The thyroid gland, located below the larynx and anterior to the trachea, secretes key hormones including thyroxine (T4), triiodothyronine (T3), and calcitonin, with T4 being the predominant hormone. Thyroid hormone production is regulated by thyroid-stimulating hormone (TSH) from the anterior pituitary, influencing metabolic rates, growth, and various bodily functions, with T3 being more potent than T4. Dysfunctions in thyroid hormone levels can lead to conditions such as hyperthyroidism and hypothyroidism, each presenting various physiological symptoms and requiring distinct treatment approaches.

1. THYROID
The thyroid gland
 below the larynx on each side of and
anterior to the trachea
15-20 gms in adults
secretes two major hormones:
 thyroxine (T4)
triiodothyronine (T3)
Also secretes calcitonin (an important
hormone for calcium metabolism)

3. Microscopic Appearance of
the Thyroid Gland
Figure 76-1; Guyton & Hall

4.  Thyroid Hormones
 ↑↑↑BMR
 Its ↓↓↓ → 40-50% BMR ↓↓
 Its ↑↑↑ → 60-100% ↑↑ BMR
 secretion is controlled by thyroid-stimulating hormone (TSH) from the
anterior pituitary gland.

5. Synthesis and Secretion of the Thyroid
Metabolic Hormones
• 93% T4 & 7% T3
• T4→T3 in tissues
• Qualitatively same
• Differ in Rapidity & Intensity of action.
• T3 is 4 times ↑potent than T4, but ↓↓↓conc. In
blood & ↓↓↓half life.

6. Physiologic Anatomy of the
Thyroid Gland.
• Composed of large numbers of closed follicles (100-
300 micrometers in diameter) filled with colloid
(major component Thyroglobulin) and lined with
cuboidal epithelial cells that secrete into the interior
of the follicles.
• The large glycoprotein Thyroglobulin contains the
thyroid hormones within its molecule.
• Secretion enters the follical→absorbed (through
epithelium)back into the blood to function.
• Blood flow/min = 5 times its wt.

7. Iodine Requirement
• 50mg/year, 1mg/week
• Common table salt is iodized with 1 part sodium
iodide to every 100,000 parts NaCl.
• Iodides (absorbed from GIT)→⅕ removed from the
blood by thyroid cells for synthesis of hormones; rest
excreted through kidneys.

8. • Basal membrane of thyroid cells has an active pump
to push iodides to interior (Iodine Pump).
– Normally 30% more conc. Inside
– Max. active 250% more conc. Inside
• The rate of Iodine trapping is influenced by conc. of
TSH.
• TSH stimulates and hypophysectomy greatly
diminishes the activity of the iodide pump in thyroid
cells.

9. Thyroid cellular mechanisms for iodine transport,
thyroxine and triiodothyronine formation, and
thyroxine and triiodothyronine release into the blood.
MIT, monoiodotyrosine; DIT, diiodotyrosine; T3, triiodothyronine;
T4, thyroxine; TG, thyroglobulin.

10. Thyroglobulin and Chemistry of T4
and T3 Formation
 Thyroglobulin
– formed by ER
– secreted by Golgi
– mol. wt. 660000
– Each mol. has 123-140 tyrosine aminoacids (Tyrosine +
Iodide = Thyroid hormone)

11.  Conversion of Iodides to oxidized form of Iodine
– Oxidation is by Peroxidase (enzyme) & H₂O₂
– Peroxidase is in apical membrane of the cell or attached to
it.
– Thyroglobulin mol. comes out of Golgi & cell membrane at
the same place.
– If Peroxidase is not present→Thyroid hormone formation
falls to zero.

12. Thyroid cellular mechanisms for iodine transport,
thyroxine and triiodothyronine formation, and
thyroxine and triiodothyronine release into the blood.
MIT, monoiodotyrosine; DIT, diiodotyrosine; T3, triiodothyronine;
T4, thyroxine; TG, thyroglobulin.

13. Iodinationof Tyrosine & Formation of Thyroid
hormones
– Binding of oxidized Iodine with Thyroglobulin =
Organification
– Enzyme Iodinase speeds up the reaction
– Iodine binds with ⅙ of Tyrosine aminoacids within
Thyroglobulin mol.
– Tyrosine→Monoidotyrosine then Diidotyrosine
– Thyroxine=major product, Triidothyroxine=⅕ of
that.

15. Chemistry of thyroxine and triiodothyronine formation.

16. Storage of Thyroglobulin
– Large amount
– Thyroglobulin mol. has 30 thyroxine and a few T3.
– Storage sufficient for 2-3 months.

18. Release of Thyroxine and
Triiodothyronine in the blood
• Cleavage required for the release.
• Pseudopod extensions from the apical surface of the thyroid cells
that close around small portions of the colloid → pinocytic vesicles
formed→ enter the apex of thyroid cell digestive
vesicles release T4 & T3 in free form→ diffuse through
the base of the thyroid cell into the blood.
• ¾ of iodinated tyroxinase never forms hormone, remains as mono or
di ido-MIT, DIT released from Thyroglobulin Tyrosine + I⁻.
• 75% MIT, DIT is recycled.
• ↓↓↓ of enzyme deiodinase can cause defficiency of hormones due
to lack recycling.
• Hormone used by tissues is Triidothyroxine 35 µgm/day.
• 99% of T3 & T4 combines with plasma proteins on entering blood.
– Thyroxine binding globulin
– Thyroxine binding prealbumins
– Thyroxine binding albumin
lysosomes
proteases
deiodinase

19. Transport of Thyroxine and
Triiodothyronine to Tissues
• ½ of T4 bound to proteins is released to
tissues every 6 days.
• ½ of T3 bound to proteins is released to
tissues daily.
• In the target cells, they bind with intracellular
protein to be released slowly.
• T4 has more stray binding.

20. Thyroid Hormones Have Slow Onset
and Long Duration of Action
T4
• No effect for 2-3 days after injection
• Long Latent Period.
• Activity peaks in 10-12 days & ↓↓ with a half
life of 15 days.
• In some cases it takes 6 weeks-2 months.
T3
• 4 times rapid
• Latent Period 6-12 hours
• Peak in 2-3 days

21. Physiologic Functions of the
Thyroid Hormones
Thyroid Hormones Increase the Transcription
of Large Numbers of Genes
• Activates Nuclear Transcription→ ↑↑Protein synthesis →
Generalised ↑↑ in function.
• More than 90% of Thyroid hormone that binds with cellular
receptors is T3.
 Thyroid Hormone Receptor usually forms a heterodimer with
Retinoid X receptor(RXR) at specific thyroid hormone response
element on DNA.
• Receptor+Hormone →Messenger RNA→Translation

22. Thyroid Hormones Increase Cellular
Metabolic Activity
• ↑↑↑ T3 & T4 →BMR ↑ 60-100%.
• Utilization of food products ↑↑↑.
• Protein formation ↑↑& protein catabolism↑↑ as well.
• Growth rate in young ↑↑.
• Endocrine gland activity in other ↑↑.
• Mental process excited.
• Increase in the no. & activity of Mitochondria.
• Mitochondria ↑ in size & no.
• Total membrane surface area of Mitochondria α ↑ BMR.
• Activity of Na⁺-K⁺ ATPase ↑ in response to Thyroid
hormones→↑↑Transport of ions through cell membranes
→ Energy consumed, heat produced.

24. Effect of Thyroid Hormone on
Growth
• In young growing children, its ↓↓causes great
retardation
• ↑↑ causes →↑↑skeletal growth at an early
age but fusion also. So, the end height may be
shortened.
• Development of brain in fetal life & early
childhood.
• ↓↓ release by Fetus → brain remains smaller
than normal & retarded.

25. Effects of Thyroid Hormone on Specific
Bodily Mechanisms
o Stimulation of all aspects of Carbohydrate
Metabolism
 ↑Uptake of glucose by cells
 Enhanced glycolysis
 Enhanced glyconeogenesis
 ↑Rate of absorption from GIT
 ↑Insulin secretion

26. o Stimulation of Fat Metabolism
– Influence of Thyroid hormone→Lipid mobilization from
fat tissues →↓↓in fat stores→ ↑↑free Fatty acids in
plasma & ↑↑their oxidation.
 ↑↑Thyroid hormone →↓↓Plasma conc. of
cholesterol, phospholipids & triglycerides + ↑↑↑free
Fatty acids.
 ↓↓Thyriod hormone →↑↑Plasma conc. of
cholesterol, phospholipids & triglycerides + excessive
deposition of fats in liver.

27. Metabolic Effects of Thyroid Hormones
Parameter ↓ T3, T4 ↑ T3, T4
Basal metabolic rate ↓ ↑
Carbohydrate metabolism ↓ Gluconeogenesis ↑ Gluconeogenesis
↓ Glycogenolysis ↑ Glycogenolysis
Normal serum [glucose] Normal serum [glucose]
Protein metabolism ↓ Synthesis ↑ Synthesis
↓ Proteolysis ↑ Proteolysis
Muscle wasting
Lipid metabolism ↓ Lipogenesis ↑ Lipogenesis
↓ Lipolysis ↑ Lipolysis
↑ Serum [cholesterol] ↓ Serum [cholesterol]
Thermogenesis ↓ ↑
Table 48-1, Boron & Boulpaep

28. – The large ↑ in circulating plasma cholesterol in
prolonged hypothyroidism is often associated
with severe atherosclerosis.
– Mechanisms by which thyroid hormone ↓plasma
cholesterol conc. is to ↑rate of cholesterol
secretion in the bile & loss in the feces.
– A possible mechanism for ↑ cholesterol secretion
is that thyroid hormone induces ↑ no. of LDL
receptors on the liver cells→Rapid removal of LDL
from the plasma by the liver & secretion of
cholesterol in these LDLs by the liver cells.

29. o Increased Requirement for Vitamins
 Thyroid hormone ↑ quantities of hormones i.e ↑in
Formation of enzymes & coenzymes→↑need for vit.
 A relative vitamin deficiency can occur when excess
thyroid hormone is secreted, unless at the same time
increased quantities of vitamins are made available.

30. o Increased Basal Metabolic Rate
– Excessive quantities of Thyroid hormone
occasionally ↑ BMR 60-100% above normal.
– When no Thyroid hormone is produced, BMR falls
almost to one-half normal.
– Extreme amounts of the hormones are required
to cause very high BMR.

31. o Increased Respiration
– ↑Rate of metabolism→ ↑Utilization of O₂→↑CO₂
production →↑Respiration
o Decreased Body Weight
– ↑ Thyroid hormone almost always ↓ body weight.
– Greatly ↓ Thyroid hormone almost always ↑ body
weight.
• These effects do not always occur, because thyroid
hormone also ↑ appetite which may counterbalance the
change in the metabolic rate.

32. o Increased Gastrointestinal Motility
– ↑Appetite→↑Rate of gastric secretions +
↑Motility of GIT.
– Hyperthyroidism often results in diarrhea.
– Lack of thyroid hormone can cause constipation.

33. o Effect of Thyroid Hormones on CVS
 Increased metabolism in tissues → Rapid utilization of O₂
& metabolites → need for heat elimination +
Vasodilation →↑blood flow→↑Cardiac
Output(sometimes ↑ 60 % or more when excessive
thyroid hormone is present & ↓50% in very severe
hypothyroidism).
 Direct effect on the excitability of the heart → ↑ heart
rate.
 Moderate ↑in Thyroid hormone →↑ Heart strength

34.  Large ↑ in Thyroid hormone→↓ strength of heart
muscle (due to long term excessive protein
catabolism).
 Some severely thyrotoxic patients die of cardiac
decompensation secondary to myocardial failure
and to increased cardiac load imposed by the
increase in cardiac output.
 The mean arterial pressure remains normal after
administration of thyroid hormone. (↑blood flow
through the tissues between heartbeats→↑pulse
pressure; e.g in hyperthyroidism 10-15 mm Hg ↑
systolic pressure & corresponding↓ diastolic
pressure.)

35. o Excitatory Effects on the Central Nervous
System
– Thyroid hormone ↑ rapidity of cerebration but also
often dissociates this.
– Lack of thyroid hormone decreases this function.
– Hyperthyroidism → extreme nervousness &
psychoneurotic tendencies e.g anxiety complexes,
extreme worry & paranoia.

36. o Effect on the Function of the Muscles
– Slight ↑in thyroid hormone→ muscles react with vigor.
– Excessive quantity of Thyroid hormone→ muscles become weakened
(due to excess protein catabolism).
– Lack of thyroid hormone→ muscles become sluggish & relax slowly
after a contraction.
– Hyperthyroidism→ ↑ reactivity of the neuronal synapses in the areas
of the spinal cord that control muscle tone → Fine muscle tremor
(occurs 10- 15 times/sec).
 This tremor is an important means for assessing the degree of thyroid
hormone effect on the central nervous system.

37. o Effect on Sleep
– In hyperthyroidism
• the exhausting effect of thyroid hormone on the musculature
and on the central nervous system →a feeling of constant
tiredness.
• excitable effects on synapses do not let person sleep.
– Hypothyroidism →Extreme somnolence with sleep
sometimes lasting 12-14 hrs/day.

38. o Effect on Other Endocrine Glands
– ↑Glucose metabolism→↑Insulin by the pancreas
– ↑Bone formation→↑Parathyroid
– ↑Rate at which adrenal glucocorticoids are
inactivated by the liver→ feedback ↑ in
adrenocorticotropic hormone production by the
anterior pituitary→ increased rate of
glucocorticoid secretion by the adrenal glands.

39. o Effect of Thyroid Hormone on Sexual Function
– In men
• Lack of Thyroid hormone→Loss of libido
• Great excess of Thyroid hormone→Impotence
– In women
• lack of thyroid hormone→ Loss of libido
• Hypothyroidism often causes menorrhagia and polymenorrhea
but strangely enough, in some women it may cause irregular
periods and occasionally even amenorrhea.
• hyperthyroidism→ oligomenorrhea and occasionally
amenorrhea

40. • The action of thyroid hormone on the gonads cannot be
pinpointed to a specific function but probably results
from a combination of direct metabolic effects on the
gonads as well as excitatory and inhibitory feedback
effects operating through the anterior pituitary
hormones that control the sexual functions.

41. Regulation of Thyroid Hormone
Secretion
Specific feedback mechanisms operate
through the hypothalamus and anterior
pituitary gland → control the rate of thyroid
secretion→ maintain normal levels of
metabolic activity in the body.
 TSH (from the Anterior Pituitary Gland) Increases
Thyroid Secretion.
 Thiocyanate, Propylthiouracil, and high
concentrations of inorganic Iodides are Antithyroid
Substances.

42. Hypothalamohypophyseal-Thyroid Axis
HypothalamusHypothalamus
ThyrotropeThyrotrope
ThyroidThyroid
TT33, T, T44
TRHTRH
TSHTSH
__
__
+
+

43. TSH (thyrotropin)
– is an anterior pituitary hormone
– a glycoprotein (mol. wt. 28,000)
– increases all the known secretory activities of the
thyroid glandular cells.

44. Specific effects of TSH on the thyroid gland
are
• ↑Proteolysis of Thyroglobulin to release
stored T3 &T4. (most imp. early effect).
• ↑Activity of Iodine Pump→↑Iodide trapping.
(Intracellular:Extracellular Ratio ↑8 times)
• ↑Iodination of Tyrosine to form Thyroid
hormone
• ↑size & ↑secretory activity of Thyroid cells

45. Mechanism of Action
Activation of the “second
messenger” cyclic adenosine
monophosphate (cAMP) system of
the cell
• Binding of hormone with specific TSH receptors
to basal membrane of Follicular cell →
Activation of Adenylyl cyclase in membrane →
Formation of cAMP in the cell → Activation of
Protein Kinase → Multiple phosphorylation
→immediate ↑ in secretion of thyroid
hormones + prolonged growth of the thyroid
glandular tissue itself.

46. Regulation of TSH
• Anterior pituitary secretion of TSH is controlled by a
hypothalamic hormone, thyrotropin-releasing
hormone (TRH), which is secreted by nerve endings
in the median eminence of the hypothalamus.
• TRH is
– is a tripeptide amide—pyroglutamyl-histidylproline-
amide
– is transported to the anterior pituitary by way of the
hypothalamichypophysial portal blood.
– directly affects the anterior pituitary gland cells to
increase their output of TSH.

49. • Blockage of blood portal system ↓↓↓↓TSH from ant. pit.
 The molecular mechanism by which TRH causes the TSH-secreting cells of
the anterior pituitary to produce TSH is
– first to bind with TRH receptors in the pituitary cell membrane.
– This in turn activates the phospholipase second messenger system
inside the pituitary cells to produce large amounts of phospholipase C,
– followed by a cascade of other second messengers, including calcium
ions and diacyl glycerol,
– which eventually leads to TSH release
• Effects of Cold and Other Neurogenic Stimuli on TRH and TSH Secretion

50. Feedback Effect of Thyroid Hormone
to Decrease Anterior Pituitary
Secretion of TSH
• ↑Thyroid → ↓ of TSH by ant. Pit.
• At 1.75 times normal the TSH ↓↓
to zero.
• Even when ant. Pit. Is seperated
from Hypothalamus; direct effect
on ant. Pit.

51. Regulation of thyroid secretion.

52. Antithyroid Substances
• Thiocyanate Ions Decrease Iodide Trapping
• Propylthiouracil Decreases Thyroid Hormone
Formation.
• Iodides in High Concentrations Decrease Thyroid
Activity and Thyroid Gland Size.

53. Diseases of the Thyroid
Hyperthyroidism
• Causes of Hyperthyroidism:
o Toxic Goiter, Thyrotoxicosis, Graves’ Disease
– Autoimmunity against Thyroid tissue
– Thyroid Stimulating Immunoglobulin
o Thyroid Adenoma

54. • Symptoms:
– (1) a high state of excitability
– (2) intolerance to heat
– (3) increased sweating
– (4) mild to extreme weight loss (sometimes as much as 100 pounds)
– (5) varying degrees of diarrhea
– (6) muscle weakness
– (7) nervousness or other psychic disorders
– (8) extreme fatigue but inability to sleep
– (9) tremor of the hands.
 Exophthalmos
• Physiology of Treatment in Hyperthyroidism (Surgery)
• Treatment of the Hyperplastic Thyroid Gland with Radioactive Iodine

55. Hypothyroidism
• Causes:
– Autoimmunity destroys the gland (Autoimmune Thyroiditis in
most cases) → Progressive deterioration & fibrosis of gland → No
secretion.
– Endemic Colloid Goiter caused by Dietary Iodide Deficiency
– Idiopathic Nontoxic Colloid Goiter

56. • Physiologic Characteristics of Hypothyroidism:
– fatigue
– extreme somnolence with sleeping up to 12 to 14 hours a day
– extreme muscular sluggishness
– slowed heart rate
– decreased cardiac output
– decreased blood volume
– sometimes increased body weight
– constipation
– mental sluggishness
– failure of many trophic functions in the body evidenced by depressed growth of hair and
scaliness of the skin
– development of a froglike husky voice
– in severe cases, development of an edematous appearance throughout the body called
myxedema.
– Atherosclerosis in Hypothyroidism.
– Cretinism (caused by extreme hypothyroidism during fetal life, infancy, or childhood

57.  Myxedema
– Total lack of Thyroid functions
– Bagginess under the eyes and swelling of the face
– Non pitting edema due to gel nature of excess
fluid(greatly increased quantities of hyaluronic acid +
chondroitin sulfate bound with protein form excessive
tissue gel in the interstitial spaces→↑ total quantity of
interstitial fluid)

58.  Atherosclerosis in Hypothyroidism
– Lack of thyroid hormone →altered fat and cholesterol
metabolism + diminished liver excretion of cholesterol in
the bile→↑ blood cholesterol (associated with increased
atherosclerosis) →peripheral vascular disease, deafness, &
coronary artery disease with consequent early death.

59. Pathophysiology of Thyroid
Hormones
• Pathophysiology of Thyroid Hormones:
• Graves’ disease – autoimmune disorder;
immune complex mimics TSH – stimulates
continual production of thyroid hormone – leads
to hyperthyroidism and goiter formation.
• Cretinism – deficiency of thyroid hormones in
childhood – results in severe growth retardation
and mental retardation.

60.  Cretinism
– Congenital Cretinism
– Endemic Cretinism
– Caused by extreme hypothyroidism during fetal life, infancy, or
childhood.
– Characterized by failure of body growth & by mental retardation.

62. Hypothalamohypophyseal-Thyroid Axis in
GraveHhs’ Disease
HypothalamusHypothalamus
ThyrotropeThyrotrope
ThyroidThyroid
TT33, T, T44
TRHTRH
TSHTSH
__
+
__
+
TSI
+

63. – Unless the cretinism is treated within a few weeks after birth,
mental growth remains permanently retarded due to
retardation of the growth, branching, andmyelination of the
neuronal cells of the central nervous system at this critical time
in the normal development of the mental powers.
– Skeletal growth in the child with Cretinism is characteristically
more inhibited than is soft tissue growth→ disproportionate
rate of growth (the soft tissues are likely to enlarge excessively,
giving the child with cretinism an obese, stocky, and short
appearance).
– Occasionally the tongue becomes very large in relation to the
skeletal growth → obstructs swallowing and breathing→
guttural breathing that sometimes chokes the child.

64. • Treatment of Hypothyroidism
– daily oral ingestion of a tablet or more containing
Thyroxine.
– Proper treatment of the hypothyroid patient →complete
normality (formerly myxedematous patients have lived
into their 90s after treatment for more than 50 years).

65. Overview of ECF Ca⁺⁺
• ECF Ca⁺⁺= q.n mg / dL
• Precise control muscle contraction, blood
clotting, nerve impulses
• ↑↑ Ca⁺⁺ depression of CNS while ↓ CNS
more excited
• 0.1 % is in ECF , 1% in cells and 99% in bones

66. Overview of PHOSPHATE
• 85 % in bones
• 14 – 15 % in cells and less than 1% ECF
• Deposition and absorption of Bone
• Osteoblasts on the surface and cavities
• Osteoclasts

67. PARATHYROID
• Poly peptide; mol. wt. 2500; 84 a.a
• Controls ECF Ca⁺⁺ & Phosphate conc. by
– Intestinal reabsorption
– Renal excretion
– Exchange between ECF & bone
• ↑Ca⁺⁺ & Phosphate absorption from bone
• ↓ Ca⁺⁺ excretion & ↑ Phosphate excretion by
kidneys
4 Parathyroid glands
– Removal of 2 doesnot affect much
– but removal of 3→hypoparathyroidism

68. Anatomy of the Parathyroid Glands
& Microscopic Appearance of Chief
Cells
Figure 79-9;
Guyton & Hall

69. Mechanism of Action
• cAMP acts as a 2nd
messenger to carry out the
effects of hormone.
Regulation
• Slightest ↓↓ in Ca⁺⁺ion concentration
→↑↑↑parathyroid
• ↑↑ In Ca⁺⁺ →↓↓ Parathyroid Hormone

70. • Bone
– ↑ resorption ( ↑ osteoclasts)
– ↑ osteocytic osteolysis
• Kidney
– ↑ Ca2+
reabsorption
– ↓ phosphate reabsorption
– ↓ Na+
reabsorption (weak effect)
– ↑ 1,25-(OH)2-D3
• Intestine
– ↑ Ca2+
absorption
– ↑ phosphate absorption
PTH Actions

71. • Plasma Calcium concentration and PTH
secretion
PlasPpma Calcium Concentration & PTH
Secretion

72. 0
6 8 10 12 14
50
100
PTHsecretion
(%maximalrate)
Total plasma [Ca2+
] (mg/dL)
Plasma Calcium Concentration
& PTH Secretion

73. Hypocalcemia
Disorder
Plasma
[PTH]
Plasma
[1,25-(OH)2-D3] UrineBone
Plasma
[Ca2+
]
Plasma
[Phosphate]
Vitamin D
deficiency
Chronic renal
failure
(2°)
*
*
Phosphate
cAMP
Phosphate
( ↓ GFR)*
Osteomalacia
Resorption
Resorption
* Primary events or disturbances
Surgical
hypoparathyroidism
(2°)
*
Osteomalacia
Resorption cAMP
Phosphate
Castanzo, Table 9-17

74. Primary Hyperparathyroidism

75. Primary Hyperparathyroidism
Plasma
[PTH]
*
Plasma
[1,25-(OH)2-D3] Urine
Phosphate
Ca2+
cAMP
Bone
Resorption
Plasma
[Ca2+
]
Plasma
[Phosphate]
* Primary disturbance
Castanzo, Table 9-17

76. CALCITONIN
• Peptide hormone
• Mol. Wt. 3400
• From thyroid gland (C cells in the interstitium
between follicles)
• Actions opposite to Parathyroid
• ↑↑ Ca⁺⁺ concentration↑↑ Calcitonin
• ↓↓ Ca⁺⁺ concentration in Plasma
• PTH overrides its effects.

77. VITAMIN D
• Increases Ca⁺⁺ absorption from GIT
• Bone deposition and bone absorption
• ↑ Intestinal Ca⁺⁺ absorption
• ↑ Intestinal phosphate absorption
• ↓ Renal Ca⁺⁺ & phosphate excretion
• In large quantities it causes bone absorption
• In ↓↓ quantities it causes bone deposition

78. Activation of vitamin D3 to form 1,25-dihydroxycholecalciferol and the
role of vitamin D in controlling the plasma calcium concentration

79. Pathophysiology
• Decreased – Osteoclasts inactive- ca
decreases- tetany