Hormone : Is the secretion of any endocrine gland is called

" HORMONE " which means to stimulate. This name is not exactly
explain the nature of the endocrine secretions as some of them
stimulate the function while other inhibit the same action.

Hormones are organic chemical substances which are classically

divided, according to their composition, into 2 groups;
nitrogenous and steroids.

Hormones can induce their effect when present. in very small

amounts.
A) Synthesis Hormone is synthesized by specific cell type which
should be physiologically capable for complete functional
activity to produce the specific hormone. The blood reaching
the producing cells containing the building units of the
hormone is a must. For example, the building stones of thyroid
hormones are the amino acid tyrosine and iodine. The thyroid
tissue (thyroid epithelium) has the ability to trap iodine from
the circulation and accumulate it in the gland. This capacity is
called iodine trap. Inside the thyroid cells, this trapped iodine is
converted into active one by oxidative enzymes as peroxidase.
Formation of the thyroid hormones (T3 and T4) takes place due
to utilization of active iodine for iodination of the amino acid
tyrosine as follows :
Tyrosine + Iodine (active)→ MIT
MIT + Iodine (active) → DIT
MIT + DIT → t3
DIT + DIT → t4
B- Storage:
- Some hormones are stored inside follicles (vesicles) located
among the same producing cells such as the thyroid gland in
which the thyroid hormones combine with a protein (globulin)
to form an inactive thyroprotein (thyroglobulin) which is
stored inside the thyroid follicles.
- Other glands like anterior pituitary, adrenal, gonads ... etc.)
store their hormones intracellularly in the form of protein -
bound hormone. Degranulation of such cells indicates the
release of the hormone (s).
- The posterior pituitary (pars nervosa) represents unique
example for storage of what is known as posterior pituitary
hormones as the actual site of secretion for these hormones
is the hypothalamus (paraventricular and supraoptic nuclei).
- T4 is considered a depot for the potent T3. Demonoiodination
takes place in the circulation. T3 is 10 times potent more than
that of T4.
C- Release:
It means the secretion of the hormone to the body fluids
mainly blood. The endocrine glands as an important regulators
for many biological activities in the body are under careful
regulation for their endocrine output. Regulation of the
hormone secretion depends .upon several .mechanisms; One
of the simplest is the metabolic concentration of the
hormone(s) itself or substances influenced by the hormone in
the circulation.
D) Transport:
The majority of hormones are transported to their targets via
blood. Even in of local or tissue hormones, besides they induce
their action at their site of production, they also have a
generalized effect.
In the circulating blood, it bound to plasma proteins (albumin
or globulin) which tend to restrict the hormonal activity. This
pound form of the hormone is biologically inactive. At the cells
of the target, the molecules are released from their binding
proteins and become free; in order to exert their action at the
intracellular level of the target.
Recycling:
- After degradation of the hormone, a part of its building stones is
excreted outside the body; while another part returns back to the
site of hormone synthesis in order to share in the formation of
new molecule of the hormone. For example, a part of iodine,
which is released during inactivation of thyroid hormones, is
excreted by the kidneys and bile while another part is trapped
again by the thyroid tissue to be used for synthesis of thyroid
hormones.
Anatomy:
This gland lies in the fossa of the upper surface of the sphenoid
bone which is callead sella turcica. It is attached to the base of
the brain (hypothalamus) by means of pituitary stalk
(infundibulum). The pituitary gland consists of a
- glandular part (adenohypophysis): the glandular part is further
subdivided into pars tuberalis of unknown function, pars distalis
(anterior pituitary) and pars intermedia.
- the nervous portion (neurohypophysis): composed of pars
nervosa and the infitndibulain.
Hormones of the pars distalis are classified into metabolic
(STH, TSH, ACTH and LTH) and gonadotropic hormones
(FSH, LH and LTH).

1- Somatotropic hormone (STH) or Growth hormone:

This hormone regulates normal growth and development in
young animals as it is responsible for retention of inorganic
elements necessary for formation of soft and hard tissues as well
as nitrogen and water. In addition, it stimulates formation of
ribosomes and RNA synthesis leading to protein formation.
Thus, STH is important for normal growth and composition of
bone and muscles. Also, the hormone plays an important role to
stimulate cellular growth and division as well as it increases the
mass of internal organs specially liver, intestines and lymph
nodes.
Hypofunction of STH, particularly in Youngs, leads to a
condition known as dwarfism which is characterized by
symmetrical retardation of growth accompanied usually by
normal mental and reproductive capacities.
On the other side, over production of STH before puberty results
in gigantism which is manifested by increased length and width
of bones as the hormone retards calcification and closure of
ossification centres. In this respect, the mass of the internal
organs as well as the animal weight increase significantly.

Increase after puberty, a condition called acromegaly takes

place which is characterized by enlargement of the flat bones
particularly the facial accompanied with enlargement of the
joints. Moreover, the diabetogenic effect accompanied with
increased STH has now been recognized as STH secretion for
long periods inhibits glucokinase enzyme and destroys the
already present beta cells. The aftermath of these sequences lead
to hyperglycemia and even glucosuria .
Control of Secretion of STH is under continuous control of
hypothalamus which secretes STH-RH reaching the pituitary
gland through the portal circulation leading to STH release. Also,
Somatostatin hormone is produced by the hypothalamus to inhibit
synthesis and secretion of STH .
2- Thyroid stimulating hormone (TSH)
This hormone activates all functions of the thyroid gland as it:
1- stimulates growth of thyroid tissue by hyperplasia and
hypertrophy leading to formation of multiple large follicles.
2- Activates the uptake of iodine and synthesis of T3 and T4.
3-Activates the proteolytic enzyme inside the lumen of the follicle
leading to hydrolysis of the thyroglobulin into free T3 and T4.
4- Increases the blood supply of the thyroid gland

•TSH is considered fat mobilization factor and a connective

Over TSH production leads to
tissue stimulator. mobilization of fat from its depots
and these sites are replaced by
connective tissue formation

- Exophthalmos due to replacement of fat in eye pad with CT

- Conversion of the corpus luteum into corpus albicans.
3- Adrenocorticotrophic hormone (ACTH):
-This hormone controls the activity of the adrenal cortex
particularly zona fasticulata.
-In mammals, ACTH has a melanocyte stimulating activity
leading to coloration and pigmentation of the skin.
- ACTH has a similar effect like glucocorticoids, so it could be
used instead of cortisone or cortisol.
Control
ACTH is under continuous control of the hypothalamic ACTH-
RH.
-In case of over production of ACTH the hypothalamus produces
an inhibiting hormone to ACTH which is known as ACTH-IH.
4) Prolactin (PRL):
This hormone exhibits both metabolic and gonadotropic activities.

Functions:
1- In female mammals:

- It initiates and maintains milk secretion on condition that the

mammary gland is previously developed, under the effect of other

hormones, for complete functional activity.

- Stimulates the growth of corpora lutea leading to secretion of

progestins mainly progesterone.

4) Prolactin (PRL):
This hormone exhibits both metabolic and gonadotropic activities.

Functions:
2- In male and female pigeon and doves:
- The hormone stimulates crop milk formation as prolactin increases food intake
of the parents and causes increased development of the alimentary tract and liver
resulting in enhanced growth and the digested extra-food intake is utilized for the
formation of crop milk.
-Prolactin also stimulates cellular proliferation of the mucosal lining of the
lateral pouches of the crop. When such cells become peripherally situated. the
blood supply is inadequate leading to detachment and degeneration of the cells
which constitute the majority of crop milk.

Over Production in male and female mature birds and

mammals for long period
leads to atrophy of the gonads as it increases the production of sex hormones which inhibit
the gonadotropins production.
5- Gonadotropic Hormones
1) Follicle stimulating hormone (FSH):

Functions:
1- In females: it stimulates growth and development of the Graafian
follicles leading to secretion of estrogens; a function which necessitates
the presence of balanced amount of luteinizing hormone (LH).
2- In males: the hormone is well known as gametogenic hormone as
it stimulates the process of spermatogenesis if present with balanced
amount of interstitial cell stimulating hormone (ICSH).
2- Luteinizing hormone (LH}:
Functions:
1- In female mammals and birds: LH stimulates the process of
ovulation and corpus luteum formation.
Also, it inhibits the luteolytic effect of oxytocin. LH augments the
stimulating action of FSH on the Graafian follicles.
2- In the male: this hormone is known as interstitial cell
stimulating hormone (ICSH) as it stimulates the Leydig cells of
the testis to secrete the male sex hormones (androgens mainly
testosterone).
Control of Gonadotropin secretion:
1- The hypothalamus: It secretes gonadotropin hormone releasing hormone
(GnRH) which regulates type and released amount of gonadotropins from the
pituitary gland

- When the pulse frequency and amplitude of GnRH are rapid and multiple this

call the release of LH

- while decreased frequency and amplitude promote the FSH release.

Control of Gonadotropin secretion:
2- Ovarian hormones:

- Estrogens have a tripple threshold effect on pituitary gonadotropins:

Low estrogens level: stimulates both synthesis and release of FSH resulting

in elevation of its level in the circulation.

High level of estrogens, Within physiological limits: inhibits synthesis and

release of FSH and permits the secretion of the already formed LH.from pars

distalis.

Abnormal high estrogens level: (as in case of cystic ovaries .or

administration): it inhibits synthesis and release of both FSH and LH, a case

which may lead after a long period to atrophy of the gonads.

Control of Gonadotropin secretion:
2- Ovarian hormones:

- Progestins
Small amounts of for short period in ovaries previously treated
with estrogens: stimulates the release of FSH with traces of LH.
Higher levels of progestins: inhibit the secretion of both
gonadotropins particularly LH leading to inhibition of ovulation and
corpus luteum formation.
The persistence of corpora lutea (of the estrous cycle or those of the
pregnancy) in domestic animals specially cows and buffaloes is considered one
of the serious problems causing infertility asthe large amounts of progestins
inhibit the release of gonadotropins leading to a serious irregularity of the
estrous cycle.
3- Inhibin: is a non-steroidal gonadal protein produced by:
-The granulosa cells of the Graafian follicles
specially the mature ones.
-The corpus luteum of some species (rat, woman
and pig)
-The placenta of rabbit and human are considered
propoable sites of inhibin production.
-In male, Sertoli cells are the main source of
inhibin production
lower concentrations of inhibin suppresses only FSH (synthesis
and release) while higher levels of the hormone inhibit both
FSH and to a lesser effect LH.
Physiological anatomy and histology:
The thyroid gland in mammals is formed of two lobes
connected together by isthmus which is a band of the thyroid
tissue.
The gland is located on either sides of the lateral aspect of the
trachea at the point of attachment to the larynx.
In birds, fish, reptiles and amphibia the thyroids consist of
two separate lobes.
- The gland is surrounded by two connective tissue capsules, from the inner
connective tissue septa emerge to divide the gland into lobules which contain
thyroid follicles (vesicles) of variable size.
- These follicles are supplied with rich network of blood capillaries.
- Sympathetic nerves enter the lobules in association with blood capillaries.
These nerves regulate only the blood supply of the gland.
- In case of normal thyroid (euthyroid), the thyroid follicle is lined by a
single layer of cuboidal cells. The lumen contains considerable amount of
thyroprotein (stored hormone).
- Subfunctional activity (hypothyroidism): the vesicles become enlarged than
the normal state, the epithelial cells become flattened and the amount of
colloid (thyroglobulin) increases.
- In hyperthyroidism, the cells are columnar in shape and the amount of
colloid decreases than normal as well as the lumen of the follicle becomes
narrow. The basal surface of the thyroid epithelial cells is in contact with
blood capillaries.
 By electron microscope, it was found that some of the
endothelial cells of blood capillaries become thick and large to
form a new cell type known C- cells (parafollicular cells).
 These cells produce a hormone called calcitonin or
thyrocalcitonin.
 In most of mammals, this hormone is produced from the
thyroid gland but in birds, reptiles, fishes and amphibia the C
cells aggregate and form a separate :endocrine gland known as
the ultimobranchial gland which produces the calcitonin
hormone.
 Hormones of the thyroid gland:

1- Thyroid hormones (T3 and T4).

2- Thyrocalcitonin.
3- Thermothyrin (Heat - reducing hormone).
Function of T3 and T4:
1- At cell level:
a- Under physiological conditions (euthyroid): T3 and T4 stimulate
the release of oxidative enzymes from the mitochondria (as they
increase the number of cristae and make them fragile) leading to
liberation of energy.
- A part of energy is used for supplying the cells with energy
required for their vital processes.
- The remaining part of energy is stored in the form of high
energy - containing bonds (like ATP). This stored energy is
further utilized for the synthesis of RNA and consequently
protein synthesis leading to stimulate the growth.
This action of the thyroid hormones is considered as anabolic one
b- In hypothyroidism: The energy produced by oxidation is
lesser than that required by the tissues; therefore there is a
continuous exhaustion of the stored energy and by time, this
condition may affect protein synthesis and growth.

c- In hyperthyroidism : All the energy produced by Oxidation is

lost in the form of CO2, H2O and heat, thus it is of catabolic
action accompanied with wasteful loss of energy.
2) On metabolism:

a- Within physiological limits (Euthyroid): T3 and T4 promote

protein synthesis due to formation of ATP and increase of nitrogen retention in

the body; therefore thyroid hormones promote growth and consequently

considered anabolic hormones.

b- Hypothyroidism:

- It is usually accompanied with reduced number of mitochondria resulting in

decreased quantity of oxidative enzymes in the cells.

- The oxygen utilization of the liver, kidneys and muscles decreases

significantly.
- The basal metabolic rate becomes lower as much as 50 % than that of the

normal animals.

- The rate of sugar absorption through the intestine is inhibited.

- Protein synthesis is also decreased and retardation of growth takes place.

- The cholesterol level in blood is inversely related to the activity of thyroid

the thyroid activity
gland Cholesterol level increases and
is lowered

generalized arteriosclerosis is common in long standing cases.

- Hypothyroidism also diminishes excretion of calcium and phosphorus from

the body.

The effect of hypothyroidism is catabolic.

C- Hyperthyroidism:
- Extra-energy production without efficient storage and utilization- of energy.
(wasteful loss of energy in the form of heat)
-The number of mitochondria and the quantity of the cellular oxidative
enzymes increases.
- Oxygen utilization by the liver, kidneys and muscles increases. The basal
metabolic rate increases as much as 50 % than normal. The rate of glucose
absorption increases.
- Glucogenolysis is stimulated leading to reduced liver and muscle glycogen.
- Hyperglycaemia and glucosuria occasionally occur.
- Fat stores are mobilized to supply the extra-energy and the blood cholesterol
is decreased.
- Mineral metabolism is also impaired as the excretion of calcium and
phosphorus in the urine and feces is increased.
- Moreover, due to the enhanced metabolism the vitamin requirement increases
(specially vitamins pi and A).
- As energy is lost without being used for protein synthesis, the plasma
proteins concentration and the protein content of the liver and muscles
decreases. in this respect, the nitrogen balance becomes negative and this
effect of thyroid hormones is catabolic.
3) On growth:
a) lack of thyroid hormones on growth differs according to the age

of the animal. In young animals (sheep, goat, horse, rabbit

and rat) and human, hypothyroidism results in a condition known

as cretinism which is characterized by:

 Asymmetrical retardation of growth, the external and internal
gentalia are like infants and when the animal reaches maturity, the
secondary sexual characters will not appear.
 Retardation in the proliferation of epiphyseal cartilage, delay in the
appearance of ossification centers, weak development of skeletal
muscles.
 Retention of excess fluid in the body are recorded in cretin.
Moreover, the tongue is enlarged and protrudes between
thickened lips.
 The skin is coarse, dry and the hair is scanty. The head becomes
larger in size and the neck
- In case of adult animals , hypothyroidism leads to a

condition comparable to myxedema in humans which is

manifested by:
 Subcutaneous edema, weakness of the muscular activity.
 Bradycardia, the ECG becomes of low voltage, the gonads
undergo slight atrophy and the secondary sexual characters are
depressed.
b- Hyperthyroidism results in retardation of growth due to
accelerated protein catabolism, decreased plasma proteins and
inhibition of protein synthesis.
5) On reproduction:
 The thyroid gland is more active at estrus as compared to the other
stages of the estrous cycle.
 During pregnancy, the thyroid becomes more active at the late stage.
 Hypothyroidism in females is accompanied with degeneration of the
ova leading to irregular estrous cycle and low fertility Silent heat
among cattle and buffaloes represent a great problem due to
hypoactivity of the thyroid gland.
 In males, hypothyroidism leads to impair the process of
spermatogenesis and consequently the semen quality becomes poor.
In ram and bull, summer sterility is a common case due to
deficiency of T3 and T4.
6) On the nervous system:
 Hypothyroidism results in depression of neuron functions and
the excitability of the nervous system decreases.
 The affected animal becomes dull, sluggish and sleepy. In
hyperthyroidism, the excitability of the nervous system
increases and the animal becomes anxious, irritable and its
reflexes are exaggerated as well as the reaction time is
reduced.
7- On the gastrointestinal tract:
 Hypoactivity of the thyroid gland is accompanied with
constipation, hypoplasia, decreased gut motility and the
absorption of glucose is reduced.
 In hyperthyroidism, diarrhea, polyphagia, increased gut
motility and accelerated absorption of glucose take place.
8) Cardiovascular system:
 Deficiency of T3 and T4 in the circulation decreases the cardiac
output and the blood flow_ Bradycardia takes place. Enlargement
and degeneration of the cardiac muscle are associated with such
case. The arterial blood pressure becomes subnormal.
 If the deficiency is prolonged, generalized arteriosclerosis takes
place. In hyperactivity of the thyroid gland, the cardiac output and
the arterial blood pressure increase.
 Tachycardia develops due to : a- Thyroxin stimulates directly the
rhythmicity of the SAN, b- The increased metabolism produces
peripheral vasodilatation leading to increased venous return and
consequently the heart rate accelerates (Bainbridge's reflex).
9- Other effects of thyroid hormones:
 Hypothyroidism results in anemia (usually of Microcytic and
hypochromic type). This anemia is due to T3 and T4 affect
protein synthesis.
 On the respiratory system, deficiency of thyroid hormones in
the blood decreases the depth and rate of respiration
accompanied with weakness of the respiratory muscles.
 Thyroid hormones are essential for normal healing of wounds
and bone fractures. Moreover, thet increase the resistance of
the body against infection.
 Control of Thyroid Gland
Nervous control:
This type of control may be direct of indirect. Direct nervous control means
stimulation of the nerve supply of the thyroid gland resulting in increased its
blood supply leading to enhance the activity of the cells to produce more
thyroid hormones, indirect nervous control means stimulation of the nerve
supply of the anterior lobe of the pituitary gland resulting' in secretion of TSI-
.1which stimulates the thyroid gland due to
1- It promotes the blood supply of the gland.
2- TSH enhances the growth of thyroid tissue by hypertrophy and hyperplasia
leading to formation of large number of vesicles.
3- It activates the uptake of iodine by the thyroid tissue.
4- TSH activates all steps of synthesis of T3 and T4.
5- It stimulates the proteolytic enzymes present in the gland resulting in
release of thyroid hormones.
2) Hormonal control:
The activity of the thyroid stimulating hormone (TSH) which is
reused from the anterior pituitary.
The role of TSH on the thyroid gland was previously mentioned.
The secretion of TSH is regulated by :
a) The feedback mechanism
b) Environmental conditions : Cold and / or light stimulate the
hypothalamus to produce TSH-RH which is transported to the
anterior pituitary via the hypothalamo-hypophyseal portal
circulation present in the pituitary stalk resulting in the release of
TSH which activates the thyroid gland.
On the other side, high environmental temperature inhibits the
release of TSH-RH and stimulates the release of TSH-IH from
the hypothalamus resulting in inhibition of the release of TSH
and consequently inhibition of the thyroid gland.
3) Chemical control:
Some chemical substances have the capacity to block the phases of
synthesis of thyroid hormones. These substances induce goiter
therefore, they are called goitergenic compounds.
The most famous goitergenic compounds are:
a- Potassium thiocyanate and potassium perchlorate: They block the
iodine trap the thyroid tissue from the uptake of iodine.
b- Thiourea: "They block the oxidative enzymes (thyroid peroxidase)
resulting in prevention of conversion of ion, , active one.
c- Sulphonamides administration: In animals these compounds prevent
the iodination of amino acid tyrosine.
4) Goitrin:
Many flowering and vascular plants of the Family Brassicae
(cabbage, sprouts) known as progoitrin that can be enzymatically
converted into a potent antithyroid compound called gottrin.
- Sufficient quantities of goitrin are absorbed from the intestine
into the blood, synthesis of thyroid hormones is impaired and
hypothyroidism accompanied with goiter takes place. Cooking
these plants normally destroys the enzymes that convert
progoitrin to goitrin; but progoitrin itself is not affected.
5) The effect of other hormones: Oxytocin and vasopressin of the
posterior pituitary beside relaxin (which is produced by the ovaries
and placenta during late pregnancy) activate all functions of the
thyroid gland.
 Goiter
Goiter is an enlargement of the thyroid gland which is not malignant and
uninflammatory.
It may be associated with hypothyroidism (simple or colloidal goiter) or
hyperthyroidism (exophthalmic goiter).
1) Simple goiter:
This type of Biter is due to iodine deficiency (soil), goiterogenic
substances, goitrin and formation of antibodies to thyroglobulin (abnormal
condition).
All these causes lower T3 and T4 in the blood resulting in increased release
of TSH from the anterior pituitary (feedback mechanism). Over production
of TSH leads to enlargement of the thyroid gland (goiter). In this type of
goiter the histological picture of the thyroid follicles resembles that of
hypothyroidism.
2) Exophthalmic goiter This type of goiter originates due to:-
a- Over production of TSH as in tumours of gland.
b- Long-acting thyroid stimulating substance, (LATS) which can activate the
thyroid gland of several species of animals:
It is one of the cause of hyperthyroidism. This substance is separated from
serum of hyperthyroid individuals. It is always bound with gamma globulin
fraction of the serum proteins.
This type of goiter is usually accompanied with very high level of TSH which
leads to protrusion of the eye ball (exophthalmos) because TSH is considered as
fat mobilization factor and connective tissue stimulating factor. Exophthalmos, is
a result of replacement of the fat bad of the eye ball by connective tissue.
Moreover, toxic symptoms of hyperthyroidism (due to increased TSH level in
the blood) may be involved in such type of goiter.
The microscopic picture of the thyroid follicles in exophthalmic goiter is similar
to that of hyperthyroidism.
 2- Thyrocalcitonin (Calcitonin):
1- Site of synthesis: Previously mentioned.
2- Action of the hormone:
Thyrocalcitonin lowers the calcium (Ca +) in the blood.
The hormone granules are stored within the cells. Degranulation
of these cells indicates release of the hormone into circulation.
3- Control of the hormone :
a) When calcium. (Ca ) level in the blood rises than the normal
level (hypocalcaemia); it stimulates C-cells to release
thyrocalcitonin.
b) b) Glucagon hormone increases the secretion rate of the
thyrocalcitonin.
Thermothyrin (heat reducing hormone): In case of danger due to
rise in body temperature, the thyroid gland produces a hormone
called thermothyrin.
This hormone decreases oxygen consumption and heat production
of the living organism in order to maintain the body temperature
within the physiological limits.
Physiological anatomy and histology:
 In mouse, cat and man: the parathyroids are embedded within
the thyroid tissue.
 In other mammals such as goat, rabbit ....etc: they are
separated glands located near to the thyroid.
 In case of birds, there are two parathyroids which are
separated from the thyroid gland.
 The parathyroid gland contains two cell types; chief (principal)
and oxyphil cells. The former cell type is responsible for
parathonnone production, while the other type does not have
an active function in the biosynthesis of the hormone
Storage of parathormone molecules takes place within the
cytoplasm of the chief cells. Degranulation of such cells indicates
the release of the hormone into the circulation:
Actions of the parathormone:
 The parathyroid hormone is considered a hypercalcaemic
agent as its primary role is to increase the calcium (Ca++) level
and lowers that of phosphorus in the blood.
 This action is due to :
1- Parathormone accelerates the absorption of both calcium and
phosphorus from the small intestine; but to lesser extent than
vitamin D does.
-2- It acts on the skeletal tissue (bone and teeth) by drawing
calcium and phosphorus from them and pour them into the blood
stream. This action is due to parathormone converts the insoluble
forms of calcium such as calcium carbonate and triphosphate of
the skeletal tissue into soluble forms like calcium citrate and
lactate which are poured into blood.
-3- Parathormone increases the reabsorption of calcium from the
renal tubules and excretion of phosphorus.
Effects of hyperparathyroidism :
A) The calcium level in the blood increases and may reach up to 22
mg %.
B) B) The phosphorus level in the blood decreases (down to 2 - 3 mg
%).
C) C) Calcium deposition takes place in the soft tissues like heart,
brain and kidneys. This effect is due to the increased level of
calcium in the blood plasma.
D) D) The calcium is drawn from the skeletal tissue leading to the
appearance of cavities in the shaft (diaphysis) of long bones. This
condition is called generalized osteitis fibrosa cystica.
E) E) The increased calcium level in the blood plasma affects the
cardiac muscle by stimulating the cardiac systole.
The effect of Hypoparathyroidism
A) The calcium level in the blood decreases down to 4 - 5 mg %.
B) Phosphorus level in the blood plasma increases up to 10 - 15 mg %.
C) The decreased calcium level in the blood plasma results in inhibition of the cardiac
systole.
D) Tetany: Normal calcium level in the blood plasma is indispensable for the
maintenance of the functional activity of the neuromuscular junction and to prevent the
continual excitability due to external continual stimuli. In hypoparathyroidism, as
calcium level in the blood decreases it leads to increase the excitability of the
neuromuscular junction. In this case the animal becomes sensitive to any external
stimulation and responds by series of muscular contractions (convulsions) and tremors
allover the animal body. Other symptoms such as loss of appetite and stiff gait are also
involved in such cases. The condition may involve (specially in dogs) persistent
contractions of the laryngeal and intercostal muscles as well as the diaphragm followed
by paralysis of the affected muscles and the animal dies due to asphexia unless it is
treated with calcium compounds at the early stages of hypocalcaemia. These symptoms
are known as tetany.
Control
Control
Control
Control
Control
Control
Control
Islets of Langerhans
 Insulin
Physiological effects:
1)On Carbohydrate metabolism:

Has hypoglycemic effect …….(How?)

1- cause glucose uptake and storage in liver cells through:
The net effect
- enhancing glucose uptake by liver cells by glucokinase.
increase
2- Inhibiting phosphorylase enzyme prevent glycogenolysis. glycogen in
liver.
3- increasing activities of enzymes that promote glycogen synthesis
(phosphofructokinase and synthetase)
4- Accelerating intracellular glucose oxidation.
2) On Protein metabolism:
Insulin prevents degradation of protein and fat→ stimulates growth in
3) On cell repair and healing of wounds:
Insulin is essential for cell repair and wound healing. Deficiency of insulin is usually

associated with prolonged time necessary for healing.

c) Effect on growth:
Insulin stimulate growth indirectly as it prevents degradation of protein and fat.
Control of insulin
secretion
1. Through chemical feed back mechanism (glucose level).

Positive caused by Negative caused by

- Hyperglycemia Hypoglycemia
- Increased blood
concentrations of other fuel
molecules; amino acids and
fatty acids

2.Some hormones that either have direct action, or potentiate glucos

(glucagon, GH, cortisol, adrenalin).

3. Autonomic:
A- parasympathetic  stimulate
---- insulin release.
B- sympathetic ----
inhibit insulin release, which potentiate the hypergly
action of adrenaline.
4. Some chemicals (e.g.,alloxan)
Destroys β- cells
5. Some Sulphonamides:
 Stimulates insulin secretion
 Glucagon

Physiological effects:
1)On carbohydrate metabolism (Hyperglycemic):
Has hyperglycemic effect …….(How?)
1- It enhances glycogenolysis in liver.
2- It activates hepatic gluconeogenesis (= formation of glucose from non hexose
substrate such as amino acids and fatty acids)
3- It accelerates intracellular glucose oxidation.

2) On Protein and fat metabolism:

1- It enhance transformation of amino acids into glucose (gluconeogenesis).
2- It enhance lipolysis of triglyceride in adipose tissue
Control of Glucagon secretion:
1) Feedback mechanism:
-Positive feedback
Decrease blood glucose below its fasting level---- increase glucagon
secretion
Exercise (exercise induces depletion of glucose)

- Negative feedback is mediated by:

- Hyperglycemia.

(2) Somatostatin hormone → inhibits glucagon release.

III - Posterior pituitary(Pars nervosa)
:(neurohypophysis)
- It acts as a store for the hormones secreted from the
hypothalamus.
- The neurosecretion of hypothalamic neurons (supraoptic and
paraventricular nuclei) transported to posterior pituitary
where it stored until released to blood.
 Antidiuretic hormone (AD
Functions:
1. It promotes reabsorption(facultative reabsorption) of water from the collecting
ducts of the kidney (facultative reabsorption 15% of glomerular filtrate).
2. High concentrations of antidiuretic hormone cause widespread constriction of
arterioles, which leads to increased arterial pressure.
Control: stimulate
3. Increase in osmotic pressure
osmoreceptor Stimulate
(specialized neurosecretory
neurons) in neurons to
hypothalamus produce ADH.

4. : Stimulates ADH secretion.

Decrease blood pressure

5. : Loss of 15 or 20% of blood volume by hemorrhage

Decrease in blood volume

results in massive secretion of antidiuretic hormone.

6. Nausea, vomiting, excessive sweating Stimulate ADH secretion

• Hypofunction : depress water reabsorption lead to
excessive loss of water in urine (polyurea) and thirst sensation
(diabetes insipidus).
 Oxytocin hormone (Pitoci
Called neurohypophyseal hormone as a neurohumeral reflex
controls its secretion
Physiologic Effects of oxytocin:
a-It stimulates contraction of the uterus, which is previously primed
by oestrogen leading to parturition.
b-It controls let down of milk by its action on the myoepithelial cells
which surround the alveoli in the mammary gland.
c-It helps the suction of spermatozoa by stimulating antiperistaltic
movements in the Fallopian tube.
d- it is secreted locally in C.L in non pregnant animal to induce
involution of C.L
Control of Oxytocin Secretion:
(1) Neuroendocrine control (Suckling, Coitus, The act of labor)

Spinal reflex arc

Brain
 Release of hypothalamic oxytocin
 Adrenal gland
or suprarenal gland
(birds and mammals)

Adrenal medulla Adrenal cortex

- The central part - Essential for life.
- Functionally related to - It secretes different groups of
sympathetic nervous system. hormones (corticosteroids).
- It secretes epinephrine (80%) - Adrenal cortex Bilateral
and nor epinephrine (20%). removal---- death with
circulatory collapse.
Adrenal cortex
Zona glomerulosa 15% of the mass----
 mineralocorticoids.

Zona fasiculata 50% of the mass----

glucocorticoids.

Zona reticularis 7% of the mass----

sex steroids
:Mineralocorticoids
• This term is because they affect electrolytes of extracellular

and K+), so they are responsible for maintaining Na+ & K+

• Mineralocorticoids are acutely critical for maintenance of li

removal of the adrenal glands can lead to death within just

aldosterone
• The principal steroid with mineralocorticoid activity .is
 Functions
Filtrate Renal tubule Plasma
Na+
Counter transport
K+ or 2K+
H+ ATPASE
3Na+

Aldosterone acts on the kidneys to

provide: an increase of
-Active reabsorption of sodium and an blood pressure and
Results in
associated passive reabsorption of water. blood volume
-Active secretion of potassium in the principal
cells of the cortical collecting tubule
• N.B: Na+ is the main ion extracelluar, K+ is the main ion
intracellular. So it is important to save Na+ and excrete K+.
• N.B: positive charge of Na+ cause positive co-transport of
negative ions (CL-) ---- creates osmotic pressure difference----
 that move water through membrane (obligatory
reabsorption for 85% water content of glomerular filtrate as
solvent so regulate water balance.
 Control of Mineralocorticoid secre

1. Increase K+ level even than Na+ ( Feedback

mechanism)  stimulate aldosterone secretion (because
K+ increase is a dangerous process (hyperkalemia) that
affect contractility of the cardiac muscle).
2. Renin angiotensin system.
Decreased renal blood flow (usually due to decreased
vascular volume) activation of the
renin-angiotensin system release of angiotensin II 
.stimulates aldosterone secretion
ACTH (usually minor in controlling aldosterone .3
.secretion)
 -They are named so because their effec
:Glucocorticoids specific on glucose metabolism.
-Cortisol and corticosterone are the ma
-In mammals----
 cortisol.
-In birds, mice, rat
 ----
corticosterone.
Functions
I) On carbohydrate:
1. Has antiglucagon effect because it inhibit phosphorylase

Favor storage of glycogen (liver)

2. Has anti-insulin effect because it inhibits glucokinase

Decrease uptake of glucose by the cell

Decrease rate of glucose utilization.

Excess cortisol---- gluconeogenesis---- hyperglycemia---- steriod diabetes.

II) On protein:
- Mobilization of A.As from extrahepatic tissue mainly
from muscles

A.As are available for gluconeogenesis in liver.

III) On fat:
- Mobilization of F.As from muscles and also from adipose
tissue (lipolytic effect)

These F.As---- gluconeogenesis.

- Oxidation of F.As ---- ketone bodies (ketogenic effect).

- Despite F.As mobilization, excess cortisol develop a

peculiar type of obesity with excess deposition of fat in
face (moon face), in trunk (buffalo hump) and abdomen
instead of hips)
IV) Anti- inflammatory action: Prevent formation of
1- It induces vasoconstriction inflammatory exudate, local
oedema and redness
2- It diminishes permeability of capillary walls
3- It inhibits proliferation of fibroblasts and connective tissue formation→ inhibition of
cellular response to inflammation and retardation of granulation tissue formation.

V) On Immune system:
- Causes atrophy of lymphoid tissue and destruction to already form
lymphocytes Lymphopnea
- It suppresses antibody production by lymphocytes

Suppress immune system so used in organ transplantation medication.

VI) On blood formed elements:

-It induces lymphopenia, eosinopenia, neutrophilia.

VII) Anti-allergic effect:

- Suppress histamine production.
Effect of hyper-adrenocorticism
(or excessive administration of glucocorticoid for prolonged period as a drug):
1-Metabolic disorders:
-Steroid diabetes.
- Excessive protein catabolism→ Muscle weakness and thin skin
- Obesity = Moon face and pendulous abdomen.
2-Inhibition of bone formation as a result of suppression of calcium absorption.
3- Delayed wound healing.
4-Effect on blood cells:
-Lymphopenia  due to atrophy of lymphoid tissue and destruction of already
present lymphocytes
- Eosinopenia due to depression of production from bone marrow
-Neutrophilia on the expanse of other types of cells.
5-Peptic ulcer due to excessive gastric secretion (both acid secretion and pepsin)
Control
(1) Feedback mechanism:
- Positive feedback is mediated by:
- Any type of physical or mental stress:
e.g., taking an examination, recovering from a broken bone, running away from an
invading army, mild starvation.
- ↓↓ glucocorticoids in circulation.
N.B: Glucocorticoids are secreted in response to ACTH from the anterior pituitary. ACTH
is itself secreted under control of the hypothalamic peptide CRH.
- Negative feedback is mediated by:
- ↑↑ glucocorticoids in circulation
(2) Diurinal variation:
In pig and mare the rhythm of glucocorticoids output is highest in the morning (4 – 10
a.m) , rises during sleep and become lowest during the afternoon and early evening.
:Sex steroids
-3
A. Androgen hormone: which represent 10% of circulating
androgen in male and about 50% in female.
B. Small amount of estrogen + progesterone.
 :B- Glucocorticoid deficiency

1- Decrease cortisol reduce mobilization of protein and fat from the tissues-
--- depress other metabolic functions.
2- Decrease cortisol --- make the patient unable to tolerate stress.
3-Decrease cortisol (increase ACTH) -------------- pigmentation in mucous
membrane and skin.
Adrenal medulla
• It forms the core of adrenal gland
• It can be considered as modified sympathetic ganglia.
• Sympathetic stimulation --- epinephrine (80%) and nor
epinephrin (20%).
• epinephrin--- anxiety, fright, fleet.
• Nor epiphrin--- aggressiveness (fight+ attack in wild animal).
• So ratio differ in species.
Catecholamine receptors on the surface of the target cells:
- The effectof epinephrine
and norepinephrine
are initiated
by theirbindingto
adrenergic receptors on the surface of target cells

Receptor Effectively Binds Effect of Ligand Binding

Alpha1 Epinephrine, Norepinphrine Increased free calcium

Alpha2 Epinephrine, Norepinphrine Decreased cyclic AMP

Beta1 Epinephrine, Norepinphrine Increased cyclic AMP

Beta2 Epinephrine Increased cyclic AMP

- Circulating epinephrine and norepinephrine released from the adrenal

have the same effects on target organs as direct stimulation by sympathet
although their effect is longer lasting
Effects of catecholamines:
1) On cardiac muscles:
 rate and force of contraction (this is

predominantly an effect of epinephrine acting through beta receptors).

2) On blood vessels:
norepinephrine, in particular, causes widespread

vasoconstriction, resulting in increased resistance and hence arterial

to provide glucose for energy production
blood pressure.

3) On bronchioles:
dilatation of bronchioles that assists ventilation

4) On carbohydrate metabolism:
promote breakdown of glycogen

in skeletal muscle
5) On fat metabolism:
Increases lipolysis to provide fatty acids for energy

production in many tissues and aids in conservation of dwindling reserves of blood

glucose.

6) On the eye:
Dilatation of the eye pubil to Accommodate for low ambient

light

7) On metabolic rate:
Increases metabolic rate, oxygen consumption and

heat production

8) On GIT:
Inhibition of gastrointestinal secretion and motor activity
Control of catecholamines:
1- Stimulation of acetylcholine
release from preganglionic

sympathetic fibers innervating the medulla  Stimulate

catecholamine release.

2- Stressors
:

- Many types of "stresses" stimulate such secretion, including

exercise, hypoglycemia and trauma.