Endocrine system

Unit: IV
Endocrine System
Presented by: Prof.Mirza Anwar Baig
Anjuman-I-Islam's Kalsekar Technical Campus
School of Pharmacy,New Pavel,Navi Mumbai,Maharashtra
1Presented by: Prof.Mirza Anwar
Baig,AIKTC's SOP,New Panvel
1

Contents:
• Classification of hormones
• Mechanism of hormone action
• Structure,functions and disorders of
– pituitary gland,
– thyroid gland,
– parathyroid gland,
– Adrenal gland,
– Pancreas,
– Pineal gland,
– Thymus and their disorders.
2Presented by: Prof.Mirza Anwar Baig,AIKTC's SOP,New Panvel

What is hormone?
❖ A hormone is a mediator molecule that is released in one part of
the body but regulates the activity of cells in other parts of the
body.
❖ Most hormones enter interstitial fluid and then the bloodstream.
Both neurotransmitters and hormones exert their effects by
binding to receptors on or in their “target” cells.
❖ Several mediators act as both neurotransmitters and hormones.
❖ One familiar example is norepinephrine, which is released as a
neurotransmitter by sympathetic postganglionic neurons and as a
hormone by chromaffin cells of the adrenal medullae.
Presented by: Prof.Mirza Anwar
3

Classification of hormones:
1. Chemical Classes of Hormones
a. Lipid soluble
b. Water soluble
a. Lipid-soluble Hormones
It includes steroid hormones, thyroid hormones, and nitric oxide.
i. Steroid hormones derived from cholesterol.
Each steroid hormone is unique due to the presence of different
chemical groups attached at various sites on the four rings at the
core of its structure. These small differences allow for a large
diversity of functions.
ii. Two thyroid hormones (T3 and T4) are synthesized by
attaching iodine to the amino acid tyrosine. The benzene ring of
tyrosine plus the attached iodines make T3 and T4 very lipid
soluble.
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iii. The gas nitric oxide (NO) is both a hormone and a
neurotransmitter: Its synthesis is catalyzed by the enzyme nitric
oxide synthase.
2. Water-soluble Hormones
i. Amine hormones: Synthesized by decarboxylating and
otherwise modifying certain amino acids.
They are called amines because they retain an amino group.
The catecholamines—epinephrine,norepinephrine, and
dopamine—are synthesized by modifying the amino acid
tyrosine.
Histamine is synthesized from the amino acid histidine by mast
cells and platelets.
Serotonin and melatonin are derived from tryptophan.
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2. Peptide hormones and protein hormones are amino
acid polymers.
The smaller peptide hormones consist of chains of 3 to 49
amino acids; the larger protein hormones include 50 to 200
amino acids.
Examples of peptide hormones: antidiuretic hormone and
oxytocin;
Examples of protein hormones include human growth
hormone and insulin.
Several of the protein hormones, such as thyroid-stimulating
hormone, have attached carbohydrate groups and thus are
Glycoprotein hormones.
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3. The eicosanoid hormones are derived from arachidonic
acid,a 20-carbon fatty acid.
The two major types of eicosanoids are prostaglandins and
leukotrienes.
The eicosanoids are important local hormones, and they
may act as circulating hormones as well.
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Mechanism of Hormone Action:
• The response to a hormone depends on both the hormone and the
target cell.
• Various target cells respond differently to the same hormone.
Example: Insulin, stimulates synthesis of glycogen in liver cells
and synthesis of triglycerides in adipose cells.
• Other hormonal effects include changing the permeability of the
plasma membrane stimulating transport of a substance into or out
of the target cells, altering the rate of specific metabolic reactions,
or causing contraction of smooth muscle or cardiac muscle.
• In part, these varied effects of hormones are possible because a
single hormone can set in motion several different cellular
responses.
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Mechanism of lipid soluble steroid hormone and
thyroid hormones
9

Mechanism of water soluble hormones (protein,
peptide, amine and eicosonides)
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11
Endocrine glands in the human head and neck
and their hormones

PITUITARY GLAND
X-RAY SKULL: LATERAL
VIEW
SAGITTAL SECTION OF HEAD
& NECK
Hypophyseal fossa
Sphenoidal air sinus
Pituitary
gland

It lies in the middle cranial
fossa
It is well protected in sella
turcica (hypophyseal fossa) of
body of sphenoid
Sella turcica
POSITION

Hypothalamus
controls the
pituitary
The HYOPTHALAMUS is the “coordinating centre” in the brain associated with
homeostasis.
The PITUITARY GLAND in the brain stem is the “master gland” that controls the
endocrine glands in the body (Control Centre)

PITUITARY GLAND
• Master Gland (controls other glands)
• Rests in the base of the skull in a structure called the
sella turcica “Turkish Saddle”
• Works with the Hypothalamus (Coordinating centre or
“secretary”)

SUBDIVISIONS OF PITUITARY GLAND
The gland is subdivided into:
1) Anterior lobe (Adenohypophysis): True gland, Secretes hormones
2) Posterior lobe (Neurohypophysis): Connected to hypothalamus
through hypothalamo-hypophyseal tract, stores hormones secreted by
hypothalamic nuclei.
Hypothalamo-hypophyseal
tract

BLOOD SUPPLY OF PITUITARY GLAND

Many
different
target
organs
and
functions

Hormones secreted by anterior pitutary:

Principal actions of anterior pitutary hormones:

Principal actions of anterior pitutary
hormones contd:

Summary of posterior pitutary hormones:

Feedback system:

Anterior Pituitary Gland Disorders
1. Pituitary Dwarfism:
• Hyposecretion of hGH during the
growth years slows bone growth,
and the epiphyseal plates close
before normal height is reached.
This condition is called pituitary
dwarfism.
• Other organs of the body also fail
to grow, and the body proportions
are childlike.
• The individual is of small stature
but is well proportioned and
mental development is not
affected.
• Puberty is delayed and there may
be episodes of hypoglycaemia.

Statistics
Worldwide estimates vary usually due to lack of reporting and
recording but estimates range from 1:30,000 to 1:1800.
Risk Factors
Pituitary dwarfism may be associated with deficiencies of other
hormones, including the following:
• Thyrotropins (control production of thyroid hormones)
• Vasopressin (controls water balance in the body)
• Gonadotropins (control production of male and female sex
hormones)
• Adrenocorticotrophic hormone or ACTH (controls the adrenal gland
and its production of cortisol and other hormones)

Diagnosis
• Charting a child's growth in comparison to age norms will help
lead to a diagnosis.
• X ray of the child's hand to determine the child's bone age by
comparing this to the child's actual chronological age. The bone
age in affected children is usually two or more years behind the
chronological age.
• X rays, MRI or computed tomography (CT), may help the
doctor make a diagnosis and may show whether there have been
any changes to the pituitary gland itself.
• Blood levels of growth hormone and IGF-1 may also be
measured with blood tests.
• A complete examination to make sure that delayed growth is not
caused by other underlying problems, such as tumor.

Etiology:
Pituitary dwarfism can be caused by:
• Genetics
• Accident-related trauma to the pituitary gland
• Surgical injury of the pituitary
• Central nervous system tumor
• Central nervous system trauma
• Central nervous system radiation
• Leukemia
• In most cases, the cause of dwarfism is not known
(idiopathic).

Treatment
• Growth hormone replacement therapy can be administered if the
child is lacking growth hormone before a child's bone growth
plates have fused or joined.
• Recombinant DNA techniques produced a safe and unlimited
supply of GH in the lab.
• A careful balancing of all of the hormones produced by the
pituitary gland is necessary for patients with panhypopituitarism,
making this form of dwarfism complex and difficult to manage.

2.Panhypopituitarism:
• Panhypopituitarism is absence of all hormones.
Causes of hyposecretion include:
tumours of the hypothalamus or pituitary
trauma, usually caused by fractured base of skull or surgery
pressure caused by a tumour adjacent to the pituitary
gland, e.g. glioma, meningioma
infection, e.g. meningitis, encephalitis, syphilis ischaemic necrosis
ionising radiation or cytotoxic drugs.

Symptoms
• It is often progressive. Although the signs and symptoms can
occur suddenly, they more often develop gradually.
They may include:
• Fatigue
• Weight loss
• Decreased sex drive
• Sensitivity to cold or difficulty staying warm
• Decreased appetite
• Facial puffiness
• Anemia
• Infertility
• Short stature in children

Diagnosis:
• Blood tests. They can help detect deficits in hormones as a result
of pituitary failure.
• Brain imaging. Magnetic resonance imaging (MRI) of your
brain can detect a pituitary tumor or other structural abnormality.
• Vision tests. These tests can determine if growth of a pituitary
tumor has impaired your sight or visual fields.

Treatment
• Successful treatment of the underlying condition causing
hypopituitarism may lead to a optimum relief.
• Replacement of deficient hormones, dosages are set to match the
amounts that your body would normally manufacture. Treatment
may be lifelong
• Hormone replacement medications may include:
• Corticosteroids (hydrocortisone or prednisone) replace the
adrenal hormones because of an adrenocorticotropic hormone
(ACTH) deficiency.
• Levothyroxine (Levoxyl, Synthroid, others). This medication
replaces deficient thyroid hormone levels caused by low or
deficient TSH production.
• Sex hormones. These include testosterone in men and estrogen or
a combination of estrogen and progesterone in women.
• Growth hormone. 33Presented by: Prof.Mirza Anwar

3.Ischaemic necrosis (Simmond's disease):
• Simmonds disease is a chronic deficiency of function of the
pituitary gland, a form of hypopituitarism.
• Leads to atrophy of many of the viscera, including the heart,
liver, spleen, kidneys, thyroid, adrenals, and gonads.
• The disease results in emaciation and death if left untreated.
• The outcome depends on the extent of pituitary necrosis and
hormone deficiency.
• In severe cases, glucocorticoid deficiency may be life threatening
or fatal.
• When this condition is associated with severe haemorrhage
during or after childbirth it is known as Sheehan's syndrome and
in this situation the other effects are preceded by failure of
lactation.

4.Frohlich's syndrome:
• In this condition there is panhypopituitarism but the main
features are associated with deficiency of GH, FSH and LH.
• In children the effects are diminished growth,lack of sexual
development, obesity with distribution of fat and retarded mental
development.
• In a similar condition in adults, obesity and sterility are the main
features.
• It may be the result of a tumour of the anterior pituitary and/or
the hypothalamus but in most cases the cause is unknown.

5.Gigantism and acromegaly:
Hypersecretion of hGH during childhood causes
giantism, having following symptoms:
an abnormal increase in the length of long bones.
The person grows to be very tall, but body proportions are about
normal.
Hypersecretion of hGH during adulthood is acromegaly
Although hGH cannot produce further lengthening of the long bones
because the epiphyseal plates are already closed.
The bones of the hands, feet, cheeks, and jaws thicken
and other tissues enlarge.
In addition, the eyelids, lips, tongue, and nose enlarge, and the skin
thickens and develops furrows, especially on the forehead and soles

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6.Cushing’s syndrome:
Oversecretion most commonly involves ACTH leading to
Cushing’s syndrome
Features include:
Masculinization & amenorrhea in women, truncal obesity,
hypertension, osteoporosis, and polycythemia.
Patients are often obese and somnolent [feeling sleepy].
Exhibit fine, scanty [inadequate] hair, dry, soft skin.
Experience headaches, and visual defects progressing to
blindness.
Other signs and symptoms include polyuria, polyphagia, and a
subnormal body temperature.

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Postarior pitutary hormone deficiancy:
7.Diabetes Insipidus:
• Diabetes insipidus is a disorder of the posterior lobe of the
pituitary gland.
• ADH is deficient.
• Causes could be head trauma, brain tumor, or irradiation of
the pituitary gland, infections of the CNS (meningitis,
encephalitis, tuberculosis) or tumors (eg, metastatic disease,
lymphoma of the breast or lung).
• Another cause is failure of the renal tubules to respond to
ADH; this may be related to hypokalemia,hypercalcemia, and
a variety of medications (eg, lithium,Declomycin).

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• Enormous daily output of very dilute, water-like urine.
• Intense thirst: The patient drinks 2 to 20 liters of fluid daily.
• Fluid intake cannot be limited; otherwise the patient will
experience crave for fluid and would develop hypernatremia
and severe dehydration.
Clinical Manifestations:

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Treatment
• Desmopressin (DDAVP), a synthetic vasopressin.
• Intramuscular administration of ADH.
• Clofibrate, a hypolipidemic agent, has an antidiuretic effect.
• Chlorpropamide (Diabinese) and thiazide diuretics are used in
mild forms of the disease as they potentiate the action of
vasopressin.
• Thiazide diuretics and prostaglandin inhibitors (ibuprofen,
indomethacin, and aspirin) are used to treat the nephrogenic
form of the disease.

CONTROL OF METABOLISM
Metabolism is the sum of all chemical rxns in the body
Growth, repair, reproduction, maintenance and response are
all part of metabolism
Thyroid: Metabolic Control

Thyroid is located in front of the larynx
Thyroid converts Iodine to hormones T3
and T4 that control metabolism
Thyroxine
Triiodothyoronine

Background
brownish-red, highly vascular gland
Location: ant neck at C5-T1
Avg width: 12-15 mm (each lobe)
Avg height: 50-60 mm long
Avg weight: 25-30 g in adults (slightly more in
women)
**enlarges during menstruation and pregnancy**

The Thyroid Gland – Histology

Thyroid Follicles

Thyroid gland is controlled by the pituitary
Pituitary releases TSH (Thyroid Stimulating hormone)
which stimulates the creation of T3 and T4 in the thyroid
T4 presence negatively feeds back and decrease TSH
production

Thyroid Hormones
• There are two biologically active thyroid hormones:
- tetraiodothyronine (T4; usually called
thyroxine)
- triiodothyronine (T3)
• Derived from modification of tyrosine.

Differences between T4 and T3
• The thyroid secretes about 80 microg of T4, but only 5
microg of T3 per day.
• However, T3 has a much greater biological activity
(about 10 X) than T4.
• An additional 25 microg/day of T3 is produced by
peripheral monodeiodination of T4.
T4
thyroid
I-
T3

Why is Iodine Important in Thyroid Hormone
Production?
Thyroid hormones are unique biological molecules in that they
incorporate iodine in their structure.
Thus, adequate iodine intake (diet, water) is required for normal
thyroid hormone production.
Major sources of iodine:
- iodized salt
-iodated bread
- dairy products
- shellfish
Minimum requirement: 75 micrograms/day

Iodine Metabolism
• Dietary iodine is absorbed in the GI tract, then taken
up by the thyroid gland (or removed from the body by
the kidneys).
• The transport of iodide into follicular cells is
dependent upon a Na+/I- cotransport system.
• Iodide taken up by the thyroid gland is oxidized by
peroxide in the lumen of the follicle:
peroxidase
I- I+
• Oxidized iodine can then be used in production of
thyroid hormones.

The Next Step: Production of Thyroglobulin
• Pituitary produces TSH, which binds to follicle cell
receptors.
• The follicle cells of the thyroid produce
thyroglobulin.
• Thyroglobulin is a very large glycoprotein.
• Thyroglobulin is released into the colloid space,
where it’s tyrosine residues are iodinated by I+.
• This results in tyrosine residues which have one or
two iodines attached (monoiodotyrosine or
diiodotyrosine).

One Major Advantage of this System
• The thyroid gland is capable of storing many
weeks worth of thyroid hormone (coupled to
thyroglobulin).
• If no iodine is available for this period, thyroid
hormone secretion will be maintained.

Regulation of Thyroid Hormone Levels
• Thyroid hormone synthesis and secretion is
regulated by two main mechanisms:
- an “autoregulation” mechanism, which
reflects the available levels of iodine
- regulation by the hypothalamus and anterior
pituitary

Autoregulation of Thyroid Hormone
Production
• The rate of iodine uptake and incorporation into
thyroglobulin is influenced by the amount of
iodide available:
- low iodide levels increase iodine transport into
follicular cells
- high iodide levels decrease iodine transport into
follicular cells
Thus, there is negative feedback regulation of iodide
transport by iodide.

Effects of Thyroid Hormones on the
Cardiovascular System
Increase heart rate
Increase force of cardiac contractions
Increase stroke volume
Increase Cardiac output

Respiratory System
Increase resting respiratory rate
Increase minute ventilation
Increase ventilatory response to
hypercapnia and hypoxia

Renal System
Increase blood flow
Increase glomerular filtration rate

Effects Thyroid Hormones in Growth
and Tissue Development
Increase growth and maturation of bone
Increase tooth development and eruption
Increase growth and maturation of epidermis,hair
follicles and nails
Increase rate and force of skeletal muscle
contraction
Inhibits synthesis and increases degradation of
mucopolysaccharides in subcutaneous tissue

Biological role of thyroid hormones

Hypothyroidism: Underactive thyroid.
Decreased rate of Body Functions
Conditions: Myxoedema (adults), Cretinism (infants)
Hyperthyroidism: Overactive Thyroid, increased rate of body functions.
Contitions: Grave’s disease & Goitre
Disorders of the Thyroid Gland
Thyroid
hormone level

Hypo and Hyper thyroidism:

65
Hyperthyroidism (thyrotoxicosis)
1. Graves Disease (exophthalmic
goitre)
• Immune system creates antibodies
that stimulate the thyroid and cause
overproduction of thyroid hormones.
Symptoms:
•increased metabolic rates
•Increased size of thyroid gland
•Bulging of eyes (Exophthalmos)
•Treatment: 131I , removal of part or all
thyroid gland, antithyroidal drugs.

Graves Disease (exophthalmic goitre) contd:
accounts for 90% of cases of thyrotoxicosis.
There is diffuse swelling (hyperplasia)
Exophthalmos is due to the deposition of excess fat and fibrous
tissue behind the eyes.
In severe cases the eyelids may not completely cover the eyes
during blinking and sleep, leading to drying of the conjunctiva
and predisposing to infection. It does not occur in other forms
of thyrotoxicosis.

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2. Toxic nodular goitre:
➢In this condition one or two nodules of a gland that is already
affected by goitre become active and secrete excess T3 and T4
causing the effects of hyperthyroidism.
➢ It is more common in women than men and after middle age.
As this condition affects an older age group than Graves'
disease,arrhythmias and cardiac failure are more common.
➢Exophthalmos does not occur
in this type of hyperthyroidism.

Hyperthyroidism: Symptoms
• Increased Heart Rate
•Heat Sensitivity
•Eye Bulging (exopthalmos)
•Weight loss and fatigue in older individuals
Hyperthyroidism: Treatment
• Taking beta blockers to reduce heart rate
•Taking drugs that reduce T3/T4 production

Hypothyroidism
1. Myxedema
FACTS
•15% of Adults
•Women 2x more often than men
•Often caused by Pituitary malfunction
SYMPTOMS
•Dry Skin
•Facial Swelling
•Achy Joints, slow reflexes
•Weight Gain in adults
•Inability to tolerate cold
•Numbness
•Can cause Myxoedema coma in severe cases

70
Myxoedema contd:
Deficiency of T3 and T4 in adults results in an abnormally low
metabolic rate.
There may be accumulation of polysaccharide substances in the
subcutaneous tissues especially of the face.
The commonest causes are:
• autoimmune thyroiditis
• severe iodine deficiency
• iatrogenic, e.g. antithyroid drugs, surgical removal of thyroid
tissue, ionising radiation.

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2.Cretinism
Infantile hypothyroidism
This condition is endemic in areas remote from the sea where
the soil and diet are severely deficient in iodine.
In some cases there is congenital absence of the thyroid gland.
In both situations retarded physical growth and mental
development become evident within a few weeks or months of
birth.
Unless treatment begins early in life the individual remains
severely mentally retarded, has disproportionately short limbs, a
large protruding tongue,
coarse dry skin, poor abdominal
muscle tone .

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3.Simple goitre:
This is enlargement of the thyroid gland without signs of
hyperthyroidism. Secretion of T3 and T4 is reduced and the low
levels stimulate secretion of TSH resulting in hyperplasia of the
thyroid gland..
Causes are:
• persistent iodine deficiency
• genetic abnormality
• iatrogenic, e.g. antithyroid drugs, surgical removal of excess
thyroid tissue.

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Parathyroid Glands

PARATHYROID GLANDS:
•Small glands that sit on the thyroid and control the
CALCIUM levels in the blood
•Parathyroid responds directly to the concentration of
blood calcium

Histology of parathyroid gland:

Biological role of parathyroid gland
hormones:

NEGATIVEFEEDBACK

Disorders of the parathyroid
glands
• Hyperparathyroidism (hypercalcemia)
• Hypoparathyroidism (hypocalcemia)

Hyperparathyroidism
1. Primary: commonly a benign tumor; increased
PTH secretions
2. Secondary: compensatory to a conditions that
causes hypocalcemia ( the main stimulus to
increased PTH secretion), eg; vitamin D
deficiency, Corticotropin releasing factor (CRF)
3. Tertiary: hyperplasia of parathyroid glands
leading to automatic PTH secretion by the
parathyroid gland.

Hyperparathyroidism
• Major signs and symptoms: depression,
fatigue, loss of appetite, constipation,
osteoporosis, fractures, kidney stones.
• Daignosis: bone x-rays, Ca & PTH levels.
• Treatment: decrease high serum levels,
surgical removal of parathyroid

Hyperparathyroidism:
Nonsurgical Treatment
1. Close follow up
2. Active lifestyle.
3. Dietary measures
4. Drugs
a. Phosphorus supplementation
b. Biphospahtes (Fosamax) – inhibit bone resorption of Ca to
normalize Ca serum levels
c. Oral phosphate –inhibit Vit D effects
d. Diuretics
e. Calcimimetic agent : increase sensitivity of calcium receptor
on parathyroid gland thus decreased PTH secretion and
serum Ca levels 8181Presented by: Prof.Mirza Anwar

Common Medications used in
Hyperparathyroidism
• Phosphorus
• Biphosphates
• Estrogen or progestin
• Oral phosphate

Signs that indicate calcium levels
are abnormal
• Trousseau’s sign: temporarily occlude arterial
blood flow (with BP cuff inflated) above the
normal systolic pressure. A Trousseau”s sign
occurs when the hand and fingers contract from
ischemia
• Chvostek’s sign: Sign is + when nose, eye, lip
& facial muscles twitch

Hypoparathyroidism
• Results from abnormally low levels of PTH,
low Ca level
• Symptoms: painful spasms of face, hands,
arms, and feet; seizures
• Treatment: IV Calcium; Cal Mag & vit D;

Adrenal gland:

What is adrenal gland?
❖ Location: Lies superior to each kidney in the retroperitoneal
space.
❖ Shape: Have a flattened pyramidal shape.
❖ Dimensions: 3–5 cm in height, 2–3 cm in width, and a little less
than 1 cm thick, with a mass of 3.5–5 g.
❖ Regions: Differentiate into two structurally and functionally
distinct regions: a large, peripherally located adrenal cortex,
comprising 80–90% of the gland, and a small, centrally located
adrenal medulla.
❖ Hormones : The adrenal cortex produces steroid hormones that
are essential for life.
❖ The adrenal medulla produces three catecholamine hormones—
norepinephrine, epinephrine, and a small amount of dopamine.
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Histology:

Mineralocorticoids
• Aldosterone is the major mineralocorticoid.
• It regulates homeostasis of two mineral ions, namely sodium
ions (Na) and potassium ions (K), and helps adjust blood
pressure and blood volume.
• Aldosterone also promotes excretion of H+ in the urine; this
removal of acids from the body can help prevent acidosis (blood
pH below 7.35).
• The renin–angiotensin–aldosterone or RAA pathway
controls secretion of aldosterone.
88

The renin–angiotensin–aldosterone or RAA pathway

Negative feedback :

Glucocorticoids
o Glucocorticoids regulates metabolism and resistance to stress.
o It include cortisol (hydrocortisone), corticosterone, and cortisone.
o Cortisol is the most abundant, accounting for about 95% of glucocorticoid
activity.
o Control of glucocorticoid secretion occurs via a typical negative feedback
system.
o Low blood levels of glucocorticoids, mainly cortisol, stimulate neurosecretory
cells in the hypothalamus to secrete corticotropin-releasing hormone
(CRH).
CRH promotes the release of ACTH from the anterior pituitary.
o ACTH flows in the blood to the adrenal cortex, where it stimulates
glucocorticoid secretion.
o A variety of physical and emotional stresses causes release of CRH from
hypothalamus which in turn increases release of ACTH and glucocorticoids.
91

Actions of Glucocorticoids:
1. Protein breakdown.
2. Glucose formation.
3. Lipolysis.
4. Resistance to stress. The additional glucose supplied by the liver cells provides
tissues with a ready source of ATP to combat a range of stresses.
5. Anti-inflammatory effects.
Glucocorticoids inhibit white blood cells that participate in inflammatory
responses. Unfortunately, glucocorticoids also retard tissue repair, and as a result,
they slow wound healing. Although high doses can cause severe mental
disturbances, glucocorticoids are very useful in the treatment of chronic
inflammatory disorders such as rheumatoid arthritis.
6. Depression of immune responses.
High doses of glucocorticoids depress immune responses. For this reason,
glucocorticoids are prescribed for organ transplant recipients to retard tissue
rejection by the immune system
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Androgens
o In both males and females, the adrenal cortex secretes small amounts of weak
androgens.
o The major androgen secreted by the adrenal gland is dehydroepiandrosterone
(DHEA) .
o After puberty in males, the androgen testosterone is also released in much greater
quantity by the testes.
o Thus, the amount of androgens secreted by the adrenal gland in males is usually so
low that their effects are insignificant.
o In females, however, adrenal androgens play important roles. They promote libido
(sex drive) and are converted into estrogens (feminizing sex steroids) by other body
tissues.
o After menopause, when ovarian secretion of estrogens ceases, all female estrogens
come from conversion of adrenal androgens.
o Adrenal androgens also stimulate growth of axillary and pubic hair in boys and girls
and contribute to the prepubertal growth spurt.
o Although control of adrenal androgen secretion is not fully understood, the main
hormone that stimulates its secretion is ACTH.
93

Principal actions:

Adrenal Gland Disorders
1. Cushing’s Syndrome
• Hypersecretion of cortisol by the
adrenal cortex.
• Causes include a tumor of the adrenal
gland that secretes cortisol, or a tumor
elsewhere that secretes
adrenocorticotropic hormone
(ACTH), which in turn stimulates
excessive secretion
of cortisol.
• The condition is characterized by
breakdown of muscle proteins and
redistribution accompanied by a
rounded “moon face,” “buffalo
hump” on the back, and pendulous
(hanging) abdomen.
• Facial skin is flushed, and the skin
covering the abdomen develops
stretch marks and wound healing is95

Signs and symptoms
• Fatty hump between the shoulders, a rounded face and pink or
purple stretch marks.
• Whole body: excess sweating, excessive hairiness, excessive
hunger, fatigue, flushing, high blood pressure, or osteoporosis
• Skin: abnormal pad of fat between the shoulder blades, acne,
darkening of the skin, stretch marks, or thinning.
• Muscular: muscle weakness or loss of muscle
• Also common: anxiety, depression, easy bruising, hair loss,
headache, infertility, insomnia, irritability, pot belly, reduced sex
drive, round face from gradual swelling, swelling in extremities,
or weight gain

Cushing’s Syndrome contd;
The elevated level of cortisol causes hyperglycemia,
osteoporosis, weakness, hypertension, increased
susceptibility to infection, decreased resistance to stress,
and mood swings.
People who need long-term glucocorticoid therapy—for
instance, to prevent rejection of a transplanted organ—may
develop a cushinoid appearance.

Treatment
• Treatment options include reducing steroid use, surgery,
radiation and medication.
1. Self-care
2. Reducing steroids
• Decreases the risk of side effects related to steroids.
3. Surgery
4. Removal of steroid producing tumor
5. Transsphenoidal surgery
• Surgery performed through the nose and sinus cavity to
remove brain tumours.

2. Addison’s Disease
• Hyposecretion of glucocorticoids and aldosterone causes
Addison’s disease (chronic adrenocortical insufficiency).
• The majority of cases are autoimmune disorders in which
antibodies cause adrenal cortex destruction or block binding of
ACTH to its receptors.
• Pathogens, such as the bacterium that causes tuberculosis, also
may trigger adrenal cortex destruction.
• Symptoms, which typically do not appear until 90% of
the adrenal cortex has been destroyed, include mental
lethargy,anorexia, nausea and vomiting, weight loss,
hypoglycemia, and muscular weakness. 99Presented by: Prof.Mirza Anwar

Addisons disease contd:
Loss of aldosterone leads to elevated potassium and
decreased sodium in the blood, low blood pressure,
dehydration, decreased cardiac output, arrhythmias, and
even cardiac arrest.
The skin may have a “bronzed” appearance that often is
mistaken for a suntan.
Treatment consists of replacing glucocorticoids and
mineralo-corticoids and increasing sodium in the diet.

3. Pheochromocytomas
Usually benign tumors of the chromaffin cells of the adrenal
medulla.
Cause hypersecretion of epinephrine and norepinephrine.
The result is a prolonged version of the fight-or-flight
response: rapid heart rate, high blood pressure, high levels of
glucose in blood and urine, an elevated basal metabolic rate
(BMR), flushed face, nervousness, sweating, and decreased
gastrointestinal motility.
Treatment is surgical removal of the tumor.

Pancreas
❖ The pancreas is both an endocrine gland (duct less, secretes secretions
directly in blood) and an exocrine gland (secretes secretion through ducts on
epithelial surface).
❖ Shape : A flattened organ that measures about 12.5–15 cm (4.5–6 in.) in
length.
❖ Location : located in the curve of the duodenum, the first part of the
small intestine.
❖ Parts: Consists of a head, a body, and a tail
❖ Major cells:
a) Acini (Clustered cells- 99% of total cells) produce digestive enzymes,
which flow into the gastrointestinal tract through a network of ducts.
b) Pancreatic islets or islets of Langerhans: 1–2 million tiny clusters of
endocrine tissue scattered among the exocrine acini .
❖ Abundant capillaries serve both the exocrine and endocrine portions
of the pancreas.
102

Cell Types in the Pancreatic Islets
• Each pancreatic islet includes four types of hormone-secreting cells:
1. Alpha or A cells (about 17% of pancreatic islet cells) and secrete glucagon
( Raises Blood glucose level)
2. Beta or B cells (about 70% of pancreatic islet cells) and secrete insulin
(Decrease blood glucose level)
3. Delta or D cells (about 7% of pancreatic islet cells) and secrete somatostatin
(Inhibit insulin and glucagon release, slows absorption of nutrients from
GIT)
4. F cells (about 6% of pancreatic islet cells) secrete pancreatic polypeptide.
(inhibits somatostatin secretion, gallbladder contraction, and secretion of
digestive enzymes by the pancreas)
103

Pancreas
104

Control of plasma glucose level:
105
Presented by: Prof.Mirza
Anwar Baig,AIKTC's
SOP,New Panvel

Biological role of pancreatic horomones:

Biological role of pancreatic
horomones:

Disorders of pancreatic hormones:
1. Type I, insulin-dependent diabetes mellitus (IDDM)
This occurs mainly in children and young adults and the onset is usually
sudden.
The deficiency or absence of insulin is due to the destruction of -islet cells.
The causes are unknown but there is a familial tendency, suggesting genetic
involvement.
In many cases an auto-immune reaction has occurred in which autoantibodies
to -islet cells are present.
Antibodies to viruses are present in some cases and these may destroy the [3-
islet cells directly or by an autoimmune mechanism.

2. Type II, non-insulin-dependent
diabetes mellitus (NIDDM)
This is the most common form of diabetes, accounting for about
90% of cases.
Most patients are obese and it tends to develop in women over 75
years and men over 65 years.
The cause is unknown. Insulin secretion may be below or above
normal.
Deficiency of glucose inside body cells may occur when there is
hyperglycaemia and a high insulin level.
This may be due to changes in cell membranes which block the
insulin-assisted movement of glucose into cells (insulin
resistance).

Pineal gland
• Location: A small endocrine gland attached to the roof of the third ventricle of
the brain at the midline .
• Weight: It has a mass of 0.1–0.2 g, and is covered by a capsule formed by the
pia mater.
• Cells: The gland consists of masses of neuroglia and secretory cells
called pinealocytes.
• Secretions: The pineal gland secretes melatonin, an amine hormone derived
from serotonin.
• In response to visual input from the eyes (retina) suprachiasmatic nucleus
stimulates sympathetic postganglionic neurons of the superior cervical ganglion
stimulate the pinealocytes of the pineal gland to secrete melatonin.
110

Functions:
• Biological Clock: Melatonin appears to contribute to the setting of the
body’s biological clock, which is controlled by the suprachiasmatic
nucleus of the hypothalamus.
• Promote sleepiness: As more melatonin is liberated during darkness than
in light, this hormone is thought to promote sleepiness.
• Small doses of melatonin given orally can induce sleep and reset daily
rhythms, which might benefit workers whose shifts alternate between
daylight and nighttime hours.
• Antioxidants: Melatonin also is a potent antioxidant that may provide
some protection against damaging oxygen free radicals.
111

Disorders of pineal gland
• Hyposecretion:
Results in insomnia, abnormal
thyroid function, anxiety,
intestinal hyperactivity, and menopause.
• Hypersecretion:
May cause low blood pressure, Seasonal Affective Disorder,
abnormal adrenal functions.
112
Ref: https://www.shutterstock.com/s/earchinsomnia

Prominent pineal gland disorders
❖ Disorders that affect sleep and mood
pineal gland dysfunction is disturbance in circadian rhythms.
• Sleeping too much or little or feeling active or restless in the night due to
abnormal pineal gland function.
• Furthermore, one study shows that the pineal gland releases several other
chemicals that cause depression, schizophrenia, or mental illness.
❖ Pineal Gland Tumors
• Pineal gland tumors are the most severe complication and account for one
percent of total brain tumors.
• Research shows that almost seventeen types of tumors arise in the pineal gland
area, but most of them are benign.
•
113
Ref: https://human-memory.net/pineal-gland/

Pineal gland tumor contd..
❖ The most common type is a germ cell tumor, which develops from residual
embryonic tissue in the gland.
❖ Other tumors include gliomas and pineal cell tumors.
❖ The pineal gland is situated near a duct called aqueduct of Sylvius.
❖ Pineal tumors block this duct (route of Cerebrospinal fluid and buildup the
pressure that expands the ventricles within the skull).
❖ This blockage will cause more complications such as
• Seizures
• Nausea
• Headache
• Visual changes
• Problems with memory recall
• Parinaud syndrome (inability to move the eyes upwards)
114
Ref: https://human-memory.net/pineal-gland

❖ Pineal Cysts:
• It happen in 10% of people who are undergone MRI scans or
CT.
• However, most people do not have any visible symptoms of
pineal cysts. Some patients rarely experience headache and
abnormal eye movements.
• Pineal cysts lead to seizures, sleep issues, and emotional
disturbances.
• Surgical removal is recommended for the removal of pineal
cysts.
115
Ref: https://human-memory.net/pineal-gland

Thymus gland
• Location: The thymus is located behind the sternum between the lungs.
• Size: In infants, the mass of about 70g .
By the time a person reaches maturity, the gland has atrophied considerably,
and in old age it may weigh only 3g .
• Secretion: The hormones produced by the thymus—thymosin, thymic
humoral factor (THF), thymic factor (TF), and thymopoietin—promote
the maturation of T cells (a type of white blood cell that destroys microbes
and foreign substances) and may retard the aging process.
116

Compiled by: Prof. Anwar Baig-
AIKTC-SOP
Thymus gland:

AIKTC-SOP
Thymus
• Capsule: separates the two lobes
• Trabeculae: Extensions of the capsule, penetrate inward and divide each
lobe into lobules
• Cortex: Immature T cells (pre-T cells) migrate from red bone marrow to
the cortex of the thymus, where they proliferate and begin to mature.
• Composed of
1. Dendritic cells: derived from monocytes, assist the maturation
process.
2. Epithelial cells help “educate” the pre-T cells in a process known as
positive selection. Additionally, they produce thymic hormones that are
thought to aid in the maturation of T cells. Only about 2% of developing T
cells survive in the cortex. The remaining cells die via apoptosis
(programmed cell death).
3. Thymic macrophages: clear out the debris of dead and dying cells.
The surviving T cells enter the medulla.

AIKTC-SOP
The medulla:
Consists of
1. Mature T cells
2. Epithelial cells
3. Dendritic cells
4. Macrophages
5. Thymic (Hassall’s) corpuscles.
Some of the epithelial cells become arranged into concentric
layers of flat cells that degenerate and become filled with
keratohyalin granules and keratin. may serve as sites of T cell
death in the medulla.
T cells that leave the thymus via the blood migrate to lymph
nodes, the spleen, and other lymphatic tissues where they
colonize parts of these organs and tissues.

Disorders of Thymus Gland
• The most common thymus diseases are
– Myasthenia gravis (MG)
– Pure red cell aplasia (PRCA)
– Hypogammaglobulinemia
Myasthenia gravis (MG):
• It occurs when the thymus is abnormally large and produces antibodies that
block or destroy the muscles' receptor sites.
• This causes the muscles to become weak and easily tired.
• Medications may be prescribed that help the communication between nerves
and muscles, such as pyridostigmine (Mestinon). Corticosteroids like
prednisone or immunosuppressants, such as azathioprine (Imuran), may be
used to inhibit the immune system.
120
Ref: https://www.livescience.com/62527-thymus.html

Disorders of Thymus Gland
❖ Pure red cell aplasia:
• Body’s own immune cells attacks blood-forming stem cells.
• This can happen when the thymus has a tumor.
• Blood transfusions to increase red blood cell levels, corticosteroids and
immunosuppressive therapy can all be treatments for this condition.
❖ Hypogammaglobulinemia:
• A disorder where the body doesn't produce enough antibodies.
❖ Thymus cancer:
• It is a disease in the thymus, rather than one caused by the thymus, like the previous
examples.
• Symptoms may include shortness of breath, cough (which may bring up bloody
sputum), chest pain, trouble swallowing, loss of appetite and weight loss, headaches,
swelling of head face or neck, a bluish color to the skin and dizziness.
• Thymus cancer is treated with surgery, radiation therapy or chemotherapy. This
cancer is typically malignant in about 35 percent of cases.
121

References:
• Principles of Anatomy and Physiology by
Tortora Grabowski. Palmetto, GA, U.S.A.
• Ross & Wilson Anatomy and Physiology in
Health and Illness 12th Ed
122

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