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Questions and Answers
What is the normal range for serum calcium levels?
What must be added to measured calcium in low albumin states to obtain the corrected calcium level?
Which condition can cause hypocalcemia with increased PTH levels?
How does hypomagnesemia affect calcium levels?
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What is the critical value of serum calcium clinically significant for hypercalcemia?
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What is the most common cause of hypoparathyroidism?
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Which condition is associated with congenital absence of parathyroid glands?
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What is the hallmark clinical manifestation of acute hypocalcemia?
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What chronic manifestation can develop due to prolonged hypoparathyroidism?
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Which sign indicates hypocalcemia when muscle contractions are elicited by tapping the facial nerve?
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Which of the following is NOT a typical clinical feature of hypoparathyroidism?
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What lab findings are essential for diagnosing hypoparathyroidism?
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Which of these may be a consequence of chronic hypoparathyroidism affecting the basal ganglia?
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What characterizes familial hypocalciuric hypercalcemia?
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Which of the following is a result of prolonged immobilization?
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What condition is associated with secondary hyperparathyroidism?
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What is a potential cause of Milk-Alkali syndrome?
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What characterizes tertiary hyperparathyroidism?
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What is the cure rate for a single adenoma when operated on by experienced surgeons?
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Which approach can help minimize hypercalcemia?
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What treatment is indicated if the 25-hydroxyvitamin D level is less than 20 ng/dL?
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Which condition is often associated with hypercalcemia due to the production of 1,25-dihydroxyvitamin D3?
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What medication can be used to block bone dissolution in hypercalcemia treatment?
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What biochemical effect does PTHrP produce that is similar to parathyroid hormone (PTH)?
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Why is the success rate for hyperplasia treatment often lower than that for adenomas?
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What is a common transient effect that may occur post-operation for gland excision?
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What is a key characteristic of a parathyroid adenoma?
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Which of the following is commonly observed in primary hyperparathyroidism related to the renal system?
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What skeletal condition is specifically associated with elevated PTH levels in primary hyperparathyroidism?
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Which symptom is least likely to be associated with the gastrointestinal manifestations of primary hyperparathyroidism?
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What laboratory finding is commonly elevated in patients diagnosed with primary hyperparathyroidism?
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What imaging technique is commonly used to localize the parathyroid gland in cases of primary hyperparathyroidism?
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What is the definitive treatment for symptomatic primary hyperparathyroidism?
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In primary hyperparathyroidism, the serum alkaline phosphatase level is expected to be elevated in which scenario?
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Which treatment approach may not be appropriate for hyperplasia in primary hyperparathyroidism?
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What symptom is most commonly related to neurologic manifestations of primary hyperparathyroidism?
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How does hypomagnesemia typically affect parathyroid hormone (PTH) production?
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What is a defining characteristic of calcium that is protein-bound?
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In cases of hypocalcemia, what effect does an elevated PTH level indicate?
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What is the primary reason for correcting serum calcium in low albumin states?
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What is the relationship between hypomagnesemia and hypoparathyroidism?
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What is the most significant clinical feature that can occur due to acute hypocalcemia?
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Which of the following conditions is least likely to contribute to the development of hypoparathyroidism?
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What is a noted ocular manifestation associated with chronic hypoparathyroidism?
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Which sign is characterized by carpal spasms elicited by the filling of a blood pressure cuff?
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Chronic hypocalcemia can lead to calcifications affecting which part of the body?
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Which genetic disorder is primarily recognized for its association with congenital absence of parathyroid glands?
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What is the most common cause of hypoparathyroidism linked to surgical procedures?
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What is a typical chronic manifestation in a child with untreated hypoparathyroidism during development?
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What is a characteristic feature of familial hypocalciuric hypercalcemia?
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Which condition is associated with renal damage and increased calcium levels?
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What causes secondary hyperparathyroidism in chronic kidney disease?
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Which condition can lead to chronic increased turnover of bone, resembling hyperparathyroidism?
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Which factor should be avoided in patients with primary hyperparathyroidism due to its effect on calcium excretion?
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What is the primary advantage of using calcium citrate over calcium carbonate in patients taking certain medications?
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In treating severe hypocalcemia, which treatment is indicated first for symptomatic patients?
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What is the typical starting dose for calcitriol in adults with hypocalcemia?
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What is a crucial step in the management of hypoparathyroidism when administering IV calcium?
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Which of the following is a potential complication of treating alkalosis in the context of hypocalcemia?
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What is the mechanism by which vitamin D aids in calcium utilization in the body?
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Which characteristic defines the typical administration guideline for calcium supplements?
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Which factor most significantly affects the choice between calcium carbonate and calcium citrate?
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What primary laboratory finding is considered the hallmark indicator of primary hyperparathyroidism?
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What is a potential consequence of hypercalcemia on renal function in primary hyperparathyroidism?
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Which of the following skeletal conditions is specifically associated with high levels of PTH in primary hyperparathyroidism?
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Which gastrointestinal symptom is least commonly associated with primary hyperparathyroidism?
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What imaging technique is known to have a sensitivity of 60% to 80% for localizing parathyroid adenomas?
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What typical neurologic symptom may occur in patients with primary hyperparathyroidism?
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In what scenario might serum alkaline phosphatase levels be elevated in primary hyperparathyroidism?
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What is the recommended treatment for symptomatic primary hyperparathyroidism?
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Which set of clinical features may indicate advanced disease in primary hyperparathyroidism?
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What condition can lead to the formation of brown tumors in primary hyperparathyroidism?
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What is the primary physiological role of parathyroid hormone (PTH) in relation to calcium levels?
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What unusual behavior characterizes parathyroid adenomas in relation to calcium levels?
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In terms of calcium regulation, what triggers the secretion of parathyroid hormone?
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Which of the following best describes the effect of parathyroid hormone on the kidneys?
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What condition is primarily characterized by insufficient secretion of parathyroid hormone?
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Which factor is primarily responsible for the control of calcium absorption from the small intestine and renal tubular reabsorption?
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What is the physiological state associated with ionized calcium concentration in the serum?
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Which of the following treatments is necessary to enhance calcium absorption in patients with hypocalcemia?
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Which condition is characterized by a serum magnesium concentration below 0.8 mEq/L and leads to decreased PTH production?
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How is total serum calcium corrected in low albumin states?
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What laboratory value indicates a vitamin D deficiency in patients suspected of having hypocalcemia?
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In the management of hypocalcemia, what serum calcium concentration is typically aimed for in treatment?
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Hypocalcemia associated with high or normal levels of PTH suggests which type of pathology?
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Which condition is characterized by skeletal abnormalities and end organ resistance to parathyroid hormone?
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Which of the following is a potential consequence of inadequate management of hypocalcemia?
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What treatment may be used to decrease bone resorption in hyperparathyroidism?
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Which electrolyte imbalance can cause a shortened QT interval on an EKG?
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Which condition is associated with the production of PTHrP leading to hypercalcemia?
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During the emergency treatment of hypercalcemia with elevated calcium levels, what is a preferred hydration method?
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What is the minimum duration that asymptomatic individuals over 50 with slightly elevated calcium can remain stable?
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What is a significant risk of failing to excise all glands during hyperplasia treatment?
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What should be monitored in patients receiving treatment for severe hypercalcemia?
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What dose of oral phosphate may help lower calcium levels in cases of primary hyperparathyroidism?
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Which calcium supplement is best absorbed with low gastric pH and should be taken during meals?
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What is the typical starting dose of calcitriol for treating hypocalcemia in adults?
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In the treatment of severe hypocalcemia, IV calcium is primarily administered for which specific purpose?
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What role does calcitriol play in calcium metabolism?
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Why is calcium gluconate preferred over calcium chloride for intravenous calcium administration?
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What is the significance of treating alkalosis in the context of hypocalcemia treatment?
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What is a critical aspect to monitor when administering IV calcium in patients with hypoparathyroidism?
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What condition may cause significant symptoms if hypocalcemia is not treated promptly?
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What is a primary action of parathyroid hormone (PTH) regarding calcium?
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In the feedback loop controlling PTH secretion, which condition will trigger PTH release?
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What is a key characteristic of a parathyroid adenoma in relation to calcium levels?
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Which of the following statements regarding hypoparathyroidism is inaccurate?
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Which physiological action is NOT associated with PTH?
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What is the role of PTH in the context of calcium absorption?
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In cases of hypomagnesemia, how is PTH production affected?
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What is the primary physiological form of calcium that is active in the body?
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How should serum calcium levels be corrected in low albumin states?
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What characterizes the clinical findings in hypocalcemia with increased PTH levels?
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Which factor is least likely to contribute to the occurrence of hypoparathyroidism?
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Severe complications of chronic hypoparathyroidism primarily affect which anatomical regions?
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Which clinical manifestation is most specific for acute hypocalcemia?
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What is the primary reason for checking magnesium levels in a patient suspected of having hypoparathyroidism?
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What is a common autoimmune cause of hypoparathyroidism?
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Which of the following is a distinguishing feature of idiopathic hypoparathyroidism compared to surgical causes?
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Which of the following is NOT a potential long-term consequence of hypoparathyroidism?
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What is the characteristic presentation of Chvostek's sign?
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What is the most effective treatment for symptomatic hypercalcemia with a calcium level greater than 14 mg/dl?
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Which condition is most likely to produce hypercalcemia without bone metastases?
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What lab result is typically a critical component when diagnosing hyperparathyroidism?
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How does estrogen impact bone health in the context of hyperparathyroidism?
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What is the primary consequence of increased PTH levels in primary hyperparathyroidism affecting the renal system?
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What is the expected effect of oral phosphate therapy in the management of primary hyperparathyroidism?
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What is a commonly observed postoperative complication following gland excision in hyperparathyroidism treatments?
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Which diagnostic method is known to localize the parathyroid gland with a sensitivity of 60% to 80%?
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In the context of primary hyperparathyroidism, what condition might indicate the need for immediate intervention if not managed effectively?
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Which symptom is indicative of osteitis fibrosa cystica as a manifestation of primary hyperparathyroidism?
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What is the role of hemodialysis in treating hypercalcemia?
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What is a typical expected lab finding in a patient with symptomatic primary hyperparathyroidism?
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In patients with primary hyperparathyroidism, which gastrointestinal symptom is frequently observed?
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What imaging technique shows a successful localization rate of at least 80% when used in combination with other methods?
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Which of the following laboratory findings may be observed in a patient with primary hyperparathyroidism?
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What condition can result from osteoclast activity due to increased PTH levels in primary hyperparathyroidism?
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What is the definitive treatment for symptomatic primary hyperparathyroidism?
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Which of these symptoms is associated with the neurologic manifestations of primary hyperparathyroidism?
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Study Notes
Hypoparathyroidism
- Most common cause: Surgical removal of parathyroid glands, often a complication of thyroid surgery or neck cancer surgery.
- Less common cause: Idiopathic hypoparathyroidism, diagnosed in childhood and often familial.
- Genetic disorders: DiGeorge syndrome, a congenital absence of parathyroid glands along with other malformations.
- Other causes: Autoimmune, radiation therapy, infiltrative diseases of the parathyroid glands, Hypomagnesemia.
Clinical Features of Hypoparathyroidism
- Hallmark: Tetany due to hypocalcemia.
- Acute symptoms of tetany: Perioral numbness, paresthesia of the hands and feet, muscle cramps, carpopedal spasm, laryngospasm, focal or generalized seizures, neuromuscular fatigue and weakness
- Chronic manifestations: Calcification of the basal ganglia and eyes, cataracts, keratoconjunctivitis, dental abnormalities (dental hypoplasia, defective enamel, and root formation), skeletal abnormalities, brittle nails, ridged nails, dryness and skin scaling.
- Clinical Signs: Chvostek sign (tapping along facial nerve induces contractions of eye, mouth, or nose muscles) and Trousseau sign (carpal spasms elicited by filling of a blood pressure cuff)
Hypoparathyroidism: Diagnostic Evaluation
- Laboratory findings: Low serum calcium, normal or low PTH, High Phosphorus, normal Magnesium and Vitamin D levels.
- Serum Calcium: Normal range is 8.4-10.2 mg/dl.
- Serum Calcium correction for low albumin: Measured calcium + 0.8 (4-serum albumin)
Differential Diagnosis of Hypocalcemia
- Hypomagnesemia: Low serum magnesium (below 0.8 mEq/L) can cause hypocalcemia by decreasing PTH production and inhibiting PTH action on bone.
- Causes of hypocalcemia with increased PTH levels: Kidney disease, a parathyroid producing adenoma, and vitamin D deficiency
Primary Hyperparathyroidism Clinical Features
- Diagnosis: Routine measurement of calcium.
- Common symptoms: Mild
- Occasionally patients can present with: Advanced kidney and bone disease.
- Patients with high serum calcium levels (11-12 mg/dl): May have gastrointestinal and neurological symptoms.
Primary Hyperparathyroidism: Manifestations by Organ System
- Renal: Hypercalcemia and increased glomerular filtration can lead to kidney stones, nephrocalcinosis, and eventual renal failure.
- Skeletal: Increased osteoclastic bone resorption can lead to osteitis fibrosa cystica, bone pain, fractures, swelling and deformities, bone cysts, brown tumors, osteopenia, osteoporosis, loss of lamina around the teeth, and subperiosteal resorption of cortical bone.
- Gastrointestinal: Anorexia, weight loss, nausea and vomiting, abdominal pain, constipation, increased incidence of peptic ulcer disease, and increased incidence of pancreatitis.
- Neurologic: Fatigue and muscle weakness, emotional changes, abnormal mentation.
Primary Hyperparathyroidism Labs
- Elevated serum calcium: Hallmark of primary hyperparathyroidism.
- Serum phosphate: May be lowered in many, but not all patients.
- Serum alkaline phosphatase level: Will be elevated in patients with bone disease.
- Urine calcium: Elevated (hypercalcuria) common (not all patients due to calcium resorption with elevated PTH).
- Elevated PTH level: Should be measured in conjunction with calcium level.
Other Primary Hyperparathyroidism Labs
- Serum creatinine, 24-hour urine calcium, 25-hydroxyvitamin D.
- Bone Mineral Density: Measured by Dexa scan.
Diagnostic imaging in Primary Hyperparathyroidism
- Localizing the Parathyroid Gland/Adenoma: Tc-sestamibi scanning, CT scanning, Magnetic resonance imaging, Ultrasound with color flow doppler.
- Accuracy: Individually, each test has a sensitivity of 60% to 80%. Used in combination, they are successful in at least 80%.
Treatment of Primary Hyperparathyroidism
- Definitive treatment: Parathyroidectomy.
- Surgical approach: Minimally invasive vs bilateral neck exploration depends on the ability of localizing studies to detect one clearly abnormal gland.
- Hyperplasia: May show multiple enlarged glands on scans, double adenomas can also occur. Multiple glands may require excision.
- Cure rate: 95% for a single adenoma. Success rate for hyperplasia is lower because missed glands can occur.
- Post-operative transient hypocalcemia: Can occur.
Primary Hyperparathyroidism: Medical Treatment
- No definitive medical treatment.
- Asymptomatic persons over 50 years old with serum calcium levels no greater than 11-12 mg/dl: Often have no progression of disease for 10 or more years. These patients can be followed and operated on if calcium rises.
- Increased fluids can help minimize hypercalcemia.
- Oral phosphate 1-2 g/day can help lower calcium.
- Estrogen decreases bone resorption.
Emergency Treatment of Hypercalcemia
- Calcium level >14 mg/dl.
- Hydration with 4-6 L of NS & large doses of furosemide: To increase renal calcium excretion & lower serum sodium.
- SQ/IM calcitonin: Effect limited to first 48 hours.
- IV Bisphosphonates: Block dissolution of bone & inhibit osteoclast activity (takes 2-4 days to see be effective, but more sustained).
- If 25-hydroxyvitamin D level is less than 20 ng/dL: Vitamin D should be cautiously replaced (eg, 400 to 800 international units daily).
- Denosumab if bisphosphonates are contraindicated (severe renal disease/allergy).
- Hemodialysis: As last resort.
- EKG monitoring: Shortening QT interval (hypocalcemia prolongs QT).
Differential Diagnosis of Hypercalcemia
- Malignant tumors and tumors with bone metastasis: PTHrP (parathyroid hormone-related peptide) acts like PTH and binds to PTH receptors.
- Sarcoidosis: Granulomatous tissue produces 1, 25-dihydroxyvitamin D3. Responds to glucocorticoids (Prednisone 40 mg daily).
- Familial Hypocalciuric hypercalcemia: Genetic disorder with mildly elevated calcium, rarely has complications. Clue: Family history and low urine calcium levels).
- Vitamin D intoxication: Usually in people receiving vitamin D with hypocalcemia.
- Milk-Alkali-syndrome: Ingestion of large doses of calcium and absorbable alkali (calcium carbonate >5 g/d). Causes renal damage/nephrocalcinosis, hypercalcemia, and systemic alkalosis.
Other Causes of Hypercalcemia
- Hyperthyroidism: Due to increased bone turnover.
- Thiazide Diuretics: Decreases urinary calcium excretion, rare. Avoid in patients with primary hyperparathyroidism.
- Prolonged immobilization: Continuous bone resorption in the absence of normal posture.
- Paget’s disease: Due to increased bone turnover.
- Recovery from acute renal failure from rhabdomyolysis
Secondary Hyperparathyroidism
- Chronic kidney disease - Mineral & bone disorder (CKD-MBD)
- Systemic disorder characterized by biochemical abnormalities: Calcium, phosphate, PTH, vitamin D, abnormalities in bone turnover, extra skeletal calcification.
Tertiary Hyperparathyroidism
- Refractory (autonomous) hyperparathyroidism: Resulting from chronic kidney disease, increased PTH, and increased calcium.
Nomogram for Parathyroid Disorders
- This is a tool used to assess parathyroid disorders based on various lab values such as serum calcium, PTH, and phosphate.
Causes of Low PTH/ Hypoparathyroidism
-
Surgical Removal of the Parathyroid Glands: Most common cause; complication of subtotal thyroidectomy; radical neck dissection for neck cancer; temporary ischemic injury to glands during surgery can resolve within weeks to months.
-
Idiopathic Hypoparathyroidism: Less common; diagnosed in childhood; familial component; genetic disorders cause defects in parathyroid development (DiGeorge syndrome: congenital absence of parathyroid glands with other malformations).
-
Autoimmune: Destruction of parathyroid glands; radiation therapy; infiltrative diseases; hypomagnesemia.
Clinical Features of Hypoparathyroidism
- Hypocalcemia related symptoms: tetany (hallmark of acute hypocalcemia: neuromuscular irritability)
- Perioral numbness
- Paresthesia of hands and feet
- Muscle cramps
- Carpopedal spasms
- Laryngospasm
- Focal or generalized seizures
- Neuromuscular fatigue and weakness
Chronic Manifestations of Hypoparathyroidism & Hypocalcemia
-
Calcifications: Basal ganglia and eye; basal ganglia calcifications can cause parkinsonism, other movement disorders (dystonia); ocular: cataracts, keratoconjunctivitis.
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Dental: Abnormalities during early development (dental hypoplasia, defective enamel, and root formation).
-
Skeletal: Abnormalities.
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Ectodermal: Brittle nails, ridged nails; dryness and skin scaling.
Signs of Hypocalcemia
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Chvostek Sign: Tapping along facial nerve induces eye, mouth, or nose muscle contractions.
-
Trousseau Sign: Carpal spasms elicited by filling a blood pressure cuff.
Diagnostic Evaluation
-
Serum Calcium: Normal: 8.4-10.2 mg/dL; Critical value: 13.5 mg/dL.
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PTH: Normal or low.
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Phosphorus: Must be verified as normal.
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Magnesium & Vitamin D Levels: Must be checked.
Serum Calcium Correction for Low Albumin
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Calcium exists in three forms: ionized (free), protein-bound, and complex-bound.
-
Calcium must be corrected for low albumin states: measured calcium + 0.8 (4 - serum albumin).
Differential Diagnosis
-
Hypomagnesemia: Serum magnesium below 0.8 mEq/L; causes hypocalcemia; decreases PTH production and inhibits PTH action on bone.
-
Causes of hypocalcemia with increased PTH levels: Kidney disease.
Hypocalcemia Treatment - Calcium Supplements
-
Calcium carbonate (Tums): 40% elemental calcium; best absorbed at low gastric pH (with meals).
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Calcium citrate: 21% elemental calcium; absorbed with or without meals; better choice for patients taking PPIs/H2-blockers, causes less GI intolerance.
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Dosage: 800-1200 mg elemental calcium daily, in divided doses.
Hypocalcemia Treatment - Calcitriol
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Biologically active form of vitamin D; needed for calcium absorption and utilization.
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Typical starting dose: 0.25 mcg twice daily; increase dose weekly by 0.25 mcg/day to achieve low-normal serum calcium.
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Many adults require up to 2 mcg daily.
Treatment of Severe Hypocalcemia
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Symptomatic acute hypocalcemia (laryngospasm, carpopedal spasm, seizures, prolonged QT intervals): IV calcium + oral calcitriol supplementation.
-
Asymptomatic or mildly symptomatic patients with rapid decline in serum corrected calcium to ≤7.5 mg/dL: IV calcium.
Hypoparathyroidism: Treatment
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IV calcium replacement +/- IV magnesium (check and replace as needed): 1-2 10mL ampules 10% Ca Gluconate in 100mL D5, infuse intravenously over 10 minutes.
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Treat alkalosis (reduces serum Ca2+ availability).
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Continuous cardiac monitoring and ABGs.
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Laboratory monitoring: albumin-corrected serum total Calcium, Magnesium, and phosphate levels.
Hyperparathyroidism
-
Primary Hyperparathyroidism: Parathyroid adenoma functions autonomously and produces excessive PTH despite high ionized calcium levels.
-
Clinical Features:
- May be diagnosed based on routine calcium measurement.
- Common to only have mild symptoms.
- Occasionally patients present with advanced kidney and bone disease.
- Patients with high serum calcium levels (11-12 mg/dL) may have GI and neurologic symptoms.
Manifestations by Organ System
-
Renal: PTH increases renal calcium reabsorption, but hypercalcemia and increased glomerular filtration can lead to:
- Kidney stones
- Nephrocalcinosis
- Renal failure
-
Skeletal: PTH increases osteoclastic bone resorption:
- Osteitis fibrosa cystica (bone pain, fractures, swelling, deformities).
- Areas of demineralization can lead to bone cysts and brown tumors.
- Radiographs show osteopenia and osteoporosis.
-
Gastrointestinal: Anorexia, weight loss, nausea and vomiting, abdominal pain, constipation, increased incidence of peptic ulcer disease and pancreatitis.
-
Neurologic: Fatigue, muscle weakness, emotional changes, abnormal mentation.
Hyperparathyroidism Labs
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Elevated Serum Calcium: Hallmark of primary hyperparathyroidism.
-
Serum Phosphate: May be lowered.
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Serum Alkaline Phosphatase: Elevated in patients with bone disease.
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Urine Calcium: Elevated (hypercalcuria).
-
Elevated PTH Level: Measured in conjunction with calcium level.
Other Hyperparathyroidism Labs
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Serum creatinine, 24-hour urine calcium, 25-hydroxyvitamin D.
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Bone Mineral Density: DEXA scan.
Diagnostic Imaging in Primary Hyperparathyroidism
- Localizing the parathyroid gland/adenoma:
- Tc-Sestamibi scanning
- CT scanning (including 4-D CT)
- MRI
- Ultrasound with color flow doppler
- Experienced professionals achieve 80% sensitivity with combined use.
Treatment of Primary Hyperparathyroidism
-
Definitive Treatment: Parathyroidectomy (indicated for symptomatic patients).
-
Approach: Minimally invasive vs bilateral neck exploration (depends on the ability of localizing studies to detect one clearly abnormal gland).
Other Hyperparathyroid Conditions
-
Familial Hypocalciuric Hypercalcemia: Genetic disorder with mildly elevated calcium; rarely has complications; clue: family history and low urine calcium levels.
-
Vitamin D Intoxication: Usually in people receiving vitamin D with hypocalcemia.
-
Milk-Alkali Syndrome: Ingestion of large doses of calcium and absorbable alkali (calcium carbonate >5 g/d); causes renal damage/nephrocalcinosis, hypercalcemia, and systemic alkalosis.
Differential Diagnosis of Hypercalcemia
- Other Causes:
- Hyperthyroidism (increased bone turnover)
- Thiazide Diuretics (decreases urinary calcium excretion)
- Prolonged immobilization (continuous bone resorption without normal posture)
- Paget's disease (increased bone turnover)
- Recovery from acute renal failure (following rhabdomyolysis).
Chronic Kidney Disease - Mineral & Bone Disorder (CKD-MBD)
-
Systemic disorder characterized by biochemical abnormalities: calcium, phosphate, PTH, vitamin D, bone turnover abnormalities, and extra-skeletal calcifications.
-
Secondary hyperparathyroidism refers to the biochemical abnormalities that characterize CKD-MBD.
Tertiary Hyperparathyroidism
- Refractory (autonomous) hyperparathyroidism: increased PTH and increased calcium, resulting from chronic kidney disease.
Parathyroid Gland Anatomy & Function
- Four parathyroid glands are responsible for producing Parathyroid hormone (PTH).
- PTH maintains calcium and phosphate balance in the body.
- PTH allows for proper nervous and muscular system function and controls bone physiology.
Parathyroid Hormone Actions
- PTH stimulates the production of vitamin D, which is important for calcium absorption in the gastrointestinal tract.
- PTH increases calcium reabsorption in the kidneys by decreasing renal tubular reabsorption of phosphate.
Normal Physiology
- Parathyroid gland activity is regulated by the levels of free calcium (Ca2+) and phosphate (PO4)3- in the blood.
- Low levels of free Ca2+ stimulate PTH secretion, which in turn:
- Increases osteoclast activity, releasing Ca++ and PO43- into the bloodstream.
- Increases calcium and phosphate absorption in the small intestine through vitamin D.
- Increases calcium reabsorption in the kidneys and phosphate excretion.
- This process results in increased levels of free Ca++, which subsequently inhibits PTH secretion, creating a feedback loop to maintain calcium homeostasis.
Parathyroid Adenoma
- A Parathyroid adenoma is a non-cancerous tumor that produces excess PTH, regardless of circulating calcium levels.
- This leads to primary hyperparathyroidism.
Hypoparathyroidism
- PTH deficiency leading to low serum calcium levels.
- The cause of PTH deficiency can be challenging to determine.
Measuring Serum Calcium
- Normal serum calcium levels are between 8.4-10.2 mg/dl.
- Critical serum calcium level is 13.5 mg/dl.
- Serum calcium levels fluctuate based on calcium absorption from the small intestine and renal tubular reabsorption rate, both influenced by PTH.
Serum Calcium Correction for Low Albumin
- Calcium exists in three forms:
- Ionized or free Ca2+, which is physiologically active.
- Protein-bound Ca2+, primarily bound to albumin.
- Complexed Ca2+, forming soluble fractions with carbonates, citrates, or phosphates.
- Calcium levels must be corrected for low albumin states with the following formula: Measured calcium + 0.8 (4 - serum albumin).
Differential Diagnosis of Hypocalcemia
- Hypomagnesemia: Low serum magnesium levels (<0.8 mEq/L) can cause hypocalcemia by decreasing PTH production and inhibiting PTH's actions on bone. This is a reversible cause of hypocalcemia that resolves after restoring normal serum magnesium levels.
-
Increased PTH Levels:
- Kidney disease: Hypocalcemia can result from multiple factors including renal phosphate retention, decreased vitamin D production, and bone resistance to PTH.
- Vitamin D deficiency: Low levels of 25-hydroxyvitamin D can lead to hypocalcemia.
- Pancreatitis: Rapid precipitation of calcium within the abdomen can occur due to fat necrosis of the pancreas.
- Hypoalbuminemia: Low albumin levels can lead to a decrease in total calcium levels, which may require correction.
- Osteoblastic metastatic disease: Cancers such as breast, lung, and prostate cancer can cause hypocalcemia due to rapid bone uptake of cancer cells.
- Pseudohypoparathyroidism: A rare hereditary condition where individuals develop end-organ resistance to PTH and hypocalcemia. This condition is associated with skeletal abnormalities (short stature, shortened metacarpals) and mental deficits.
Treatment Goals of Hypocalcemia
- Relieve symptoms of hypocalcemia.
- Normalize serum calcium levels, aiming for a low-normal range of 8.0 to 8.5 mg/dL.
- Avoid hypercalciuria, nephrocalcinosis, and kidney stones.
- Prevent hyperphosphatemia.
Treatment of Hypocalcemia
- Calcium supplementation: 1-2 g of elemental calcium per day.
-
Types of calcium supplements:
- Calcium carbonate (Tums): 40% elemental calcium, best absorbed with meals.
- Calcium citrate: 21% elemental calcium, absorbed with or without meals, less GI intolerance than calcium carbonate.
- Calcitriol: Biologically active form of Vitamin D, required for calcium absorption and utilization. Typical starting dose is 0.25 mcg twice daily.
Treatment of Severe Hypocalcemia
- IV calcium: First-line treatment for symptomatic acute hypocalcemia (laryngospasm, carpopedal spasm, seizures).
- Oral calcitriol: Used in conjunction with IV calcium.
- IV calcium can also be used in asymptomatic patients with a rapid decline in serum calcium levels ≤7.5 mg/dL to prevent the development of severe symptoms.
Hypoparathyroidism: Treatment
- IV Calcium replacement: 1-2 10ml ampules of 10% calcium gluconate infused intravenously over 10 minutes.
- IV Magnesium: Check and replace magnesium as needed.
- Treat Alkalosis: Alkalosis can worsen hypocalcemia by increasing calcium binding to albumin.
- Cardiac Monitoring: Continuous cardiac monitoring to detect arrhythmias associated with hypocalcemia.
- Laboratory Monitoring: Monitor albumin-corrected serum calcium, magnesium, and phosphate levels.
Hypoparathyroidism: Treatment (Continued)
-
IV Calcium (gluconate and chloride):
- Chloride is more likely to cause tissue necrosis than gluconate.
- Administer slowly through a large vein (central venous catheter preferred).
- **Calcitriol: ** Biologically active form of Vitamin D, preferred over Vitamin D2/D3 due to rapid onset and shorter half-life, leading to less toxicity.
Hyperparathyroidism
- Primary Hyperparathyroidism: Characterized by excess PTH secretion due to a parathyroid adenoma, hyperplasia, or carcinoma.
-
Medical Treatment:
- No definitive medical treatment available.
- Asymptomatic individuals with serum calcium levels no greater than 11-12 mg/dL often experience no disease progression for 10 years or more. These individuals can be monitored and treated surgically if their calcium levels increase.
Primary Hyperparathyroidism: Medical Treatment (Continued)
- Increased Fluids: Help minimize hypercalcemia.
- Oral Phosphate: 1-2 g/day can lower serum calcium levels.
- Estrogen: Decreases bone resorption, which can help manage hypercalcemia.
Emergency Treatment of Hypercalcemia
- Severe Hypercalcemia: Serum calcium levels >14 mg/dL.
- Hydration: 4-6 liters normal saline (NS) and large doses of furosemide to increase renal calcium excretion.
- Calcitonin: SQ/IM injection, effective for the first 48 hours.
- Bisphosphonates: Inhibit osteoclast activity and block bone resorption ( takes 2-4 days for effect).
- Vitamin D: Replace cautiously if 25-hydroxyvitamin D levels are less than 20 ng/dL.
- Denosumab: Can be used if bisphosphonates are contraindicated.
- Hemodialysis: Last resort treatment.
- EKG Monitoring: Monitor for shortening of QT interval.
Differential Diagnosis of Hypercalcemia
- Malignant Tumors and Bone Metastases: Tumors that cause hypercalcemia in the absence of bone metastases often produce PTH-related peptide (PTHrP).
- PTHrP: Acts like PTH and binds to PTH receptors, producing similar biochemical effects.
- Sarcoidosis: Can cause Hypercalcemia through production of 1,25-dihydroxyvitamin D3 by granulomatous tissue. May respond to a therapeutic trial of glucocorticoids.
Parathyroid Glands
- The parathyroid glands produce parathyroid hormone (PTH)
- PTH maintains calcium and phosphate balance
- PTH allows the nervous and muscular systems to function properly
- PTH controls bone physiology
Parathyroid Hormone Actions
- PTH raises serum calcium levels by stimulating vitamin D production and increasing renal reabsorption of calcium
- PTH decreases renal tubular reabsorption of phosphate
Normal Physiology
- Low levels of free calcium (Ca2+) stimulate PTH secretion
- PTH increases osteoclast activity, releasing calcium and phosphate
- PTH increases small bowel calcium and phosphate absorption through vitamin D
- PTH increases renal resorption of calcium (distal tubule) and phosphate excretion (proximal tubule)
- Increased free calcium levels inhibit PTH secretion
Parathyroid Adenoma
- A parathyroid adenoma will make PTH autonomously despite high levels of circulating ionized calcium
- This leads to primary hyperparathyroidism
Hypoparathyroidism
- PTH deficiency causes low levels of serum calcium
- The most common cause is surgical removal of the parathyroid glands
Causes of Hypoparathyroidism
- Most common cause: Surgical removal of the parathyroid glands
- occurs as a complication of subtotal thyroidectomy
- occurs as a complication of radical neck dissection in cases of cancer of the neck
- ischemic injury to the glands during surgery can be temporary and recover in weeks to months
- Idiopathic Hypoparathyroidism
- much less common
- diagnosed in childhood
- can be familial
- genetic disorders associated with defects in parathyroid development
- DiGeorge syndrome: congenital absence of parathyroid glands in association with thymic aplasia, cardiovascular defects
- autoimmune
- other: destruction by radiation therapy, infiltrative diseases of the parathyroid glands, hypomagnesemia
Clinical Features of Hypoparathyroidism
- Tetany
- hallmark of acute hypocalcemia
- neuromuscular irritability
- Produces acute symptoms:
- perioral numbness
- paresthesia of the hands and feet
- muscle cramps
- carpopedal spasm
- laryngospasm
- focal or generalized seizures
- neuromuscular fatigue and weakness
- Chronic Manifestations of Hypoparathyroidism and Hypocalcemia
- Calcifications of the basal ganglia and eye
- over time can lead to parkinsonism and other movement disorders
- Dental: abnormalities seen if hypocalcemia is during early development
- dental hypoplasia
- defective enamel
- root formation
- skeletal abnormalities
- ectodermal manifestations: brittle nails, ridging of the nails
- dryness and skin scaling
- Calcifications of the basal ganglia and eye
Hypocalcemia Signs
- Chvostek sign: tapping along the facial nerve induces contractions of eye, mouth, or nose muscles
- Trousseau sign: carpal spasms elicited by filling a blood pressure cuff
- Chvostek and Trousseau sign are classic signs of hypocalcemia
Hypoparathyroidism Diagnostic Evaluation
- Lab findings:
- serum calcium
- serum PTH
- serum phosphorus (must verify normal magnesium and vitamin D levels)
Serum Calcium Normal Values
- Normal: 8.4-10.2 mg/dl
- Critical value: 13.5 mg/dl
- The plasma level varies with the rate of calcium absorption from the small intestine and the proximal renal tubular reabsorption rate under the control of PTH
Serum Calcium Correction for Low Albumin
- Calcium is present in three forms:
- ionized or free Ca2+ (physiologically active)
- protein-bound or non-diffusible Ca2+ (mostly loosely bound to plasma albumin)
- complexed or complex-bound Ca2+ (forms relatively soluble fractions complexed with carbonates, citrates, or phosphates)
- Calcium must be corrected for low albumin states:
- measured calcium + 0.8 (4-serum albumin)
Hypocalcemia Differential Diagnosis
- Hypomagnesemia
- Hypomagnesemia causes hypocalcemia by decreasing production of PTH and inhibiting the actions of PTH on the bone
- A reversible cause of hypocalcemia
- Hypoparathyroidism should resolve within minutes or hours after restoration of normal serum magnesium concentrations if hypomagnesemia was the cause
- Hypercalcemia: Causes of hypocalcemia with increased PTH levels
- Kidney disease: hypocalcemia multifactorial
Primary Hyperparathyroidism
- Primary hyperparathyroidism is due to a parathyroid-producing adenoma
- An adenoma can function autonomously and produce excessive PTH despite high ionized calcium levels
- This causes the abnormalities of primary hyperparathyroidism
Primary Hyperparathyroidism Clinical Features
- May be diagnosed based on routine measurement of calcium
- Common to only have mild symptoms
- Occasionally, patients can present with advanced kidney and bone disease
- Patients with high serum calcium levels of 11-12 mg/dl may have GI and neurologic symptoms
Primary Hyperparathyroidism Manifestations by Organ System
-
Renal:
- Although PTH increases renal calcium reabsorption
- The resulting hypercalcemia and increased glomerular filtration can lead to the formation of kidney stones
- Calcium deposits within the renal parenchyma can cause nephrocalcinosis and eventual renal failure
-
Skeletal:
- PTH increases osteoclastic bone resorption and can lead to osteitis fibrosa cystica
- Symptoms include:
- bone pain
- fractures
- swelling and deformities
- Areas of demineralization in the bone can lead to bone cysts and brown tumors
- Radiographs show osteopenia and osteoporosis
- Loss of lamina around the teeth
- Subperiosteal resorption of cortical bone seen in the phalanges
- similar problems in the skull can cause a salt and pepper appearance
-
Gastrointestinal:
- Symptoms include:
- anorexia
- weight loss
- nausea & vomiting
- abdominal pain
- constipation
- increased incidence of peptic ulcer disease
- increased incidence of pancreatitis
- Symptoms include:
-
Neurologic:
- Symptoms include:
- fatigue and muscle weakness
- emotional changes
- abnormal mentation
- Symptoms include:
Hyperparathyroidism Labs
- Elevated serum calcium is the hallmark of primary hyperparathyroidism
- Serum phosphate may be lowered in many, but not all patients.
- Serum alkaline phosphatase level will be elevated in patients with bone disease.
- Urine calcium elevated (hypercalcuria) is common (not all patients due to calcium resorption with elevated PTH).
- Elevated PTH level should be measured in conjunction with calcium level.
- Other labs:
- serum creatinine
- 24-hour urine calcium
- 25-hydroxyvitamin D
- bone mineral density (DEXA scan)
Diagnostic Imaging in Primary Hyperparathyroidism
- Localizing the parathyroid gland/adenoma:
- Tc-sestamibi scanning, CT scanning (including 4-D CT)
- Magnetic resonance imaging
- Ultrasound with color flow Doppler
- Individually, each has a sensitivity of 60% to 80% in experienced hands.
- When used in combination, they are successful in at least 80%.
Treatment of Primary Hyperparathyroidism
- The definitive treatment is parathyroidectomy and is indicated for symptomatic patients
- Surgical approach: minimally invasive vs bilateral neck exploration depends on the ability of the localizing studies to detect one clearly abnormal gland
- Hyperplasia: may show multiple enlarged glands on scans, double adenomas also can occur. Multiple glands may require excision
- Success rate for hyperplasia is lower because missed glands can occur.
- Transient hypocalcemia can occur post-operatively.
Primary Hyperparathyroidism Medical Treatment
- No definitive medical treatment.
- Asymptomatic people >50 with serum calcium level no greater than 11-12 mg/dl often have no progression of disease for 10 or more years.
- These patients can be followed and can be operated on if calcium rises.
Primary Hyperparathyroidism Medical Treatment
- Increased fluids can help minimize hypercalcemia.
- Oral phosphate 1-2 g/day can help lower calcium.
- Estrogen decreases bone resorption.
Emergency Treatment of Hypercalcemia
- Calcium level > 14 mg/dl
- Hydration with 4-6 L of NS and large doses of furosemide to increase renal calcium excretion and lower serum sodium
- SQ/IM calcitonin (effect limited to the first 48 hours)
- IV bisphosphonates block dissolution of bone and inhibit osteoclast activity (takes 2-4 days to be effective, but more sustained)
- If the 25-hydroxyvitamin D level is less than 20 ng/dL, vitamin D should be cautiously replaced (e.g., 400 to 800 international units daily).
- Denosumab if bisphosphonates are contraindicated (severe renal disease/allergy).
- Hemodialysis as last resort.
- EKG monitoring - Shortening QT interval (hypocalcemia prolongs QT).
Differential Diagnosis of Hypercalcemia
- Malignant tumors and tumors with bone metastasis
- Tumors that cause hypercalcemia in the absence of bone metastasis make PTH-related peptide (PTHrP)
- PTHrP acts like PTH and binds to PTH receptors; may produce similar biochemical effects as PTH.
- Sarcoidosis
- Causes hypercalcemia via the production of 1, 25-dihydroxyvitamin D3 by granulomatous tissue.
- Will respond to a therapeutic trial of glucocorticoids (prednisone 40 mg daily).
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Description
Explore the causes and clinical features of hypoparathyroidism, including its hallmark symptoms such as tetany and hypocalcemia. This quiz covers various genetic disorders and the impact of surgical interventions on parathyroid function.
