Disorders of the Parathyroid Gland

EMBRYOLOGY AND ANATOMY

Parathyroid Embryology
In humans, the superior parathyroid glands are derived from the fourth branchial pouch, which also gives rise to the thyroid gland. The third branchial pouches give rise to the inferior parathyroid glands and the thymus

Parathyroid Embryology
The position of normal superior parathyroid glands is more consistent, with 80% of these glands being found near the posterior aspect of the upper and middle thyroid lobes, at the level of the cricoid cartilage. Enlarged superior glands may "descend by gravity" in the tracheoesophageal groove and come to lie caudal to the inferior glands.

Parathyroid Embryology
As the embryo matures, the thymus and inferior parathyroids migrate together caudally in the neck. The most common location for inferior glands is within a distance of 1 cm from a point centered where the inferior thyroid artery and recurrent laryngeal nerve cross.

Parathyroid Embryology
The position of the inferior glands, however, tends to be more variable as a consequence of their longer migratory path. Undescended inferior glands may be found near the skull base, angle of the mandible, or superior to the superior parathyroid glands, along with an undescended thymus.

Parathyroid Anatomy
The usual weight, size, and fat content of a normal parathyroid gland vary. The weight of a normal gland has been recorded to be as low as 40 mg, and a limit of 50 to 60 mg has been suggested Chronic illness, race, and other individual variations may affect the weights of normal parathyroid glands.
In patients with chronic illness, total glandular weights are lower male and black patients, total glandular weights are higher.

Normal dimensions of 3 to 6 mm in length, 2 to 4 mm in width, and 0.5 to 2 mm in thickness, and an average of three dimensions of 5 mm 3 mm 1 mm have been proposed.

Parathyroid Anatomy
The stromal fat content of parathyroid glands is the hallmark in the evaluation of their functional status. Detailed studies of normal glands have shown wide variations in fat content The variability of fat content reported by different studies suggests that measurement of stromal fat within parathyroid glands has become nearly useless as an indicator of function. In children and adolescents, parathyroid glands contain very sparse amounts of fat. After adolescence, stromal fat progressively increases until 25 to 30 years of age; subsequently fat content is largely determined by constitutional factors. Women seem to have a tendency to have higher glandular fat content, which may be related to total body fat concentrations.

Parathyroid Anatomy
The characteristic cellular content of the normal gland is dominated by chief cells with rare water clear cells. Oxyphil cell concentrations tend to increase with age and are noted to be rare in young individuals. Oxyphil cell concentrations seem to be more common in adults older than 40 years.

Parathyroid Anatomy
Four parathyroid glands is the usual number found in humans The presence of supernumerary parathyroid glands is rare, and may have important clinical consequences, especially with respect to patients with hyperparathyroidism resulting from multiple-gland disease.
In a series of 2015 patients who were operated on for primary hyperparathyroidism, a hyperfunctioning supernumerary ffith parathy roid gland was the source of hypercalcemia in 15 patients (0.7%). Nine of these patients required reoperation to remove the supernumeriary gland representing the parathyroid tumor. Most of these fifth gland tumors were located in the mediastinum, either in the thymus (seven tumors) or related to the aortic arch (three tumors).

Parathyroid Anatomy
The location of parathyroid glands may vary, as a consequence of the variation in degree of migratory descent during development. Additional infuences on these variable locations involves displacement of enlarged parathyroid glands during the development of hyperparathyroidism. Enlarged parathyroid glands tend to migrate in a fbroareolar plane, which offers little resistance as a result of gravity and the action of swallowing and variations in intrathoracic pressure

Parathyroid Anatomy
Eighty percent of the superior parathyroid glands are found at the cricothyroid junction approximately 1 cm cranial to the juxtaposition of the recurrent laryngeal nerve and the inferior thyroid artery. The superior parathyroids, which are intimately associated with the posterior capsule of the superior thyroid pole, are usually covered by an extension of the pretracheal fascia that envelopes the thyroid gland and connects it to the hypopharynx and esophagus and the carotid sheath. The relationship of these superior parathyroid glands with the pretracheal fascia is such that the glands themselves are allowed freedom of movement under this pseudocapsule. This feature discriminates parathyroid glands from thyroid nodules, which cannot move freely because they are enveloped by the true capsule of the thyroid gland

Parathyroid Anatomy
Normal superior parathyroid glands may be found in the retroesophageal or paraesophageal space in approximately 1% of all instances. These spaces represent sites where enlarged superior parathyroid glands potentially descend to the superior and posterior mediastinum.

Parathyroid Anatomy
The inferior parathyroid glands tend to have a more variable location. Greater than 50% of the inferior parathyroid glands are situated neighboring the lower pole of the thyroid gland. Twenty-eight percent of the inferior parathyroids are found within the thyrothymic ligament or within the anterior superior mediastinal thymic gland. The migratory pattern of inferior parathyroid glands tends to follow a pathway into the anterior superior mediastinum, where one third of all missed parathyroid tumors may be found.

Parathyroid Anatomy
The incidence of intrathyroidal parathyroid glands is controversial. Wang considered the superior parathyroid gland the most likely to be intrathyroidal primarily because of the close embryologic relationship of the primordium of the superior parathyroid gland with the lateral complex of the thyroid.

Parathyroid Anatomy
The overall incidence of intrathyroidal parathyroid glands ranges from approximately 0.5% to 3% as reported in the literature

 Parathyroid glands that are located in loose connective tissue generally are more characteristically ovalshaped, bean-shaped, or teardrop-shaped. The color of normal parathyroid glands ranges from yellowish brown to reddish brown. Generally, the color may depend on the amount of stromal fat, oxyphil cell concentration, and degree of vascularity Normal glands tend to be more reddish brown or rustcolored in younger patients, whereas older individuals have parathyroid glands of a more yellow-brown or tobacco color.

 Enlarged hyperfunctional parathyroid glands have a color variation from dark brown to light yellow. Enlarged glands occurring in either secondary or tertiary hyperparathyroidism may have a lighter gray tone to the coloration. Parathyroid carcinoma can also show a mottled gray-to-white surface appearance

 Normal parathyroid glands most commonly are supplied by a single dominant artery (80%). The length of the dominant artery supplying the parathyroid gland may vary from 1 to 40 mm. In most instances, the superior and inferior parathyroid glands derive their dominant arterial blood supply from the inferior thyroid artery.

 Abundant arterial anastomoses exist between the parathyroid glands and include anastomoses with thyroid arteries and dominant arteries of the larynx, pharynx, esophagus, and trachea. Of the superior parathyroid glands, 20% or more may be vascularized solely by the superior thyroid artery. 10% of the inferior parathyroid glands derived their dominant arterial supply from a branch of the superior thyroid artery. In most of these instances, the inferior thyroid artery was noted to be absent.

 The venous drainage distribution of the parathyroid glands generally runs parallel to the arterial vessels and drains via the neighboring thyroid venous tributaries into the internal jugular system. Similarly, lymphatics from the parathyroid glands drain with the lymphatics of the thyroid gland into the paratracheal and deep cervical lymphatic basins.

 The parathyroid glands are enveloped in their own thin collagenous connective tissue capsule. This capsule extends septa into the gland, which separate the parenchyma into elongated chords or clusters of functional secretory cells. Blood vessels, lymphatics, and nerves travel along the septa to reach the interior of the gland

 The major functional parenchymal cells of the parathyroid glands are the chief cells, which are slightly eosinophilic staining and measure 5 to 8 in diameter. These granules contain PTH, which is synthesized from a precursor of prepro-PTH. With increasing age, the secretory cells of the parathyroid glands may be replaced by adipose cells, which may make up 50% to 60% of the gland in older individuals.

 The second cell type making up parathyroid glandular parenchyma is the oxyphil cell. Although their function is unknown, it is believed that oxyphil cells and a third cell type, sometimes described as intermediate cells, may represent inactive phases of a single cell type Oxyphil cells are less numerous, are larger (6 to 10 millimicrons in diameter), and stain more deeply with eosin than chief cells.

Parathyroid Gland Physiology

Calcium Homeostasis
Produce parathyroid hormone which maintains extracellular fluid calcium level on a normal range It acts on bones, kidneys and intestines

 Acts directly on bones which promotes calcium resorption, produces remodelling effect of osteoclast and osteoblast activity. Acts directly on kidneys promotes calcium reabsorption and decrease tubular reabsorption of phosphorus Increase synthesis of 1,25 dihydroxyvitamin D, increase gastrointestinal calcium absorption

Bone
osteoblasts have receptor proteins for binding PTH PTH activate the calcium pump, causing rapid removal of calcium phosphate salts amorphous bone crystals that lie near the cells. PTH stimulate by increasing calcium permeability of the bone fluid of the osteocytic membrane, allowing calcium ions to diffuse into the membrane cells from the bone fluid

Kidneys
PTH also increases renal tubular reabsorption of calcium at the same time that it diminishes phosphate reabsorption increased calcium absorption occurs mainly in the late distal tubules, the collecting tubules

 Vitamin D in promotes bone calcification One of the ways in which it does this is to increase calcium and phosphate absorption from the intestines

 effect of PTH is mediated by the cyclic adenosine monophosphate (cAMP) second messenger mechanism the concentration of cAMP increases in the target cells

 Calcium most potent regulator of parathyroid hormone secretion ECF Calcium controls PTH secretions by interaction of with calcium sensor, GPCR Receptors are present in parathyroid glands and calcitonin producing cells of thyroid gland

Negative feedback control

parathyroid glands have calcium-binding surface receptors that are the same as the receptors found on calcitonin-secreting cells of the thyroid and on the calcium-absorbing cells of the kidneys Ca binding to the receptors depresses the release of PTH

 slightest decrease in calcium ion concentration in the extracellular fluid causes the parathyroid glands to increase their rate of secretion within minutes conditions that increase the calcium ion concentration above normal cause decreased activity and reduced size of the parathyroid glands

 excess quantities of calcium in the diet increased vitamin D in the diet Bone absorption caused by factors other than PTH

 Blood Ca2+ is low, receptors on parathyroid cells are activated, and PTH is produced high calcium concentration inhibits the secretion of preformed PTH from storage granules in the parathyroids calcitonin, which is produced in parafollicular cells (C cells) of the thyroid gland, works in opposition to PTH and acts to decrease blood calcium concentration

Calcitonin
peptide hormone secreted by the thyroid gland, tends to decrease plasma calcium concentration and, effects opposite to those of PTH primary stimulus for calcitonin secretion is increased plasma calcium ion concentration

 immediate effect is to decrease the absorptive activities of the osteoclasts and possibly the osteolytic effect of the osteocytic membrane throughout the bone decrease the formation of new osteoclasts minor effects on calcium handling in the kidney tubules and the intestines

DISEASE ENTITIES AND CLINICAL PRESENTATION FOR PTG DISEASES

Outline
Hyperparathyroidism
Primary Secondary Tertiary

Hypercalcemic Crisis Hypoparathyroidsm Inherited Parathyroid Disease

Hyperparathyroidism
Incidence increased after the introduction of routine serum calcium assessment (1970s) Common among women, usually beyond menopause
Every woman has a 1% risk of experiencing primary hyperparathyroidism during her lifetime

Hyperparathyroidism
Classification Primary Secondary Tertiary Definition Autonomous secretion Response to normal regulatory stimuli Refractory secondary HPT with hypercalcemia

Clinical Manifestations
Classic Pentad:
Kidney stones Painful bones Abdominal groans Psychic moans Fatigue overtones

Clinical Manifestations
Two populations may be identified:
Disease progresses insidiously over several years and eventually manifests as renal colic Symptoms manifest over a considerably shorter time with marked elevations in serum calcium leading to weight loss, acute gastrointestinal symptoms, anorexia, bone pain, and occasionally pathologic fracture

Clinical Manifestations
Minimally symptomatic
Non-specific complaints
Emotional complaints Muscular fatigue Constipation Bone and joint pain Asymptomatic renal calculi Decreased bone mineral density

Eliminated by parathyroidectomy

Clinical Manifestations
Kidney and Urinary Tract
Nephrolithiasis or nephrocalcinosis
Majority: Calcium oxalate Calcium phosphate

S/Sx:
Renal Colic Hematuria Pyuria Metabolic acidosis

Clinical Manifestations
Skeletal System
Osteitis Fibrosis Cystica (now rare, <10%)
Subperiosteal erosion of the distal phalanges Bone wasting and softening Distal tappering of the clavicles salt and pepper appearance of the skull Bone cysts and brown tumors of the long bones Chondrocalcinosis

S/Sx: Bone pain, pathologic fracture, cystic bone changes, focal areas of bone swelling (epulis of the jaw or brown tumors) Bone loss occurs at cortical bone sites generally sparing the trabecular bone

Clinical Manifestations
Neuromuscular System
Proximal muscle weakness Progressive fatigue and malaise EMG changes with atrophy of the skeletal muscle on biopsy specimens

Clinical Manifestations
Neurologic
Spectrum: from anxiety and mild emotional disturbance to frank psychosis Depression, nervousness, and cognitive dysfunction in primary hyperparathyroidism Cerebral dysfunction is more common in elderly patients with an underlying mild cognitive abnormality exposed to hypercalcemia Others: deafness, dysphagia, dysosmia, and dysesthesia

Clinical Manifestations
Gastrointestinal
Peptic Ulcer Disease
Hypercalcemia Gastrin Gastric acid secretion

Pacreatitis Cholelithiasis
biliary calcium calicium bilirubinate stones

Sluggish bowels or constipation in asymptomatic

Clinical Manifestations
Cardiovascular
Hypertension

Primary Hyperparathyroidism
Third most common endocrine disorder Results from a hyperfunction of the parathyroid glands Generalized disorder of calcium, phosphate, and bone metabolism

Primary Hyperparathyroidism
Causes
Hyperplasia Adenoma, lipoadenoma Carcinoma
Primary Multiple Endocrine Neoplasia [MEN] Type 1 Multiple Endocrine Neoplasia [MEN] Type 2a

Lithium therapy

Primary Hyperparathyroidism

Secondary Hyperparathyroidism
Refers to the excessive secretion of PTH by the parathyroid glands in response tohypocalcemia and associated hypertrophy of the glands Especially seen in patients with chronic renal failure

Secondary Hyperparathyroidism

Tertiary Hyperparathyroidism
Long standing renal failure s/p renal transplant Autonomous parathyroid gland function and tertiary HPT. Can cause problems similar to primary hyperparathyroidism

Summary

Hypercalcemic Crisis
Hypercalcemia may decompensate from a more or less chronic status into a critical and life-threatening condition Majority of cause: Primary HPT

Hypercalcemic Crisis

Other Causes of Hypercalcemia

Benign Tumors
Parathyroid hormoneresecreting ovarian dermoid cyst or uterine fibroid

Endocrine Disease
Thyrotoxicosis Pheochromocytoma Addisons disease Islet cell pancreatic tumors VIPoma

Other Causes of Hypercalcemia

Granulomatous Disorders

Sarcoidosis Wegeners granulomatosis Berylliosis Silicone-induced and paraffin-induced granulomatosis Eosinophilic granuloma Tuberculosis (focal, disseminated, Mycobacterium avium complex in AIDS) Histoplasmosis Coccidioidomycosis Candidiasis Leprosy Cat-scratch disease

Other Causes of Hypercalcemia

Drugs
Vitamin D excess (oral or topical) Vitamin A excess Thiazide diuretics Lithium Estrogens and antiestrogens Androgens Aminophylline, theophylline Ganciclovir Recombinant growth hormone treatment of AIDS patients Foscarnet 8-Chloro-cyclic adenosine monophosphate

Other Causes of Hypercalcemia

Miscellaneous
Familial hypocalciuric hypercalcemia Immobilization with or without Pagets disease of bone End-stage liver failure Total parenteral nutrition Milk-alkali syndrome Hypophosphatasia Systemic lupus erythematosus Juvenile rheumatoid arthritis Recent hepatitis B vaccination Gauchers disease with acute pneumonia Aluminum intoxication (long-term hemodialysis) Manganese intoxication Primary oxalosis

Hypercalcemia of Malignancy

Hypoparathyroidism
Deficient secretion of PTH which manifests itself biochemically by hypocalcemia, hyperphospatemia diminished or absent circulating iPTH and clinically the symptoms of neuromuscular hyperactivity

Hypoparathyroidism
Causes
Surgical hypoparathyroidism (most common) Idiopathic hypoparathyroidism Functional hypoparathyroidism (hypomagnesemia)

Clinical Features
Neuromuscular
The rate of decrease in serum calcium is the major determinant for the development of neuromuscular complications When nerves are exposed to low levels of calcium they show abnormal neuronal function which may include decrease threshold of excitation, repetitive response to a single stimulus and rarely continuous activity

Clinical Features
Neuromuscular
Parathesia Tetany Hyperventilation Adrenergic symptoms Convulsion (More common in young people and it can take the form of either generalized tetany followed by prolonged tonic spasms or the typical epileptiform seizures.) Signs of latent tetany
Chvostek sign Trousseau sign Extrapyramidal signs (due to basal ganglia calcification)

Clinical Features

Clinical Features

Clinical Features
Other
1. Posterio lenticular cataract 2. Cardiac manifestation:
1. Prolonged QT interval in the ECG 2. Resistance to digitalis 3. Hypotension 4. Refractory heart failure with cardiomegally can occur.

Clinical Features
Other
3. Dental Manifestation
Abnormal enamel formation with delayed or absent dental eruption and defective dental root formation. Presumably secondary to decreased calcium level and may lead to steatorrhoea with long standing untreated disease.

4. Malabsorption syndrome

Pseudohypoparathysoidism and Pseudopseudohypoparathyroidism

Rare familial disorders with target tissue resistance to PTH. There is hypocalcaemia, hyperphosphataemia, with increased parathyroid gland function. There is also a variety of congenital defects in the growth and development of skeleton including:
Short statue Short metacarpal and metatarsal bones

Pseudohypoparathysoidism and Pseudopseudohypoparathyroidism

In pseudopseudohypoparathyroidism they have the developmental defects without the biochemical abnormalities

Other Causes of Hypocalcemia

Dietary deficiency of vitamin D or calcium Decreased intestinal absorption of vitamin D or calcium due to primary small bowel disease, short bowel syndrome, and postgastrectomy syndrome. Drugs that cause rickets or osteomalacia such as phenytoin, phenobarbital, cholestyramine, and laxative.

Diagnosis of Hyperparathyroidism

 Diagnosis of hyperparathyroidism is based upon 2 laboratory tests: serum calcium, and serum parathyroid hormone.

Other Tests
Laboratory Albumin Alkaline Phosphatase Rationale the level of total serum calcium is directly proportional to serum albumin if elevated prior to parathyroidectomy, these patients are more likely to require calcium supplementation post-operatively Normally low; if high suspect renal failure or high intake Normally elevated; because PTH decreases the renal resorption of bicarbonate, resulting in increased renal resorption of chloride; a chloride:phosphorous ratio >33 suggests hyperparathyroidism

Phosphorus Chloride

BUN and Creatinine

24-hour urine calcium Bone Densomitry

To assess renal function

High in the majority of hyperparathyroidism cases A Z-score of 2 is considered indicative of clinically significant HPT in an otherwise asymptomatic patient.

Localization Studies and Their Application

Localization studies has permitted surgeons to employ more limited procedures in neck exploration, while achieving the same, or improved, surgical outcomes Operationally classified as preoperative (invasive or non invasive)or intraoperative

Non Invasive Preoperative Localization

1. 2. 3. 4. 5. 6. 7. Pertechnetate Thallous Chloride Imaging Technetium 99m Sestamibi Scintigraphy Technetium 99m Sestamibi with SPECT CT- Sestamibi Fusion Ultrasonography Compiuted Tomography MRI

1. Pertechnetate Thallous Chloride Imaging

This technique requires prolonged patient immobilization Sensitivity: 27-82% Widespread availability, minimal irradiation, and low risk

2. Technetium 99m Sestamibi Scintigraphy

Late phase is preferable for detecting PT adenomas because the thyroid and thyroid nodules clear of uptake is faster than do parathyroid neoplasms No need to immobilize the patient between images 100% sensitivity, 90% specificity

3. Technetium 99m Sestamibi with SPECT

It uses a camera collimator that rotates 360 around the patient in the axial plane Portrays a 3D image as the sequence progresses from the mandible to thorax Images appear to have a higher resolution

4. CT Sestamibi Fusion
It is a combined imaging modality whereby anatomic and physiologic images are combined to create a single image providing concise anatomic localization of physilogically hyperactive parathyroid tissue

5. Ultrasonography
Easy to perform, well tolerated by the patient, does not require radiotracer, rapid and at low cost. Sensitivity depends on the ultrasonographers experience, frequency of transducer, resolution of image, parathyroid gland size

CT vs. MRI
Computed Tomography Less sensitive expensive Exposure to radiation Requires administration of a contrast material With interference from surgical clips Useful for ectopic parathyroid glands Offer limited application in preop localization Non exposure to radiation Does not require contrast material No interference from surgical clips left in the neck after initial exploration Useful for ectopic parathyroid glands Offer limited application in preop localization MRI More sensitive (50-80%)

Invasive Preoperative Localization

1. Parathyroid Arteriography 2. Selective Venous Sampling for PTH 3. USG guided Fine Needle aspiration

1. Parathyroid Arteriography
Includes examination of both thyrocervical trunks, the int. mammary arteries, and carotids 60% sensitivity

2. Selective Venous Sampling for PTH

Angiography is performed to outline the venous drainage, facilitating sampling for PTH assay Expensive and technically difficult Generally believed to be the most sensitivity lateralizing about 80% of the parathyroid tumors

3. Ultrasound Guided Fine Needle Aspiration

May provide for direct cytologic exam May facilitate the use of a bioassay of the aspirate to determine PTH level
When the aspirate is positive for PTH, it confirms the presence of parathyroid tissue within the enlarged gland

Surgical Management of Hyperparathyroidism

 Medical surveillance vs. Surgical treatment

If severe hypercalcemia (>11.5mg/dl) is present, surgery is mandatory According to NIH, patients <50 should undergo surgery Other considerations that favored surgery:
Concern that consistent follow up would be unlikely Presence of coexisting illness that would complicate management

No specific recommendations about medical therapy were made

 Asymptomatic Hyperparathyroidism
Defined as documented HPT without signs or symptoms attributable to the disease

2000 Guidelines for Parathyroid Surgery in Asymptomatic Primary HPT

Measurement Serum Ca 24-h urine Ca Creatinine Clearance Bone Mineral Density Age Other 2000 Guidelines >1.0 mg/dl above normal >400mg/dl Reduced by 30% T score <-2.5 at any site <50 Patients request surgery, or patients are unsuitable for long-term surveillance.

Parathyroidectomy Technique

1. Anesthesia and Preparation

General anesthesia with endotracheal intubation The patients neck should be hyperextended dorsally to provide optimal access to the neck The table may be adjusted in the reverse Trendelenburg position to decrease venous congestion around the thyroid bed and central neck.

2. Exploration of the neck

A low transverse cervical incision (Kocher) is designed two finger breadths above the suprasternal notch In any event, the incision should not extend beyond the SCM muscles Depending on the surgical preference, the usual trend is to identify the inferior glands initially (larger and more anterior)

 Most PTG have a light brown or tobacco color PTG have a freedom of mobility Lymph nodes are more firm, translucent white gray Parathyroid adenomas appear rust red or beefy red in situ, mottled Hyperplastic glands appear darker than adenoma After abnormal gland is removed, it is sent for pathologic analysis

3. Closure of the Incision

Operative field is irrigated with warm saline solution and inspected for adequate hemostasis An occlusive dressing is placed to prevent fluid collection under the incision.

Post operative Care

Successful parathyroid exploration with removal of a solitary adenoma results in a decrease in total serum calcium level, which usually reaches a nadir at approximately 48 hours after the operation. Normocalcemia at 6 months postop is the usual standard assessment for surgical success. Total serum calcium level and intact PTH level should be assessed at 1 month and 6 months postoperatively.

Medical Management of Hyperparathyroidism

 Symptom complex, age, overall medical condition and health status Hypercalcemia
Hydration by loop diuretics Meds that reduce osteoclastic bone resorption: bisphosphonates, calcitonin, plicamycin

Enhancement of urinary calcium excretion is the initial approach for Ca>12mg/dl

Diagnosis of Hypoparathyroidism

Types of Hypoparathyroidism
Laboratory Results Primary Hypoparathyroidism Secondary Hypoparathyroidism Pseudohypoparathyroidism Low PTH, Low Ca Low PTH, High Ca High PTH, Low Ca

Laboratory Tests Measurement of ionized calcium concentration in the plasma Albumin Serum 25-hydroxy vitamin D

Rationale It is the ideal measurement Hypoalbuminemia causes a drop in total calcium concentration to exclude vitamin D deficiency as a cause of hypocalcemia

Serum Magnesium

Hypomagnesemia may cause PTH deficiency and subsequent hypocalcemia. Exclude it in any patient with primary hypoparathyroidism.
PTH is a phosphaturic hormone. In its absence, phosphorus levels in the blood rise.

Serum Phosphorus

Physical Examination
Chvosteks (Weisss) and Trousseaus signs indicate latent tetany.

 A grading system exists for Chvosteks sign:

Grade I=twitching of lip at angle of mouth (8% of normals) Grade II=Grade I with twitching of ala nasi Grade III=Grade II with twitching of lateral angle of eye Grade IV=twitching of all facial muscles

Management of Hypoparathyroidism

Medical Care
Currently, treatment of patients with hypoparathyroidism involves correcting the hypocalcemia by administering calcium and vitamin D.

Surgical Care
Patients may be treated with an autotransplant of a segment of parathyroid gland to prevent hypoparathyroidism. This autotransplant is usually placed subcutaneously in the forearm or in the neck.

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