.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 increasesintestinal 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 hyperparathyroidismAdenomas- 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 surgicaltherapy 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 bemonitored 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, andlithium) 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 techniquesHave 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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HyperparathyroidismSecondry
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 Dsufficiency.
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 formationwithin 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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PATHOPHYSIOLOGYObserved 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.
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