Download MBBS General Surgery PPT 7 Parathyroid Gland Lecture Notes

PARATHYROID GLAND

Anatomy and Embryology

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.4 parathyroid glands situated posterior to the thyroid.

.Superior glands:

Found just superior to the intersection of the inferior thyroid artery and the recurrent

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laryngeal nerve.

Derived from the fourth pharyngeal pouch.

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Occasional y found within the substance of the thyroid gland.

.Inferior glands

Derived from the third pharyngeal pouch.

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Embryologic association with the thymus, the inferior glands are often found adjacent to or

within the thymus.

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Usual y located near the inferior pole of the thyroid.
Physiology

.Parathyroid Hormone:

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Primarily responsible for maintaining extracel ular calcium concentrations.

Secretion is regulated directly by the plasma conc. of ionized calcium.

.Effects of parathyroid hormone

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Increase the concentration of plasma calcium by-

o Increasing the release of calcium and phosphate from bone matrix.
o Increasing calcium reabsorption by the kidney.

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o And increasing renal production of 1,25-dihydroxyvitamin D-3 (calcitriol), which increases

intestinal absorption of calcium.

Also causes phosphaturia, thereby decreasing serum phosphate levels.

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Primary Hyperparathyroidism

.Unregulated overproduction of parathyroid hormone (PTH) resulting in

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abnormal calcium homeostasis.

.Etiology:

Hyperplasia Or Adenoma

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85% of cases- a single adenoma.

15% of cases- multiple glands are involved (ie, either multiple adenomas or hyperplasia)

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Rarely- parathyroid carcinoma.
Primary Hyperparathyroidism

.Most cases- sporadic.

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.Familial cases can occur either as part of-

Multiple endocrine neoplasia syndromes (MEN 1 or MEN 2a).

Hyperparathyroid-jaw tumor (HPT-JT) syndrome.

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Familial isolated hyperparathyroidism (FIHPT).

Pathophysiology

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.In primary hyperparathyroidism

Adenomas- the normal feedback on parathyroid hormone production by

extracel ular calcium seems to be lost.

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In parathyroid hyperplasia- an increase in the cel numbers is probably the

cause.

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.The chronic excessive resorption of calcium from bone-

Result in osteopenia/ osteoporosis.
Pathophysiology....

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.In severe cases-

May result in Osteitis Fibrosa Cystica.

Subperiosteal resorption of the distal phalanges.

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Tapering of the distal clavicles.

Salt-and-pepper appearance of the skul .

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And brown tumors of the long bones.

The chronical y increased excretion of calcium in the urine-

Can predispose to the formation of renal stones.

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Pathophysiology....

.Other symptoms due to the hypercalcemia itself-

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Muscle weakness, fatigue.

Volume depletion, nausea and vomiting.

And in severe cases- coma and death.

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Neuropsychiatric manifestations are particularly common and may include

depression.

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Can increase gastric acid secretion-

o may have a higher prevalence of peptic ulcer disease.

Pancreatitis.

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Symptoms

.The clinical syndrome of primary hyperparathyroidism:

"Bones, stones, abdominal groans, and psychic moans."

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.Skeletal manifestations include-

Bone and joint pain, pseudogout, and chondrocalcinosis.

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Osteitis fibrosa cystica.

.Renal manifestations include-

Polyuria, kidney stones, hypercalciuria and rarely nephrocalcinosis.

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Symptoms....

.Gastrointestinal manifestations include-

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Anorexia, nausea, vomiting.

Abdominal pain, constipation, peptic ulcer disease.

And acute pancreatitis.

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.Neuromuscular and psychologic manifestations include-

Proximal myopathy, weakness and easy fatigability.

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Depression, inability to concentrate, and memory problems.

.Cardiovascular manifestations include-

Hypertension, bradycardia, and left ventricular hypertrophy

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Examination

.Physical examination findings- usually noncontributory.

.Examination may reveal- muscle weakness and depression.

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.A palpable neck mass-

not usual y expected with hyperparathyroidism

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in rare cases, it may indicate parathyroid cancer.

Workup
Blood

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.Total serum calcium and albumin levels or ionized calcium levels.

Hypercalcemia should be documented on more than one occasion before a

diagnostic workup is undertaken.

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.An elevated intact parathyroid hormone level with an elevated ionized

serum calcium level-

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Diagnostic of primary hyperparathyroidism.

.A 24-hour urine calcium measurement- is necessary to rule out FHH.

.Mild hyperchloremic acidosis, hypophosphatemia, and mild-to-moderate

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increase in urinary calcium excretion rate.

Imaging

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.Imaging studies are used to guide the surgeon once surgical

therapy has been decided.

.Nuclear medicine scanning with Radiolabeled Sestamibi-

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A widely used technique.

Radionuclide concentrated in thyroid and parathyroid tissue-

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Usually washes out of normal thyroid tissue in under an hour.

Persists in abnormal parathyroid tissue.

Therefore, on delayed images, an abnormal parathyroid is seen as a persistent focus

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of activity.
Imaging....

.Ultrasonography of the neck-

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May be equivalent or superior to sestamibi scanning.

.CT scanning and MRI-

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Now been largely replaced by sestamibi scanning and ultrasound.

.Dual-energy X-ray absorptiometry (DXA)-

A useful tool to demonstrate the skeletal involvement in primary

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hyperparathyroidism.

Treatment
Hypercalcemic Crisis

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.Intravascular volume expansion with sodium chloride.

.Loop diuretics such as furosemide once the intravascular volume is

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restored.

.Drugs such as calcitonin and IV bisphosphonate have been used as a

temporary measure prior to surgical treatment.

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Medical Treatment

.Monitoring:

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Patients who do not meet the guidelines for surgical intervention can be

monitored safely.

.Annual assessment:

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For overt signs and symptoms of primary hyperparathyroidism.

Serum creatinine level

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And 3-site dual-energy x-ray absorptiometry (DXA) study.

.Serum calcium should be checked every 6 months.
Medical Treatment....

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.Diet and lifestyle:

Patients should maintain a moderate daily elemental calcium intake of

800-1000 mg and a vitamin D intake appropriate for their age and sex.

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Maintaining good hydration.

Participation in regular exercise activity.

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And avoidance of certain medications (such as thiazides, diuretics, and

lithium) are desirable.

Medical Treatment....

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.Pharmacotherapy:

Estrogen therapy.

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Selective estrogen receptor modulators-

such as raloxifene.

Bisphosphonates-

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Alendronate.

Calcimimetic drugs-

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such as cinacalcet.
Medical Treatment....

.Other treatments:

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Percutaneous alcohol injection and other percutaneous ablation techniques

Have been suggested as an alternative treatment in patients who

cannot or wil not undergo surgery.

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Percutaneous techniques have high complication rates in smal

numbers of patients

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Their routine use cannot yet be supported.

Surgery

.Indications for surgery-

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1.0 mg/dL above the upper limit of the reference range for serum

calcium.

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24-hour urinary calcium excretion greater than 400 mg.

A 30% reduction in creatinine clearance.

Bone mineral density T-score below -2.5 at any site.

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Age younger than 50 years.
Surgery....

.Standard operative approach:

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Complete neck exploration with identification of al parathyroid glands.

OR

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Removal of al abnormal glands with autotransplantation.

In the case of 4-gland hyperplasia-

3.5-gland parathyroidectomy is performed.

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A nonabsorbable suture is left as a tag to identify the gland.

Secondry

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Hyperparathyroidism
Secondry

Hyperparathyroidism

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.Secondary hyperparathyroidism:

Overproduction of parathyroid hormone

Secondary to a chronic abnormal stimulus for its production.

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.Typically, this is due to chronic renal failure.

.Another common cause is vitamin D deficiency.

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Etiology

.In chronic kidney disease-

Overproduction of parathyroid hormone occurs in response to

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hyperphosphatemia, hypocalcemia.

And impaired 1,25-dihydroxyvitamin D production by the diseased kidneys.

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.Hyperphosphatemia-

Directly stimulate parathyroid hormone synthesis and parathyroid

hyperplasia.

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And indirectly promotes secondary hyperparathyroidism by decreasing free

calcium level.
Clinical Features

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.Virtually all patients with renal failure have

Hyperparathyroidism to some degree

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Clinical presentation is often that of renal failure.

.In secondary hyperparathyroidism due to vitamin D deficiency

Symptoms are mainly due to the vitamin deficiency

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E.g.- osteomalacia with increased fracture risk, myopathy.

.In advanced cases- some patients may have bone pain.

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Workup

.Serum level of parathyroid hormone, calcium, phosphorus, and 25-

hydroxyvitamin D should be measured.

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.Patients with secondary hyperparathyroidism usually have

A low-normal calcium and elevated parathyroid hormone.

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.The phosphate level may vary based on the etiology-

High values in renal insufficiency

And low values in vitamin D deficiency.

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Treatment

.Medical management is the mainstay of treatment for secondary

hyperparathyroidism.

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.Correcting vitamin D deficiency can be achieved using-

50,000-IU capsule of vitamin D-2 once a week for 8 weeks

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and repeating the course for another 8 weeks if needed to achieve vitamin D

sufficiency.

Treatment

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.Current nonsurgical treatment options for management of secondary

hyperparathyroidism in chronic kidney disease:

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Dietary phosphate restriction .

Phosphate binders can be used if hyperphosphatemia persists despite dietary

phosphate restriction.

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Calcium-based phosphate binders such as calcium carbonate or calcium acetate

Non-calcium-based phosphate binders such as sevelamer hydrochloride or lanthanum carbonate

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Calcium supplementation should be limited to less than 2 g/d.

Vitamin D and its analogs.

Treatment with calcimimetics such as cinacalcet.

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Treatment

.Indications for surgery include-

Bone pain or fracture

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Pruritus, calciphylaxis

And extraskeletal nonvascular calcifications with elevated PTH levels

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despite appropriate medical therapy.

Tertiary

Hyperparathyroidism

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Tertiary Hyperparathyroidism

.Tertiary disease is characterized by-

Development of autonomous hypersecretion of parathyroid hormone causing

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hypercalcemia.

.Etiology is unknown.

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. but may be due to monoclonal expansion of parathyroid cells (nodule formation

within hyperplastic glands).

. A change may occur in the set point of the calcium-sensing mechanism to

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hypercalcemic levels.

. Four-gland involvement occurs in most patients.

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PATHOPHYSIOLOGY
Observed most commonly in-

Patients with chronic secondary hyperparathyroidism and often after renal

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transplantation.

Hypertrophied parathyroid glands fail to return to normal-

Continue to over secrete parathyroid hormone, despite serum calcium levels that

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are within the reference range or even elevated.

Hypertrophied glands become autonomic and cause hypercalcemia, even after

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withdrawal of calcium and calcitriol therapy.

This type of tertiary disease is particularly dangerous because the
phosphate level is often elevated.
TREATMENT

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.Total parathyroidectomy with autotransplantation

.Subtotal parathyroidectomy.