Hyperparathyroidism: Clinical sciences

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Introduction0:00–0:58

Hyperparathyroidism is when excess parathyroid hormone, or PTH for short, is produced. PTH is produced by the parathyroid glands, which lie behind the thyroid, and it controls calcium balance in the body.
Now, primary hyperparathyroidism occurs when the parathyroid glands autonomously make too much PTH. In contrast, secondary hyperparathyroidism is caused by an appropriate rise in PTH levels, as the parathyroid glands attempt to correct hypocalcemia caused by other conditions, such as vitamin D deficiency, or chronic kidney disease.
Finally, there’s tertiary hyperparathyroidism, which is usually caused by long-standing secondary hyperparathyroidism that eventually results in parathyroid hyperplasia and unregulated, autonomous PTH overproduction.Now, if your patient presents with a chief concern suggesting hyperparathyroidism, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.

Unstable Patient0:58–2:06

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry, as well as cardiac telemetry.
Finally, if needed, provide supplemental oxygen.Here’s a high-yield fact to keep in mind! Patients with hyperparathyroidism can develop severe or rapidly progressing hypercalcemia, which can cause lethargy, stupor, or even coma.
Additionally, an ECG may reveal bradycardia, atrioventricular block, or a shortened QT interval. To normalize serum calcium, you should start intravenous hydration; and diuretics, like furosemide; or bisphosphonates, like zoledronic acid can also be used.Now, let’s go back to the ABCDE assessment and discuss the stable patients.

Stable Patient2:06–3:57

First, obtain a focused history and physical examination. Many patients with hyperparathyroidism are asymptomatic, but some may report personality and mood changes, trouble concentrating, and even altered mental status.
They might also experience gastrointestinal issues, such as abdominal pain, nausea, anorexia, and constipation. Additionally, history might reveal musculoskeletal pain as well as polyuria and polydipsia.
Finally, there could be a history of chronic kidney disease, vitamin D deficiency, nephrolithiasis, or low-impact bone fractures.
On the flip side, physical exam findings are typically nonspecific and might include muscle weakness, diminished deep tendon reflexes and signs of dehydration, like dry mucous membranes and poor skin turgor.
Now, here’s another high-yield fact! There’s a mnemonic for the signs and symptoms of hypercalcemia: “groans, bones, stones, thrones, and psychiatric overtones.” Groans represent constipation and muscle weakness, which occur due to decreased muscle contractions.
Bones is for bone pain resulting from chronic bone demineralization, while stones refers to nephrolithiasis, since hypercalcemia can lead to hypercalciuria in an attempt to excrete the excess calcium.
Finally, thrones refers to the toilet, to remind you of polyuria; and psychiatric overtones remind you of mood changes or altered mental status.If your patient presents with these signs and symptoms, suspect hyperparathyroidism, and order labs, including a CMP and serum PTH level.

Suspect hyperparathyroidism3:57–4:18

Once you’ve got the results, assess the serum PTH and calcium levels, and don’t forget to correct the serum calcium if albumin levels are abnormal!Consider alternative diagnosisNow, if the patient’s PTH is low or normal, your patient does not have hyperparathyroidism, so consider alternative diagnoses.On the flip side, if the serum PTH and calcium are both elevated, diagnose primary hyperparathyroidism.

Consider alternative diagnosis4:18–4:29

Primary HPT4:29–7:27

Next, assess for features of multiple endocrine neoplasia, or MEN, types 1 and 2A. If the personal or family history reveals a pituitary or pancreatic tumor, order genetic testing to look for mutations in the MEN1 gene.
If the mutation is present, diagnose MEN1.On the other hand, if history reveals pheochromocytoma, or medullary thyroid cancer, order genetic testing to look for mutations in the RET gene.
If the mutation is present, diagnose MEN2A.If an MEN syndrome is diagnosed, be sure to treat any coexisting conditions.And if the history reveals no coexisting endocrine disorders, we’re looking at sporadic primary hyperparathyroidism.
For both sporadic and MEN-related cases, after primary hyperparathyroidism is confirmed, you should order imaging studies like a neck ultrasound and a Tc-99m sestamibi scintigraphy to localize the affected parathyroid gland; and a DEXA scan to assess bone mineral density.
Now, the preferred treatment for primary hyperparathyroidism is parathyroidectomy, so consult the surgical team. Alternatively, if your patient is asymptomatic, or not a surgical candidate, you can consider medical management.
This includes vitamin D supplementation, bisphosphonates to improve bone mineral density, and calcimimetics to reduce serum calcium levels.
Monitor serum calcium and 24-hour urine calcium levels annually, and order regular abdominal ultrasounds to screen for nephrolithiasis; and DEXA scans to monitor bone mineral density.Now, here’s a clinical pearl!
Some rare conditions that cause elevated PTH and serum calcium can mimic primary hyperparathyroidism, including familial hypocalciuric hypercalcemia and lithium-induced hypercalcemia.
Familial hypocalciuric hypercalcemia is a genetic condition caused by a mutation in the calcium-sensing receptor, resulting in high PTH levels despite hypercalcemia.
It can be distinguished from primary hyperparathyroidism by measuring the urine calcium to creatinine ratio, which is decreased with this condition; and genetic testing confirms the diagnosis.
Similarly, lithium can mimic primary hyperparathyroidism by raising the threshold of calcium required to suppress PTH release, causing elevated serum PTH and calcium levels.Alright, now let’s go back to the PTH and calcium, and consider cases in which there’s high PTH, but low serum calcium.

Secondary HPT7:27–7:56

In this case, diagnose secondary hyperparathyroidism and assess for the underlying cause by calculating the glomerular filtration rate, or GFR, and ordering labs, including a 25-hydroxy vitamin D level.
Now, if the GFR is less than 60 and the 25-hydroxy vitamin D is low, diagnose chronic kidney disease. When kidney function is impaired, vitamin D conversion to its physiologically active form is also impaired, as is renal excretion of phosphate; and this stimulates PTH secretion.

CKD7:56–8:53

To lower serum phosphate levels, recommend a low phosphate diet, and begin oral phosphate binders. Supplement your patient with active vitamin D, like alfacalcidol, and consider calcimimetics to reduce serum PTH levels.Next, assess your patient’s treatment response by checking serum PTH and calcium levels.
Low or normal serum calcium means your patient has an adequate response, so continue current management, and monitor serum calcium levels regularly.However, if serum calcium level becomes elevated and the PTH remains very high, there’s an inadequate response to treatment.
In this case, diagnose tertiary hyperparathyroidism, which is a common consequence of long-standing secondary hyperparathyroidism, and consult the surgery team to evaluate the patient for parathyroidectomy.

Tertiary hyperparathyroidism8:53–9:16

Alright, now let’s go back and consider cases in which the GFR is normal, but the 25-hydroxy vitamin D is low. In this case, diagnose nutritional vitamin D deficiency, which can occur because of low dietary intake, or in conditions associated with malabsorption, such as celiac disease and cystic fibrosis.

Malabsorption/malnutrition9:16–9:49

In these patients you should ensure an adequate intake of calcium and provide vitamin D supplementation.However, if the patient has normal GFR and 25-hydroxy vitamin D levels, suspect pseudohypoparathyroidism.
This is a genetic condition that causes resistance to PTH in the proximal tubules of the kidney. In this case, order genetic testing for mutations in GNAS, and if a mutation is detected, diagnose pseudohypoparathyroidism.

Pseudohypoparathyroidism9:49–10:24

Treat your patient with calcium and vitamin D supplementation, with a goal of maintaining serum calcium levels in the low-normal range.Finally, if your patient is taking loop diuretics, anticonvulsants, phosphates, or bisphosphonates, diagnose medication-induced secondary hyperparathyroidism.
These medications can lower serum calcium levels and trigger increased PTH secretion. Consider adjusting the medication dose, or switching to an alternative medication to normalize serum calcium and PTH levels.Alright, now let’s go all the way back to the CMP and PTH.

Medication-induced secondary hyperparathyroidism10:24–10:53

If the PTH is elevated but the serum calcium is normal, diagnose normocalcemic hyperparathyroidism. Next, assess for an underlying cause, and if you can’t identify any, diagnose normocalcemic primary hyperparathyroidism.

Normocalcemic Hyperparathyroidism10:53–11:47

For these patients, just annual monitoring of serum calcium and PTH levels is enough. On the other hand, if you identify an underlying cause, such as chronic kidney disease, vitamin D deficiency, or medication use, diagnose normocalcemic secondary hyperparathyroidism.
Treatment aims to correct the underlying cause, and serum calcium and PTH levels should be monitored annually.Alright, as a quick recap… When suspecting hyperparathyroidism, order a serum PTH and calcium level.
If they’re both elevated, diagnose primary hyperparathyroidism. If the PTH is elevated but the calcium is low, diagnose secondary hyperparathyroidism and check the GFR and 25-hydroxy vitamin D levels.
If the GFR is under 60, diagnose chronic kidney disease and begin medical management. If the serum calcium becomes elevated in these patients, diagnose tertiary hyperparathyroidism.

Review11:47–13:01

If the GFR is normal and vitamin D is low, diagnose nutritional vitamin D deficiency. On the flip side, when GFR and vitamin D levels are normal, it suggests pseudohypoparathyroidism.
Finally, if your patient takes a medication that lowers serum calcium, suspect medication-induced secondary hyperparathyroidism.
On the flip side, if the PTH is elevated and the calcium is normal, diagnose normocalcemic hyperparathyroidism. D deficiency On the flip side when G Fr and Vitamin D levels are normal it suggests pseudohypoparathyroidism If your patient takes a medication that lowers serum calcium suspect medication induced secondary hyperparathyroidism on the flip side If the P TH is elevated and the calcium is
Hyperparathyroidism: Clinical Sciences: Video | Osmosis