Endocrine: Parathyroid Gland Flashcards
Parathyroid Gland: Anatomy
- surgical treatment of parathyroid disease relates mainly to hyperparathyroidism.
- are normally small, yellowish- brown tissues measuring 2 35 mm.
- each gland on average weighs 30 to 40 mg.
- Pathologic glands, whether they are parathyroid adenomas or hyperplasia, appear grossly enlarged and reddish-brown.
- Both are hypercellular microscopically.
- At least four parathyroid glands are present in all individuals, residing posterior to the thyroid.
- Embryologically, the upper or superior paired glands arise from the fourth branchial pouch, located in a plane posterior to the recurrent laryngeal nerve (RLN), usually within 1 cm where the RLN and inferior thyroidal artery cross.
- The lower or inferior paired glands along with the thymus arise from the third branchial pouch, located in a plane anterior to the RLN within 2 cm of the lower thyroid pole.
- Superior glands can also be found more lateral than inferior glands.
- All four glands receive their blood supply from the inferior thyroidal artery, sharing it with the thyroid gland (Figs. 13-1, 13-2, and 13-3).
- Ectopic locations of parathyroid glands are based on embryology and are the key to localization.
- Aberrant lower glands rarely are intrathyroidal but can be found undescended, with thymic tissue high in the neck near the hyoid bone (Fig. 13-4)
Parathyroid Gland: Physiology
- are endocrine organs regulating calcium and phosphate metabolism.
- The parathyroid hormone (PTH), which can be biochemically detected in its intact 84 amino acid form, works on bone as well as kidney tubules to increase blood calcium.
- PTH is regulated through a feedback system.
- Hyperparathyroidism exists in several forms.
- Primary hyperparathyroidism (HPT) results from excess PTH, which causes mobilization of calcium deposits from bone, inhibition of renal phosphate reabsorption, and stimulation of renal tubular absorption of calcium.Overall, both total body calcium and phosphate wasting occur, leading to osteoporosis and bony mineral loss.
- Secondary HPT is from hyperplasia of the parathyroid glands, occurring in those with chronic hypocalcemia, as is usually seen in patients with renal disease. The hyperphosphatemia suppresses calcium levels, leading to excess PTH production.
- Tertiary HPT is the consequence of secondary HPT becoming autonomous. Long after a renal dialysis patient undergoes successful renal transplantation, the hyperplastic parathyroid glands will eventually function normally. Therefore, it is rare to intervene surgically.
- Pseudohyperparathyroidism or humoral hypercalcemia of malignancy leads to hypercalcemia as well as hypophosphatemia similar to primary HPT; however, it is PTH-related protein that is the cause.
- This latter molecule is not detected in the assays for PTH. The malignancy causes hypercalcemia as a result of these mechanisms: PTH-related protein, lytic bone metastases, and ectopic calcitriol secretion.
Parathyroid Gland: Epidemiology
- HPT is the most common cause of hypercalcemia, fol-
lowed by malignant disease. The majority of HPT cases
occur sporadically or in a nonfamilial form, often from
a single hyperfunctioning gland or adenoma.
- Patients with multiple endocrine neoplasia 1
(involvement of the three Ps: parathyroid, pituitary, pan-
creas) and multiple endocrine neoplasia 2A (hyper-
parathyroidism, pheochromocytoma, and medullary
cancer of the thyroid) have HPT involving multigland
hyperplasia of the parathyroids.
Parathyroid Gland: Pathology
- olitary parathyroid adenoma accounts for 80% of
primary HPT. Nearly 15% of cases are due to hyper-
plasia, where up to all four glands are involved. It is
thought that single-gland disease and multigland
disease lie within a spectrum. Double adenoma
lies between solitary adenoma and hyperplasia.
Parathyroid carcinoma is rare, occurring in fewer than
2% of cases. Typically the hypercalcemia is more
pronounced in value and presentation. The lesions
can be encapsulated like their benign counterparts
but tend to be more ill defined, possibly invading the
thyroid or nearby structures.
Parathyroid Gland: History
- Historically, patients presented with long-term
complications related to “stones, bones, groans, and
moans.”
- Renal stones/nephrocalcinosis
- Bones: aches and arthralgias
- Groans: abdominal pain from constipation, pan-
creatitis, or peptic ulcer disease
• Psychic moans: mood swings, fatigue, anxiety, or
memory loss
Today’s surgical treatment of parathyroid disease is
seen more in asymptomatic individuals rather than
those sustaining long-term complications. Presently it
is not uncommon to see postmenopausal women
who have abnormal bone mineral densitometry to
detect osteoporosis be screened on calcium blood tests
and are found to be normal or hypercalcemic. This
then prompts a workup for hypercalcemia where the
PTH is elevated. The 2002 updated National Institutes
of Health Consensus Development Conference on the
Management of Asymptomatic Primary Hyperpara-
thyroidism issued guidelines for surgery of the hyper-
parathyroid patient:
- Serum calcium greater than 1.0 mg/mL above upper limit of normal
- greater than 400 mg/d hypercalciuria
- Sequelae of hypercalcemia resulting from primary
hyperparathyroidism, such as nephrolithiasis, osteitis
fibrosa cystica, classic neuromuscular disease, severe
psychoneurologic disorder
• Cortical bone density reduction with T score less than 2.5
standard deviation (SD) of lumbar spine, hip, or wrist
- less than30% reduction of renal function in the absence of other cause
- Inability to have appropriate follow-up
- Age less than 50 years
Parathyroid Glad: Physical Examination
- Rarely will any abnormalities be found on the physical
examination, as the early diagnosis is captured biochem-
ically. Should a palpable neck mass be associated with
HPT, one would then suspect parathyroid carcinoma.
Parathyroid Gland: Differential Diagnosis
- In addition to medical conditions associated with
hypercalcemia that must be excluded, it is important
to distinguish benign familial hypocalciuric hypercal-
cemia (BFHH) from HPT, as the former is not treated.
Thus surgical intervention will be of no benefit.
BFHH can present with hypercalcemia associated
with mildly elevated PTH levels. The test of choice for
exclusion of BFHH is presence of low urinary calcium
(Table 13-1).
Parathyroid Gland: Diagnostic Evaluation
- A combination of elevated calcium and PTH levels is
highly suggestive of primary HPT. Again, BFHH can
be ruled out by presence of low urinary calcium.
Parathyroid Gland: Treatment
- Primary HPT is a surgical disease, and only parathyroidectomy can successfully treat the disease. The success of the operation is measured by the return of calcium to normal limits. Those with hypercalcemic crisis such as coma, delirium, anorexia, vomiting, and abdominal pain must be initially stabilized with vigorous intravenous hydration and forced diuresis with furosemide. Associated hypokalemia and hyponatremia must also be corrected. Once HPT is confirmed, preoperative localization of the suspecting gland may be performed in an attempt to perform minimally invasive surgery or assist in determining whether the source is from adenoma versus hyperplasia. Moreover, localization studies are indicated in those undergoing reoperative surgery for persistent or recurrent HPT. The preferred modality is technetium (Tc)-sestamibi scanning, including oblique and single photon emission computed tomography scans, but ultrasound and computed tomography may also be complementary. To maximize the success of surgery, preoperative Tc-sestamibi scanning and intraoperative rapid PTH assay are recommended. The intraoperative rapid PTH assay is a means to monitor adequate removal of the abnor-mal parathyroid gland. Once the tumor is removed, PTH levels should decrease to less than 50% of the baseline value in as short as 10 minutes. These two modalities also allow for a minimally invasive approach, decreasing operative time and length of stay.
Parathyroid Gland: Surgery
- Traditionally, the four gland bilateral neck exploration has been implemented without prior localization studies. Recently, with the assistance of preoperative Tc-sestamibi where a single adenoma is localized,a patient may undergo minimally invasive surgery, during which the gland of concern is targeted via a smaller incision, sometimes under regional anesthesia and as an outpatient procedure under experienced hands. If level of experience is sufficient, endoscopic parathyroidectomy is also used.If there is no localization preoperatively and ultra-sound is also nonrevealing, the likely finding is hyper-plasia. Four-gland exploration should be used. All four glands are identified in their usual locations before any removal; their size, appearance, and color will usually determine presence of abnormality without resorting to biopsy and pathologic confirmation. If all glands arehyperplastic, a subtotal parathyroidectomy, which is the equivalent to 3.5-gland removal, or total parathyroidec-tomy with autotransplantation is performed. If a missing gland is not identified in its usual loca-tion, the search for ectopic sites should be performed. These ectopic sites are related to the embryologic development. Thymic and thyroidal tissues may need to be encompassed as well.After surgery, although calcium levels may return to normal, the patient may still develop symptoms of hypocalcemia, such as perioral numbness/tingling,distal extremity paresthesias, and signs of a positive Chvostek, where the facial muscle twitches with tap-ping of the facial nerve.Calcium should be replen-ished, even if normal,in these instances.
Parathyroid Gland: Key Points
- Hyperparathyroidism is the most common cause of
hypercalcemia for which surgical intervention can
successfully treat the disease.
- There are many forms of hyperparathyroidism; however,
primary HPT is usually due to single-gland adenoma.
- Embryologic migration of parathyroid tissue deter-
mines resting location as well as ectopic sites.
- Hyperparathyroidism is diagnosed biochemically
using blood studies as well as urine tests.
- Minimally invasive surgery is possible as a result of
localization studies and rapid parathyroid hormone
assay availability.
