What is the most abundant mineral

in the body?
What is the smallest endocrine
gland in the body?
Parathyroid Hormones
*Secretes Parathyroid Hormones
*Four small pieces of tissue embedded in the thyroid gland
in the neck (2 parathyroid glands in each thyroid gland)
**Primary role:
Regulates Blood CALCIUM level
________________________
**Promotes Bone Resorption – release calcium into the blood stream
**Increase Renal Reabsorption of Calcium
**Stimulates conversion of Inactive Vit. D to activated Vit. D3
 Calcium
- the most abundant mineral
in the human body
- The ave. adult body contains approx.
25,000mmol (1 kg), of which 99% is
bound in the skeleton
 Calcium
Functions:
• Activator of the coagulation system
• Contributor to structure of bone and teeth
• Activator for enzymes
• Neurotransmission regulator
 Skin 0.3mmol/24h
Food
25 mmol/24h
25,000 mmol exchange
100 mmol rapidly 500 mmol/24h ECF 22.5 mmol
exchangeable absorption
Bone formation 12 mmol/24h
7.5 mmol/24h Plasma
Bone resorption 9 mmol
secretion
7.5 mmol/24h 6 mmol/24h

Reabsorption Glomerular filtration

234 mmol/24h 240 mmol/24h

Loss or input Feces 19 mmol/24hr

Where held
Urine 6mmol/24h
3 forms:
 bound (mainly albumin) : 40%
 complexed (with citrate and phosphate) : 10%
 Ionized (physiologically active) : 50%
Urine calcium : 85% ionized and 15% complexed
- isN-terminal
a polypeptide
portioncomposed
of
the first 34
of 84 amino acids amino
acids. This fragment is
- Synthesized as a
believed to confer all
larger
precursor, pre-pro-PTH
the biological actions
(115
of amino
the acids)
full-length
peptide
- is secreted by the chief cells of the parathyroid glands in
response to a fall in plasma (ionized) calcium
- PTH : plasma calcium and plasma phosphate
- Hypercalcemia & Calcitriol inhibit Calcium secretion & synthesis
- PTH half-life in blood :
 3 – 4 minutes (5mins) – N-terminal
 1 hour – C-terminal
Major PTH breakdown  Liver, kidney, bone
Liver  the primary location for fragmentation
of the intact 84-amino acid PTH chain
• From this hydrolysis comes the major
amount of C-terminal PTH fragments
found in the circulation
• A decrease in the serum ionized calcium level triggers
the release of PTH
• This release is very sensitive to the ionized calcium
since a drop of 0.1 mg/dL below the normal limit is
sufficient to trigger an increase of PTH in the circulation.

• Magnesium is another essential ingredient for PTH

release. If serum Mg drop much below the normal limits,
PTH is inhibited
 Target Action Effect
Organ
Bone • Rapid release of calcium  Increase plasma [Ca++]
• Increases osteoclastic
resorption
PTH
Kidney • increases calcium (and  Increase plasma [Ca++]
magnesium) reabsorption

• Decreases phosphate  decrease plasma [Pi]

reabsorption
 Increase calcium and phosphate
absorption from gut
• Decreases bicarbonate
 acidosis
 Calcitonin
- Produced by the C cells of the thyroid gland
- Half-life : 10 minutes
- Filtered at the glomerulus, partially reabsorbed in
the tubules and apparently metabolized to small
fragments (or amino acids) while still in the
kidney
- Lower blood levels of calcium
- When calcitonin interacts with
bone, calcium is absorbed by bone
and bone mass increases
 Effects of Vitamin D on Calcium metabolism:
• Increased absorption from intestine
• Increased resorption from bones
• Increased reabsorption from kidney
tubules
Vit. D is obtained in :
• Diet
• Formed in the skin through
conversion of 7-dehydrocholesterol
by UV radiation (sunlight)
 Vit. D3 metabolism and activation

Skin synthesis

Diet Vit. D3 25-hydroxy- D3 1, 25-hydroxy- D3

Bloodstream liver kidney

(globulin)
*Derived from Vitamin D by successive hydroxylation in the
liver (25-hydroxylation) and kidney (1a-hydroxylation)
*It stimulates the reabsorption of calcium & phosphate (gut)
*Promotes mineralization (bone) :
it stimulates osteoclastic bone resorption,
which releases calcium and phosphate into the ECF
 PTH PTH
phosphate phosphate
Ca and Pi
reabsorption

+ – gut
–
25-OH cholecalciferol calcitriol

bone

Calcitriol regulation Bone

resorption
Clinical Disorders
 Hyperparathyroidism
1. Primary hyperparathyroidism

2. Secondary hyperparathyroidism

3. Tertiary hyperparathyroidism
PRIMARY Hyperparathyroidism

• physiologic defects lies with the parathyroid gland

• The most common cause of hypercalcemia
• Due to the presence of parathyroid adenoma or
hyperplasia
• If goes undetected, severe demineralization my
occur (osteopenia, osteitis fibrosa cystica)
 PRIMARY Hyperparathyroidism
Lab diagnosis
•Increased PTH
•Increased ionized blood calcium
•Hypercalciuria
•Hypophosphatemia (fasting state)
•Phosphaturia
 SECONDARY Hyperparathyroidism

• Overproduction of Parathyroid hormone:

due to :Chronic abnormal stimulus for its production
Chronic Renal Failure or Vit. D deficiency
• There is a diffuse hyperplasia of all 4 glands
• The patient develops severe bone disease
SECONDARY Hyperparathyroidism
Lab diagnosis

•Increased PTH
•Decreased ionized blood calcium
TERTIARY Hyperparathyroidism
• Occurs with secondary hyperparathyroidism
• is a state of excessive secretion of parathyroid hormone
after longstanding secondary hyperparathyroidism
and resulting in hypercalcemia
• observed most commonly in patients with chronic
secondary hyperparathyroidism and often
after renal transplantation
TERTIARY Hyperparathyroidism
Lab diagnosis
•Phosphate levels are normal to high
•Calcium phosphates precipitate in
soft tissues
Thank you! 