Parathyroid disease Flashcards
1
Q
Hyperparathyroidism definition
A
hyperparathyroidism is characterised by excessive production of parathyroid hormone by the parathyroid glands.
2
Q
Classification of hyperparathyroidism
A
- Primary - excessive production of PTh by one or more of the parathyroid glands. This is usually the result of a small PTH secreting adenoma
- Secondary- result of a normal phsiological response to hypocalcaemia, which may be due to a myria of different causes:
- Chronic renal failure
- chronic pancreatitis
- small bowel absorption
- tertiary
- secretion of PTH autonomously- often as result of chronic kidney disease
3
Q
Physiology
A
- low serum calcium is detected by the parathyroid glands
- this promotoes production of PTH
- PTH is release into the blood
- PTH promotoes osteoclast acitivty in the bones
- osteoclasts dissolve bone and calcium from this move into the serum
- PTH also increases calcium reabsorption by the kidneys and decreases phosphate reabsorption
- PTH also promotes the conversion of vitamin D in the kidney into its more active form
- Increased levels of active vitamin D promote increased reabsorption of calcium in the bowel
- bone resorption alongside increased renal and bowel reabsoprtion results in increased serum calcium levels
- increased serum calcium levels inhibit further production of PTH via negative feedback
4
Q
Investigations
A
Bloods
- calcium - this is raised in all forms of hyperparathyroidism
- parathyroid hormone- PTH is also raised
- phosphate - this is low in all types of hyperparathyroidism due to the effect of PTH on the kidneys
- U and Es - may show increased creatinine suggesting chronic renal disease- a common cause of 2o and tertiary hyperaprathyroidism
Review patients medications for drugs promoting hypercalcaemia
- lithium
- thiazide diuretics
Imaging
- Dexa scan -measures bone mineral density (BMD), patient with hyperparatyroidism often have low BMD due to the effect of PTH on osteoclasts, a dexa will therefore be useful in assessing the severity of the disease as well as response to treatment
- MIBI scan- scan used in suspected primary hyperparathyroidism, aim is to identify secreting PTH adenomas, The contrast used is a complex of technetium-99m with the ligand methoxyisobutylisonitrile (MIBI), The parathyroid gland takes up this complex after intravenous injection, The patient’s neck is then imaged with a gamma camera to show the location of all glands.A second image is obtained after a washout time (approximately 2 hours, Abnormal PTH secreting adenoma glands retaining the 99mTc and are seen with the gamma camera, The test can detect 75% to 90% of abnormal parathyroid glands in primary hyperparathyroidism
- Neck USS
- An USS scan of the parathyroid glands is often done in addition to the MIBI scan
- It looks for enlarged parathyroid glands suggestive of adenoma
- Use of both USS & MIBI can increase the sensitivity & specificity of identifying single adenomas
- The biggest issue is that Neck USS is far more operator dependent than a MIBI scan
- So the USS operator skill significantly influences the usefulness of the test
- Renal tract imaging
- Patients who are hypercalcaemic are significantly more likely to develop renal stones
- This can often be the way hyperparathyroidism first presents
- As a result, those who are diagnosed with hyperparathyroidism often have a KUB x-ray performed
- Biopsy
- Parathyroid biopsies are sometimes performed if carcinoma is suspected
Carcinoma is rare however
5
Q
Symptoms and signs of primary hyperparathyroidism
A
“Stones, Bones, Abdominal Groans & Psychiatric Moans” is a useful aide-mémoire
- Stones
- Kidney stones – stones made of calcium salts which can block the urinary tract
- Nephrocalcinosis – deposition of calcium in the renal parenchyma – can lead to renal failure
- Acquired Diabetes Insipidus – hypercalcaemia causes increased sodium loss in the urine & therefore loss of more water with it
- Bones
- Osteoporosis:
- Excessive PTH promotes the destruction of bone by osteoclasts
- As a result bone mineral density decreases
- Osteitis fibrosa cystica:
- Bone pain – especially the long bones e.g. Tibia
- Peritrabecular fibrosis – replacement of bone with fibrous tissue
- Brown cyst-like tumours form throughout the skeleton
- Osteoporosis:
- Abdominal Groans
- Constipation
- Indigestion
- Nausea & Vomiting
- Peptic ulcers
- Pancreatitis
- Psychiatric Moans
- Lethargy
- Fatigue
- Depression
- Poor memory
- Delirium
- Psychosis
6
Q
Diagnosis of hyperparathyroidism
A
- Serum Calcium – ↑
- Parathyroid Hormone – ↑
- U&E’s – renal function may be normal or impaired if hypercalcaemia has been longstanding
- MIBI – may show a single enlarged parathyroid gland suggestive of adenoma
- DEXA – depends on length & severity of disease – usually less than norma
7
Q
Management of hyperparathyroidism
A
- conservative- in mild/asymptatic disease
- check calcium every 6 months
- also creatinine for renal damage
- annual dexa scan
- advise high fluid intake- keeps calcium lower and reduces risk of renal stone
- moderate calcium intake
- surgical - if the patient has any of the following
- symptomatic hypercalcaemia
- significant loss of bone density
- renal stones
- Single parathyroid gland hyperplastic then
- directed parathyroidectomy
- single gland not identified all though to be hyperplastic
- more invasice incision over thyroid, to remove 3 and a 1/2 parathyroid glands
- medical
- is not first line in majority
- reserved when surgery is not appropriate
- cinacalet - calcimimetic (mimics action of callcium, by binding to the same recepto, resulting in negative feedback effect reducing PTH)
- bisphosphanates - alendronate, protects from bone loss and increases bone density (promote apoptosis of osteoclasts)
8
Q
Complications of surgery
A
- hypocalcaemia- rapid fall in PTH results in reversal of inhibitory effects of osteoblasts
- haematoma - increasingly significant due to anatomical position of glands (haematoma in the pre-tracheal space can raidly result in airway occlusion)
- reccurent laryngeal nerve palsy- nerve runs close tot he operatie site, resulting in hoarse voice
9
Q
Secondary hyperaprathyroidism definition
A
Secondary hyperparathyroidism occurs as a result of chronic hypocalcaemia
Because of continous stimulation, the parathyroid glands become hyperplastic
The most common causes of chronic hypocalcaemia are:
- Renal failure
- Malabsorption
- Vitamin D deficiency
10
Q
Diagnosis of secondary hyperparathyroidism
A
- hypocalcaemia
- raised PTH
- phosphate- raised in renal disease- low in vitamin D deficiency
11
Q
Management of secondary hyperparathyroidism
A
- medical management is first line
- treatment of underlying pathology
- vitamin D deficiency replacement with supplements
- chronic kidney disease
- calcium and vitamin D supplement (calcichew D3)
- cincacalet- only recommende in end stage renal disease
12
Q
hypoparathyroidism
A
decreased function of the parathyroid glands characterised by:
- hypocalcaemia
- hyperphosphataemia
- low or inapproriately normal levels of PTH
13
Q
Aetiology hypoparathyroidism
A
Most common aetiology in adults is post-surgical:
- During thyroid resection, parathyroids may suffer unplanned resection or compromise of their blood supply.
- Remaining parathyroid tissue may temporarily continue to be suppressed after thyroidectomy for hyperthyroidism, [2] or after parathyroidectomy of a hyperfunctioning parathyroid adenoma.
- After parathyroidectomy for secondary hyperparathyroidism, resection of the glands almost always unmasks a chronic bone deficit and consequent hypocalcaemia.
Other aetiologies are uncommon and include:
- Congenital (e.g., DiGeorge’s syndrome [neither the parathyroids nor the thymus develop]), gene mutations affecting PTH receptor [3] or PTH, autoimmune polyglandular syndrome type 1, [4] and polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome. [5] [6]
- Infiltration of the gland by heavy metals, metastatic tumours or Riedel’s thyroiditis.
- Impaired PTH secretion (e.g., hypomagnesaemia), alcoholism, or alcohol withdrawal.
- Neonates from hypercalcaemic mothers can suffer in utero suppression of their developing parathyroids by high maternal calcium. [7]
- HIV infection
14
Q
Physiology hypoparathyroidism
A
- PTH is released from the paratyroid gland when a calcium-sensing receptor perceives decreased ionised calcium
- PTH acts to increase serum calcium by
- literating calcium from bone
- increasing intestinal calcium absorption by promoting vitamin D synthesis and conversion to active from
- promoting calcium reabsorpition in the kidneys
- inadequate PTH secretion in response to low calcium levels results in hypoca,acemia, with symptoms of hypersensitivity of nerve and muscle
15
Q
Classification hypoparathyroidism
A
- Primary hypoparathyroidism - low concentration of PTH with low calcium levels
- Secondary hypoparathyroidism- the serum PTH concentration is low and the serum calcium concentration is elevated
- Psuedohypoparathyroidism - serum PTH concentration is low and the serum calcium concentration is elevated
