increased PTH secretion.

What are the typical laboratory findings in secondary hyperparathyroidism?

PTH is elevated, serum calcium is low or normal, and serum phosphorus is often elevated in CKD-related secondary hyperparathyroidism. Vitamin D may be low if deficiency is the underlying cause.

Why can serum calcium be low or normal in secondary hyperparathyroidism?

PTH secretion increases as a compensatory response to low calcium or another problem affecting calcium regulation, but the underlying condition may prevent calcium from returning to normal.

Why is serum phosphorus often high in secondary hyperparathyroidism caused by CKD?

Damaged kidneys cannot excrete phosphorus effectively, causing phosphorus to accumulate in the blood.

What condition affecting the bones is associated with secondary hyperparathyroidism in CKD?

Renal osteodystrophy, a bone disorder caused by disturbances in mineral and bone metabolism associated with chronic kidney disease.

How is secondary hyperparathyroidism treated?

Treatment focuses on the underlying cause and may include phosphorus-binding medications, vitamin D supplementation or activated vitamin D, and management of calcium and phosphorus levels.

Why are phosphorus-binding medications used in secondary hyperparathyroidism?

They bind phosphorus in the gastrointestinal tract and reduce its absorption, helping lower serum phosphorus levels.

Why may vitamin D supplementation be prescribed for secondary hyperparathyroidism?

Vitamin D helps improve calcium absorption from the gastrointestinal tract and can reduce the stimulus for excessive PTH secretion when vitamin D deficiency contributes to the condition.

What is tertiary hyperparathyroidism?

Tertiary hyperparathyroidism develops after long-standing secondary hyperparathyroidism causes the parathyroid glands to enlarge and secrete excessive PTH independently of normal calcium feedback.

What causes tertiary hyperparathyroidism?

Long-standing secondary hyperparathyroidism causes parathyroid gland hyperplasia, leading to excessive PTH secretion that no longer responds appropriately to calcium levels.

What is parathyroid gland hyperplasia?

Hyperplasia is an increase in the number of cells in the parathyroid glands, causing the glands to enlarge and potentially produce excessive PTH.

What happens to the normal negative feedback mechanism in tertiary hyperparathyroidism?

The enlarged parathyroid glands become less responsive to calcium feedback and continue secreting excessive PTH despite normal or elevated serum calcium.

What is the most common underlying condition associated with tertiary hyperparathyroidism?

Long-standing chronic kidney disease, often after years of secondary hyperparathyroidism.

What are the typical laboratory findings in tertiary hyperparathyroidism?

PTH is elevated, serum calcium is elevated, and serum phosphorus is often elevated, particularly when advanced CKD continues to impair phosphorus excretion.

How does secondary hyperparathyroidism progress to tertiary hyperparathyroidism?

Persistent stimulation of the parathyroid glands can cause hyperplasia. Over time, the glands may begin secreting excessive PTH without responding normally to calcium levels, leading to tertiary hyperparathyroidism.

How is tertiary hyperparathyroidism treated?

Treatment may include cinacalcet or parathyroidectomy, depending on disease severity and response to medical treatment.

What are the typical PTH, calcium, and phosphorus levels in primary hyperparathyroidism?

PTH is high, calcium is high, and phosphorus is usually low or normal.

What are the typical PTH, calcium, and phosphorus levels in secondary hyperparathyroidism?

PTH is high, calcium is low or normal, and phosphorus is often high in CKD-related disease.

What are the typical PTH, calcium, and phosphorus levels in tertiary hyperparathyroidism?

PTH is high, calcium is high, and phosphorus is often high, especially in patients with advanced CKD.

What is the common cause of primary hyperparathyroidism?

A benign parathyroid adenoma; parathyroid carcinoma is a less common cause.

What are the common causes of secondary hyperparathyroidism?

CKD, vitamin D deficiency, malabsorption disorders, renal failure, poor calcium absorption, and hyperphosphatemia.

What is the common cause of tertiary hyperparathyroidism?

Long-standing secondary hyperparathyroidism, commonly associated with chronic kidney disease.

How can laboratory findings help distinguish primary from secondary hyperparathyroidism?

Both usually have elevated PTH, but primary disease typically has high calcium and low or normal phosphorus, while secondary disease often has low or normal calcium and high phosphorus in CKD-related cases.

How can laboratory findings help distinguish tertiary from secondary hyperparathyroidism?

Both can occur in CKD and have elevated PTH, but tertiary disease typically has elevated calcium because the parathyroid glands continue secreting excessive PTH despite high calcium levels.

Why must laboratory findings be interpreted with the underlying cause when diagnosing hyperparathyroidism?

Calcium and phosphorus patterns can vary depending on kidney function, vitamin D status, and other contributing conditions, so lab results must be considered together with the patient's clinical history.

What is a parathyroidectomy?

A surgical procedure involving partial or complete removal of one or more parathyroid glands.

Why might a patient need a parathyroidectomy?

It may be indicated for primary hyperparathyroidism or severe or persistent hyperparathyroidism that does not respond adequately to other treatments.

What are potential indications for parathyroidectomy in hyperparathyroidism?

Serum calcium more than 1 mg/dL above the upper limit of normal, hypercalciuria greater than 400 mg/day according to the provided notes, decreased bone density, neuromuscular effects, or kidney stones.

What does hypercalciuria mean?

Hypercalciuria means excessive calcium excretion in the urine.

What is the purpose of removing the parathyroid glands during a parathyroidectomy?

To reduce excessive PTH secretion and help correct the abnormal calcium balance.

What happens to serum calcium levels after parathyroidectomy?

Serum calcium can decrease rapidly because the source of excessive PTH has been removed, increasing the risk of postoperative hypocalcemia.

Why can hypocalcemia occur after parathyroidectomy?

Removal of the overactive glands can cause a sudden decrease in PTH secretion. The remaining parathyroid tissue may not produce enough PTH immediately to maintain normal calcium levels.

Where may normal parathyroid tissue be reimplanted during surgery?

Normal parathyroid tissue may be reimplanted in the forearm or near the sternocleidomastoid muscle, depending on the surgical plan.

Why might a patient need lifelong calcium supplementation after parathyroidectomy?

If the remaining or reimplanted parathyroid tissue does not produce enough PTH to maintain calcium levels, long-term or lifelong calcium supplementation may be needed.

What education should be provided to a patient after parathyroidectomy?

Teach incision care, taking prescribed calcium supplements, reporting numbness or tingling around the mouth, reporting muscle cramps or spasms immediately, and keeping follow-up appointments for calcium monitoring.

Why should a patient report numbness or tingling around the mouth after parathyroidectomy?

These can be early signs of hypocalcemia, which can progress to muscle spasms, tetany, or airway-threatening laryngospasm.

Why should a patient report muscle cramps or spasms after parathyroidectomy?

Muscle cramps and spasms can indicate hypocalcemia and require prompt assessment and treatment.

Why are follow-up appointments important after parathyroidectomy?

Follow-up appointments allow healthcare providers to monitor serum calcium levels, assess recovery, and adjust calcium or vitamin D supplementation as needed.

What is the priority nursing concern after thyroidectomy or parathyroidectomy?

Airway and breathing, because postoperative neck swelling, hemorrhage, or laryngospasm can obstruct the airway.

What should the nurse assess to monitor for airway compromise after thyroidectomy or parathyroidectomy?

Assess respiratory status, work of breathing, oxygenation, neck swelling, and signs of bleeding or hemorrhage.

Why must the nurse monitor for neck swelling after thyroidectomy or parathyroidectomy?

Swelling or a hematoma can compress the airway and cause respiratory distress.

What postoperative complications should the nurse monitor for after thyroidectomy or parathyroidectomy?

Airway obstruction, hemorrhage, hypocalcemia, muscle spasms, tetany, and laryngospasm.

What are the signs and symptoms of postoperative hypocalcemia?

Perioral numbness or tingling, tingling in the fingers, muscle cramps, spasms, tetany, and potentially laryngospasm.

What emergency medication should be readily available after parathyroidectomy when hypocalcemia is a concern?

IV calcium gluconate, which can be used to treat symptomatic or severe hypocalcemia as prescribed.

Why should IV calcium gluconate be readily available after parathyroidectomy?

A rapid decrease in serum calcium can cause severe neuromuscular irritability, tetany, and laryngospasm that require urgent treatment.

What emergency equipment may need to be at the bedside after thyroidectomy or parathyroidectomy?

A tracheostomy tray may be kept at the bedside when indicated by the patient's risk and facility protocol.

Why is airway monitoring a priority even when the patient initially appears stable after neck surgery?

Bleeding, swelling, or laryngospasm can develop and quickly compromise the airway.

What is hypoparathyroidism?

Hypoparathyroidism occurs when the parathyroid glands produce insufficient PTH, causing decreased serum calcium and increased serum phosphorus.

What is the most common cause of hypoparathyroidism?

Injury to or removal of the parathyroid glands during thyroid or parathyroid surgery.

What are the typical laboratory findings in hypoparathyroidism?

PTH is low, serum calcium is low, and serum phosphorus is high.

Why does hypoparathyroidism cause hypocalcemia?

Low PTH decreases calcium release from bones, reduces calcium reabsorption in the kidneys, and decreases activation of vitamin D, reducing calcium absorption from the gastrointestinal tract.

Why is serum phosphorus elevated in hypoparathyroidism?

Low PTH reduces phosphorus excretion by the kidneys, causing more phosphorus to remain in the bloodstream.

How does hypocalcemia affect neuromuscular excitability?

Hypocalcemia increases neuromuscular excitability, which can cause paresthesias, muscle spasms, tetany, hyperreflexia, and potentially laryngospasm.

What are the neuromuscular signs and symptoms of hypoparathyroidism?

Tetany, muscle spasms, hyperreflexia, and paresthesias such as numbness or tingling.