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Parathyroid gland

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Parathyroid gland Dr G S Randhawa Associate professor of surgery
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Parathyroid gland

Dr G S RandhawaAssociate professor of surgery

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Parathyroid gland I

HistorySurgical anatomyPhysiologyCalcium metabolismHypercalcemiaHyperparathyroidism

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Parathy.....History The parathyroid gland was first recognized in 1850 by Richard

Owen during a dissection of an Indian rhinoceros at the London Zoo.

The credit for the discovery of the parathyroid has, however, been given to the Uppsala anatomist Ivar Sandström, who was the first to demonstrate the gland in man.

His dissection studies were undertaken between 1877 and 1880, when he still was a medical student in Uppsala.

Ivar Sandström, the man behind the discovery of the parathyroid gland, often called the last anatomical discovery, was a disharmonious person with psychiatric problems and he committed suicide in 1889 at the age of 37 years.

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Para...Anatomy• 4 in no. Two superior two inferior on

posteromedial aspects of thyroid lobes.• Flat, ovoid and red-brown to yellow.• Size-5-7mm x 3-4mm x 0.5-2mm• Weight-30-50 mg• Lower larger than upper ones.• Superiors- embedded in fat on posterior

surface of each lobe near the insertion of RLN into larynx.

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Para..Anat.• Inferiors-more ventral on infero-posterior

aspect of the thyroid lobules lie close to or within the paranchyma of cervical extension of thymus.

• Fairly constant anatomy but variations are there, due to embryogenetic pattern.

• Embryology- superiors from 4th pharyngeal pouch and inferiors from 3rd along with thymus .

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Para..Anat.• Supernumery glands found in about 15%

of cases, mostly in conjunction with thymus.

• Arterial supply- usually from inferior thyroid artery for all four. Rarely by arteria thyroidea ima or anastomosis around trachea oesophagus and larynx.

• Venous drainage through inferior, middle and superior veins and then into internal jugular vein.

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Para..Anat.• Histology- half parenchyma and half

stroma including fat cells.• In children- cheif cells only.• At puberty adepocytes

appear>acidophilic ,mitochondria-rich oxyphilic cells>intermixed with glycogen-laden, polygonal, water-clear cells.

• Waterclear cells and oxyphilic cells derive(?) from chief cells and secrete PTH.

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Para..Physiology• Primary physiologic role of the gland

is endocrine regulation of calcium and phosphate metabolism.

Schematic sketch of Ca+ daily turnover

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Calcium metabolism• Plays critical role in all biologic systems.• Participates in enzymatic reactions,

mediater in hormone metabolism.• Intimately involved in physiology of

neurotransmission, muscle contraction and blood coagulation.

• Major cation in bone and teeth.• 2% of body weight and almost all

contained in skeleton.

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Calcium metabolism• Normal range- 9-10.5mg%(4.5-5.2mEq/L)• Daily variation <10%• Half in ionic form-biological active; 40% bound to

serum protein(mainly albumin) and 10% to organic ions such as citrate.

• Serum calcium is measurement of protein-bound calcium. Hydrogen ion competes with ca+ for same site on albumin, hence any change in bodyfluid pH alters ca+ levels

• For every change in 1gm/dl of albumin changes; Ca+ changes by 0.8mg/dl.

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Calcium metabolism• Almost all physiologic activity is by ionic unbound

calcium.• Absorbed from duodenum and proximal jejunum

in ionic form.• Absorption rate regulated by body calcium status.• Ca+ in extra-cellular fluid is constantly exchanged

with- intracellular fluid, exchangeable bone and glomerular filtrate.

• Ca+ reabsorption from kidney is directly related to Na+ transport and 99% Ca+ gets reabsorbed from filtered load.

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Calcium metabolismRegulation- effected by-1. PTH(parathyroid hormone or parathormone)• Single most imp. Hormonal regulator of Ca+ and PO4. Direct effect on

bones and kidneys while indirect effect on intestine mediated through vit D.

• In target tissue- PTH binds to membrane recepter>activates adenyl cyclase>generates cAMP which regulates other intracellular enzymes.

• Bone-stimutes both reabsorption and formation of new bone. However , sustained high levels stimulate only osteoclasts and inhibits osteoblasts.

• Kidney- promotes reabsorption from extracellular fluid irrespective of its concentration.

• Reabsorption in proxomal tubule and loop of Henle is affected by sodium transport such that factors that alter Na+ transport alter Ca+ reabsorption concommitantly.

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Calcium metabolism• Distal tubule reabsorption is independent of Na+ and

influnced by PTH only.• Promotes renal excretion of phosphates.• GI tract- indirect effect by stimulating the hydroxylation

of 25- hydroxyvitamin D to 1,25-dihydroxyvitamin D in the kidney.

• Synthesis- PTH precurser>cleaved in parathyroid >proPTH>PTH 84-amino-acid PTH, secretion of this molecule is controlled by feedback loop from extracellular Ca+ levels. Half life of this molecule is 4 minutes.

• Further cleaved to N- and C-terminal fragments . N-terminus contains most of biologic activity and rapidly degraded by liver.C-terminus slowly metabolized in kidney.

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Calcium metabolism• Vit D-• Acts at two major sites – 1. promotes intestinal

absorption of Ca+ and phosphates 2.-promotes mineralization in bone and enhances PTH mediated resorption from bone.

• Probably no effect on kidney.• Calcitonin-produced by C-cells of thyroid. Its not

essential for control of calcium in humans. Total thyroidectomy does not lead to any disturbances of calcium homeostasis.its physiological as well as therapeutic function is to promote excretion of Ca+ and thus reducing blood calcium levels.

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Hypercalcemia• Relatively common clinical problem• In general population and OPD patients

incidence is-0.1% and 0.5% respectively.

• Most patient in this group have primary hyperparathyroidism.

• Incidence in hospitalized patients is 5% and 2/3 of them are suffering from malignancy.

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Hyper...• Clinical features- varied and non-

specific. Magnitude and rapidity determines severity .

• Many of the manifestations are suble and evident in retrospect when the hypercalcemia is corrected.

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Clinical features of hypercalcemia

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Causes of hypercalcemia

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Hyperparathyroidism• Definition- excessive secretion of

parathyroid hormone due to any cause called hyperparathyroidism.

• Three types-• Primary, • Secondary and• tertiary

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Primary hyperparathyroidism Unstimulated inappropriate high

secretion of PTH is referred to as primary form. Major causes are –

• Parathyroid hyperplasia(20-24%)• Adenoma(75-90%)• Parathyroid carcinoma(1%)

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Secondary hyperparathyroidism• It’s due to following causes-• Chronic renal failure• Malabsorption • Vit D deficiency state• These causes lead to hypocalcemia which in

turn triggers hyperplasia of gland and hence hypersecretion of PTH.

• CRF causes hyperphosphataemia and reduces conversion of 25-monohydrovit D to 1,25-dihydrovit D.

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Tertiary hyperparathyroidism• Due to prolonged secondary

stimulation sometimes gland becomes autonomous and does not respond to calcium levels.

• It continues to secrete PTH in high quantities even after correction of calcium homeostasis.

• It happens in about 2% cases of renal transplantation.

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Clinical features• “Bones,stones,abdominal groans and

psychic moans”. Classical vignatte of hyperparathyroidism.

• Common in middleaged women• >50% are asymptomatic• Nonspecific symtoms dismissed as neurotics• Behavioral problems• Osteitis fibrosa cystica( Von Recklinghausen

disease) 5% cases showing multiple cysts or pseudotumours in jaws, skull or radial aspects of middle phalanges.

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Clinical features..• Lamina dura of tooth is first bone to show

changes.• In kidneys bilateral multiple stones or even

renal calcinosis leading to renal failure.• May be associated with peptic ulcer,

pancreatitis, MEN I syndrome.• Skin necrosis, band keratopathy,pseudogout,

myalgia, arthralgia, polyuria, glycosuria and hypertension may be the associated problems.

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Investigations • High serum calcium >10.5mg%• Low serum phosphate• High urinary calcium excretion

>250mg/24hrs• High serum PTH levels >0.5mg/L(diagnostic)• X-ray skull shows salt-pepper appearance.• X-ray phalanges and jaw are specific.• US abdomen for kidney, pancreas• CT/MRI neck and chest

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Investigations • Thallium-Tc scan to detect hotspot

which is diagnostic of adenoma.• Tc-99 labelled Sestamibi isotope scan

is more sensitive but very expensive.• Urinary cAMP levels increases in 90%

of cases.• FNAC

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Differential diagnosis• Bone secondaries- due to secretion of PTH-like

peptide causes hypercalcemia. Actual PTH is suppressed.

• Multiple myeloma• Vit D intoxication• Sarcoidosis• Functioning carcinoma• Familial hypocalciuric hypercalcemia- autosomal

dominant disease where mutation of cell membrane receptor leads to mild hypercalcemia and high PTH levels with low urinary excretion of calcium. Does not need any treatment.

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Treatment • Surgery is the treatment of choice- partial

or total parathyroidectomy is done according to the aetiological factor.

• All four glands need to be removed in hyperplasia with implantation of about 5gm tissue in brachioradialis or sternocleidomastoid muscle.

• Adenoma affecting single gland will require excision of affected gland only.

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Treatment • If carcinoma, remove ipsilateral lobe of

thyroid too.• When all four glands are involved remove

thymus as well for better results.• Medical treatment- not very effective

hence not popular. Used only in crisis state and in patients unfit to undergo surgery due to concommitant co-morbidities.

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Medical treatment• Drugs used to reduce serum Ca+ levels

are-• Estrogens ,progestogens and

raloxifene(estrogen receptor modulater)• Mithramycin,calcitonin,• Mithramycin used once a week but

causes hepatotoxicity and thrombocytopenia in therapeutic doses

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Parathyroid gland II

Dr. G S RandhawaAssociate professor of surgery

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Parathyroid gland II• Hypocalcemia• Hypoparathyroidism• Tetany • Hungary bone syndrome

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Hypocalcemia • May be acquired or congenital origin• Deficiency or defect in the action of

either PTH or vit D.• Most common cause radical

thyroidectomy.• Chronic vit D deficiency leads to

compensatory increase in PTH levels. The end result is rickets in chidren and osteomalacia in adults.

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Hypocalcemia clinical features- major clinical

signs and symptoms are due to decreased levels of ionized Ca+ which increases neuromuscular excitability.

The earliest are numbness and tingling in the circumoral area.

Anxiety, depression, confusion Teteny

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Clinical featu..• Chvostek sign• Trousseau sign

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hypo,..causes• Causes- hypoparathyroidism• -post-operative• -idiopathic • Vit D deficiency• Pseudohypoparathyroidism • Hypomagnesemia • Malabsorption • Pancreatitis• Hypoalbumenemia• Chelation of calcium• Toxic shock syndrome• Hyperphosphatemia

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Treatment • Symptomatic – oral calcium carbonate or

iv calcium gluconate. Supplemented with vit D prepation for better absorption.

• Tetany – iv calcium gluconate• Correction of hypomagnesemia-iv MgCl2.• Long-term therapy-calcium

carbonate,lowphosphate,lowoxalate,parathyroid grafting(immunosuppressed or cryopreserved autograft.

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Hypoparathyroidism • Sign and symptom-complex that

follows due to low levels of PTH is referred to as hypoparathyroidism. Almost all features thereof are due to hypocalcemia.

• May be – congenital or acquired; temporary or permanent.

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Hypo..causes• Congenital –Digeorge syndrome-

partial or complete agenesis of thymus and parathyroid glands. Disorder involving the branchial pouches.

• Prenatal suppression of fetal parathyroid as a consequence of maternal hypercalcemia. Also common in premature infants.

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Hypo..causes • Aquired – most common cause is

totalthyroidectomy with neck dissection .

• It may include total removal, trauma or devascularization of glands.

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Hypo.. types• Temporary- more common about 2-50%

average 10%. Lasts from 2-6 months. Shows decrease in calcium and increase in phosphates.

• Permanent- less common about 0.4-13% average 1%.

• Hungary-bone syndrome- common about 5-13%. Begins immediately in post-operative period, rapid. Decrease in calcium and phosphate levels.

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Hypo..types• Cause of transient hypocalcemia after

surgery is temporary hypoparathyroidism caused by reversible ischemia of gland, hypothermia of gland and release of endothelin-I an acute-phase reactant causes suppression of PTH secretion.

• Calcitonin by C-cells causes inhibition of bone breakdown and promotes renal excretion of calcium.(opposes PTH).

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Hypo.. Specific lab test• Assess ionized as well as albumin

bound Ca+• PTH levels• If PTH<1.5pmol/L and serum calcium

<2.0mmol/L then patient is at risk of hypocalcemia.

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Hypo..clinical features• Circumoral tingling,numbness,

paraesthesia.mm • Carpopedal spasm, clonic-tonic

convulsions, laryngeal stridor.• Respiratory muscle spasm, suffocation.• Blurred vision due to intraocular

muscle spasm.• Cataract formation as late feature.

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Treatment • Essentially treatment of

hypocalcemia• In acute cases postoperatively- 10 ml

of 10% calcium gluconate given slowly over a period of 10 minutes. An infusion can be started at a rate of 1-2mg/kg/hr if symtoms do not resolve. Monitored by repeated analysis of serum calcium.

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Treat..• Oral- 1-2 gm of elemental Ca+ should be

given. 1250 mg of Ca+ prepation provides 500mg of elemental Ca+. So a dose of 2500-5000mg should be given daily in divided doses.

• Vit D supplementation to ensure better absorption. 0.25-1 mcg/day.

• Iv/im magnesium o.5gm/kg/day for 5 days later magnesium gluconate tablet 500mg/day.

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Treat..• Trial weaning of calcium after 2

months to ascertain whether the problem is temporary or permanent.

• If calcium therapy needed for more than 6 months a diagnosis of permanent hypothyroidism is made.

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Prevention of hypothyroidism• Accurate preoperative parathyroid

localization.• Maintenence of blood supply of

thyroids.• Ligation of inferior thyroid arteries as

low as possible to retain endarteries which supply parathyroids.

• Parathyroid autotransplantation if all 4 glands needed to be removed.

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Teteny • Symptom-complex due to decreased

levels of calcium in blood.• Causes- hypoparathyroidism after

thyroidectomy. Usually temporary lasts for 4-6 months. Commonest.

• Neck dissection• Haemochromatosis• Wilson’s disease• DiGeorge syndrome contd....

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Tetany..causes• Severe vomiting• Hyperventilation due to respiratory

alkalosis• Metabolic alkalosis• Rickets, osteomalacia• CRF• Acute pancreatitis• Multiple blood transfusions

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Tetany.. Clinical features• Circumoral parasthesia• Parasthesia of neck, fingers, toes.• Twitching and weakness of tongue

muscles,muscles of forearm, hand foot and digits- carpopedal spasm.

• Fingers are extended except at MCP joints thumb is strongly adducted.

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Tetany..clini.• Extension of feet due to carpopedal

spasm.• Chvostek’s sign- tapping above the

angle of jaw will cause twitching of angle of mouth and eyelids due to stimulation of facial nerve(positive in 10% normal subjects)

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Teteny..clini..• Trousseau’s sign- blocking blood supply

to distal upper limb by applying sphygmomanometer (Hg raised upto 200mm) will cause carpal spasm.

• Stridor and difficulty in breathing due to weakness of respiratory muscles.

• Generalized twitching resembling convulsions.

• Prolonged QT interval and QRS complex in ECG.

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Tetany..management • Serum calcium-<7mg%• Iv calcium gluconate 10ml of 10% in 10

minutes 6 to 8 hrly.• Later oral calcium 1g t.i.d• Vit D 1-3 ug/day• Follow-up with regular serum calcium

monitoring.• Magnesium supplementation 10 ml 10%

iv or 500mg o.d. Orally.

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Hungary bone syndrome

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Hungary bone syndrome• Rapid reuptake of calcium and

phosphate by bones once the cause of resorption is removed leading to a state of hypocalcemia.

• Causes• Post-thyroidectomy for toxic disease.• Post- parathyroidectomy• Carcinoma prostate on oestrogen


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Hungary..• Bones suck back Ca+,Pho4 and

magnesium leadind to-• Hypocalcemia,• Hypophosphatemia,• Hypomagnesemia and• Hyperkalemia• Bone-specific alkaline phosphatase

contnues to rise indicating increased bone formation.

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Hungary..management • High calcium demand meted by infusion

of calcium along with magnesium.• Hyperkalemia delt with extra care.• Once settled then oral calcium

supplemented with vit D and magnesium is needed for 6 months then gradually reduced.

• Monitored by serum Ca+,phosphates,Mg+ and s. Alk. phosphatase.

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