Transcript Parathyroid Gland

THE
PARATHYROID
GLAND
Parathyroid Hormone,
Calcitonin, Calcium
and Phosphate
Metabolism, Vitamin D,
Bone
The physiology of calcium
and phosphate Metabolism,
formation of bone and teeth,
and regulation of vitamin D,
parathyroid hormone (PTH)
and calcitonin are all closely
intertwined
Overview of Calcium and Phosphate
Regulation in the ECF and Plasma
CALCIUM – 1100 GM – 1.5% of body weight
1.
Skeleton (99%)
a. Rapidly Exchangeable reservoir
b. Stable calcium
2. Blood (1%) 9 – 10 mg%, Average 9.4
mg%, 2.4 mmol per liter
a. 41% ( 1 mmol/L) - combination with
plasma protein and is non-diffusible
through capillary membrane
b. 9% ( 0.2 mmol/L ) - diffusible , not
ionized
c. 50% - diffusible and ionized
Absorption and Excretion of Calcium and
Phosphate
Intestinal Absorption and Fecal
Excretion of Calcium and Phosphate
Renal Excretion of Calcium and Phosphate
Bone and Its Relation to Extracellular Calcium and
Phosphate
Composition of Compact Bone
1. Organic Matrix (30%)
- 90 to 95% collagen fibers
- Remainder is ground substance ( composed
of ECF plus proteoglycans esp.
chondroitin sulfate and hyaluronic acid
2. Bone Salts (70)
- crystalline salt is composed principally of
calcium and phosphate, known as
Hydroxyapatite
Tensile and Compressional Strength of Bone
Collagen fibers of bone have great tensile strength
Calcium salts have great compressional strength
Deposition and Absorption of Bone
Deposition of Bone by the Osteoblast
Absorption of Bone by the Osteoclast
The Osteoclast send out villus-like projections
toward the bone. The villi secrete:
1. proteolytic enzyme released from
lysosome of the osteoclast
2. several acids including lactic acid and
citric acid, released from the
mitochondria and secretory vesicles
VITAMIN D
Steps that Lead to the Formation of
Substances from Vitamin D
- Cholecalciferol (Vitamin D3) is
Formed in the Skin
- Cholecalciferol is Converted to 25Hydroxycholecalciferol in the
liver
- Formation of 1,25Dihydroxycholecalciferol in the
Kidneys and Its Control by
Parathyroid Hormone
- Calcium Ion Concentration Controls
the Formation of 1,25
Dihydrocholecalciferol
Actions of Vitamin D
1. “Hormonal “ Effect of Vitamin D to Promote
Intestinal Calcium Absorption
2. Vitamin D Promotes Phosphate Absorption
by the Intestine
3. Vitamin D Decreases Renal Calcium
Absorption and Phosphate Excretion
4. Effect of Vitamin D on Bone and its Relation
to Parathyroid Hormone Activity
PARATHYROID
HORMONE
Physiologic Anatomy of the Parathyroid Gland
Effect of Parathyroid Hormone on Calcium and
Phosphate Concentrations in the ECF
The rise in calcium concentration is
caused by two Effects
1. an effect of PTH to increase calcium and phosphate
absorption from the bone
2. a rapid effect of PTH to decrease the excretion of
calcium by the kidneys
- Parathyroid Hormone Increased Calcium and Phosphate
Absorption from the Bone
- Rapid Phase of Calcium and Phosphate Absorption – Osteolysis
- Slow Phase of Bone Absorption and Calcium Phosphate Release
– Activation of the Osteoclasts
- Parathyroid Hormone Decreases Calcium Excretion and
Increase Phosphate Excretion in the Kidneys
- Parathyroid Hormone Increases Intestinal absorption of
Calcium and Phosphate
- Cyclic Adenosine Monophosphate Mediates the Effects of
Parathyroid Hormone
ACTIONS OF PTH ON TARGET ORGANS
1. BONES OR SKELETON
Calcium and Phosphate absorption from bones
a. Rapid Phase – osteolysis
b. Slow Phase – activation of osteoclasts
1. immediate activation of osteoclasts
that are already formed
2. formation of new osteoclasts from
osteoprogenator cells
2. INTESTINES
Enhances both Ca and PO4 absorption from the
intestines by increasing formation of 1, 25
dihydroxycholecalciferol from vitamin
3. KIDNEYS
a. Increased renal tubular reabsorption of calcium in the
distal tubules and collecting ducts
b. diminished proximal tubular reabsorption of PO4
EFFECTS OF PTH ON TARGET
ORGANS
1.
Blood Calcium and Phosphate
a. Hypercalcemia
b. Hypophosphatemia
2. Urine
a. Hypocalciuria
b. Hyperphosphatemia - phosphaturic
Control of Parathyroid Hormone Secretion
CALCITONIN
Peptide hormone secreted by the thyroid
gland that tends to decrease plasma calcium
concentration.
Two ways:
1. decrease absorptive activities of the osteoclasts
and the osteocytic effect of the osteocytic
membrane – immediate effect
2. decrease formation of new osteoclasts – more
prolonged effect
Increased Plasma Calcium Concentration
Stimulates Calcitonin Secretion
Calcitonin Has a Weak Effect on Plasma Calcium
Concentration in Adult Human
SUMMARY OF CONTROL OF
CALCIUM ION CONCENTRATION
1. Buffer Function of the Exchangeable Calcium
in Bones - the First Line of Defense
2. Hormonal Control of Calcium ion
concentration – the Second Line of Defense
a. PTH
b. Calcitonin
PARATHYROID HORMONE and BONE
DISEASE
1. Hypoparathryroidism
a.Tetany – Calcium concentration is 6-7
mg% - Larygospasm
Signs of Latent Tetany
1. Chvostek’s sign
2. Trousseau’s sign
b. Impairment of blood clotting
2. Hyperparathyroidism
a. Bone Disease
- broken bones
- Cystic bone disease – Osteitis Fibrosa Cystica or
Von Recklinghausen’s Disease
b. Effects of Hypercalcemia
1. Rise of calcium to 12-15 mg%
- depression of central and peripheral nervous
system
- muscular weakness, constipation, abdominal
pain, peptic ulcer, lack of appetite,
depressed relaxation of the heart
during diastole
2. Formation of kidney stones
3. Parathyroid hormone poisoning and
metastatic calcification- 17 mg%
Calcium
•alveoli of the lungs – tubules of
kidneys
•thyroid gland – walls of the arteries
•stomach mucosa
BONE DISEASES
Rickets – Vitamin D Deficiency
- occurs mainly in children
- results from calcium or phosphate
deficiency in the ECF caused by lack of
VitaminD
- develops tetany
Osteomalacia – “Adult Rickets”
- deficiency of both vitamin D and calcium occurs as
aresult of steatorrhea (failure to absorb fat) because
vitamin D is fat soluble
- “Renal rickets” is a type of osteomalacia that
results from kidney damage
Osteoporosis – Decreased Bone Matrix
- the most common of all bone disease in adults
especially in old age
- results from diminished bone matrix rather
than poor bone calcification
Causes:
a. lack of physical stress on the bones due to
inactivity
b. malnutrition – sufficient protein matrix
cannot be formed
c. lack of vitamin C – necessary for secretion
of intercellular substances
d. postmenopausal lack of estrogen secretion
– estrogen have osteoblast-stimulating
activity
e. old age – diminished growth hormone
f. Cushing’s syndrome – massive
glucocorticoids cause
decreased deposition of protein thus
depressing osteoblastic activity
PHYSIOLOGY OF THE TEETH