This document provides information on the parathyroid gland including its history, anatomy, physiology, calcium metabolism, hypercalcemia, and hyperparathyroidism. Some key points: - The parathyroid gland regulates calcium and phosphate levels in the body through secretion of parathyroid hormone (PTH). - It consists of usually four small glands located on the posterior surface of the thyroid gland. - Hyperparathyroidism is excessive secretion of PTH, which can be primary (autonomous secretion), secondary (compensatory to low calcium), or tertiary (persistent after secondary cause is resolved). - Primary hyperparathyroidism is usually caused by a single adenoma and

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

2. Parathyroid gland I
History
Surgical anatomy
Physiology
Calcium metabolism
Hypercalcemia
Hyperparathyroidism

3. 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.

5. 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.

7. 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 .

8. 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.

9. 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.

11. Para..Physiology
• Primary physiologic role of the gland
is endocrine regulation of calcium
and phosphate metabolism.
Schematic sketch of Ca+ daily turnover

12. 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.

13. 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.

14. 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.

15. Calcium metabolism
Regulation- 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.

16. 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.

17. 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.

18. 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.

19. 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.

20. Clinical features of
hypercalcemia

21. Causes of hypercalcemia

22. Hyperparathyroidism
• Definition- excessive secretion of
parathyroid hormone due to any
cause called hyperparathyroidism.
• Three types-
• Primary,
• Secondary and
• tertiary

23. 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%)

24. 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.

25. 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.

26. 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.

27. 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.

28. 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

30. 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

31. 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.

32. 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.

33. 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.

34. 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

36. Parathyroid gland II
Dr. G S Randhawa
Associate professor of surgery

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

38. 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.

39. 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

40. Clinical featu..
• Chvostek sign
• Trousseau sign

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

42. 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,par
athyroid grafting(immunosuppressed or
cryopreserved autograft.

43. 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.

44. 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.

45. Hypo..causes
• Aquired – most common cause is
totalthyroidectomy with neck
dissection .
• It may include total removal, trauma
or devascularization of glands.

46. 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.

47. 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).

48. 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.

49. 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.

50. 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.

51. 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.

52. 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.

53. 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.

54. 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....

55. Tetany..causes
• Severe vomiting
• Hyperventilation due to respiratory
alkalosis
• Metabolic alkalosis
• Rickets, osteomalacia
• CRF
• Acute pancreatitis
• Multiple blood transfusions

56. 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.

57. 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)

59. 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.

61. 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.

62. Hungary bone syndrome

63. 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
therapy.

64. 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.

65. 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.