Thyroid, Parathyroid THYROID Developmental Abnormalities Thyroglossal Duct Cyst and Sinus. Thyroglossal duct cysts may occur anywhere along the migratory path of the thyroid, although 80% are found in juxtaposition to the hyoid bone. usually asymptomatic but occasionally become infected by oral bacteria. hyroglossal duct sinuses result from infection of the cyst secondary to spontaneous or surgical drainage of the cyst and are accompanied by minor inflammation of the surrounding skin. Histologically, thyroglossal duct cysts are lined by pseudostratified ciliated columnar epithelium and squamous epithelium, with heterotopic thyroid tissue present in 20% of cases. The diagnosis usually is established by observing a 1- to 2-cm, smooth, well-defined midline neck mass that moves upward with protrusion of the tongue. Routine thyroid imaging is not necessary, although thyroid scintigraphy and ultrasound have been performed to document the presence of normal thyroid tissue in the neck. Treatment involves the “Sistrunk operation,” which consists of en bloc cystectomy and excision of the central hyoid bone to minimize recurrence.

Lingual Thyroid.: A lingual thyroid represents a failure of the median thyroid anlage to descend normally and may be the only thyroid tissue present. Ectopic Thyroid: Normal thyroid tissue may be found anywhere in the central neck compartment, including the esophagus, trachea, and anterior mediastinum. Thyroid tissue situated lateral to the carotid sheath and jugular vein, previously termed lateral aberrant thyroid, almost always represents metastatic thyroid cancer in lymph nodes, and not remnants of the lateral anlage that had failed to fuse with the main thyroid, as previously suggested by Crile. Even if not readily apparent on physical examination or ultrasound imaging, the ipsilateral thyroid lobe contains a focus of papillary thyroid cancer (PTC), which may be microscopic. Pyramidal Lobe: normally the thyroglossal duct atrophies, although it may remain as a fibrous band. In about 50% of individuals, the distal end that connects to the thyroid persists as a pyramidal lobe projecting up from the isthmus, lying just to the left or right of the midline. In the normal individual, the pyramidal lobe is not palpable

Thyroid Anatomy: The normal thyroid gland weighs approximately 20 g, but gland weight varies with body weight and iodine intake. an isthmus that is located just inferior to the cricoid cartilage. The strap muscles (sternohyoid, sternothyroid, and superior belly of the omohyoid) are located anteriorly and are innervated by the ansa cervicalis (ansa hypoglossi). The thyroid gland is enveloped by a loosely connecting fascia that is formed from the partition of the deep cervical fascia into anterior and posterior divisions. The true capsule of the thyroid is a thin, densely adherent fibrous layer that sends out septa that invaginate into the gland, forming pseudolobules. The thyroid capsule is condensed into the posterior suspensory or Berry’s ligament near the cricoid cartilage and upper tracheal rings. Blood Supply. The superior thyroid arteries. The inferior thyroid arteries. A thyroidea ima artery arises directly from the aorta or innominate in 1% to 4%. Nerves. the recurrent laryngeal nerve (RLN): The left & The right. Along their course in the neck, the RLNs may branch, and pass anterior, posterior, or interdigitate with branches of the inferior thyroid artery. The right RLN may be nonrecurrent in 0.5% to 1% of individuals and often is associated with a vascula anomaly. Nonrecurrent left RLNs are rare but have been reported in patients with situs inversus and a right-sided aortic arch. The RLN may branch in its course in the neck, and identification of a small nerve should alert the surgeon to this possibility. The last segments of the nerves often course below the tubercle and are closely approximated to the ligament of Berry. The RLNs terminate by entering the larynx posterior to the cricothyroid muscle . The superior laryngeal nerves also arise from the vagus nerves. Parathyroid Glands. Lymphatic System

Thyroid Physiology: Iodine Metabolism Thyroid Physiology: Iodine Metabolism. Thyroid Hormone Synthesis, Secretion, and Transport. T4 is produced and released entirely by the thyroid gland, whereas only 20% of the total T3 is produced by th thyroid. Most of the T3 is produced by peripheral deiodinati (removal of 5′-iodine from the outer ring) of T4 in the liver, muscles, kidney, and anterior pituitary, a reaction that is catalyzed by 5′-mono-deiodinase. Some T4 is converted to rT3, the metabolically inactive compound, by deiodination of the inner ring of T4. In conditions such as Graves’ disease, toxic multinodular goiter, or a stimulated thyroid gland, the proportion of T3 released from the thyroid may be dramatically elevated

Thyroid hormones are transported in serum bound to carrier proteins such as T4-binding globulin, T4-binding prealbumin, and albumin. Only a small fraction (0.02%) of thyroid hormone (T3 and T4) is free (unbound) and is the physiologically active component. T3 is the more potent of the two thyroid hormones, although its circulating plasma level is much lower than that of T4. T3 is less tightly bound to protein in the plasma than T4, and so it enters tissues more readily. T3 is three to four times more active than T4 per unit weight, with a half-life of about 1 day, compared to approximately 7 days for T4.

The thyroid gland also is capable of autoregulation, which allows it to modify its function independent of TSH. As an adaptation to low iodide intake, the gland preferentially synthesizes T3 rather than T4, thereby increasing the efficiency of secreted hormone. In situations of iodine excess, iodide transport, peroxide generation, and synthesis and secretion of thyroid hormones are inhibited. Excessively large doses of iodide may lead to initial increased organification, followed by suppression, a phenomenon called the Wolff-Chaikoff effect. Epinephrine and human chorionic gonadotropin hormones stimulate thyroid hormone production. Thus, elevated thyroid hormone levels are found in pregnancy and gynecologic malignancies such as hydatidiform mole. In contrast, glucocorticoids inhibit thyroid Lower parathyroid Upper parathyroid Int. jugular v. Recurrent laryngeal n. Thyroid Inferior thyroid a. Common carotid a. Figure 38-5. Relationship of the parathyroids to the recurrent laryngeal nerve. a. = artery; v. = vein. VRG RELEASE: tahir99 https://kickass. hormone production. In severely ill patients, peripheral thyroid hormones may be reduced, without a compensatory increase in TSH levels, giving rise to the euthyroid sick syndrome.

Thyroid Hormone Function: Thyroid hormones affect almost every system in the body. Thyroid hormones affect almost every system in the body. They are important for fetal brain development and skeletal maturation. T3 increases oxygen consumption, basal metabolic rate, and hea production by stimulation of Na+/K+ ATPase in various tissues. It also has positive inotropic and chronotropic effects on the heart by increasing transcription of the Ca2+ ATPase in the sarcoplasmic reticulum and increasing levels of β-adrenergic receptors and concentration of G proteins. Myocardial α receptors are decreased, and actions of catecholamines are amplified. Thyroid hormones are responsible for maintaining the normal hypoxic and hypercapnic drive in the respiratory center of the brain. They also increase gastrointestinal (GI) motility, leading to diarrhea in hyperthyroidism and constipation in hypothyroidism. Thyroid hormones also increase bone and protein turnover and the speed of muscle contraction and relaxation. They also increase glycogenolysis, hepatic gluconeogenesis, intestinal glucose absorption, and cholesterol synthesis and degradation.

Evaluation of Patients with Thyroid Disease Tests of Thyroid Function. TSH is the only test necessary in most patients with thyroid nodules that clinically appear to be euthyroid. Serum Thyroid-Stimulating Hormone (Normal 0.5–5 μU/mL) : There is an inverse relationship between the free T4 level and the logarithm of the TSH concentration— small changes in free T4 lead to a large shift in TSH levels. The ultrasensitive TSH assay has become the most sensitive and specific test for the diagnosis of hyper- and hypothyroidism and for optimizing T4 therapy. Total T4 (Reference Range 55–150 nmol/L) and T3 (Reference Range 1.5–3.5 nmol/L): Total T4 levels reflect the output from the thyroid gland, whereas T3 levels in the nonstimulated thyroid gland are more indicative of peripheral thyroid hormone metabolism, and are, therefore, not generally suitable as a general screening test. Total T4 levels are increased not only in hyperthyroid patients, but also in those with elevated Tg levels secondary to pregnancy, estrogen/progesterone use, or congenital diseases. Similarly, total T4 levels decrease in hypothyroidism and in patients with decreased Tg levels due to anabolic steroid use and protein-losing disorders like nephrotic syndrome.

Free T4 (Reference Range 12–28 pmol/L) and Free T3 (3–9 pmol/L): These radioimmunoassay-based tests are a sensitive and accurate measurement of biologically active thyroid hormone. Use of this test is confined to cases of early hyperthyroidism in which total T4 levels may be normal but free T4 levels are raised. Free T3 is most useful in confirming the diagnosis of early hyperthyroidism, in which levels of free T4 and free T3 rise before total T4 and T3. Thyrotropin-Releasing Hormone: his test is useful to evaluate pituitary TSH secretory function. Thyroid Antibodies: nclude anti-Tg, antimicrosomal, or anti-TPO and thyroid-stimulating immunoglobulin (TSI). Anti-Tg and anti-TPO antibody levels do not determine thyroid function, but rather indicate the underlying disorder, usually an autoimmune thyroiditis. About 80% of patients with Hashimoto’s thyroiditis have elevated thyroid antibody levels; however, levels may also be increased in patients with Graves’ disease, multinodular goiter, an occasionally, thyroid neoplasms. Serum Thyroglobulin Tg is only made by normal or abnormal thyroid tissue. It normally is not released into the circulation in large amounts but increases dramatically in destructive processes of the thyroid gland, such as thyroiditis, or overactive states such as Graves’ disease and toxic multinodular goiter. The most important use for serum Tg levels is in monitoring patients with differentiated thyroid cancer for recurrence, particularly after total thyroidectomy and RAI ablation. Tg antibodies can interfere with the accuracy of serum Tg levels and should always be measured when interpreting Tg levels.

Serum Calcitonin (0–4 pg/mL Basal) secreted by the C cells and functions to lower serum calcium levels, although in humans, it has only minimal physiologic effects. It is also a sensitive marker of MTC.

Thyroid Imaging Radionuclide Imaging: Both iodine-123 (123I) and iodine-131 (131I) are used to image the thyroid gland. Technetium Tc 99m pertechnetate (99mTc) 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) combined with computed tomography (CT) Ultrasound FNAB Computed Tomography/Magnetic Resonance Imaging Scan CT Combined PET-CT scans are increasingly being used for Tg positive, RAI-negative tumors.

Benign Thyroid Disorders Hyperthyroidism. Increased Hormone Synthesis (Increased RAIU) Release of Preformed Hormone (Decreased RAIU) Graves’ disease (diffuse toxic goiter) Toxic multinodular goiter Toxic adenoma Drug induced—amiodarone, iodine Thyroid cancer Struma ovarii Hydatidiform mole TSH-secreting pituitary adenoma Thyroiditis—acute phase of Hashimoto’s thyroiditis, subacute thyroiditis Factitious (iatrogenic) thyrotoxicosis “Hamburger thyrotoxicosis” RAIU = radioactive iodine uptake; TSH = thyroid-stimulating hormone.

Clinical Features: Hyperthyroid symptoms include heat intolerance, increased sweating and thirst, and weight loss despite adequate caloric intake. Symptoms of increased adrenergic stimulation include palpitations, nervousness, fatigue, emotional lability, hyperkinesis, and tremors. The most common GI symptoms include increased frequency of bowel movements and diarrhea. Female patients often develop amenorrhea, decreased fertility, and an increased incidence of miscarriages. Children experience rapid growth with early bone maturation, whereas older patients may present with cardiovascular complications such as atrial fibrillation and congestive heart failure.

On physical examination, weight loss and facial flushing may be evident. The skin is warm and moist. Tachycardia or atrial fibrillation is present, with cutaneous vasodilation leading to a widening of the pulse pressure and a rapid falloff in the transmitted pulse wave (collapsing pulse). A fine tremor, muscle wasting, and proximal muscle group weakness with hyperactive tendon reflexes often are present. The clinical manifestations of Graves’ disease can be divided into those related to hyperthyroidism and those specific to Graves’ disease.

Approximately 50% of patients with Graves’ disease also develop clinically evident ophthalmopathy, and dermopathy occurs in 1% to 2% of patients. It is characterized by deposition of glycosaminoglycans, leading to thickened skin in the pretibial region and dorsum of the foot (Fig. 38-12). Eye symptoms include lid lag (von Graefe’s sign), spasm of the upper eyelid revealing the sclera above the corneoscleral limbus (Dalrymple’s sign), and a prominent stare, due to catecholamine excess. True infiltrative eye disease results in periorbital edema, conjunctival swelling and congestion (chemosis), proptosis, limitation of upward and lateral gaze (from involvement of the inferior and medial rectus muscles, respectively), keratitis, and even blindness due to optic nerve involvement. Gynecomastia is common in young men. Rare bony involvement leads to subperiosteal bone formation and swelling in the metacarpals (thyroid acropachy). Onycholysis, or separation of fingernails from their beds, is a commonly observed finding. On physical examination, the thyroid usually is diffusely and symmetrically enlarged, as evidenced by an enlarged pyramidal lobe. There may be an overlying bruit or thrill over the thyroid gland and a loud venous hum in the supraclavicular space.

Treatment. Graves’ disease may be treated by any of three treatment modalities: antithyroid drugs, thyroid ablation with radioactive 131I, and thyroidectomy. propylthiouracil (PTU, 100 to 300 mg three time daily) and methimazole (10 to 30 mg three times daily, then once daily). 40% to 80% of patients developing recurrent disease after a 1- to 2-year course. The catecholamine response of thyrotoxicosis can be alleviated by administering β-blocking agents. Propranolol is the most commonly prescribed medication in doses of about 20 to 40 mg four times daily. Calcium channel blockers are useful for rate control in patients in whom β-blockers are contraindicated.

Riedel’s Thyroiditis Goiter. Any enlargement of the thyroid gland I referred to as a goiter.

Etiology of nontoxic goiter Classification Specific Etiology Endemic Medications Thyroiditis Familial Neoplasm Resistance to thyroid hormone Iodine deficiency, dietary, goitrogens (cassava, cabbage) Iodide, amiodarone, lithium Subacute, chronic (Hashimoto’s) I mpaired hormone synthesis from enzyme defects Adenoma, carcinoma __

Solitary Thyroid Nodule History. Details regarding the nodule, such as time of onset, change in size, and associated symptoms such as pain, dysphagia, dyspnea, or choking, should be elicited. Pain is an unusual symptom and, when present, should raise suspicion for intrathyroidal hemorrhage in a benign nodule thyroiditis, or malignancy. Patients with MTC may complain of a dull, aching sensation. A history of hoarseness is worrisome, risk factors for malignancy, such as exposure to ionizing radiation and family history of thyroid and other malignancies associated with thyroid cancer.

Physical Examination: Nodules that are hard, gritty, or fixed to surrounding structures such as the trachea or strap muscles are more likely to be malignant. The cervical chain of lymph nodes should be assessed as well as the nodes in the posterior triangle. Diagnostic Investigations: Fine-Needle Aspiration Biopsy FNAB. Laboratory Studies Serum calcitonin levels should be obtained in patients with MTC or a family history of MTC or MEN2. Imaging: Ultrasound is helpful. CT and MRI are unnecessary in the routine. Scanning the thyroid with 123I or 99mTc is rarely necessary, and thyroid scanning currently is recommended in the assessment of thyroid nodules only in patients who have follicular thyroid nodules on FNAB and a suppressed TSH. PET scanning does not play a major role in the primary evaluation of thyroid nodules.

Malignant Thyroid Disease Specific Tumor Types: Papillary Carcinoma PTC: 80% of all thyroid malignancies in iodine-sufficient areas and is the predominant thyroid cancer in children and individuals exposed to external radiation. Lymph node metastases are common. The diagnosis is established by characteristic nuclear cellular features. Psammoma bodies, which are microscopic, calcified deposits representing clumps of sloughed cells, also may be present.

Follicular Carcinoma : Follicular carcinomas account for 10% of thyroid cancers and occur more commonly in iodine-deficient areas. Unlike papillary cancers, cervical lymphadenopathy is uncommon at initial presentation (about 5%), although distant metastases may be present. In <1% of cases, follicular cancers may be hyperfunctioning. FNAB is unable to distinguish benign follicular lesions from follicular carcinomas. Malignancy is defined by the presence of capsular and vascular invasion. Surgical Treatment and Prognosis: Patients diagnosed by FNAB as having a follicular lesion should undergo thyroid lobectomy because at least 80% of these patients will have benign adenomas. older patients with follicular lesions >4 cm. atypia on FNA. a family history. history of radiation exposure. Total thyroidectomy should be performed when thyroid cancer is diagnosed. completion of total thyroidectomy primarily so that 131I can be used to detect and ablate metastatic disease.

Hürthle Cell Carcinoma: under the World Health Organization classification, are considered to be a subtype of follicular thyroid cancer. characterized by vascular or capsular invasion and, therefore, cannot be diagnosed by FNAB. they are more often multifocal and bilateral (about 30%), usually do not take up RAI (about 5%), metastasize to local nodes (25%) and distant sites. Management is similar to that of follicular neoplasms, with lobectomy and isthmusectomy being sufficient surgical treatment for unilateral Hurthle cell adenomas. When Hurthle cell neoplasms are found to be invasive on definitive paraffinsection histology, then total thyroidectomy should be performed. should undergo routine central neck node removal.

External-Beam Radiotherapy and Chemotherapy Postoperative Management of Differentiated Thyroid Cancer Radioiodine Therapy: RAI is more sensitive than chest x-ray or CT scanning for detecting metastases; however, it is less sensitive than Tg measurements for detecting metastatic disease in most differentiated thyroid cancers except Hurthle cell tumors. External-Beam Radiotherapy and Chemotherapy Thyroid Hormone: T4 is necessary as replacement therapy in patients after total or near-total thyroidectomy, and also has the additional effect of suppressing TSH and reducing the growth stimulus

Follow-Up of Patients with Differentiated Thyroid Cancer Thyroglobulin Measurement Tg and anti-Tg antibody levels should be measured initially at 6-month intervals. Imaging diagnostic whole-body scans, cervical ultrasound

Medullary Carcinoma MTC: arises from the parafollicular or C cells of the thyroid, C cells secrete calcitonin, most MTCs occur sporadically. However, approximately 25% occur within the spectrum of several inherited syndromes such as familial MTC, MEN2A, and MEN2B. Pain or aching is more common in patients with these tumors, and local invasion may produce symptoms of dysphagia, dyspnea, or dysphonia. Distant blood-borne metastases to the liver, bone (frequently osteoblastic), and lung occur later in the disease. Diagnosis. The diagnosis of MTC is established by history, physical examination, raised serum calcitonin, or CEA levels, and FNAB cytology of the thyroid mass.

Treatment: Pheochromocytomas need to be excluded Treatment: Pheochromocytomas need to be excluded. If patients are found to have pheochromocytoma, this must be operated on first. Total thyroidectomy is the treatment of choice for patients with MTC. Postoperative Follow-Up and Prognosis. Patients are followed by annual measurements of calcitonin and CEA levels, in addition to history and physical examination. Other modalities used to localize recurrent disease include ultrasound, CT, MRI, and more recently, FDG-PET/CT scans.

Anaplastic Carcinoma: The tumor is large and may be fixed to surrounding structures or may be ulcerated with areas of necrosis, Lymph nodes usually are palpable at presentation. Diagnosis is confirmed by FNAB. Core or incisional biopsy occasionally is needed to confirm the diagnosis, especially when there is necrotic material on the FNA. Treatment and Prognosis. This tumor is one of the most aggressive thyroid malignancies, with few patients surviving 6 months beyond diagnosis. A total or near-total thyroidectomy with therapeutic lymph node dissection is recommended for patients with an intrathyroidal mass. Cytotoxic chemotherapy.

Lymphoma can arise as part of a generalized lymphomatous condition, most thyroid lymphomas develop in patients with chronic lymphocytic thyroiditis. Treatment and Prognosis: thyroid lymphoma respond rapidly to chemotherapy. Combined treatment with radiotherapy and chemotherapy often is recommended. Thyroidectomy and nodal resection are used to alleviate symptoms of airway obstruction in patients who do not respond quickly to the above regimens or who have completed the regimen before diagnosis. Metastatic Carcinoma

PARATHYROID Parathyroid Physiology and Calcium Homeostasis: Calcium is the most abundant cation in human beings and has several crucial functions. Calcium is absorbed from the small intestine in its inorganic form. Extracellular calcium (900 mg) accounts for only 1% of the body’s calcium stores, the majority of which is sequestered in the skeletal system. Approximately 50% of the serum calcium is in the ionized form, which is the active component. The total serum calcium levels range from 8.5 to 10.5 mg/dL (2.1 to 2.6 mmol/L). The total serum calcium level must always be considered in its relationship to plasma protein levels, especially serum albumin.

Parathyroid Hormone PTH: PTH secretion by sensing extracellular calcium levels. PTH secretion also is stimulated by low levels of 1,25-dihydroxy vitamin D, catecholamines, and hypomagnesemia. PTH is synthesized in the parathyroid gland. PTH functions to regulate calcium levels via its actions on three target organs, the bone, kidney, and gut. PTH increases the resorption of bone by stimulating osteoclasts and promotes the release of calcium and phosphate into the circulation. PTH acts to limit calcium excretion at the distal convoluted tubule. PTH also inhibits phosphate reabsorption (at the proximal convoluted tubule) and bicarbonate reabsorption. It also inhibits the Na+/H+ antiporter, which results in a mild metabolic acidosis in hyperparathyroid states. PTH and hypophosphatemia also enhance 1-hydroxylation of 25-hydroxyvitamin D,

Calcitonin: functions as an antihypercalcemic hormone by inhibiting osteoclastmediated bone resorption. Calcitonin plays a minimal, if any, role in the regulation of calcium levels in humans. Vitamin D: Vitamin D refers to vitamin D2 and vitamin D3, both of which are produced by photolysis of naturally occurring sterolprecursors. Vitamin D2 is available commercially in pharma-ceutical preparations, whereas vitamin D3 is the most important physiologic compound. Vitamin D stimulates the absorption of calcium and phosphate from the gut and the resorption of calcium from the bone.

Hyperparathyroidism Hyperfunction of the parathyroid glands may be classified as primary, secondary, or tertiary. PHPT arises from increased PTH production from abnormal parathyroid glands and results from a disturbance of normal feedback control exerted by serum calcium. Elevated PTH levels may also occur as a compensatory response to hypocalcemic state resulting from chronic renal failure or GI malabsorption of calcium. This secondary HPT can be reversed by correction of the underlying problem. chronically stimulated glands may occasionally become autonomous, resulting in persistence or recurrence of hypercalcemia after successful renal transplantation, resulting in tertiary HPT.

Primary Hyperparathyroidism: Increased PTH production leads to hypercalcemia via increased GI absorption of calcium, increased production of vitamin D3, and reduced renal calcium clearance. PHPT is characterized by increased parathyroid cell proliferation and PTH secretion that is independent of calcium levels. PHPT results from the enlargement of a single gland or parathyroid adenoma in approximatel 80% of cases, multiple adenomas or hyperplasia in 15% to 20% of patients, and parathyroid carcinoma in 1% of patients. It should be emphasized that when more than one abnormal parathyroid gland is identified preoperatively or intraoperatively, the patient has hyperplasia (all glands abnormal) until proven otherwise. inherited disorders such as MEN1, MEN2A, isolated familial HPT.

Primary Hyperparathyroidism (cont.): Clinical Manifestations: PHPT formerly presented with the “classic” pentad of symptoms (i.e., kidney stones, painful bones, abdominal groans, psychic moans, and fatigue overtones). Currently, most patients present with weakness, fatigue, polydipsia, polyuria, nocturia, bone and joint pain, constipation, decreased appetite, nausea, heartburn, pruritus, depression, and memory loss. An increased incidence of pancreatitis. cholelithiasis, chondrocalcinosis, gout, and pseudogout. Calcification at ectopic sites such as blood vessels, cardiac valves, and skin

Primary Hyperparathyroidism (cont.): Physical Findings: Parathyroid tumors are seldom palpable. A palpable neck mass in a patient with PHPT is more likely to be thyroid in origin or a parathyroid cancer.

Differential diagnosis of hypercalcemia Hyperparathyroidism Malignancy—hematologic (multiple myeloma), solid tumors (due to PTHrP) Endocrine diseases—hyperthyroidism, Addisonian crisis, VIPoma Granulomatous diseases—sarcoidosis, tuberculosis, berylliosis, histoplasmosis Milk-alkali syndrome Drugs—thiazide diuretics, lithium, vitamin A or D intoxication Familial hypocalciuric hypercalcemia Paget’s disease Immobilization PTHrP = parathyroid hormone-related protein; VIP = vasoactive intestinal peptide.

The presence of an elevated serum calcium and intact PTH or two-site PTH levels, without hypocalciuria, establishes the diagnosis of PHPT with virtual certainty. FNAB of such a tumor for PTH levels or selective venous catheterization of the veins draining such tumors can help clarify the diagnosis. Treatment: ndications for Parathyroidectomy and Role of Medical Management. Developed complications and have “classic” symptoms of PHPT should undergo parathyroidectomy.

Preoperative Localization Tests. noninvasive or invasive modalities Commonly used parathyroid localization studies Preoperative, noninvasive: Sestamibi-technetium-99m scan Ultrasound CT scan MRI scan Four-dimensional CT scan Preoperative, invasive: Preoperative, invasive Angiogram Venous sampling Intraoperative: PTH assay

Secondary Hyperparathyroidism. Secondary HPT commonly occurs in patients with chronic renal failure but also may occur in those with hypocalcemia secondary to inadequate calcium or vitamin D intake or malabsorption. These patients generally are treated medically with a low-phosphate diet, phosphate binders, adequate intake of calcium and 1, 25-dihydroxy vitamin D, and a high-calcium, low-aluminum dialysis bath. Assessment of parathyroid mass is thought to be an important factor for predicting the response to medical management. Therefore, some groups recommend parathyroidectomy if the glands are >1 cm (or >500 mm3) on ultrasound. These glands are apparently more likely to have developed nodular hyperplasia and hence might be refractory to medical management. Following the introduction of calcimimetics, there appears to have been a reduction in parathyroidectomy rates.

Tertiary Hyperparathyroidism Generally, renal transplantation is an excellent method of treating secondary HPT, but some patients develop autonomous parathyroid gland function and tertiary HPT. Tertiary HPT can cause problems similar to PHPT. Similar to patients with secondary HPT, many patients with tertiary HPT are being treated with cinacalcet. operative intervention is indicated for symptomatic disease or if autonomous PTH secretion persists for >1 year after a successful transplant in patients who are deemed operative candidates. All parathyroid glands should be identified. The traditional surgical management of these patients consisted of subtotal or total parathyroidectomy with autotransplantation and an upper thymectomy.

Hypoparathyroidism By far, the most common cause o hypoparathyroidism is thyroid surgery, particularly total thyroidectomy with a concomitant central neck dissection. often develop transient hypocalcemia due to ischemia of the parathyroid glands; permanent hypoparathyroidism is rare. Hypoparathyroidism also may occur after parathyroid surgery, which is more likely if patients undergo a subtotal resection or total parathyroidectomy with parathyroid autotransplantation.

Acute hypocalcemia results in decreased ionized calcium and increased neuromuscular excitability. Patients initially develop circumoral and fingertip numbness and tingling. Mental symptoms include anxiety, confusion, and depression. Physical examination reveals positive Chvostek’s sign (contraction of facial muscles elicited by tapping on the facial nerve anterior to the ear) and Trousseau’s sign (carpopedal spasm that is elicited by occluding blood flow to the forearm with a blood pressure cuff for 2–3 minutes). Tetany, which is characterized by tonic-clonic seizures, carpopedal spasm, and laryngeal stridor, may prove fatal and should be avoided. Most patients with postoperative hypocalcemia can be treated with oral calcium and vitamin D supplements; IV calcium infusion is rarely required except in patients with preoperative osteitis fibrosa cystica.

Conditions causing hypocalcemia • Surgical • Neonatal • Familial Hypoparathyroidism • Surgical • Neonatal • Familial • Heavy metal deposition • Magnesium depletion Resistance to the action of parathyroid hormone • Pseudohypoparathyroidism • Renal failure • Medications—calcitonin, bisphosphonates, mithramycin Failure of normal 1,25-dihydroxy vitamin D production Resistance to the action of 1,25-dihydroxy vitamin D Acute complex formation or deposition of calcium • Acute hyperphosphatemia • Acute pancreatitis • Massive blood transfusion (citrate overload) • “Hungry bones”