THE

ENDOCRINE
SYSTEM

Dr. Yaser Ashour

 THE ENDOCRINE SYSTEM
By
Dr. Yaser Mohamed Ashour
Prof. of Physiology Al Azhar
Faculty of Medicine (Assuit)

Dr. Yaser Ashour

 Introduction
• The body functions are regulated by nervous
and endocrine systems aiming for homeostasis.
• Both systems represent two parts of continuum
of control systems.
• The difference between the two systems is in
their speed and time needed to exert their
action.
• The nervous system responds within a fraction
of seconds whereas the endocrine system
responds from a fraction of second up to over
cycles of days, month or even years.

Dr. Yaser Ashour

• The difference in time factor because
the nervous system depends upon an
action potential as a conductor of its
signal, which travel along the nerve
fibers within a fraction of seconds
while the endocrine system depends
upon a chemical substance called
hormone which travel allover the body
with blood to exert the signal which it
carries.

Dr. Yaser Ashour

• Both systems are integrated
to control homeostasis and
this principle is clearly seen
in the hypothalamus and
pituitary gland where the
two systems are linked

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• (1) The
nervous system
mediate its activity
through nerves that
directly innervate the
cells being controlled,
by releasing regulatory
molecules known as
neurotransmitters to
achieve the desired
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 • (2) Both systems enable the body to
respond to a wide range of internal and
external stimuli by electing appropriate
responses to these stimuli that ensure
that the physiological functioning of the
body is done to achieve homeostasis.

HOMEOSTASIS
keeping the parameters of the body
in a steady, same state.
Dr. Yaser Ashour
 The endocrine system consists of glands,
which secrete hormones directly into blood
stream.
Major Endocrine Glands
• Hypothalamus • Adrenal medulla
• Anterior pituitary • Adrenal cortex
• Posterior pituitary • Pancreas
• Pineal • Ovaries
• Thyroid • Testes
• Parathyroids • Placenta

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Dr. Yaser Ashour
THE HORMONES

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• The endocrine gland secrete a chemical
substance called hormone
• Hormone is a chemical transmitter
(messenger) synthesized by specialized
cells (glandular cells) and carried by
bloodstream after its secretion in
response to a specific stimulus to exert
its physiological control on other
distant target cells.

Dr. Yaser Ashour

Dr. Yaser Ashour
Hormones are grouped into three classes:
• Steroids: These are derivatives of
cholesterol e.g. testosterone,
estrogen, cortisol, and Aldosterone.
• Peptides: These are short chains of
amino acids e.g. growth hormone,
insulin, and ADH.
• Amines: These are formed of amino
acid as T3 – T4 and adrenaline.
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 Properties of Hormones
1- Hormones are synthesized continuously.
2- Hormones may be stored within the cytoplasm
of the cells as inactive granule e.g. pituitary
hormones or in the form of colloid mass as in
thyroid acini.
3- Some hormones are secreted by more than
one gland e.g. estrogenic hormones are
secreted by (ovary, placenta and adrenal
cortex).
4 -Most hormones are released from their glands
in short burst (pulses) that maintain basal
definite level for each
Dr. Yaser Ashour hormone in blood.
 5- The hormone secretion show diurnal variation
(circadian rhythm) e.g. growth hormone
secretion is markedly increased in early
hours of sleep, while plasma cortisol rise in
early morning.
6- Reciprocal chemical regulation: The stimuli
which produce secretion of one hormone
inhibits the release of its antagonistic e.g. fall
in plasma calcium stimulate secretion of
parathormone and inhibit the secretion of
thyrocalcitonin hormone.
7- Hormones produce their physiological effect by
a very low concentration in blood.
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 8- Hormones act on a very specific
receptors.
9- Hormones act as trigger substances,
which initiate biochemical reactions that
persist after disappearance of hormone
from blood.
10- Hormones may affect many cells of the
body e.g. insulin & thyroxine.
11- Hormones may produce specific action
e.g. insulin lowers blood glucose.
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 12- Hormones can be classified into local and
general hormones:-
- Local hormones → which have specific local
effects at or near their site of release e.g. G.I.T.
hormones.
- General hormones → which have generalized
effects away from its site of release e.g.
pituitary hormone.
13- Antigenic property: protein and peptide
hormones stimulate the formation of
antihormone when injected to another species
due to difference in the arrangement of amino
acids
Dr. Yaser at parts of molecule.
Ashour
 1. STEROID HORMONES (LIPID
SOLUBLE)
-Pass
through the
cell
membrane
to a
receptor in
the nucleus .
-Activates
genes that
cause the
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production
PEPTIDE (PROTEIN) HORMONESwater soluble

-Bind to cell
membrane
receptor.
-series of
reactions that
alter cell
activity.

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 The Mechanisms of Hormones Action
• The chemical nature of a hormone has implications
for its transport in blood and its mechanism of
action at the target cell.
The hormones are classified as fallow:-
• Hydrophilic hormones:
(water soluble hormones), which include peptide
and adrenaline.
• Lipophilic hormones:
(Lipid soluble hormones), which include the steroid
and T3, T4.

Dr. Yaser Ashour

 • The hormone action starts by binding of the
hormone to the receptor, which they are located
either on the cell membrane, cytoplasm or
nucleus of the cell.
• The binding of a hormone molecule with a
specific receptor leads to the formation of a
receptor hormone complex.
• Receptors on target cell membranes bind only to
one type of hormone.
• More than fifty human hormones have been
identified.
• All act by binding to receptor molecules.
• The binding hormone changes the shape of the
receptor causing the response to the hormone.

Dr. Yaser Ashour

 The mechanism of hydrophilic hormone
action (water soluble).

• Hydrophilic hormones bind to external

receptors found in the cell membrane of
the target cells.
• Binding of the hormone to the receptor
activates the receptor which leads to one
of the following reactions:-

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 Cell surface receptors
• Peptide hormones and catecholamines
bind to cell surface receptors
• Receptors have extracellular,
transmembrane and intracellular domains
• Extracellular domain contains ligand
(hormone) binding site

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Cell surface receptors

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G protein –linked receptors

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 Non-G linked receptors
• Cell surface receptors with intracellular
domains with intrinsic enzymatic activity
– Protein kinase (serine or tyrosine kinases)
• Or intracellular domains that link closely to
other enzymes

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Non-G protein Receptors

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 Second messengers
• Binding to cell surface receptors releases
second messenger molecules inside cell
• Second messengers include
– cAMP or cGMP
– phopholipids diacylglycerol and inositol triphosphate
(DAG and IP3)
– calcium

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cAMP as second messenger

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Phospholipids as Second Messengers

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 Biological effects
• Second messengers create phenotypic
changes in target cells
– Alter phosphorylation (activity) of proteins
– Alter permeability of membranes
– Indirectly influence gene expression

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 Receptor Down-regulation

• After hormone binding receptors may be

internalized (coated pits)
• Leads to reduced responsiveness of
target cell (usually temporary)
• Receptor may be recycled to cell surface
or degraded

Dr. Yaser Ashour

 Intracellular Receptors
• Steroid and thyroid hormones act via
intracellular receptors
• Hormone-receptor complex interacts
directly with DNA in chromatin fiber at
the promoter of specific genes
• H-R complex acts as a transcription
factor to enhance (or decrease) rate of
transcription

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Intracellular Receptors

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 Steroid Receptor Domains

Steroid receptors interact with the grooves in DNA

double-helix via ‘zinc fingers’ formed as loops in
the receptor
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 Response Elements in Genes
• Steroid hormone receptors recognize specific
DNA elements in genes
• Short elements are steroid specific

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 Endocrine Dysfunction
• At level of endocrine
gland
• At level of target cell
– Structure, secretion,
stability, elimination of
hormone
– Primary problems in gland
of origin
– Secondary due to signals
from Hypo-Pit
– Presence of other agonists
/ antagonists
– Structure, stability of
receptor
– Downregulation
reduces sensitivity
– Post-receptor signal
transduction defects
• Second messengers
• Gene expression
• HRE

Dr. Yaser Ashour

 Regulation of endocrine system
Direct negative feedback:
• There is direct interaction between the
controlling hormone and the controlled
metabolite: - e.g.:- Plasma calcium level.
• E.g. In case of decreased plasma calcium
level → this is detected directly by
parathyroid cells lead to synthesis of
parathormone hormone leads to increase
calcium level by increased secretion.
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Indirect negative Feedback:
• Some peripheral endocrine glands (thyroid,
adrenal cortex and gonads) are dependent on
the regulation provided by hormones released
from the anterior pituitary, whose release is in
turn dependent on the endocrine activity of
hypothalamus.
• In this situation, the hypothalamic
neuroendocrine cells are frequently integrating
information from a variety of sources, including
the circulating levels of the hormone secreted
by the peripheral endocrine gland.

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 Negative Feedback:
A self-correcting system
Upper limit

Bl normal
glu

Lower limit

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A Negative Feedback System

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 Positive Feedback:
• Positive feedback exists when a hormone is able
to stimulate its own production.
• Such situations are rare and the only example that
is well documented, relates to ovulation and 17 b-
oestrdiol, which achieves positive feedback by
stimulating the release of hypothalamic GnRH;
this causes the release of pituitary FSH and LH,
which in turn stimulates the production of more
17 b-oestradiol by the ovary.

Dr. Yaser Ashour

Positive Feedback?

This is a NON-correcting system. A little

becomes more. Less becomes a lot less.
Examples: Oxytocin and Prolactin hormones
.

Dr. Yaser Ashour

Hypothalamus and
Pituitary
 Hypothalamus and Pituitary
• The hypothalamus-pituitary unit is the
most dominant portion of the entire
endocrine system.
• The output of the hypothalamus-pituitary
unit regulates the function of the thyroid,
adrenal and reproductive glands and also
controls somatic growth, lactation, milk
secretion and water metabolism.

Dr. Yaser Ashour

Hypothalamus and pituitary gland

Dr. Yaser Ashour

Hypothalamus and pituitary gland

Dr. Yaser Ashour

 Hypothalamus and Pituitary
• Pituitary function depends on the hypothalamus
and the anatomical organization of the
hypothalamus-pituitary unit reflects this
relationship.
• The pituitary gland lies in a pocket of bone at the
base of the brain, just below the hypothalamus
to which it is connected by a stalk containing
nerve fibers and blood vessels. The pituitary is
composed to two lobes-- anterior and posterior

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 Posterior Pituitary:
neurohypophysis
• Posterior pituitary: an outgrowth of the
hypothalamus composed of neural tissue.
• Hypothalamic neurons pass through the
neural stalk and end in the posterior
pituitary.
• The upper portion of the neural stalk
extends into the hypothalamus and is
called the median eminence.

Dr. Yaser Ashour

Hypothalamus and
posterior pituitary

Midsagital view illustrates that

magnocellular neurons
paraventricular and supraoptic
nuclei secrete oxytocin and
vasopressin directly into
capillaries in the posterior lobe

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 ADH = ANTIDIURETIC HORMONE
 1. low water concentration of blood (causes  of  
dehydration?)
2. hypothalamus osmoreceptors fire
 3. posterior pituitary secretes ADH and 
increases  thirst.
 4.     ADH ­ increases permeability of kidney 
tubules to water, increasing  reabsorption of 
water from urine into  blood.. (stealing water from 
the urine)
 5.      High water concentration of blood
Dr. Yaser Ashour
  ­DIURETICS (caffeine, alcohol) interfere with ADH, 
so water remains in urine and is not returned to 
blood.  Results in dehydration.  
 ­DIABETES INSIPIDUS –very little ADH is made, so 
water is not reabsorbed from urine. 
 Symptoms:  excessive urination (12L) thirst, copious 
dilute urine. 
­Bedwetting:  due to low ADH? Nosespray?
­What medical conditions could be treated  with 
diuretics?
-Why are athletes advised against cola and
coffee? Dr. Yaser Ashour
 Anterior pituitary:
adenohypophysis
• Anterior pituitary: connected to the
hypothalamus by the superior hypophyseal
artery.
• The antererior pituitary is an amalgam of
hormone producing glandular cells.
• The anterior pituitary produces six peptide
hormones: prolactin, growth hormone (GH),
thyroid stimulating hormone (TSH),
adrenocorticotropic hormone (ACTH),
follicle-stimulating hormone (FSH), and
luteinizing hormone (LH).
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 Hypothalamus and
anterior pituitary
Midsagital view
illustrates
parvicellular
neurosecretory
cells secrete
releasing factors
into capillaries of
the pituitary portal
system at the
median eminence
which are then
transported to the
anterior pituitary
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gland to regulate
 neocortex

Reituclar
Thalamus Limbic
activating Optical
substance system system
pain Emotion, fright,
Sleep/ rage, smell vision
wake

Heat regulation Energy Autonomic

(temperature) regulation regulation
(hunger, (blood pressure

Water balance (blood

volume, intake--thirst,
BMI) etc)

Metabolic rate, stress

Regulation
response, growth,

of
output—urine volume)
reproduction, lactation)

Hypothalamus

Anterior
pituitary
posterior hormones
pituitary
hormones

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 Hypothalamus/Pituitary
Axis

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 Hypothalamic releasing factors for
anterior pituitary hormones

 Travel to adenohypophysis via hypophyseal-

portal circulation
 Travel to specific cells in anterior pituitary to
stimulate synthesis and secretion of trophic
hormones

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Hypothalamic releasing hormones
Hypothalamic releasing
hormone
Corticotropin releasing hormone
(CRH)
Thyrotropin releasing hormone
(TRH)
Growth hormone releasing
hormone (GHRH)
Somatostatin
Gonadotropin releasing hormone
(GnRH) a.k.a LHRH
Prolactin releasing hormone (PRH)
Prolactin inhibiting hormone
(dopamine)
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Effect on pituitary
Stimulates ACTH secretion
Stimulates TSH and Prolactin
secretion
Stimulates GH secretion
Inhibits GH (and other hormone)
secretion
Stimulates LH and FSH
secretion
Stimulates PRL secretion
Inhibits PRL secretion
 Characteristics of hypothalamic
releasing hormones
• Secretion in pulses
• Act on specific membrane receptors
• Transduce signals via second messengers
• Stimulate release of stored pituitary hormones
• Stimulate synthesis of pituitary hormones
• Stimulates hyperplasia and hypertophy of target
cells
• Regulates its own receptor

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 Hypothalamus
and anterior
pituitary

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 Anterior pituitary
• Anterior pituitary: connected to the
hypothalamus by hypothalmoanterior pituitary
portal vessels.
• The anterior pituitary produces six peptide
hormones:
– Prolactin.
– Growth hormone (GH),
– thyroid stimulating hormone (TSH),
– adrenocorticotropic hormone (ACTH),
– follicle-stimulating hormone (FSH),
– luteinizing hormone (LH).

Dr. Yaser Ashour

 Anterior pituitary cells and hormones
Cell type Pituitary Product Target
populatio
n
Corticotroph 15-20% ACTH Adrenal gland
β- Adipocytes
lipotropin Melanocytes
Thyrotroph 3-5% TSH Thyroid gland
Gonadotroph 10-15% LH, FSH Gonads
Somatotroph 40-50% GH All tissues,
liver
Breasts
Lactotroph 10-15% PRL gonads
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Anterior pituitary hormones

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 THYROXIN
-Produced by the thyroid
gland
-increases rate of
metabolism (cell
respiration)
-provides more energy,
uses up glucose and
oxygen, produces heat.
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1.  low metabolic rate-
Control of
2. hypothalamus secretes
TSHR
thyroxin
3.      ant. Pit secretes TSH
secretion
4.      thyroid secretes TSHRF – Thyroid
thyroxine stimulating hormone
releasing factor
5.      increase in metabolic rate
6.      too high metabolic rateTSH – Thyroid
stimulating hormone
7.      hypoth. decreases TSHRF
8.      ant pit decreases TSH
9.      thyroid gland decreases
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  hypothyroidism – low thyroxine
­Symptoms: fatigue, weight gain in 
adults, cold, slow thought, possible 
goiter.
­called Cretinism in kids.  Retarded 
and small.
Goiter: Results from low dietary 
Iodine. 
Thyroid needs lots of Iodine to  
make thyroxine. With no iodine, 
high TSHRF and TSH continue to 
stimulate thyroid making it large 
and over­worked. Dr. Yaser Ashour
Hyperthyroidism = high thyroxin

Exophthalmos
Symptoms:  due to
High energy, weight  hyperthyroidism
loss, hunger, 
very alert and unable 
to sleep.
Exophthalmos

Dr. Yaser Ashour

 THE PARATHYROID GLANDS
AND
CALCIUM HOMEOSTASIS
Plasma calcium levels are maintained within very narrow
limits in order to support the many physiological
functions in which calcium is involved:
• Calcium ions play an essential role in the regulation of
membrane permeability, and hence influence
neuromuscular excitability.
• They participate in the release of neurotransmitters,
and are a vital component in the excitation –
contraction process in muscle cells.

Dr. Yaser Ashour

• They are also involved in many intracellular metabolic
pathways where they act as coenzymes and
regulators, and in both endocrine and exocrine cells
they are often implicated in excitation-secretions
pathways.
• Blood coagulation is dependent on normal levels of
calcium, as are bone & teeth formation and milk
production.
• More than 99% of total body calcium is contained in
bone and, although it provides the principle store
of calcium most is incorporated into a complex crystal
structure called hydroxyapatite, which means that it
cannot be released quickly when required.

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 • The remaining 1% of the calcium in bone can
be readily exchanged, being in the form of
calcium phosphate salts that are in equilibrium
with plasma calcium and hence provide a
convenient buffer to sudden changes in calcium
levels.
• Normally, plasma calcium is maintained at 2.3-
2.6 m mol/L and is present in three forms:-
• Diffusible ionized= ionic Ca++= 50%= 1.2 m
mol/L* non diffusible= protein bound= 41%= 1.0
m mol/LDiffusible= combined with
citrate/phosphate= 9%= 0.2 m mol/LTotal= 2.4
m mol/L
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 • The daily loss of calcium from the
body in nails, dead cells and hair, is
added to daily flux of calcium across
the gastrointestinal and kidney
epithelia.
• The net result is daily loss of 1000 mg
of calcium which needs to be
replaced in the diet.

Dr. Yaser Ashour

 Regulation of plasma calcium
depends upon:-
• Parathormone (PTH) → ↑ plasma Ca++ level.
• Calcitonin → ↓ plasma Ca++ level.
• 1, 25 dihydrocholecalciferol → ↑ plasma Ca++
level.
• Adrenal glucocorticoids → ↓ plasma Ca++
level act as anti vitamin D.
• Growth hormone → ↑ plasma Ca++ level by
↑ Ca++ excretion & ↑ Ca++ absorption.
• Thyroid hormone → ↑ plasma Ca++ level.

Dr. Yaser Ashour

 Parathormone Hormone:
• This hormone is secreted by the parathyroid
glands.
• The parathyroid glands are four, and they are
embedded in the posterior surface of thyroid
gland. Two in each lobe.
• There are two cells in the parathyroid gland:
• Chief cells → producing parathormone
hormone.
• Oxyphilic cells → whose function is not yet
clear.

Dr. Yaser Ashour

 Action of the parathormone:
• The parathormone is a major regulating
factor for both calcium (Ca++) and
phosphate (PO4--) concentrations in body
fluids.
• Normally, the plasma PO4—concentration
is inversely related to the Ca++
concentration Ca++ 1/a PO4--.
• Ca++ X PO4 = constant = solubility
product.

Dr. Yaser Ashour

 • The main function of PTH is to
increase the plasma Ca++ level and
decrease the plasma PO4-- level.
• A reciprocal relationship exists
between plasma calcium and
phosphate, such that a decrease in
one results in an elevation of the
other, and vice versa.

Dr. Yaser Ashour

 PTH exerts its actions by working on (kidney, bone & intestine).

Kidney:
• More than 95% of the filtered calcium load is
reabsorbed via a number of active and passive
transport mechanisms.
• PTH: inhibits reabsorption of calcium in the
proximal tubule & stimulate reabsorption in the
distal nephron → there is overall effect of
increased reabsorption and increased plasma
calcium concentration.
• PTH inhibit phosphate reabsorption by the
proximal convoluted tubules → this lead to:-
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 ∀ ↑ Phosphate excretion in urine.
∀ ↓ Phosphate level in plasma.
∀ ↑ Calcium level in plasma to maintain the
solubility product constant i.e. Ca++ X PO-- =
constant.
• PTH activates renal 1-hydroxylase which
converts 25-hydroxycholecalciferol to active 1,
25 dihydroxycholecalciferol.
• PTH increase Mg++ and H+ reabsorption by
renal tubules.

Dr. Yaser Ashour

 Gastrointestinal tract (intestine):
• PTH has no direct effect on the intestine.
• PTH has an indirect effect on the intestine
through its stimulation of kidney to form 1,
25 dihydroxycholecalciferol which in turn
stimulate Ca++ & PO4-- absorption from
upper small intestine.

Dr. Yaser Ashour

 Bone:
• 99% of the body’s calcium is in bone, and 99% of
this calcium is contained in a complex mineralized
matrix of hydroxyapatite crystals from which calcium
ions cannot readily be removed.
• However, a small proportion of bone is constantly
remodeled throughout life, which is why bones are
able to heal following a fracture.
• This remodeling is a dynamic equilibrium in which
bone resorption roughly equals bone formation.
• PTH is able to influence the buffering capability
provided by the calcium phosphate salts present in
this readily exchangeable bone.

Dr. Yaser Ashour

Control of parathormone secretion:
PTH is regulated by:-
(1) Ca++ ions level in plasma:
∀ ↓ Ca++ level by 0.5 mg % → stimulate PTH
secretion.
∀ ↑ Ca++ level → inhibit PTH secretion.
(2) PO4-- Level in plasma:
∀ ↑ PO4—plasma level → stimulates PTH secretion.
(3) Mg++ level in plasma:
∀ ↓ Mg++ level → stimulate PTH secretion.
∀ ↑ Mg++ level → inhibit PTH secretion.

Dr. Yaser Ashour

 Calcitonin:
• Calcitonin (CT) is a calcium lowering
hormone.
• It is a polypeptide secreted from the
Parafollicular cells of the thyroid gland.
• It was found that (CT) also found in the
brain, pituitary, thymus, lung, liver and gut.
• The plasma level of CT is 2-4 mg %.
• Its half life in circulation is less than 10
minutes.

Dr. Yaser Ashour

 Actions of calcitonin:
(1) Effect on Bone:
• Inhibits bone resorption by:
• Inhibit the permeability of osteoclasts and osteocytes
to calcium i.e. decrease mobilization of calcium from
both.
∀ ↓ The activity and numbers of osteoclast.
(2) Effect on G.I.I.:
• Inhibit intestinal absorption of Ca++ & PO4--.
∀ ↓ Gastric acid secretion.
(3) Effect on kidney:
∀ ↑ Urinary excretion of PO4--, Ca++ and Na+, Cl-.
• Inhibit renal 1 a-hydroxylase activity.

Dr. Yaser Ashour

 Vitamin D
• Vitamin D → It is word refer to a group of a
closely related sterols, the commonest of which
are vitamin D2 (calciferol) and vitamin D3
(cholecalciferol).
• Vitamin D3: is formed in the skin by the effect
of ultraviolet rays of the sun, also it is taken in
the diet (e.g. cod liver oil and egg yolk).
• Vitamin D2: is taken in food and it has the
metabolism as VD3.

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 Action of Vitamin D3:
It increases absorption of both Ca++ &
PO4—from intestine.
It mobilizes both Ca++ & PO4—from
bone.
It facilitates Ca++ reabsorption in the
kidneys.
It helps development of normal bone and
teeth.
It stimulates differentiation of immune
cells and keratinocytes
Dr. Yaser Ashour in the skin.
 Other hormones affecting calcium metabolism:
• Glucocorticoids → ↓ Ca++ level.
• Growth hormone → ↑ Ca++ level.
• Thyroxine → hypercalcaemia – hypercalciuria
& osteoprosis.
• Sex hormones → Androgen → * calcium
retention
• Oestrogen → * ↓ plasma Ca++ level.
* prevent osteoprosis.

Dr. Yaser Ashour

 Control of Ca++ blood
concentration is by PTH
and Calcitonin.

-Calcium can move between the blood

and the storage pools in bones and
teeth depending on the body’s needs.
……..What Dr.
isYaser
calcium
Ashour needed for?
 PARATHYROID HORMONE
-Produced by parathyroid glands when
blood calcium is low.
PTH increases blood calcium by
1. Dissolving Ca from bones and teeth
into blood.
2. Causing increased absorption of Ca
from the gut into the blood
When would you expect PTH blood
concentrations to be high?
Dr. Yaser Ashour
 OSTEOPOROSI
S is Calcium
loss from
bone.
If your diet
and thus your
blood is low in
calcium then
PTH will be
dissolving
your bones
resulting in
osteoporosis.
Dr. Yaser Ashour Low estrogen
 CALCITONIN HORMONE
Produced by thyroid gland when
blood Ca levels are high.
Calcitonin decreases blood Ca by:
1. Increasing Ca deposition in bones
and teeth.
4. Reducing Ca absorption from the gut
into the blood.

When would you expect Calcitonin

blood concentrations to be high?
Dr. Yaser Ashour
 Where is calcitonin and PTH
released?

Blood
calciu
m

Dr. Yaser Ashour

 Disorders of Calcium Homeostasis
Hypovitaminosis D:
• Vitamin D deficiency causes Rickets in children
and osteomalacia in adults.
Causes:
• Inadequate intake of vitamin D in diet.
• Inadequate exposure to ultraviolet rays.
• Inadequate absorption in the intestine e.g.
celiac disease or obstructive jaundice.

Dr. Yaser Ashour

• Renal failure → there is failure of hydroxylase
25 – hydroxycholcalciferol to calcitrol.
Manifestations:
• Lack of vit D → decrease Ca++ absorption
from the intestine → hypocalcaemia →
failure of mineralization of new bone and
more secretion PTH lead to more bone
demineralization and mobilization of Ca++
from bone lead to Rickets in children and
osteomalacia in adult

Dr. Yaser Ashour

 Rickets:
• This is a common disease in poor community
due to malnutrition.
Characteristic of Rickets:
• Growth retardation or stoppage.
• Swelling near the joints (due to continuous
growth of epiphyseal plates).
• Bone deformities:
* Bowing of leg.
* Pelvis deformity.

Dr. Yaser Ashour

 Osteomalacia:
• This is a disease which occurs in
adult due to hypocalcaemia and
usually it occurs in multipart ladies,
and their bones become brittle, tender
and painful.

Dr. Yaser Ashour

 Hypervitaminosis D:
Prolonged administration of large doses of vitamin D
produce:-
• Hypercalcaemia and deposition of calcium in soft
tissues.
∀ ↑ Calcium and phosphate excretion in urine →
polyuria + polydipsia.
• Renal ischemia → due to deposition of calcium in
renal blood vessel → hypertension.
• Renal failure → due to calcium deposition in renal
tubules.
• Other symptoms (anorexia, nausea, vomiting,
headache, drowsiness).
• Bone resorption → osteoporosis.
Dr. Yaser Ashour
 Hyperparathyroidism:
• Hyperfunction of parathyroid gland is produced by
parathyroid hyperplasia or adenoma with excess PTH
secretion.
Manifestations:
* Urine & blood changes:
∀ ↑ Phosphate excretion in urine (hyperphosphaturia).
∀ ↓ Plasma phosphate (hypophosphatatemia).
∀ ↑ Plasma calcium (Hypercalcaemia).
∀ ↑ Calcium excretion in urine (hypercalciuria).
∀ ↑ Plasma alkaline phosphatase.
• * ↑↑ bone resorption → ↑ decalcification of bones:
• Bone becomes fragile bone show multiple cysts
Dr. Yaser Ashour(ostitis fibrosa cystica).
∀ ↓↓ Neuromuscular excitability → (due to
hypercalcaemia).
• Mental retardation.
• Depression of reflexes.
• Muscle weakness.
• Constipation.
• * Renal changes:
• Polyuria.
• Renal stones.
• Renal failure.

Dr. Yaser Ashour

 Hypoparathyroidism
This is due to faulty removal of parathyroid
during thyroidectomy.
Manifestations:
• * Urine and blood changes:
∀ ↓ phosphate excretion in urine.
∀ ↑ phosphate level in plasma.
∀ ↓ calcium level in plasma.
∀ ↓ calcium excretion in urine.
• * ↓ ionized Ca++ level in plasma:

Dr. Yaser Ashour

• Tetany.
∀ ↑ H.R., cardiac arrhythmia, prolongation of
S-T segment, and prolongation of Q-T
interval.
• Intestinal and biliary colic.
• Opacity of eye lens (cataract).
• Hair falls & brittle nails.

Dr. Yaser Ashour

 TETANY
• It is a disease characterized by increased
neuromuscular excitability due to ↓ ionized calcium
level in plasma.
• It is characterized by attacks of spasmodic
contractions which may involve the laryngeal and
respiratory muscles.
Causes of tetany:
• Hypocalcaemia: → ↓ calcium level in blood due to:-
- Hypoparathyroidism.
- ↓ calcium intake.
- Calcium need (pregnancy & lactation).
- ↓ absorption of calcium as in:-
- steatorrhea (fatty diarrhea) → due to combination
of fat with calcium
Dr. Yaser forming calcium soaps.
Ashour
 • Deficiency of vitamin D.
∀ ↑ alkalinity of intestinal content which precipitates
calcium.
• Administration of oxalate or citrate
• Oxalate → precipitate calcium.
• Citrate → form unionized calcicitrate.
Types of Tetany
• Upon the calcium level in the blood there are two
types of tetany:-
1- Manifest tetany → when the calcium level is below 7
mg %.
2- Latent tetany → when the calcium level drops
between 9 mg % → 7 mg%.
Dr. Yaser Ashour
 Manifest tetany:
Manifestations:
1- Fibrillary twitches of skeletal muscles and
attacks of clonic & tonic contractions.
• These tonic contractions may lead to
generalized convulsions.
• Spasmodic contraction of laryngeal muscles
leads to respiratory distress and cyanosis.
• If this spasmodic contraction prolonged it leads
to death as a result of asphyxia (laryngeal
stridor).
Dr. Yaser Ashour
 2- Carpopedal spasm = obstetrician hand =
Accoche’s hand.= carpal spasm = stiffness of
hand muscles.
There is flexion of wrist
Flexion of metacorpo-phalngeal joints.
Extension of interphalngeal joints.
Adduction of thumb into hand
Pedal spasm = dorsiflexion of foot toes are
planter flexed.

Dr. Yaser Ashour

carpopedal spasm

Dr. Yaser Ashour

 Latent tetany:
• Plasma calcium level is above 7 mg %
and ↓ 9 mg %.
• Manifestations of tetany are absent at
rest.
• These manifestations appear when there
is an increase of body need to calcium.
• Or there is exposure to stress e.g.
pregnancy, lactation, emotion and
hyperventilation.
Dr. Yaser Ashour
 Diagnosis of latent tetany:
1- Determination of ionized calcium level in
plasma.
Trousseau’s sign: on application of occlusion of
blood supply to the arm by sphygmomanometer
cuff → Trousseau’s sign.
Chvostek’s sign: Tapping the facial nerve in
front of the ear results in twitch of facial
muscles especially the upper lip due to
increased excitability to mechanical stimuli.

Dr. Yaser Ashour

Erb’s sign: ↑ excitability of motor nerves to galvanic
current.
• On application of a signal electric stimulus of any
superficial motor nerve → produce prolonged
spasmodic contraction in the supplied muscles in
positive cases.
Treatment:
* Acute tetanic attacks → are treated by slow I.V.
calcium chloride injection.
* After attack:
– * Vitamin D.
– * Diet rich in calcium.
– * Ammonium chloride.
– * PTH injection.* A.T.10

Dr. Yaser Ashour

 GLUCAGON
• Alpha cells secrete glucagon -
peptide of 29 amino acids.
– Stimulus for release is decrease in blood
glucose levels
– Synthesized as a larger proglucagon
molecule and then clipped down by enzymes
– Potent hyperglycemic agent - major target
organ is the liver
– Stimulates glycogenolysis and lipolysis

Dr. Yaser Ashour

 INSULIN
• Beta cells secrete insulin - peptide of
51 amino acids.
– Synthesized as a larger proinsulin molecule and
then clipped down by enzymes.
– Lowers blood glucose by enhancing membrane
transport of glucose into body cells (especially
muscle and fat cells). The brain, kidney and liver
have easy access to glucose and do not require
insulin.
– Inhibits glycogenolysis and gluconeogenesis

Dr. Yaser Ashour

 INSULIN
• After glucose enters a target cell, insulin
binding triggers enzymatic activity that:
– Catalyze the oxidation of glucose for ATP
production
– Join glucose molecules together to form
glycogen
– Convert excess glucose to fat

Dr. Yaser Ashour

INSULIN
• Diabetes mellitus results
from hyposecretion of
insulin or hypoactivity of
insulin.
• When insulin is absent or
deficient, blood sugar
levels remain high after a
meal because glucose is
unable to enter most
tissue cells.
Dr. Yaser Ashour
 DIABETES
• Type I diabetes mellitus (insulin-
dependent) afflicts 750, 000 Americans.
– Autoimmune disease (beta cells are attacked
by immune cells). May be due to a virus
entering the body and mimicking beta cell
antigens.
– Insulin is not produced or secreted, requiring
regular insulin injections.

Dr. Yaser Ashour

 DIABETES
• Type II diabetes mellitis (non-insulin-
dependent) afflicts 7.5 million
Americans.
– Insulin resistance - Insulin is usually
produced but the receptors do not respond.
– The membrane protein PC-1 may be a culprit
– it has been shown to inhibit the tyrosine
kinase receptor, but its mechanisms of action
are unknown.
Dr. Yaser Ashour
 DIABETES
Heredity plays a role - an estimated 30% of
poples carry a gene that predisposes them to
Type II diabetes.
Lifestyle play a role - Type II diabetics are
almost always obese and sedentary.
Adipose tissue produces a hormone-like
chemical called tumor necrosis factor-
alpha, which depresses synthesis the cellular
glucose transporter (glut-4).
Cells cannot take up glucose in the absence of
Dr. Yaser Ashour glut-4.
ANTAGONISTIC HORMONE
PAIRS
work together to keep a parameter
from becoming too high or too low.
Eg. Insulin decreases blood
glucose
Glucagon increases blood
glucose
Eg. PTH increases blood Ca++
CalcitoninDr.decreases
Yaser Ashour
blood
Dr. Yaser Ashour
CONTROL OF BLOOD GLUCOSE - Where
are insulin and glucagon secreted
from? The islets of Langerhans in the
pancreas.

Alpha islet cells secrete glucagon.

Beta islet cells
Dr. secrete
Yaser Ashour insulin.
WHEN BL. GLUCOSE IS HIGH, INSULIN
GLUCOSE
GGGGGG
DECREASES IT BY:
1. Increasing glucose permeability of cell CELL
(open glucose gates on cell membranes). LIVER

2 Causes liver to remove excess glucose from the blood

and store it as liver glycogen and fat.

Dr. Yaser Ashour

 INSULIN UNLOCKS
THE GLUCOSE
GATES ON THE CELL
SO GLUCOSE CAN
ENTER THE CELL
FROM THE
BLOODSTREAM.
If there is no
insulin, glucose
remains in the
blood (high bl. Glu)
and the cell
starves, producing
no energy. The
Dr. Yaser Ashour victim becomes
 WHEN GLUCOSE IS LOW, GLUCAGON
INCREASES IT BY:
1. Decreasing permeability of cells to
glucose (close glucose gates on cells).
GGGGGGGGG

cell

2. Releasing stored glucose from the liver

liver into the blood.

Dr. Yaser Ashour

 When are insulin and
glucagon released?

A
Blood
glucose
B

Dr. Yaser Ashour

What happens when insulin isn’t secreted
or cells become insulin resistant?
Disease DIABETES MELLITUS
Type I: juvenile – due to lack of insulin
Type II: adult onset – due to insulin
resistance (Associated with obesity).
Symptoms:
• High blood glucose, fatigue, high glu in 
urine, high urine volume, weight loss.

Dr. Yaser Ashour

What’s the physiology behind these
symptoms?
High blood glucose
Fatigue
High glu in urine
High urine volume
Dry, itchy skin
Thirst
Weight loss.Dr. Yaser Ashour
High blood glucose – glucose from food can not enter
cells so it remains in blood.
Fatigue – cells lack glucose for cell respiration so no
ATP energy is made.
High glu in urine – XS glu spills into urine and is not
returned completely to blood by active transport.
High urine volume – Normally water from the urine
follows glucose back into the blood by osmosis, but
because some glu remains in the urine, the water
remains with it.
Dry, itchy skin – The increased loss of water in urine
dehydrates the blood stream.
Thirst – Same as above
Weight loss – The glucose lost in the urine is from
your meals. Dr. Yaser Ashour
• Treatment
    Injection of insulin, oral
hypoglycemic pills, control of
exercise, diet, weight reduction.

Continuous Blood
Glucose monitoring .

Insulin
Pump
automa
t-ically
injects
insulin
into
Dr. Yaser Ashour
the
 DIABETES
TECHNOLOGIES
• Recombinant DNA technology:
Human insulin gene transfered
into bacteria?
http://www.angelfire.com/dc/apgenetics/rec.dna.plasmid.gif

• Transplanting normal human islet

cells into liver of diabetic patient?
http://www.ianblumer.com/islet_cell_transplants.htm

• Gene Therapy: Transplanting

insulin genes into embryos or
fetuses?
Dr. Yaser Ashour
The
Edmonto
n
Protocol

Dr. Yaser Ashour

What happens if you can’t make
Glucagon ? HYPOGLYCAEMIA:

Blood glucose can’t be raised-

it stays low.
Symptoms:
·       Low blood glucose, fatigue,
passing out.
 Treatment?
Dr. Yaser Ashour
 Hormones
• Regulatory molecules
secreted into the blood
or lymph by endocrine
glands. “Ductless”
– Lack ducts.
– Derived from epithelium
but lose connection with
surface.
• Carry hormone to
target tissue where it
produces its effects.

Dr. Yaser Ashour

 Chemical Classification of
Hormones
• Amines
• Polypeptides
• Glycoproteins
• Steroids

Dr. Yaser Ashour

 Amines
• Hormones derived from tyrosine and
tryptophan.
• Include hormones secreted by
adrenal medulla, thyroid, and pineal
glands.

Dr. Yaser Ashour

 Polypeptides

• Chains of amino acids (< 100 amino

acids in length).
– ADH
– Insulin

Dr. Yaser Ashour

 Glycoproteins
• Long polypeptides (>100) bound to
one or more carbohydrate (CHO)
groups.
– FSH
– LH

Dr. Yaser Ashour

 Steroids
• Lipids derived from
cholesterol.
• Are lipophilic
hormones.
– Testosterone
– Estradiol
– Cortisol
– Progesterone

Dr. Yaser Ashour

 Thyroid Hormones

• Tyrosine derivatives
bound together.
• Contain 4 iodine
atoms (T4).
• Contain 3 iodine
atoms (T3).
• Small, non-polar
molecules.
– Soluble in plasma
membranes.

Dr. Yaser Ashour

 Hormonal Interactions
• Synergism:
• Two hormones work together to produce a
result.
– Additive:
• Each hormone separately produces response, together at
same concentrations stimulate even greater effect.
– Epinephrine and norepinephrine.
– Complementary:
• Each hormone stimulates different step in the process.
– FSH and testosterone.

Dr. Yaser Ashour

 Hormonal Interactions

• Permissive effects:
– Hormone enhances the responsiveness of
a target organ to second hormone.
– Increases the activity of a second
hormone.
• Prior exposure of uterus to estrogen induces
formation of receptors for progesterone.

Dr. Yaser Ashour

 Hormonal Interactions
• Antagonistic effects:
• Action of one hormone antagonizes the
effects of another.
– Insulin and glucagon.

Dr. Yaser Ashour

 Effects of Hormone
Concentration
• Concentration of hormones in blood
reflects the rate of secretion.
• Half-life:
– Time required for the plasma concentration
is reduced to ½ reference level.
• Physiological range of concentration
produces normal tissue response.

Dr. Yaser Ashour

 Effects of Hormone
Concentration
• Varying hormone concentration within
normal, physiological range can affect
the responsiveness of target cells.
• Priming effects (upregulation)
– Increase number of receptors formed on
target cells.
– Greater response by the target cell.

Dr. Yaser Ashour

 Effects of Hormone
Concentration
• Desensitization (downregulation):
– Decrease in number of receptors on target
cells.
– Produces less of a target cell response.
• Insulin in adipose cells.
• Pulsatile secretion may prevent
downregulation.
– GnRH and LH.

Dr. Yaser Ashour

 Mechanisms of Hormone
Action
• Hormones of same chemical class have
similar mechanisms of action.
– Location of cellular receptor proteins.
• Target cell must have specific receptors
for that hormone (specificity).
• Hormones bind to receptors with high
bond strength (affinity).
• Low capacity of receptors (saturation).

Dr. Yaser Ashour

 Hormones That Bind to
Nuclear Receptor Proteins
• Lipophilic steroid and thyroid hormones
bound to plasma carrier proteins.
• Hormones dissociate from carrier
proteins to pass through lipid
component of the target cell membrane.
• Receptors for the lipophilic hormones
are known as nuclear hormone
receptors.

Dr. Yaser Ashour

 Nuclear Hormone
Receptors
• Function within cell to activate genetic
transcription.
• mRNA directs synthesis of specific enzyme
proteins that change metabolism.
• Receptor must be activated by binding to
hormone before binding to specific region of
DNA called HRE (hormone responsive
element).
– Located adjacent to gene that will be transcribed.

Dr. Yaser Ashour

 Mechanisms of Steroid
Hormone Action
• Steroid receptors
located in cytoplasm.
• Bind to steroid
hormone.
• Translocates to
nucleus.
• DNA-binding domain
binds to specific HRE
of the DNA.
• Dimerization occurs.
• Stimulates
transcription. Dr. Yaser Ashour
Dr. Yaser Ashour
Dr. Yaser Ashour
 Hormones That Use 2nd
Messengers
• Cannot pass through plasma membrane.
• Catecholamines, polypeptides, and
glycoproteins bind to receptor proteins on
the target cell membrane.
• Actions are mediated by 2nd messengers
(signal-transduction mechanisms).
– Extracellular hormones are transduced
into intracellular second messengers.

Dr. Yaser Ashour

Dr. Yaser Ashour
Dr. Yaser Ashour
Dr. Yaser Ashour
Endocrine
Glands

Dr. Yaser Ashour

Anterior and posterior pituitary glands.
Dr. Yaser Ashour
 Posterior Pituitary
• Also called the neurohypophysis.
• Formed by downgrowth of the brain during
fetal development.
• Is in contact with the infundibulum.
• Nerve fibers extend through the
infundibulum.

Dr. Yaser Ashour

 Hypothalamic Control of
Posterior Pituitary
• Hypothalamus produces:
– ADH: paraventricular
nucleus
– Oxytocin: supraoptic
nucleus
• Hormones transported
along the hypothalamo-
hypophyseal tract.
• Stored in posterior
pituitary.
• Release controlled by
neuroendocrine reflexes.
Dr. Yaser Ashour
 Anterior Pituitary
• Master gland (also called
adenohypophysis).
• Derived from a pouch of epithelial tissue
that migrates upward from the mouth.
• Consists of 2 parts:
• Pars distalis: anterior pituitary.
• Pars tuberalis: thin extension in contact
with the infundibulum.

Dr. Yaser Ashour

 Anterior Pituitary
• Trophic effects:
– Health of the target glands, depends
upon stimulation by anterior pituitary
for growth.
– High plasma hormone concentration
causes target organ to hypertrophy.
– Low plasma hormone concentration
causes target organ to atrophy.

Dr. Yaser Ashour

Dr. Yaser Ashour
 Hypothalamic Control of the
Anterior Pituitary
• Hormonal control rather than neural.
• Hypothalamus synthesizes releasing
hormones and inhibiting hormones.
• Hormones are transported to axon
endings of median eminence.
– Delivers blood and hormones to anterior
pituitary via portal system.

Dr. Yaser Ashour

 Feedback Control of the
Anterior Pituitary
• Anterior pituitary and hypothalamic
secretions are controlled by the target
organs they regulate.
• Negative feedback inhibition by target
gland hormones.

Dr. Yaser Ashour

 Feedback Control of the
Anterior Pituitary

• Negative feedback at 2 levels:

– The target gland hormone can act on the
hypothalamus and inhibit releasing
hormones.
– The target gland hormone can act on the
anterior pituitary and inhibit response to the
releasing hormone.

Dr. Yaser Ashour

Dr. Yaser Ashour
Dr. Yaser Ashour
 Adrenal Glands
• Paired organs that cap the kidneys.
• Each gland consists of an outer cortex and inner
medulla.
• Adrenal medulla:
– Derived from embryonic neural crest
ectoderm (sympathetic ganglia).
– Synthesizes and secretes:
• Catecholamines (mainly epinephrine but some
norepinephrine).

Dr. Yaser Ashour

Dr. Yaser Ashour
 Adrenal Medulla
• Innervated by sympathetic nerve fibers.
– Increase respiratory rate.
– Increase heart rate, cardiac output; and
vasoconstrict blood vessels, thus increasing
venous return.
– Stimulate glycogenolysis.
– Stimulate lipolysis.

Dr. Yaser Ashour

Dr. Yaser Ashour
Dr. Yaser Ashour
 Thyroid Hormones
• Thyroid gland located just below the
larynx.
• Thyroid is the largest of the pure
endocrine glands.
• Follicular cells secrete thyroxine.
• Parafollicular cells secrete calcitonin.

Dr. Yaser Ashour

 Production of Thyroid
Hormones
• I- (iodide) actively transported into the
follicle and secreted into the colloid.
• Oxidized to (Io) iodine.
• Iodine attached to tyrosine.
– Attachment of 1 iodine produces
monoiodotyrosine (MIT).
– Attachment of 2 iodines produces
diiodotyrosine (DIT).
• MIT and DIT or 2 DIT molecules
coupled. Dr. Yaser Ashour
 Production of Thyroid
Hormones
• T3 and T4 produced.
• TSH stimulates pinocytosis into the
follicular cell.
– Enzymes hydrolyze to T3 and T4 from
thyroglobulin.
• Attached to thyroid-binding protein and
released into blood.

Dr. Yaser Ashour

 T3 Effects
• Stimulates cellular respiration by:
– Production of uncoupling proteins.
– Stimulate active transport Na+/ K+ pumps.
– Lower cellular [ATP].
• Increases metabolic heat.
• Increases metabolic rate.
– Stimulates increased consumption of
glucose, fatty acids and other molecules.

Dr. Yaser Ashour

Dr. Yaser Ashour
 Parathyroid Hormone
• Parathyroid glands embedded in the
lateral lobes of the thyroid gland.
• Only hormone secreted by the
parathyroid glands.
• Single most important hormone in the
control of plasma Ca++ concentration.
• Stimulated by decreased plasma Ca++
concentration.

Dr. Yaser Ashour

Dr. Yaser Ashour
Dr. Yaser Ashour
Dr. Yaser Ashour
 Pancreas
• Endocrine portion consists of islets of
Langerhans.
• Beta cells secrete insulin
– Stimulus is increase in plasma glucose
concentrations
– Promotes entry of glucose into cells
• Alpha cells secrete glucagon
– Stimulus is decrease in plasma glucose
concentrations
– Stimulates lipolysis.
Dr. Yaser Ashour
Dr. Yaser Ashour
 Pineal Gland
• Melatonin:
– Production stimulated by the suparchiasmatic
nucleus (SCN) in hypothalamus.
– SCN is primary center for circadian rhythms.
• May inhibit GnRH.

Dr. Yaser Ashour

Dr. Yaser Ashour
 Thymus
• Site of production of T cells (thymus-
dependent cells), which are lymphocytes.

Dr. Yaser Ashour

 Gonads and Placenta
• Gonads (testes and ovaries):
– Secrete sex hormones.
• Testosterone.
• Estradiol.
• Progesterone.
• Placenta:
– Secretes large amounts of estrogen and
progesterone.

Dr. Yaser Ashour

 Prostaglandins
• Most diverse group of autocrine regulators.
• Produced in almost every organ.
• Wide variety of functions.
– Immune system:
• Promote inflammatory process.
– Reproductive system:
• Play role in ovulation.
– Digestive system:
• Inhibit gastric secretion.

Dr. Yaser Ashour

 Prostaglandins
– Respiratory system:
• May bronchoconstrict or bronchodilate.
– Circulatory system:
• Vasoconstrictors or vasodilators.
– Urinary system:
• Vasodilation.

Dr. Yaser Ashour

Dr. Yaser Ashour
Good Luck ya
2ooroood

Dr. Yaser Ashour