Endocrine Physiology pituitary

1. Endocrine
system
Physiology

2. Presented by/
Dr/ dina hamdy merzeban

3. Pituitary
The pituitary gland also called the hypophysis, is a small
gland, that lies in the sella turcica, a bony cavity at the base
of the brain, and is connected to the hypothalamus by the
pituitary (or hypophysial) stalk. Physiologically, the pituitary
gland is divisible into two distinct portions: the anterior
pituitary, also known as the adenohypophysis, and the
posterior pituitary, also known as the neurohypophysis.
Between these is a small, relatively avascular zone called the
pars intermedia, which is much less developed in the human
beings.

4. ANTERIOR
PITUITARY
Somatotropes secrete:
human growth hormone
Corticotropes secrete:
adrenocorticotropin
Thyrotropes secrete:
thyroid-stimulating
hormone
Gonadotropes secrete:
gonadotropic hormones,
which include both
luteinizing hormone (LH)
and follicle-stimulating
hormone (FSH)
Lactotropes secrete:
prolactin (PRL)

5. POSTERIOR
PITUITARY
Antidiuretic hormone controls
the rate of water excretion into
the urine, thus helping to
control the concentration of
water in the body fluids
Oxytocin helps express milk
from the glands of the breast to
the nipples during suckling and
helps in the delivery of the baby
at the end of gestation

6. • Hypothalamic-Hypophysial
Portal circulation connects
Hypothalamus to the Anterior
Pituitary.
• Hypothalamo-hypophyseal tract
connects Hypothalamus with
posterior pituitary.

7. Hypothalamic-Hypophysial
Portal circulation
• Thyrotropin-releasing hormone , which causes release of thyroid-
stimulating hormone
• Corticotropin-releasing hormone , which causes release of
adrenocorticotropin
• Growth hormone–releasing hormone , which causes release of growth
hormone, and growth hormone inhibitory hormone , also called
somatostatin, which inhibits release of growth hormone
• Gonadotropin-releasing hormone , which causes release of the two
gonadotropic hormones, luteinizing hormone and follicle- stimulating
hormone
• Prolactin inhibitory hormone , which causes inhibition of prolactin
secretion

8. Hypothalamic-Hypophysial Portal
circulation
Thyrotropin-releasing
hormone TRH.....
release of thyroid-
stimulating hormone
Corticotropin-releasing
hormone CRH.....
release of
adrenocorticotropin
Growth hormone–
releasing hormone ,
which causes release of
growth hormone
growth hormone
inhibitory hormone , also
called somatostatin,
which inhibits release of
growth hormone
Gonadotropin-releasing
hormone GRH , which
causes release of the
two gonadotropic
hormones LH & FSH
Prolactin inhibitory
hormone , which causes
inhibition of prolactin
secretion

9. GROWTH HORMONE
It is a polypeptide hormone also called Somatotropin

10. Mechanism of
action :
(JACK-STAT
pathway)
• GH receptor is composed of large extracellular and
cytoplasmic domains with a small transmembrane
domain. Binding of Growth Hormone (GH) to its
receptor induces receptor dimerization forming
homodimer, and activation of the tyrosine kinase
JAK2 (Janus family of cytoplasmic tyrosine kinase).
JAK2 phosphorylate tyrosine in themselves (auto
phosphorylation) and in GH receptor leading to
activation of signaling molecules such as:

11. Mechanism of
action :
(JACK-STAT
pathway)
• STAT5 transcription factors, , which leads to initiation
of transcription of certain genes for protein synthesis
• Insulin receptor substrates 1 that lead to
the activation of enzymes involved in the
metabolic processes in the cell
• Phosphorylation of MAPK

12. PHYSIOLOGICAL
FUNCTIONS OF
GROWTH HORMONE
• It causes growth of almost all tissues of the body that are capable of
growing by increasing the number and the size of the cells.
• GH also has many metabolic actions:

13. PHYSIOLOGICAL FUNCTIONS OF
GROWTH HORMONE
Protein: Protein sparer”
“Anabolic effect”
Lipids: GH Enhances
Fat
Utilization “Ketogenic”
Effect
Carbohydrates: GH
Decreases
Carbohydrate
Utilization
Growth Hormone
Stimulates Cartilage
and Bone Growth
Growth Hormone
Stimulates visceral
growth

14. PHYSIOLOGICAL FUNCTIONS OF
GROWTH HORMONE
• Protein: Growth Hormone Promotes Protein Deposition in Tissues. ”Protein
sparer” “Anabolic effect”
• Increased Nuclear Transcription of DNA to Form RNA.
• Enhancement of RNA Translation to Cause Protein Synthesis by the Ribosomes.
• Enhancement of Amino Acid Transport through the Cell Membranes.
• Decreased Catabolism of Protein and Amino Acids.

15. PHYSIOLOGICAL FUNCTIONS OF
GROWTH HORMONE
• Lipids: Growth Hormone Enhances Fat Utilization for Energy and leading to
release of ketone bodies “Ketogenic” Effect.

16. PHYSIOLOGICAL FUNCTIONS OF
GROWTH HORMONE
Carbohydrates: Growth Hormone Decreases Carbohydrate Utilization
• Decreased glucose uptake in tissues such as skeletal muscle and fat.
• Increased glucose production by the liver.
• Increased insulin secretion.
• Each of these changes results from growth hormone– induced “insulin resistance,” which
oppose insulin’s actions and leads to increased blood glucose concentration and a
compensatory increase in insulin secretion. For these reasons, growth hormone’s effects
are called Hyperglycemic and diabetogenic.
• Insulin and Carbohydrate are NECESSARY for the Growth-Promoting Action of Growth
Hormone. Growth hormone fails to cause growth in animals that lack a pancreas.

17. PHYSIOLOGICAL FUNCTIONS OF
GROWTH HORMONE
Growth Hormone Stimulates Cartilage and Bone Growth
• Although growth hormone stimulates increased deposition of protein and
increased growth in almost all tissues of the body, its most obvious effect is to
increase growth of the skeletal frame.
• growth hormone increases deposition of protein both in cartilage and bones
causing formation of new cartilage and bone cells. These effects lead to
increased length of the bones before puberty and increased thickness of the
bones after puberty.
Growth Hormone Stimulates visceral growth (heart, lung,
stomach etc….).

18. PHYSIOLOGICAL FUNCTIONS OF
GROWTH HORMONE
“Somatomedins”
• Growth Hormone Exerts Much of Its Effect through
Intermediate Substances Called “Somatomedins”
• Growth hormone causes the liver to form several small proteins called somatomedins
• have potent effect of increasing all aspects of bone growth.
• Many of the somatomedin effects on growth are similar to the effects of insulin on growth.
Therefore, the somatomedins are also called insulin-like growth factors (IGFs).
• At least four somatomedins have been isolated, but by far the most important of these is
somatomedin C (also called insulin-like growth factor-1, or IGF-I).

19. • Regulation of GH secretion:
• Most of the control of growth hormone secretion is probably mediated
through GHRH rather than through the inhibitory hormone somatostatin.
• GHRH stimulates growth hormone secretion by attaching to specific cell
membrane receptors on the outer surfaces of the growth hormone cells
in the pituitary gland.
• The receptors activate the adenylyl cyclase system inside the cell
membrane, increasing the intracellular level of cyclic adenosine
monophosphate (cAMP).

20. Regulation
of GH
secretion:
Stimulate GH secretion Inhibit GH secretion
• Decreased blood glucose
• Decreased blood free fatty
acids
• Increased blood amino
acids (arginine)
• Starvation or fasting, protein
deficiency
• Trauma, stress, excitement
• Exercise
• Testosterone, estrogen
• Deep sleep (stages II and
IV)
• Growth hormone–releasing
hormone
• Ghrelin
• Increased blood glucose
• Increased blood free
fatty acids
• Aging
• Obesity
• Growth hormone inhibitory
hormone (somatostatin)
• Growth hormone
(exogenous)
• Somatomedins (insulin-like
growth factors)

21. Abnormalities
of GH
secretion
Decreased
secretion
◦ PANHYPOPITUITARISM: This term means decreased secretion of all
the anterior pituitary hormones. The decrease in secretion may be
congenital (present from birth), or it may occur suddenly or slowly
at any time during life, most often resulting from a pituitary tumor
that destroys the pituitary gland.
◦ SHEEHAN’S SYNDROME: Happens as a result of sever postpartum
hemorrhage that leads to destruction of anterior pituitary
hormones. Sheehan’s syndrome is manifested by rapidly progressive
senility.
◦ PITUITARY DWARFISM. Most instances of dwarfism result from
deficiency of GH secretion during childhood. In general, all the
physical parts of the body develop in appropriate proportion to one
another, but the rate of development is greatly decreased. They are
normal both mentally and sexually.

22. Abnormalities
of GH
secretion
increased
secretion
GIGANTISM
Occasionally, growth hormone– producing cells of the anterior
pituitary gland become excessively active
As a result, large quantities of growth hormone are produced. All
body tissues grow rapidly, including the bones. If the condition
occurs BEFORE adolescence, before the epiphyses of the long
bones have become fused with the shafts, height increases so
that the person becomes a giant. Gigantism is usually
accompanied by Diabetes Mellitus and hyperglycemia, and the
beta cells of the islets of Langerhans in the pancreas are prone
to degenerate because they become overactive owing to the
hyperglycemia.

23. Abnormalities
of GH
secretion
Increased
secretion
ACROMEGALY
If a tumor occurs AFTER adolescence— that is, after the
epiphyses of the long bones have fused with the shafts—the
person cannot grow taller, but the bones can become thicker
and the soft tissues can continue to grow.
◦ Enlargement is especially marked in the bones of the hands
and feet and in the membranous bones, including the
cranium, nose, bosses on the forehead, supraorbital ridges,
lower jawbone, and portions of the vertebrae, because their
growth does not cease at adolescence
◦ In females: Amenorrhea and galactorrhea
◦ In males: Infertility
◦ In both sexes: decreased libido
◦ Treatment of hyperprolactinemia:Dopamineagonist

24. prolactin
• It is a polypeptide hormone with great similarity to GH
• Mechanism of Action: JAK2-STAT pathway
• Prolactin (PRL) hormone is secreted by the mother’s anterior
pituitary gland, and its concentration in her blood rises steadily from
the fifth week of pregnancy until birth of the baby, at which time it
has risen to 10 to 20 times the normal level.
• The placenta secretes large quantities of human chorionic
somatomammotropin, which stimulates milk production, The fluid
secreted during the last few days before and the first few days after
parturition is called colostrum;
• After birth of the baby, the basal level of prolactin secretion returns
to the non-pregnant level over the next few weeks. However, each
time the mother nurses her baby, nervous signals from the nipples
to the hypothalamus causes a 10- to 20-fold surge in prolactin
secretion that lasts for about 1 hour.

25. Physiological Actions of PRL: In
females:
A- Milk secretion: after
priming action of estrogen
and progesterone during
pregnancy increased
production of Casien and
Lactalbumin
B- Prevention of
Ovulation: inhibits the
effect of gonatotropin
hormones on the ovaries
(amenorrhea & infertility)-
during lactation.

26. Regulation of
PRL secretion:
Increased secretion Decreased
secretion
Pregnancy and lactation period
Suckling
Stress
Dopamine

27. Hyperprolactinemia
In females: Amenorrhea and galactorrhea
In males: Infertility
In both sexes: decreased libido
Treatmentofhyperprolactinemia:Dopamineagonist

28. POSTERIOR PITUITARY GLAND
• The posterior pituitary gland, also called the neurohypophysis, hormones are
secreted from terminal nerve endings from nerve tracts that originate in the
supraoptic and paraventricular nuclei of the hypothalamus. These endings secrete
two posterior pituitary hormones:
• Antidiuretic hormone (ADH), also called vasopressin, formed primarily in the supraoptic
nuclei.
• Oxytocin. is formed primarily in the paraventricular nuclei

29. ANTIDIURETIC HORMONE
V1 : Acts via G coupled
protein by inositol
phosphate pathway , to
increase intracellular
Ca2+
V2 : Acts through G
coupled protein of
Adenyl cyclase pathway
that increases the
intracellular cAMP
V3 : Acts through G
coupled protein on
phospholipase

30. ANTIDIURETIC HORMONE
• RENAL EFFECTS
• ON BLOOD VESSELS
• In case of STRESS

31. Physiological Functions of
Antidiuretic Hormone:
A- On renal tubules : (V2
receptors)
Distal tubules (principle cells): It
causes translocation of water
channels (Aquaporin 2) …......
(water
reabsorption)…... (antidiuresis).
Cortical collecting duct: ADH
stimulates urinary K+ secretion.
Medullary collecting duct:
insertion of Urea transporter
(UT1) to increase flow of urea
to medullary interstitium to
increase the concentration of
interstitial solutes to and help
more water reabsorption.

32. Physiological Functions of
Antidiuretic Hormone:
ON BLOOD VESSELS : ( V1
receptors)It increases intracellular Ca2+
which stimulates Vasoconstriction of
blood vessels in cases of hemorrhage
to raise the dropped blood pressure.
This effect is minor compared to renin
Angiotensin & sympathetic nervous
system which are considered as the
primary regulators of the blood
pressure.
In case of STRESS :ADH can
stimulate corticotropes to secret ACTH
which in turn causes Cortisol release to
produce stress response.

33. Control of ANTIDIURETIC
HORMONE secretion
Hypovolemia Hypotension
Hypothalamic
osmoreceptors

34. Control of ADH secretion:
Hypovolemia
• Hypovolemia, (during hemorrhage and dehydration) >> results in a decrease in
atrial pressure and central venous pressure (CVP) >> decreased firing of atrial
stretch receptors (cardiopulmonary baroreceptors) >> Afferent nerve fibers
from these receptors synapse within the nucleus tractus solitarius of the medulla,
which sends fibers to the hypothalamus, a region of the brain that controls AVP
release by the pituitary. Atrial receptor firing normally inhibits the release of AVP
by the posterior pituitary. With hypovolemia or decreased central venous
pressure, the decreased firing of atrial stretch receptors leads to an increase in
AVP release.

35. Control of ADH secretion:
• Hypotension, which decreases arterial baroreceptor firing, leads to enhanced
sympathetic activity that increases AVP release.
• Hypothalamic osmoreceptors sense extracellular osmolarity and stimulate
AVP release when osmolarity rises, as occurs with dehydration.
• Angiotensin II receptors located in a region of the hypothalamus regulate AVP
release – an increase in angiotensin II simulates AVP release.
• Stress: increases ADH through CRH-ADH.
• Drugs: Morphine, Nicotine, Anesthesia (increase ADH).

36. Stimuli that decrease ADH
secretion:
• Low osmolarity of the plasma.
• Hypervolemia.
• α- Adrenergic stimulation
• Ethyl Alcohol.

37. Disturbance of
ADH secretion:
1.Diabetes
insipidus
(decreased A
DH secretion-
excessive
water loss)
Central diabetes insipidus Nephrogenic diabetes insipidus
Insufficient ADH due to problem with
production at the level of the
hypothalamus.
X- linked mutation of V2 receptors
gene or Autosomal mutation of
Aquaporin 2.
This leads to absence of response to
ADH.
Manifestations : Polyuria • Polydipsia • Hypernatremia • Urine osmolality
less than serum osmolality

38. DisturbanceofADH secretion:
SyndromeofInappropriateAntidiureticHormoneSecretion(SIADH)
The syndrome of inappropriate antidiuretic hormone
secretion (SIADH) involves the continued secretion or
action of ADH despite normal or increased plasma volume.
This leads to retention of water and hyponatremia.
Causes: Drugs (Antidepressants) Cancer (lung).

39. OXYTOCIN
Mechanism of Action: Binds to G-protein coupled receptor to increase cytoplasmic Ca+ level which in order increases smooth muscle
contraction
In Male: contraction of the vas deferens
Females: Contraction of the uterus
helps semen transport into the uterus
During labor: Strong uterine contraction
to expel the baby
During lactation: myoepithlial cells
contraction to squeeze the milk
Conditioned reflex: Higher centers stimulation: Seeing, Hearing the cry of baby, smelling, or just thinking of the baby
Mechanism of secretion: Neurohormonal reflex
Unconditioned reflex
• Genital manipulation
• Massage of the nipple during lactation

40. OXYTOCIN
Mechanism of secretion: Neurohormonal reflex
Unconditioned reflex
•Genital manipulation
•Massage of the nipple during lactation
Conditioned reflex: Higher centers stimulation: Seeing, Hearing the cry of baby, smelling, or just thinking of the baby
Mechanism of Action: Binds to G-protein coupled receptor to increase cytoplasmic Ca+ level which in order increases smooth muscle contraction
In Male: contraction of the vas deferens
Females: Contraction of the uterus helps semen transport into the uterus
During labor: Strong uterine contraction to expel the baby
During lactation: myoepithlial cells contraction to squeeze the milk

41. THYROID
GLAND
GLUT4 is insulin dependent, it’s contained in vesicles in the
cytoplasm, these vesicles move to the cell membrane once
Insulin binds to its receptor
Non- insulin dependent tissues , have glucose transporters on
the cell membrane in absence of Insulin
EXERCISE increases the movement of GLUT4 vesicles towards
cell membrane through the action of 5’AMP activated kinase

42. MECHANISM OF INSULIN
SECRETION
The beta cells have a large number of glucose transporters that permit a rate of glucose influx that is
proportional to the blood concentration in the physiological range
Glucose is phosphorylated to glucose-6-phosphate by glucokinase
The glucose-6-phosphate is subsequently oxidized to form adenosine triphosphate
ATP inhibits the ATP-sensitive potassium channels of the cell
Opening voltage-gated calcium channels, which are sensitive to changes in membrane voltage
Influx of calcium that stimulates fusion of the docked insulin- containing vesicles with the cell
membrane and secretion of insulin into the extracellular fluid by exocytosis
ON CARBOHYDRATE METABOLISM
N.B: There is Lack of Effect of Insulin on Glucose Uptake and Usage by the Brain

43. MECHANISM OF INSULIN
SECRETION
ON LIPID METABOLISM
◦ Insulin has several effects that lead to fat storage in adipose tissue
◦ Increases Fat synthesis in the liver, the glucose is first split to pyruvate in the
glycolytic pathway, and the pyruvate subsequently is converted to acetyl coenzyme A
, the substrate from which fatty acids are synthesized
◦ Most of the fatty acids are then synthesized within the liver and used to form
triglycerides, the usual form of storage fat
◦ Insulin inhibits the action of hormone-sensitive lipase
◦ Insulin promotes glucose transport through the cell membrane into the adipose
tissue cells in the same way that it promotes glucose transport into muscle cells

44. MECHANISM OF INSULIN
SECRETION
ON PROTEIN METABOLISM AND GROWTH
◦ Insulin stimulates transport of many of the amino acids into the cells
◦ Insulin increases the translation of messenger RNA, thus forming new proteins
◦ Over a longer period of time, insulin also increases the rate of transcription of
selected DNA genetic sequences in the cell nuclei, thus forming increased quantities
of RNA and still more protein synthesis
◦ Insulin inhibits the catabolism of proteins, thus decreasing the rate of amino acid
release from the cells, especially from the muscle cells
◦ In the liver, insulin depresses the rate of gluconeogenesis
◦ Insulin and Growth Hormone Interact Synergistically to Promote Growth

45. MECHANISM OF INSULIN
SECRETION
Promotes Muscle Glucose Uptake and Metabolism to produce energy during exercise
Promotes glucose uptake and oxidation by all tissues
Storage of Glycogen in Muscle
Insulin Promotes Liver Uptake, Storage, and Use of Glucose
◦ Insulin inactivates liver phosphorylase, the principal enzyme that causes liver glycogen to split
into glucose
◦ Increases the activity of the enzyme glucokinase, which is one of the enzymes that causes the
initial phosphorylation of glucose
◦ Promotesglycogensynthesis,includingespeciallyglycogen synthase
◦ Insulin Promotes Conversion of Excess Glucose into Fatty Acids and Inhibits Gluconeogenesis in
the Liver

46. CONTROL OF
INSULIN
SECRETION
Insulin causes K+ to enter the cells
through its activation of Na+-K+
ATPase
K+ depletion causes inhibition of
Insulin secretion , this happens in 1ry
Hyperaldosteronism and patients
treated with thiazide diuretic)

47. INSULINOMA—
HYPERINSULINISM About 10 to 15 percent of these adenomas are
malignant, In case of high levels of insulin cause
blood glucose to fall to low values, the metabolism
of the central nervous system becomes depressed
Consequently, in patients with insulin-secreting
tumors or in patients with diabetes who administer
too much insulin to themselves, the syndrome
called insulin shock may occur as follows
Proper treatment for a patient who has
hypoglycemic shock or coma is immediate
intravenous administration of large quantities of
glucose

48. GLUCAGON
Breakdown of liver glycogen
Increased gluconeogenesis in the liver

49. PHYSIOLOGICAL ACTIONS OF
GLUCAGON
Increased Blood Glucose Concentration
◦ Glucagon activates adenylyl cyclase in the hepatic cell
membrane
◦ Which causes the formation of cyclic adenosine
monophosphate
◦ Which activates protein kinase regulator protein
◦ Which activates protein kinase
◦ Which activates phosphorylase b kinase
◦ Which converts phosphorylase b into phosphorylase a
◦ Which promotes the degradation of glycogen into
glucose-1- phosphate
◦ Which is then dephosphorylated; and the glucose is
released from the liver cells

50. Glucagon Increases
Gluconeogenesis
Stimulates lipolysis, Keogenesis and fat
utilization for energy production

51. Regulation of Glucagon
Secretion
Increased Blood Glucose Inhibits
Glucagon Secretion

52. Regulation of
Glucagon
Secretion
Increased Blood Amino Acids Stimulate Glucagon Secretion
Exercise Stimulates Glucagon Secretion

53. SOMATOSTATIN
Somatostatin acts locally within the islets of Langerhans in
a paracrine way to depress the secretion of both insulin
and glucagon
Somatostatin decreases the motility of the stomach,
duodenum, and gallbladder
Somatostatindecreasesbothsecretionandabsorptioninthe
gastrointestinal tract

54. SUMMARY OF BLOOD
GLUCOSE
REGULATION
The liver acts as a Glucostat : That is, when the blood glucose rises to a
high concentration after a meal and the rate of insulin secretion also
increases, as much as two thirds of the glucose absorbed from the gut is
almost immediately stored in the liver in the form of glycogen
Both insulin and glucagon function as important feedback control
systems for maintaining a normal blood glucose concentration
Also, in severe hypoglycemia, a direct effect of low blood glucose on the
hypothalamus stimulates the sympathetic nervous system
And finally, over a period of hours and days , both growth hormone and
cortisol are secreted in response to prolonged hypoglycemia

55. Importance of Blood Glucose
Regulation
In case of hypoglycemia: Glucose is the only nutrient that normally
can be used by the brain, retina, and germinal epithelium of the
gonads in sufficient quantities to supply them optimally with their
required energy

56. In case of
hyperglycemi
a
Glucose can exert a large amount of osmotic pressure in the
extracellular fluid, and if the glucose concentration rises to
excessive values, this can cause considerable cellular
dehydration
An excessively high level of blood glucose concentration causes
loss of glucose in the urine
Loss of glucose in the urine also causes osmotic diuresis by the
kidneys, which can deplete the body of its fluids and
electrolytes
Long-term increases in blood glucose may cause damage to
many tissues, especially to blood vessels

57. DIABETES MELLITUS
Type I diabetes, also called
insulin-dependent diabetes
mellitus , is caused by lack of
insulin secretion
Type II diabetes, also called
non-insulin-dependent
diabetes mellitus , and is
initially caused by decreased
sensitivity of target tissues to
the metabolic effect of insulin

58. DIABETES
MELLITUS
Microvasularcomplications:retinopathy,peripheralneur
opathy, Nephropathy
Macrovasular complications: Atherosclerosis, Ischemic
heart diseases, cerebrovascularStrokes
Fasting blood glucose more than: 126 mg/dl
HBA1C more than: 6.4 %
Homeostatic model assessment index: evaluates B-cell
function and Insulin resistance

59. Adrenal gland There are two adrenal glands, one
at the superior pole of each
kidney
The adrenal glands are essential
for life
Severe illness results from their
atrophy and death follows their
complete removal

60. CELL SURFACE RECEPTROS
Ion Channel–Linked Receptors: Virtually all the neurotransmitter
substances, such as acetylcholine and norepinephrine, combine
with receptors in the postsynaptic membrane
GTP-binding proteins : The trimeric G proteins are named for their
ability to bind guanosine nucleotides
Enzyme-Linked Hormone Receptors
Second Messenger Mechanisms for Mediating Intracellular
Hormonal Functions

61. Adenylyl Cyclase cAMP Second
Messenger System
Binding of the hormones with the receptor causes Stimulation of
adenylyl cyclase, a membrane-bound enzyme then catalyzes the
conversion of a small amount of cytoplasmic adenosine
triphosphate into cAMP inside the cell
This then activates cAMP-dependent protein kinase, which
phosphorylates specific proteins in the cell, triggering biochemical
reactions that ultimately lead to the cell’s response to the
hormone

62. Cell Membrane
Phospholipid Second
Messenger System
Calcium-
Calmodulin
Second
Messenger
System
Another second
messenger
system operates
in response to the
entry of calcium
into the cells
Changes in
membrane
potential that
open calcium
channels
A hormone
interacting with
membrane
receptors that
open calcium
channels

63. INTRACELLULAR
RECEPTROS

64. “GENOMIC ACTIONS”
Intracellular Hormone
Receptors and
Activation of Genes
Cytoplasmic receptors:
Steroid Hormones : Sex
hormones, Adrenal,
Vitamin D
Nuclear receptors:
Thyroid hormone

65. Pituitary
The Pituitary Gland Has Two Distinct Parts— The Anterior and
Posterior Lobes

66. ANTERIOR PITUITARY
Somatotropes
secrete: human
growth hormone
Corticotropes
secrete:
adrenocorticotropin
Thyrotropes
secrete: thyroid-
stimulating
hormone

67. ANTERIOR PITUITARY
Gonadotropes secrete: gonadotropic hormones, which include
both luteinizing hormone and follicle-stimulating hormone
◦ Lactotropes secrete: prolactin

68. POSTERIOR PITUITARY
Antidiuretic hormone controls the rate of water excretion into the
urine, thus helping to control the concentration of water in the
body fluids

69. POSTERIOR PITUITARY
Oxytocin helps express milk from the glands of the breast to the nipples during suckling and
helps in the delivery of the baby at the end of gestation
◦ Thyrotropin-releasing hormone , which causes release of thyroid- stimulating hormone
◦ Corticotropin-releasing hormone , which causes release of adrenocorticotropin
◦ Growth hormone–releasing hormone , which causes release of growth hormone, and
growth hormone inhibitory hormone , also called somatostatin, which inhibits release of
growth hormone
◦ Gonadotropin-releasing hormone , which causes release of the two gonadotropic
hormones, luteinizing hormone and follicle- stimulating hormone
◦ Prolactin inhibitory hormone , which causes inhibition of prolactin secretion

70. POSTERIOR PITUITARY
Oxytocin helps express milk from the glands of the breast to the
nipples during suckling and helps in the delivery of the baby at the
end of gestation
◦ Hypothalamo-hypophyseal tract connects Hypothalamus with
posterior pituitary

71. GROWTH HORMONE
It is a polypeptide hormone also called Somatotropin

72. Mechanism
of action :
STAT5 transcription factors, , which
leads to initiation of transcription
of certain genes for protein
synthesis
Insulin receptor substrates 1 that
lead to the activation of enzymes
involved in the metabolic
processes in the cell
Phosphorylation of MAPK

73. PHYSIOLOGICAL
FUNCTIONS OF
GROWTH
HORMONE
Protein: Growth Hormone Promotes Protein Deposition in Tissues
Lipids: Growth Hormone Enhances Fat Utilization for Energy and leading to release of ketone bodies “Ketogenic” Effect
Enhancementof Amino Acid Transport through the Cell Membranes
Enhancementof RNA Translation to Cause Protein Synthesis by the Ribosomes
Increased Nuclear Transcription of DNA to Form RNA
Carbohydrates: Growth Hormone Decreases Carbohydrate UtilizationGrowth hormone causes multiple effects that influence
carbohydrate metabolism, including
Decreased glucose uptake in tissues such as skeletal muscle and fat
Increased glucose production by the liver
Increased insulin secretion

74. Growth Hormone
Stimulates Cartilage and
Bone Growth
Although growth hormone stimulates increased
deposition of protein and increased growth in
almost all tissues of the body, its most obvious
effect is to increase growth of the skeletal frame
This results from multiple effects of growth
hormone on bone, including increased deposition
of protein both in cartilage and bones causing
formation of new cartilage and bone cells
These effects lead to increased length of the bones
before puberty and increased thickness of the
bones after puberty

75. GROWTH HORMONE EXERTS MUCH
OF ITS EFFECT THROUGH
INTERMEDIATE SUBSTANCES
CALLED “SOMATOMEDINS”
Growth Hormone Stimulates visceral growth

76. PROLACTIN Thyroglobulin synthesis : glycoprotein produced by the follicular cells of the
thyroid and used entirely within the thyroid gland to form T3 and T
Iodide trapping
The basal membrane of the thyroid cell has the specific ability to pump the
The energy for transporting iodide against a concentration gradient comes from
the sodium-potassium ATPase pump, which pumps sodium out of the cell,
thereby establishing a low intracellular sodium concentration and a gradient for
Iodide is transported out of the thyroid cells across the apical membrane into
the follicle by a chloride-iodide ion counter-transporter molecule

77. PROLACTIN Oxidation: The first essential step in the formation of the thyroid
hormones is conversion of the iodide ions to an oxidized form of iodine,
that is then capable of combining directly with the amino acid tyrosine
Iodination of Tyrosine and Formation of the Thyroid Hormones
“Organification” of Thyroglobulin: The binding of iodine with the
thyroglobulin molecule is called organification of the thyroglobulin
COUPLING
Thyroxine , which is formed when two molecules of diiodotyrosine are
joined together; the thyroxine then remains part of the thyroglobulin
molecule
Triiodothyronine , one molecule of monoiodotyrosine couples with one
molecule of diiodotyrosine

78. PROLACTIN
Release of Thyroxine and Triiodothyronine from the Thyroid Gland:
Thyroglobulin itself is not released into the circulating blood in
measurable amounts; instead, thyroxine and triiodothyronine
must first be cleaved from the thyroglobulin molecule, and then
these free hormones

79. PROLACTIN
Daily Rate of Secretion of Thyroxine and Triiodothyronine: About
93 percent of the thyroid hormone released from the thyroid
gland is normally thyroxine and only 7% is triiodothyronine
However, during the next few days, about one half of the
thyroxine is slowly deiodinated to form additional triiodothyronine

80. Mechanism of Action
Non-Genomic Actions: include the
regulation of ion channels and
oxidative phosphorylation and appear
to involve the activation of
intracellular secondary messengers
such as cyclic AMP or protein kinase
signaling cascades

81. PHYSIOLOGICAL FUNCTIONS OF THE THYROID
HORMONES
Increase the
metabolic activities
of almost all the
tissues of the body
Effect of Thyroid
Hormone on
Growth

82. PHYSIOLOGICAL FUNCTIONS OF THE
THYROID HORMONES
Effects of Thyroid Hormone on Metabolism
Effect of Thyroid Hormone on Sexual Function : For normal sexual function, thyroid secretion needs to be approximately
normal
Increased Requirement for Vitamins
On Body Weight: Greatly increased thyroid hormone almost always decreases the body weight, and greatly decreased
thyroid hormone almost always increases the body weight
On plasma lipids: thyroid hormones decrease plasma cholesterol and increase its secretion in bile and stool
Effect on CVS
On CNS : Thyroid has an excitatory effect on the CNS functions : A- Muscle tremors
Other endocrine glands: thyroid hormone increases the levels of insulin, cortisol and parathyroid hormone

83. REGULATION OF THYROID
HORMONE SECRETION
TSH : Increases Thyroid Secretion
◦ Cyclic Adenosine Monophosphate Mediates the Stimulatory Effect of
TSH
◦ Increased proteolysis of the thyroglobulin that has already been stored
in the follicles
◦ Increased activity of the iodide pump, which increases the rate of
“iodide trapping” in the glandular cells
◦ Increased iodination of tyrosine to form the thyroid hormones
◦ Increased size and increased secretory activity of the thyroid cells

84. N.B. ANTERIOR PITUITARY
SECRETION OF TSH IS
REGULATED BY THYROTROPIN-
RELEASING HORMONE FROM
THE HYPOTHALAMUS
Effect of change in temperature

85. N.B. ANTERIOR PITUITARY
SECRETION OF TSH IS
REGULATED BY THYROTROPIN-
RELEASING HORMONE FROM
THE HYPOTHALAMUS
Feedback mechanism

86. ABNORMALITIES OF
THE THYROID
HORMONE

87. Hyperthyroidism
Graves’ disease, the most common
form of hyperthyroidism, is an
autoimmune disease in which
antibodies called thyroid-stimulating
immunoglobulins
Thyroid Adenoma

88. Hyperthyroidism
Nervousness and high excitability

89. Hyperthyroidism
Intolerance to heat and increased sweating
◦ Weight loss
◦ Tremors of the hands
◦ Exophthalmos
◦ Tachycardia and palpitations

90. Hypothyroidism
Myxedema: Hypothyroidism
in adult life, characterized by
cold intolerance, depressed
mental and sexual functions,
husky voice, and weight gain
Cretinism: Hypothyroidism
in the neonatal period, lead
to irreversible mental,
physical and sexual growth
retardation

91. ENDOCRINE PANCREAS
The acini, which secrete digestive juices into the duodenum

92. ENDOCRINE PANCREAS
The islets of Langerhans, which secrete insulin and glucagon
directly into the blood

93. ENDOCRINE
PANCREAS
The beta cells, constituting about 60 percent
of all the cells of the islets, lie mainly in the
middle of each islet and secrete insulin
The alpha cells, about 25 percent of the total,
secrete glucagon
The delta cells, about 10 percent of the total,
secret somatostatin
The PP cell, is present in small numbers in the
islets and secretes a hormone called
pancreatic polypeptide

94. INSULIN
Insulin receptor is a combination of
four subunits held together by
disulfide linkages: two alpha
subunits that lie entirely outside the
cell membrane and two beta
subunits that penetrate through the
membrane, protruding into the cell
cytoplasm
NB: Overlap in the secretions of
androgens and glucocorticoids exist
between the fasciculata and
reticularis
Being lipophilic, the adrenocortical
hormones are all carried in the blood
extensively bound to plasma proteins
Cortisol is bound mostly to a plasma
protein specific for it called
corticosteroid binding globulin ,
about 15% is bound to albumin, only
10% is free

95. INSULIN
Rapid : Cell membrane becomes more
permeable to Glucose, K+

96. INSULIN
Intermediate : Change the activity of intracellular enzymes
◦ Secondary Active transport: – SGLT1, SGLT2; SGLT2 inhibitors are widely used for lowering blood glucose as they
increase glucose loss in urine
◦ Facilitated Diffusion: GLUT 1- GLUT7
◦ Zona glomerulosa
◦ Zona fasciculata
◦ Zona reticularis
◦ Hormones produced by the adrenal cortex are steroids derived from the common precursor cholesterol
◦ These comprise mineralocorticoids, glucocorticoids and sex hormones
◦ The three categories of adrenal steroids are produced in anatomically distinct portions of the adrenal cortex as a
result of differential distribution of the enzymes required to catalyze the different biosynthetic pathways leading to
the formation of each of these steroids
◦ Zona Glomerulosa

97. INSULIN
Intermediate : Change the activity of intracellular enzymes
◦ Outermost zone – just below the adrenal capsule is very thin and secretes
mineralocorticoids
◦ They maintain Na+ and K+ balance and ECF volume
◦ Mineralocorticoid of most importance is aldosterone
◦ Zona Fasciculata
◦ It is the middle widest zone – between the glomerulosa and reticularis
◦ Primary secretion is glucocorticoids
◦ Glucocorticoids play a major role in glucose metabolism, as well as protein and lipid
metabolism
◦ Zona Reticularis

98. Mineralocorticoids
¯It regulates the electrolyte
concentrations of extracellular fluids
¯Mineralocorticoids include mainly
aldosterone and deoxy-
corticosterone
¯Mineralocorticoids are essential for
life, without aldosterone, a person
rapidly dies from circulatory shock

99. Action of aldosterone
NB: Aldosterone also increases Na+ absorption from other body
fluid as well as from GIT mucosa
Angiotensin II stimulates conversion of corticosterone to
aldosterone in the zona glomerulosa cells and secretion of
aldosterone from these cells
Direct stimulation of adrenal cortex by a rise in plasma K+
concentration

100. Glucocorticoids
Physiological actions of glucocorticoids

101. GLUCOCORTICOIDS
Effect on metabolism

102. Glucocorticoids
Stimulation of gluconeogenesis by the
liver
Decrease the utilizationof glucose by
muscle and adipose tissue and lowers
their sensitivity to insulin
Increase protein degradation in many
tissue especially muscle, increases the
blood amino acid concentration, thus
providing more amino acids to liver or
for tissue repair
Decreased protein synthesis
Increase lipolysis (the mobilized fatty
acids are available as an alternative
metabolic fuel for tissues that can use
this energy source as an alternativeto
glucose, conserving glucose for the
brain
In diabetics, it increases ketone body
formation
Permissive action
Role in adaptation to stress

103. Glucocorticoids
Gluconeogenesis
Rises in blood
glucose, fatty
acids, and amino
acids

104. Glucocorticoids Other effects
Cortisol has a very slight mineralocorticoid activity
During fetal life, cortisol accelerates the maturation of surfactant in the lung
When cortisol or synthetic cortisol like compounds are administered to yield higher than
physiologic concentrations of glucocorticoids during treatment of certain diseases; or in case
of its hypersecretion by adrenal cortex
Corticosteroids are anti-inflammatory and immunosuppressive
It suppress the inflammatory reaction by reducing phagocytic action of white blood cells ,
inhibiting release of the lysosomal enzymes and decreasing capillary permeability
Suppresses allergic reactions by preventing release of histamine from the mast cells

105. Glucocorticoids Other undesirable effects may be observed with
prolonged exposure to higher than normal
concentrations of glucocorticoids
Cortisol increases the production of red blood cells by
mechanisms that are unclear
The administration of large doses of cortisol causes
significant atrophy of all the lymphoid tissue
throughout the body, which in turn decreases the
output of both T cells and antibodies from the
lymphoid tissue

106. Glucocorticoids
NB: This occasionally can lead to fulminating infection and death
from diseases that would otherwise not be lethal, such as
fulminating tuberculosis in a person whose disease had previously
been arrested

107. Glucocorticoids
Hypothalamic control is via CRH
CRH is secreted into the hypothalamic-hypophyseal portal blood and sent to the anterior pituitary
CRH binds to receptors causing synthesis of POMC a precursor of ACTH
POMC is a large precursor of MSH, and β- endorphin
ACTH being tropic to zona fasciculata and zona reticularis
Negative feedback system involving the hypothalamus and anterior pituitary
Diurnal rhythm: The plasma cortisol concentration display a characteristic diurnal rhythm, with the
highest level occurring in the morning and lowest level at mid night
Stress: The magnitude of the increase in plasma cortisol concentration is proportional to intensity of
the stressful stimuli

108. THE ADRENAL SEX
HORMONES
Adrenal androgen “Dehydroepiandrosterone” and
androstenedione

109. The adrenal sex hormones
Development and
maintenance of
female sex drive
Have no
masculinizing
effect in their
normal amount

110. The adrenal
sex hormones ACTH controls
adrenal androgen
secretion
Adrenal androgens
feedback outside
the hypothalamus
pituitary adrenal
cortex loop
Instead of inhibiting
CRH, it inhibits
gonadotropin
releasing hormone,
just as testicular
androgen do
Adrenal androgen
secretion undergoes
a marked surge, at
the time of puberty,
and peaks between
the ages 25 and

111. Disorders of the
adrenal cortex
Is most commonly caused by autoimmune destruction of the adrenal cortex by erroneous
production of adrenal cortex – attacking antibodies
Characterized by deficiency of all adrenocortical hormones and hyper- pigmentation
Pituitary or hypothalamic abnormality
Does not exhibit hyper-pigmentation
Aldosterone levels are normal
Decreased sodium
Decrease ECF volume
Hyperkalemia → disturbs cardiac rhythm and metabolic acidosis
Patient dies in shock if untreated
Disruption in glucose concentration

112. Disorders of
the adrenal
cortex
Reduction in metabolism of fats and proteins
Decreased resistance to different types of stress
Pigmentation of mucous membranes, pressure areas of
skin areola & nipple due to increased ACTH secretion
Loss of pubic and axillary hair in females
Anemia

113. NB: Addisonian
crisis
Primary hyperaldosteronism
Caused by over activity of the zona
glomerulosa as a result of hypersecreting
adrenal tumor
Caused by inappropriately high activity of the
renin – angiotensin system
The symptoms of both are related to
exaggerated effects of aldosterone

114. NB: ADDISONIAN
CRISIS
High blood pressure

115. NB: Addisonian
crisis
Metabolic alkalosis , decreases the plasma
Ca++
Overstimulation of the adrenal cortex by
excessive amount of CRH or ACTH
Adrenal tumors that uncontrollably secrete
cortisol independent of ACTH
ACTH secreting tumors located in places other
than the pituitary, most commonly in the lung
Administration of pharmacological doses of
glucocorticoids

116. NB: Addisonian
crisis
↑ Cortisol and androgen levels
↑ ACTH , ↓ ACTH
Hyperglycemia, glucosuria
Central obesity , round face supraclavicular fat
↑ Protein catabolism leads to muscle wasting and fatigue
Poor wound healing and easy bruisability
Hypertension
Osteoporosis
The protein poor thin skin of the abdomen becomes over overstretched by the excessive
underlying fat deposits forming irregular reddish purple linear streaks
Virilization of women

117. Adrenogenital syndrome
Male pattern of
body hair
Deepening of the
voice and more
muscular arms
and legs

118. Adrenogenital syndrome
The breast become smaller, and menstruation may cease , and
sterility occur
◦ Female infants born with a male – type external genitalia

119. ADRENOGENITAL
SYNDROME
Pre-pubertal males: Precocious pseudo-puberty

120. Adrenogenita
l syndrome
Over activity of adrenal androgens in adult
males has no apparent effect
The adrenogenital syndrome is most
commonly caused by enzymatic defect in
the cortisol steroidogenic pathway
The decline in cortisol secretion removes –
ve feedback effect on the hypothalamus
and anterior pituitary →↑ CRH and ACTH
→↑ androgen pathway

121. Adrenal
medulla
The adrenal medulla forms about 20% of the
adrenal gland
It is a modified postganglionic sympathetic
neuron where the neurons have lost their
axons and become secretory cells
Controlled by preganglionic sympathetic
innervation
Secretes epinephrine and norepinephrine

122. Adrenal medulla
Hormones are secreted and stored in the adrenal medulla and released in response to
appropriate stimuli by exocytosis
◦ Epinephrine is primarily a hormone produced by the adrenal medulla, whereas
norepinephrine is also a neurotransmitter of major importance in sympathetic nervous
system
◦ Adrenomedullary hormones are not essential for life, but virtually all organs in the body
are affected by these catecholamines
◦ The effects of epinephrine and norepinephrine are brought about by actions on two
classes of and β adrenergic receptors
◦ Epinephrine and norepinephrine exert similar effects in many tissues, with epinephrine
generally reinforcing sympathetic nervous activity
Both hormones increase the force and rate of contraction via β1 receptors

123. Adrenal
medulla
Both hormones also increase myocardial excitability
Increase arterial blood pressure
Norepinephrine produces vasoconstriction in almost all organs via a1
Epinephrine promotes vasodilation of the blood vessels that supply skeletal
muscle and the heart through β2 receptor activation
Epinephrine constricts blood vessels which have α-adrenergic receptors in their
smooth muscle
A central role of epinephrine is to increase the availability of metabolites for the
intensive physical activity involved in the acute stress situation described
The release of glucose from the liver to the blood is increased by epinephrine in
several ways: it increases glycogenolysis, and stimulates gluconeogenesis

124. Adrenal
medulla
Epinephrine stimulates glycogenolysis in skeletal
muscles, leading to the formation of lactic acid
In pancreatic beta cells, epinephrine inhibits the
production of insulin, and stimulates glucagon
In adipose tissue, epinephrine stimulates the lipolysis
Epinephrine increases the overall metabolic rate
Catecholamines affect the central nervous system to
promote a state of arousal and increased CNS alertness

125. Endocrine control of
calcium metabolism
About 99% of the Ca 2+ in the body is in crystalline
form within the skeleton and teeth
◦ About 0.9% is found intra-cellular within the
soft tissues
◦ Less than 0.1 % is present in the ECF
◦ Half of the ECF Ca2+ either is bound to
plasma proteins and therefore restricted to
the plasma or is complexed with PO4 3
◦ The other half of the ECF Ca2+ is freely
diffusible and can readily pass from the
plasma into the interstitial fluid and interact
with the cells

126. Endocrine control of
calcium metabolism
Neuromuscular excitability

127. Endocrine control of calcium metabolism
Excitation-
contraction
coupling in cardiac
and smooth muscle
Stimulus-secretion
coupling

128. Endocrine control of
calcium metabolism
Maintenance of tight junctions
between cells

129. Endocrine control of
calcium metabolism
Clotting of Blood

130. Endocrine
control of
calcium
metabolism
Calcium homeostasis: Involves the immediate
adjustments required to maintain constant free
plasma Ca2+ concentration on a minute
Calcium balance: Involves the more slowly
responding adjustments required to maintain a
constant total amount of Ca2+ in the body
The principal regulator of Ca2+ metabolism is
the parathyroid hormone
Vitamin D also contributes in important ways
to Ca2+ balance, and the third hormone is
calcitonin

131. Parathyroid
gland
Location: Four glands imbedded on
posterior surface of Thyroid
Secretes: Parathyroid hormone
Function: Calcium regulation
Produce parathyroid hormone
Increases blood concentration of Ca2+

132. Parathyroid
hormone The primary hormone
controlling Ca2+ is
parathyroid hormone,
PTH is essential for
life
PTH raises the Ca++
concentration in the
plasma
This hormone also
lowers PO4 3- in the
blood
There is an inverse
relationship between
Ca++ & PO4 3- levels
in the blood plasma;
the product of their
two concentrations
must be constant

133. Mechanism
of action of
PTH
BONE
PTH uses bone as a bank from which it withdraws Ca2+ as needed to maintain
plasma Ca2+ level
PTH has two major effects on the bone that raise plasma Ca2+ concentration
PTH quickly releases Ca++ from the small labile pool in bones
It stimulates the transfer of Ca2+ from the bone fluid across the osteocytic-
osteoblastic bone membrane into the plasma by means of PTH activated Ca2+
pumps located in the osteocytic osteoblastic bone membrane
Ca2+ is quickly replaced in this area from mineralized bone

134. Second
Under conditions of chronic hypocalcemia
PTH influences the slow exchange of Ca2+
between bone itself and ECF by promoting
actual localized dissolution of bone
It stimulates osteoclast to eat up bone,
increasing the formation of more osteoclasts,
and transiently inhibiting the bone forming
activity of osteoblast
Prolonged excess PTH secretion over months
or years eventually lead to the formation of
cavities throughout the bone, that are filled
with very large, overstuffed osteoclasts
KIDNEY
PTH increases reabsorption of calcium &
reduces reabsorption of phosphate
Net effect of its action is increased calcium &
reduced phosphate in plasma
It enhances the activation of vitamin D by the
kidney

135. Second
INTESTINE
◦ PTH indirectly increases both Ca2+ and PO43- absorption from the
small intestine by helping active vitamin D
◦ The PTH induced removal of extra PO43- from the body fluids is
essential for preventing reprecipitation of Ca2+ freed from bone

136. The solubility product plasma
concentration of Ca2+ X plasma
concentration of PO 3- constant.

137. A rise of their concentrations will raise this value above the
solubility product and results in the precipitation of the salt
When plasma PO43- level rises, some plasma Ca2+ is forced back
into bone through hydroxyapatite crystal formation, reducing
plasma Ca level and keeping constant the calcium phosphate
product

138. A rise of their concentrations will raise this
value above the solubility product and results
in the precipitation of the salt
PTH secretion is increased in response
to a fall in plasma Ca2+ concentration
and decreased by a rise in plasma
Ca2+ levels
A rise in PO43- will decrease
extracellular Ca2+ causing an increase
in PTH
1, 25 2 D3 inhibits the formation of
PTH and so decreases its secretion

139. Calcitonin Calcitonin is a polypeptide hormone secreted by the
parafollicular or “C” cells of the thyroid gland
It is released in response to high plasma calcium
Calcitonin acts on bone osteoclasts to reduce bone
resorption
Net result of its action is a decline in plasma calcium &
phosphate
It is not essential for maintaining either Ca2+ homeostasis
or balance, it is important in extreme hypercalcemia

140. Calcitonin First: On short term basis calcitonin decreases Ca2+ movement
from the bone fluid into the plasma
Second: On long term basis calcitonin decreases bone
resorption by inhibiting the activity of osteoclasts
It stimulates secretion of Ca2+ and PO43- in urine
It inhibits 1a hydroxylase activity of the proximal tubules
Increase plasma Ca2+ stimulates calcitonin secretion and a fall
in plasma Ca2+ inhibits calcitonin secretion
Calcitonin plays a role in protecting skeletal integrity when
there is a large Ca2+ demand as in pregnancy or breast feeding

141. Vitamin D
Food
UV light mediated cholesterol
metabolism

142. Vitamin D
It must be activated by two sequential
biochemical alterations that involve
the addition of two hydroxyl groups
The first of these reactions occurs in
the liver and the second in the kidneys

143. VITAMIN D3
Increase Ca2+ and PO43-
absorption in the intestine

144. Vitamin D3
It stimulates Ca2+
and PO43-
reabsorption in
the kidney
Increases the
responsiveness of
bone to PTH

145. Calcium
Disorders Hyperparathyroidism: can occur by excess PTH secretion
The affected individual can be asymptomatic or symptoms can be severed
Hypercalcemia reduces the excitability of muscle and nervous tissue, leading
to muscle weakness, decreased alertness, poor memory and depression
Other effects are the thinning of bones, development of kidney stones and
digestive disorders such as peptic ulcers, nausea and constipation
Hyperparathyroidism has been called a disease of bones, stones and
abdominal groans
PTH hyposecretion leads to hypocalcemia and hyperphosphatemia

146. Calcium Disorders
Causes: Iatrogenic or
autoimmune attack against
the parathyroid glands
Tetany is a clinical state of
increased neuro-muscular
excitability caused by a
slight decrease in the
plasma level of ionized
calcium
In complete absence of PTH:
Death results within a few
days, usually because of
asphyxiation caused by
hypocalcemic spasm of
respiratory muscles
A deficiency of vitamin D
decreases intestinal
absorption of calcium