1 MLS 418 - LECTURE
2021-2022
PARATHYROID GLAND
ANATOMY AND HISTOLOGY
• the parathyroid gland is located posteriorly to the
thyroid gland
• flattened and oval in shape situated external to the
thyroid gland but within the pre-tracheal fascia
• most individuals have four (4) parathyroid glands but
variation in number may occur (some have 2 or 6)
• superior thyroid artery - supply blood for superior
parathyroid gland
• inferior thyroid artery – supply blood for inferior
parathyroid gland
• Follicles – circular part with colloid inside
• Parathyroid gland is composed of two cells:
o Chief cells - responsible for the production
of parathyroid hormone
o Oxyphil cells - responsible for the
production of PTH-RP or parathyroid
hormone-related protein
2ND SEMESTER | S.Y.
PARATHYROID HORMONE
• Function: Increase serum calcium
• Secreted by parathyroid glands (chief cells)
▪ rapid response to reduced calcium
(minutes)
• Polypeptide
▪ 84 amino acid residues (9,500 Da)
• Operates in tissues via the cAMP second messenger
• Net effect: increased total/ionized calcium
▪ Negative feedback: lowers PTH secretion
REGULATION
• Happens in the parathyroid cell
• Calcium binds to a receptor (calcium-sensing
receptor) coupled to a G protein
▪ activation of phospholipase C (PLC)
• PLC converts phosphoinositides to inositol
triphosphate (IP3) and diacylglycerol (DAG)
• IP3 - releases calcium from internal stores
• DAG - stimulates protein kinase C (PKC) activation
▪ Calcium/PKC: inhibited PTH release and
synthesis
• INCREASED SERUM CALCIUM:
o Increased serum calcium will result in
negative feedback to bring lower the calcium
levels
o Calcium binds to the calcium-sensor receptor,
coupled with G protein
o The complex will activate phospholipase C to
inhibit the parathyroid hormone secretion
• DECREASED SERUM CALCIUM:
o Low level of calcium will not attach to the
calcium-sensor receptor, which will remain
inactivated
o Therefore, parathyroid hormone secretion
will be stimulated
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• Conclusion:
o Calcium-sensor activation will result in
parathyroid inhibition
o Calcium-sensor inactivation will result in
o parathyroid stimulation
• Effects of PTH: (increase Ca2+)
o increase in kidney calcium resorption
o increase in bone calcium resorption
o increase vitamin D secretion in kidney
▪ results in gut calcium absorption
FUNCTIONS
• Bone
o osteoblast stimulation to produce RANKL*
which will activate RANK in osteoclasts
o (end point: increased bone resorption and
increased calcium/osteoporosis risk)
▪ There will be osteoclastic activity;
where our bone loses Calcium
towards the blood
o RANKL: receptor activator of nuclear factor
ĸB ligand
o When PTH is stimulated PTH will be
released to the blood and will have a target
tissue in your bone. In your bone your PTH
stimulates osteoclastic activity bone is
resorbed which releases calcium in the
bloodstream.
o Increases serum calcium
• Kidneys
o increased urine excretion of phosphates,
calcium reabsorption in the nephron,
vitamin D activation
o Decreases serum phosphate
PTH LABORATORY METHODS
• Measurement of intact PTH (using 2 antibodies that
measure the N-terminal and C-terminal)
o Using ELISA
o Intact parathyroid hormone is biologically
active in its form, however the half-life of
intact parathyroid hormone is only less than
4-minutes.
o The kidneys and liver will clear the intact
parathyroid hormone rapidly and it will be
cleaved into different fragments, and these
smaller peptides are released in the
circulation.
• PTH-related peptide (PTH-rP)
o produced by tumors
▪ lung, breast, kidney, and other
solid tissues
o 141 AA (shares the same homology with
PTH in the first 13 AA)
o same PTH receptor/functions (increase
serum calcium)
o present in patients with malignancy-
associated hypercalcemia
DISEASES
HYPERCALCEMIA
• Increased serum calcium
• Common causes:
o Hyperparathyroidism
o Malignancy-associated: PTH-rp
o Vitamin D intoxication
o Hypercalcemia in granulomatous disorders
o Milk-alkali syndrome/Burnett syndrome
PRIMARY HYPERPARATHYROIDISM
• Primary: the organ that produces the hormone has
the problem
• The problem is within the parathyroid gland
• Excessive secretion of PTH with no stimulus and no
response to negative feedback
• Caused by: parathyroid adenoma, hyperplasia,
carcinoma
• Increased calcium (high risk of heart problems,
atherosclerosis, osteoporosis, kidney stones)
o Calcium will be lodged or stored in your
coronary arteries or in your blood vessels.
o Increased osteoclastic activity
o Calcium may be stored in your kidneys
• Hereditary factors (complex endocrine tumor)
o Combination with other carcinoma of the
body!
o Multiple endocrine neoplasia type 1: (PPP)
▪ parathyroid, pituitary, pancreas
tumors
o Multiple endocrine neoplasia type 2A:
(TPH)
▪ thyroid cancer,
pheochromocytoma (adrenal
gland), hyperparathyroidism
(parathyroid)
OTHER CAUSES OF HYPERCALCEMIA
VITAMIN D INTOXICATION
• Increased calcium absorption in the intestines,
increased bone resorption
HYPERCALCEMIA IN GRANULOMATOUS DISORDERS
• Sarcoidosis patients
o Sacroidosis = an inflammatory disorder that
affects multiple organs in the body; px will
have a severe respiratory distress because
of inflammation in lung parenchyma
o Most common affected organ: lungs and
other organ system
• Unregulated generation of vitamin D in
granulomatous tissues
o Producing increased amount of vitamin D =
hypercalcemia
MILK-ALKALI SYNDROME
• In peptic ulcer patients
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 • Increased calcium absorption/absorbable alkali
(antacids/calcium carbonate)
o Calcium carbonate is very rampant
nowadays because some patients will take
this as prophylaxis for osteoporosis
o Taking too much calcium carbonate or
antacids from peptic ulcer disease will cause
Milk-alkali syndrome
• Can be a manifestation of hypercalcemia,
hypocalciuria, alkalosis, azotemia, and soft tissue
calcification
HYPOCALCEMIA
• Causes:
o Decreased PTH production/secretion
o Resistance to PTH action
▪ You have a normal level of
parathyroid hormone. However,
our body failed to response to the
parathyroid hormone itself
o Deficiency of vitamin D
• Cardiac anomaly, abnormal facial feature / fasci
(hooded eyes, relatively long face, small and low-set
ears), thymic hypoplasia (px prone to infection), cleft
palate, hypocalcemia,
• DiGeorge syndrome, also known as 22q11.2 deletion
syndrome, is a syndrome caused by the deletion of a
small segment of chromosome 22.
• Common in young individual who have recurrent
infection
PSEUDOHYPOPARATHYROIDISM
• aka Albright hereditary osteodystrophy
• genetic disorder where the body fails to respond to
PTH
o Parathyroid hormone resistancy
o Body do not respond to PTH
• low blood calcium and high phosphate levels
• characteristics:
o short height
o short hand bones (bone below the 4th
finger)

HYPOPARATHYROIDISM
• Diminished or absent PTH production
• Acquired: neck surgeries/thyroidectomy
o Thyroidectomy: removal of thyroid either
partial or total (entire gland is being
removed)
• Parathyroid gland is situated posterior to thyroid
gland so there is a big chance that your parathyroid
gland can also be transected or can be damaged
during the procedure. That is why patient may take
Calcium supplements after thyroidectomy
• Inherited:
o Defective thymus and parathyroid gland
(DiGeorge syndrome) CATCH 22
o Hereditary autoimmune syndrome:
autoimmune polyglandular deficiency

DiGeorge syndrome is a combination of:

• Cardiac anomaly
o Px may manifest with cardiac problem or
murmur
• Abnormal facial feature or Abnormal fascia
• Thymic hypoplasia
o Px has hypoplastic thymus = poor
differentiation of T cells
o T cells are differentiated in thymus gland
o Without T cells, px may have severe
infection or recurrent infection
• Cleft palate
• Hypocalcemia
o Because of defective parathyroid gland
• Chromosome 22
o Since it is inherited, chromosome 22 is
affected

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