36 | The complete guide to parathyroid disorders for vet nurses

PodcastEndocrine
Written By Laura Jones

Today, we’re talking all about parathyroid disorders - diseases of the parathyroid gland affecting calcium balance within the body.

 

Though we don’t see these as commonly as other endocrine diseases, it’s still really important we understand these disorders - especially hypoparathyroidism, which can cause life-threatening hypocalcaemia. By the end of this episode, you’ll feel more confident caring for these patients, but before we jump into the disorders, let’s travel back to a little bit of A&P and chat about what the parathyroid gland does.

So, what are our parathyroid glands?

The parathyroid glands are two pairs of small, oval-shaped glands located next to each thyroid gland (one cranial and one caudal on each side). 

These are responsible for secreting parathyroid hormone, or PTH. PTH then converts vitamin D to its active form, vitamin D3 (aka calcitriol), which increases circulating calcium levels through 3 mechanisms:

  • Increasing calcium absorption from the GI tract

  • Increasing calcium conservation in the kidneys

  • Promoting the release of calcium from bony stores.

The ultimate goal and overall effect of PTH release is to increase blood calcium levels back to within normal limits.

We know that most of our hormones exist in pairs, with one hormone counteracting the effects of the other. And PTH is no exception - there’s a hormone called calcitonin, released from parafollicular cells in the thyroid gland. Calcitonin decreases circulating calcium levels, returning them to normal when they’re too high.

The most common parathyroid disorders we see in practice are hyperparathyroidism and hypoparathyroidism.

Let’s start by looking at hyperparathyroidism.

Hyperparathyroidism is an abnormal increase in the amount of parathyroid hormone. It can be primary or secondary in nature.

Secondary hyperparathyroidism

Secondary hyperparathyroidism is seen either due to renal disease or due to nutritional deficiencies.

Renal secondary hyperparathyroidism occurs because the kidneys lose the ability to eliminate phosphate, causing hyperphosphataemia. Because calcium and phosphate are inversely related, calcium levels decrease when phosphate levels increase.

As calcium levels drop, the body releases parathyroid hormone to try to increase them. This causes calcium levels to increase but also decreases bone density since calcium is fired up from bony stores. This causes the classic softened bones we see with this condition, especially the jaw.

Nutritional secondary hyperparathyroidism occurs when patients are fed an inappropriate diet with an incorrect calcium-to-phosphate ratio. This condition is most commonly associated with feeding an all-meat diet since it is both high in phosphate and low in calcium. We commonly see this condition in young cats, and as the trend for ‘alternative’ diets to commercial pet food has grown, so too has the prevalence of this disease.

As parathyroid hormone is released in an attempt to correct the low calcium level, calcium is freed up from bony stores, causing pathological fractures, osteopenia and bone deformities.

What about primary hyperparathyroidism?

Primary hyperthyroidism is usually caused by a benign parathyroid nodule secreting excessive PTH. This causes hypercalcaemia since the nodule’s ongoing release of PTH stimulates calcium retention and absorption in the body.

This is the most common form of hyperparathyroidism seen in dogs.

What signs do we see in a hyperparathyroid patient?

The main signs we see in dogs with primary hyperparathyroidism are polyuria and polydipsia, alongside lethargy and weight loss.

In patients with secondary hyperparathyroidism, we’ll also see signs of underlying renal disease.

In patients with nutritional secondary hyperparathyroidism, we can also see fractures, softened bones, and even neurological signs in severe cases.

How do we diagnose hyperparathyroidism?

Depending on the type of hyperparathyroidism our patient has, we’ll perform a combination of bloodwork and diagnostic imaging.

Biochemistry and haematology

Biochemistry and haematology do not usually reveal specific changes for hyperparathyroidism, except for demonstrating high total calcium levels +/- low phosphate levels in primary hyperparathyroidism, and evidence of renal disease and hyperphosphataemia in patients with renal-secondary hyperparathyroidism. In patients with nutritional-secondary hyperparathyroidism, calcium levels may be low or normal, and phosphate levels are often low.

Ionised calcium should be measured wherever possible since this is more accurate than total calcium levels. Ionised calcium is usually measured on a blood gas analyser but can also be submitted to an external lab if you don’t have one of those - just make sure there is no air in your sample tube, as this can affect the result.

The rest of our biochemistry is used to rule out other causes of hypercalcaemia, such as Addison’s disease. 

Parathyroid hormone and Vitamin D metabolites

In most cases, we’ll measure parathyroid hormone levels +/—PTH-rp (parathyroid hormone-related peptide) alongside vitamin D metabolites where needed.

Patients with primary hyperparathyroidism have an increased PTH level alongside hypercalcaemia and normal or low phosphate levels.

Patients with renal secondary hyperparathyroidism have an increased PTH level alongside low or normal calcium levels and high phosphate levels.

And patients with nutritional secondary hyperparathyroidism have an increased PTH alongside a normal or low calcium and normal or low phosphate level.

PTH-rp is used to detect paraneoplastic hypercalcaemia. Neoplasia should be excluded as a differential diagnosis in any patient presenting with hypercalcaemia.

And then there’s imaging…

Diagnostic imaging is often performed in patients with hyperparathyroidism. Primary hyperparathyroid patients require a cervical ultrasound to look for an enlarged parathyroid gland compatible with a parathyroid nodule. Renal-secondary hyperparathyroid patients will have evidence of renal disease on abdominal ultrasound, and patients with nutritional-secondary hyperparathyroidism should have survey X-rays taken to identify pathological fractures.

So, how do we treat these patients?

Treatment depends on the type of hyperparathyroidism our patient has:

Treating primary hyperparathyroidism

The initial treatment aims to reduce calcium levels where appropriate. We do this through intravenous fluid therapy (with 0.9% Saline since Hartmann’s solution contains calcium). On rare occasions, we might need to give bisphosphonate medications to reduce circulating calcium levels.

Once the patient is stable, they’ll return for a parathyroidectomy, which removes the parathyroid nodule surgically. The risk of postoperative hypocalcaemia is very high in these patients, so calcium and vitamin D supplementation is generally started early in recovery and then weaned depending on ionised calcium levels.

Speaking of ionised calcium, this is measured regularly in the recovery period while we, as nurses and technicians, observe the patient closely for signs of hypocalcaemia (such as neurological changes, muscle twitching, facial itching or rubbing, and seizure activity).

Long-term treatment with vitamin D or calcium is not usually required in these patients, as PTH levels typically equilibrate over a few weeks.

Treating secondary hyperparathyroidism

The way we treat secondary hyperparathyroidism depends on the underlying cause. Patients with renal disease need to have this managed, restricting their phosphate intake and adding a phosphate binder where needed to restore a normal calcium-to-phosphate ratio.

Patients with nutritional secondary hyperparathyroidism require a complete, balanced diet with an appropriate calcium-to-phosphorus ratio for the individual patient and their life stage. We also need to provide analgesia and handle these patients carefully since they are at a high risk of fractures. If they present with hypocalcaemia, this needs to be corrected carefully as a priority.

And what about hypoparathyroidism?

Patients with hypoparathyroidism have a loss of functional parathyroid tissue. Like hyperparathyroidism, there are two main types: primary and secondary.

Primary hypoparathyroidism

Patients with primary hypoparathyroidism have immune-mediated damage to their parathyroid glands, causing a lack of PTH release and, therefore, hypocalcaemia. This is a common form of hypoparathyroidism in dogs, and toy poodles, in particular, are overrepresented.

Secondary hypoparathyroidism

Secondary hypoparathyroidism occurs when there has been iatrogenic damage to or removal of the parathyroid glands, for example, after a thyroidectomy if the parathyroids have been accidentally removed too, or after a parathyroidectomy in a patient with primary hyperparathyroidism.

What signs do we see in these patients?

Regardless of the type of hypoparathyroidism your patient has, the clinical signs will be the same since they result from one thing: hypocalcaemia. The main presenting signs are mostly neurological and include:

  • Weakness

  • Lethargy

  • Muscle twitching

  • Seizures

  • Facial itching

Signs are usually acute in onset.

How do we diagnose these patients?

Diagnosis is made by measuring calcium and parathyroid hormone levels. Because total calcium levels don’t always accurately reflect biologically ‘available’ calcium, measuring ionised calcium levels is preferred. These are often low, alongside low PTH levels.

So that’s your patient diagnosed with hypoparathyroidism - how do we treat them?

First up, if they’re hypocalcaemic and showing clinical signs of this, we’ll need to stabilise them and correct this. We do this by administering calcium gluconate, usually as a slow IV injection or CRI, and then starting the patient on oral calcitriol +/- calcium carbonate.

When using IV calcium solutions, it’s really important that your patient be monitored continuously by ECG since cardiac arrhythmias can occur.

Alongside this, we’ll provide supportive care and withdraw IV calcium administration once the patient is normocalcaemic on oral medications alone.

Medication doses are monitored with regular re-examinations and assessment of ionised calcium levels. As the patient reaches stable doses, the frequency of recheck appointments is reduced to every six months. 


So those are the most common parathyroid disorders we see in practice, how they affect our patients, and how we treat and nurse them! Which of these do you see most commonly in practice? Let me know - drop me a DM on Instagram, and let’s chat about it!

Thanks so much for joining us for another episode of the podcast. Until next time, keep up the great nursing care!

Did you enjoy this episode? If so, I’d love to hear what you thought - screenshot it and tag me on Instagram (@vetinternalmedicinenursing) so I can give you a shout-out and share it with a colleague who’d find it helpful!

Thanks for learning with me this week, and I’ll see you next time!

References and Further Reading

Laura Jones
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