this is a brief talk about the endocrine system. i couldnt tell in detail about that topic

1. Welcome to Our Presentation

2. Endocrine System
Group members Student id
1.Ishrat jahan jui 11915026
2.Sayed bin mamun 11915030
3.Gazi mehedi hasan rakib 11915034
4.Ramim mia 11915036
5. Reza at tanzil 11915037

3. Content
Pituitary glands
Thyroid glands
Parathyroid glands
Adrenal cortex
Adrenal medulla
Islets of langerhans

4. Pituitary gland
• The master gland
• The pituitary gland is called the “master
gland” because its hormones regulate other
important endocrine glands—including the
adrenal, thyroid, and reproductive glands
(e.g., ovaries and testes)—and in some cases
have direct regulatory effects in major tissues,
such as those of the musculoskeletal system.

5. • Anatomy
• Location
• Lies at the base of brain sella turcica.
• Connected with the hypothalamus by the
pituitary stalk or hypophyseal stalk.
• Devision
• Anterior lobe ( adenohypophysis)
• Intermediate lobe ( not present or very small in
humans dispersed within anterior lobe)
• • Posterior lobe ( neurohypophysis)

6. Anterior and posterior pituitary are situated in
very approximate position. But they are entirely
different in their :
• Structure
• Funcition

7. Anterior pituitary ( adenohypophysis)
• Consists of three devisions
1. Pars distalis
2. Pars tuberalis
3. Pars intermedia
Posterior pituitary
• Consist of two parts
1.Infundibular stalks
2.Pars nervosa

8. • Pituitary hormone secretion
Secretory hormones of anterior pituitary

9. Hormone Target organ Principal effect
FSH - Follicle stimulating hormone Ovaries, testes  Female : Growth of ovarian follicles
and secretion of estrogen hormone.
 Male : Sperm production.
LH - Luteinizing hormone Ovaries, testes  Female : Ovulation , maintenance
of corpus luteum .
 Male : Testosterone secretion.
TSH - Thyroid stimulating hormone Thyroid gland Growth of thyroid, secretion of
hormone
ACTH - Adrenocorticotropic hormone Adrenal cortex Secretion of glucocorticoids,
growth of adrenal cortex.
Prolactin Mammary glands, testes  Female : Milk synthesis.
 Male : Increased LH sensitivity and
testosterone secretion.
GH - Growth hormone Liver Somatostatin secretion and
widespread growth of tissues.

10. Secretory hormones of posterior
pituitary
Hormones Target organ Principal effects
ADH - Antidiuretic hormone Kidneys Water retention
OT - Oxytocin Uterus, mammary glands Female : labour contractions, milk release.
Male : possibly invovled in ejaculation, sperm
transport and sexual affection.

11. Pituitary gland disorders
Causes of disorders of pituitary gland
• Hyperactivity
• Hypoactivity
Hyperpituitarism
• Hyperfunctioning of anterior pituitary gland -
• Gigantism and acromegaly
• Hyperfunctioning of posterior pituitary gland -
• In appropriate release of ADH

12. Hypopituitarism
• Hypofunctioning of anterior pituitary
• Dwarfism.
• Hypofunctioning of posterior pituitary
• Diabetes insipidus

13. Gigantism
Characterized signs and symptoms :
• - Excess Growth of body
• - Average height is approximately 7-8 feet
• - Headache due to tumor of pituitary
• - Hyperglycemia, visual disturbance and pituitary
diabetes mellitus.
• Cure : Gigantism can be cured by hypopituitarism
( burning cells of anterior pituitary)

15. Acromegaly
Characterised symptom & causes
• - Enlargement, thickening amd broadening of
bones.
• - particularly extremities of the body.
• - Hypersecretion of growth hormone, thyroid,
parathyroid hormone.
• - Hypertension, headache amd visual disturbance
are seen.
• Cure : as like as gigantism.

16. Dwarfism
Deficiency of growth hormone in children
before growth is completed resulting retarted
growth.
• short stature.

17.  Thyroid gland
The thyroid gland is a butterfly-shaped gland located at the base
of the base of the neck and wrapped around the lateral sides of
the trachea.
The thyroid gland produces 3 major hormones:
• Calcitonin: Reduce the concentration of calcium ions in the
blood by aiding the absorption of calcium into the matrix of
bones.
• Triiodothyronine (T3)
• Thyroxine (T4)
The hormones T3 and T4 work together to regulate the body’s
metabolic rate. Increased levels of T3 and T4 lead to increased
cellular activity and energy usage in the body.

19.  Thyroid Hormone Synthesis
There are six steps in the synthesis of thyroid hormone-
• Active transport of Iodide into the follicular cell via
Sodium-Iodide Symporter (NIS). This is actually
secondary active transport, and the sodium gradient
driving it is maintained by a Sodium-Potassium ATPase.
• Thyroglobulin (Tg), a large protein rich in Tyrosine, is
formed in follicular ribosomes and placed into secretory
vesicles.
• Exocytosis of Thyroglobulin into follicle lumen, where it
is stored as colloid. Thyroglobulin is the scaffold upon
which thyroid hormone is synthesised.

20. • Iodination of the Thyroglobulin. Iodide is made reactive by
the enzyme thyroid peroxidase. Iodide binds to the benzene
ring on Tyrosine residues of Thyroglobulin. First formed is
monoiodotyrosine (MIT) then diiodotyrosine (DIT).
• Coupling of MIT and DIT to give Triiodothyronine (T3)
hormone and coupling of DIT and DIT to give
Tetraiodothyronine (T4) hormone, also known as
Thyroxine.
• Endocytosis of iodinated thyroglobulin back into the
follicular cell. Thyroglobulin undergoes proteolysis in
lysosomes to cleave the iodinated tyrosine residues from the
larger protein. Free T3 or T4 is then released, and the
Thyroglobulin scaffold is recycled.

21.  Secretion of thyroid hormone-
• Thyroid hormones are released as part of a hypothalamic-
pituitary-thyroid axis. The Hypothalamus detects a low
plasma concentration of thyroid hormone and releases
Thyrotropin-Releasing Hormone (TRH) into the
hypophyseal portal system.
• TRH binds to receptors found on thyrotrophic cells of the
anterior pituitary gland, causing them to release Thyroid
Stimulating Hormone (TSH) into the systemic circulation.
TSH binds to TSH receptors on the basolateral membrane
of thyroid follicular cells and induces the synthesis and
release of thyroid hormone.

22.  Function-
The thyroid gland is one of the main regulators of metabolism.
T3 and T4 typically act via nuclear receptors in target tissues
and initiate a variety of metabolic pathways. High levels of
them typically cause these processes to occur faster or more
frequently.
Metabolic processes increased by thyroid hormones include:
• Basal Metabolic Rate
• Gluconeogenesis
• Glycogenolysis
• Protein synthesis
• Lipogenesis
• Thermogenesis

23.  Thyroid Conditions-
• Goiter: A general term for thyroid swelling. Goiters can be harmless, or
can represent iodine deficiency or a condition associated with thyroid
inflammation called Hashimoto’s thyroiditis.
• Thyroiditis: Inflammation of the thyroid, usually from a viral infection
or autoimmune condition. Thyroiditis can be painful, or have no
symptoms at all.
• Hyperthyroidism: Excessive thyroid hormone production.
Hyperthyroidism is most often caused by Graves disease or an
overactive thyroid nodule.
• Hypothyroidism: Low production of thyroid hormone. Thyroid damage
caused by autoimmune disease is the most common cause of
hypothyroidism .

24. • Graves disease: An autoimmune condition in which the
thyroid is overstimulated, causing hyperthyroidism.
• Thyroid cancer: An uncommon form of cancer, thyroid
cancer is usually curable. Surgery, radiation, and hormone
treatments may be used to treat thyroid cancer.
• Thyroid nodule: A small abnormal mass or lump in the
thyroid gland. Thyroid nodules are extremely common. Few
are cancerous. They may secrete excess hormones, causing
hyperthyroidism, or cause no problems.
• Thyroid storm: A rare form of hyperthyroidism in which
extremely high thyroid hormone levels cause severe illness

25.  Thyroid function tests-
• Thyroid function tests are a series of blood tests used to
measure how well your thyroid gland is working. Available
tests include the T3, T3RU, T4, and TSH.

26.  T4 & TSH results-
• The T4 test and the TSH test are the two most common thyroid function tests.
They’re usually ordered together.
• The T4 test is known as the thyroxine test. A high level of T4 indicates an
overactive thyroid (hyperthyroidism). Symptoms include anxiety, unplanned
weight loss, tremors, and diarrhea. Most of the T4 in your body is bound to
protein. A small portion of T4 is not and this is called free T4. Free T4 is the
form that is readily available for your body to use. Sometimes a free T4 level
is also checked along with the T4 test.
• The TSH test measures the level of thyroid-stimulating hormone in your
blood. The TSH has a normal test range between 0.4 and 4.0 milli-
international units of hormone per liter of blood (mIU/L).
• .

27. • If you show signs of hypothyroidism and have a TSH reading
above 2.0 mIU/L, you’re at risk for progressing to
hypothyroidism. Symptoms include weight gain, fatigue,
depression, and brittle hair and fingernails. Your doctor will
likely want to perform thyroid function tests at least every
other year going forward. Your doctor may also decide to
begin treating you with medications, such as levothyroxine, to
ease your symptoms.
• Both the T4 and TSH tests are routinely performed on
newborn babies to identify a low-functioning thyroid gland. If
left untreated, this condition, called congenital
hypothyroidism, can lead to developmental disabilities.

28.  T3 result-
• The T3 test checks for levels of the hormone triiodothyronine.
It’s usually ordered if T4 tests and TSH tests suggest
hyperthyroidism. The T3 test may also be ordered if you’re
showing signs of an overactive thyroid gland and your T4 and
TSH aren’t elevated.
• The normal range for the T3 is 100–200 nanograms of
hormone per deciliter of blood (ng/dL). Abnormally high
levels most commonly indicate a condition called Grave’s
disease. This is an autoimmune disorder associated with
hyperthyroidism.

29. Parathyroid Gland

30. Organisation
• 4 tiny parathyroid glands, in the neck, on the posterior surface
of the thyroid gland. Have 2 supiriorly & 2 infiriorly.
• Small in size, measuring about 6 mm long,
3 mm wide and 2 mm thick with dark brown colour

32. Histology
➤ Made up of chief cells & oxyphil cells
• Chief cells
➤ secrate parathormone
• Oxyphil cells
➤ degenerated chief cells and their function is
unknown
➤ may secrate parathormone during physiological
condition called parathyroid adenoma

33. Parathormone
➤ secreted by the chief cells of the parathyroid glands
➤ essential for the maintenance of blood calcium
level within a very narrow critical level
➤ maintenance of blood calcium level is necessary
because calcium is an inorganic ion for many
physiological functions

34. ➤ Chemistry
➤ Parathormone is protein in nature, having
84 amino acids
➤ It’s Molecular weight in 9,500
➤ Half life & Plasma level
➤ Parathormone has a half-life of 10 minutes
➤ Normal plasma level of PTH is about 1.5-5.5 mg/dL

35. Actions of PTH on Blood Calcium Level
➤ Primary action of the PTH is to maintain the blood calcium
level within the critical range of 9-11 mg/dL
➤ PTH control blood calcium level by
1. Reabsorption of Ca from Bones
2. Reabsorption of Ca from renal tubules (Kidney)
3. Absorption of Ca from Gastrointestinal tract

36. ➤ On bones
> PTH enhances the reabsorbtion of Ca from the bones by acting
on osteoblasts and osteoclasts of the bone
> Increase the number and activity of osteoclasts (bone destroying cells).
> Increased collagen synthesis
> Increased alkaline phosphatase activity
> Increased local growth factors: IGF and transforming factors

37. ➤ On Kidney
> PTH increases the reabsorbtion of Ca from the renal
tubules along with magnesium ions and hydrogen ions
> Increases Ca reabsorbtion mainly from distal convoluted tubule
and proximal part of collecting duct
> PTH also increases the formation of 1, 25-di-hydroxycholecalciferol
(activated form of vitamin D) from 25-hydroxycholecalciferol
in kidneys
> Decreased phosphate, sodium and bicaronate reabsorbtion from
the proximal tubule

38. ➤ On Gastrointestinal Tract
> PTH increases the absorption of Ca ions from
the GI tract indirectly.
> The activated vitamin D is very essential for the
absorption of Ca from the GI tract
> PTH also increase the absorption of PO4 & mg

39. Role of Ca ion in regulating 1,25-Dihydroxycholecalciferol
> When blood Ca level Increases, it inhibits the formation of 1,25-
Dihydroxycholecalciferol. The mechanism involved in the inhibition
of the formation of 1,25-Dihydroxycholecalciferol as folows
• Increase in Ca ion concentration directly suppresses of
25-Dihydroxycholecalciferol into 1,25-Dihydroxycholecalciferol
• Increase in Ca ion concentration decreases the PTH secretion
which in turn suppresses the convertion of
25-Dihydroxycholecalciferol into 1,25-Dihydroxycholecalciferol

40. Blood level of Calcium
• Increase in blood calcium level decreases PTH secretion
• Parathormone secretion is inversely proportional to blood
calcium level
• Conditions when PTH secretion decreases are :
> excess quantities of calcium in the diet
> increased vitamin D in the diet
> increased reabsorbtion of Ca from the bones

42. Disorders
of
Parathyroid Gland

43. Hypoparathyroidism
➤ Characterized by:
– Hypocalcaemia
– Increase neuro-muscular excitability (tetany)
➤ Mechanism:
➤ Decrease plasma Ca2+ ions < 9 mg/dl
– Increase the excitability of Nervous system due to
• ↑ neuronal membrane permeability to Na+
– Hyperexcitable nerve fibres, spontaneously initiate nerve impulses to peripheral sk ms
– thus eliciting tetanic contraction.

44. Tetany
• Manifested by ↑ed neuromuscular excitability due to ↓ plasma ionized Ca2+
Causes:
a) Hypoparathyroidism
b) Alkalaemia, decrease the solubility product of Ca2+& PO4 and leads to
• reduced ionized Ca2+.
• precipitation of CaPO4;

45. c) Decreased Ca2+ absorption from the intestine:
– 1. Low calcium intake.
– 2. Excess intake of antiacids (peptic ulcer) lead to Ca2+ precipitation and decreased
absorption.
– 3. Steatorrhea (fatty diarrhea), where Ca2+ is lost in stools.0

46. Manifestation of Tetany
• These depend on the degree of ↓ed blood Ca2+ level:
1. Manifest tetany:
– Blood Ca2+ level is below 7 mg% (N 9-11 mg%).
– Muscular spasms in the hands and feet (Carpo-pedal spasm).
2. Latent tetany:
– Blood Ca2+ level is at 7-9 mg%,
– Muscle spasms only occur when the patient is exposed to stress.

47. Treatment of Tetany
1. IV injection of Ca2+ gluconate during ms spasm.
stops immediately the tetanic spasms.
2. Calcium level is then maintained by:
– giving vitamin D and administration of oral calcium.
3. Acidifying salts as ammonium chloride
– help Ca2+ absorption as they increase the ionization of Ca2+.

48. • 4. In hypoparathyroidism:
• Repeated administration of parathormone leads to
– formation of antihormone which antagonizes its action.
• A synthetic steroid ‘dihydrotachysterol (or AT 10)’
– Has similar effects as parathormone and vitamin D,
– Not produce antihormone.

49. Islets of Langerhans
of
Pancreas

50. Pancreas
• A triangular gland, which has both exocrine and endocrine cells, located behind the
stomach
• Strategic location
• Acinar cells produce an enzyme-rich juice used for digestion (exocrine product)
• Pancreatic islets (islets of Langerhans) produce hormones involved in regulating
fuel storage and use.

52. Islets of Langerhans
• 1 million islets
• 1-2% of the pancreatic mass
• Beta (β) cells produce insulin
• Alpha (α) cells produce glucagon
• Delta (δ) cells produce somatostatin
• F cells produce pancreatic polypeptide

54. Insulin
• Hormone of nutrient abundance
• A protein hormone consisting of two amino
acid chains linked by disulfide bonds
• Synthesized as part of proinsulin (86 AA) and
then excised by enzymes, releasing functional
insulin (51 AA) and C peptide (29 AA).

55. Insulin Structure
1- Large polypeptide 51 AA (MW 6000)
2- Tow chains linked by disulfide bonds.
A chain (21 AA)
B chain (30 AA)
3- disulfide bonds.

57. Regulation of Insulin Secretion
• No insulin is produced when plasma glucose below 50 mg/dl
• Half-maximal insulin response occurs at 150 mg/dl
• A maximum insulin response occurs at 300 mg/dl
• Insulin secretion is biphasic:
– Upon glucose stimulation– an initial burst of
secretion (5-15 min.)
– Then a second phase of gradual increment that
lasts as long as blood glucose is high

58. Insulin secretion is biphase

59. Insulin Action on Cells
• Insulin is the hormone of abundance.
• The major targets for insulin are:
– liver
– Skeletal muscle
– adipose tissue
• The net result is fuel storage

60. Insulin Action on Carbohydrate Metabolism
Liver:
• Stimulates glucose oxidation
• Promotes glucose storage as glycogen
• Inhibits glycogenolysis
• Inhibits gluconeogenesis
Muscle:
• Stimulates glucose uptake (GLUT4)
• Promotes glucose storage as glycogen

61. Adipose Tissue:
• Stimulates glucose transport into adipocytes
• Promotes the conversion of glucose into
triglycerides and fatty acids

62. Glucagon
• A 29-amino-acid polypeptide hormone that is a
potent hyperglycemic agent
• Produced by α cells in the pancreas
• Its major target is the liver, where it promotes:
– Glycogenolysis – the breakdown of glycogen to
glucose
– Gluconeogenesis – synthesis of glucose from lactic
acid and noncarbohydrates
– Release of glucose to the blood from liver cells

63. Physiological Action of Glucagon
• Stimulates glycogenolysis, gluconeogenesis &
inhabits glycogenesis
• Promotes lepolysis & ketogenesis
• Increases calorigenesis

64. Somatostatin
• Secreted from D cells of pancreas
• Also secreted from hypothalamus & GIT
• A peptide hormones with 2 forms, one with
14 AAs & the other with 28 Aas
Functions
➤ inhibits secretion of insulin & glucagon
➤ inhibits GI motility & GI secretions
➤ regulates feedback control of gastric emptying

65. Diabetes Mellitus (DM)
• A serious disorder of carbohydrate metabolism
• Results from hyposecretion or hypoactivity of insulin
• The three cardinal signs of DM are:
– Polyuria – huge urine output
– Polydipsia – excessive thirst
– Polyphagia – excessive hunger and
food consumption

66. Diabetes Mellitus Type l
Type 1: beta cells destroyed- no
insulin producedchronic
fasted state, "melting flesh",
ketosis, acidosis,
glucosurea, diuresis & coma

67. Diabetes Mellitus Type ll
• Over 15 million diabetics in USA- 10% type I, 90% type II
• More common is some ethnic groups
• Insulin resistance keeps blood glucose too high
• Chronic complications: atherosclerosis, renal failure& blindness

69. Symptoms of Diabetes Mellitus
➤ Hyperglycemia
➤ Polyuria
➤ Polydipsia
➤ Polyphagia
➤ Ketoacidosis
➤ Hyperlipidemia
➤ Muscle wasting
➤ Electrolyte depletion

70. Diagnosis
• Demonstrating persistence hyperglycemia & glycosuria
• Glucose Tolerance Test (GTT) – oral is preferred
• Estimation of Fasting Blood Glucose (FBG)
• FBS more than 126 mg% inmore than
two occasions confirms DM

71. Treatment
• Insulin therapy
• Oral hypoglycemic agents
• Life style modifications

72. Our body has two adrenal (suprarenal) glands, each located
on the superior pole of each kidney.Each adrenal gland is
Structurally and functionally differentiated into two regions
or zones:
1.Adrenal Cortex
2. Adrenal medulla

73. Adrenal Cortex:
This is the outer or peripheral zone of the adrenal
gland,which makes up the bulk of the gland.
The adrenal cortex is divided into three zones.Each
zone has a different cellular arrangements and secrets
different groups of steroid hormones.
There are three layers in the adrenal cortex. These are:

75. 1. Zona-glomerulosa
2. Zon-fasciculata
3. Zona-reticulata
Zona-glomerulosa:
• This is the outermost layer of the adrenal cortex which secrets
mineralocorticoid hormones.
• Immediately beneath the capsule.
• Colomnar or pyramidal cells
• Arranged in closely packed,rounded, arched cords or small clumps.
• Occupy 15% of the adrenal cortex.

76. Zona-fasciculata :
– This is the middle zone of the adrenal cortex which secrets glococorticoids
hormone.
– Occupy 65% of the adrenal cortex.
– Polyhedral,often binucleated cells with lipid droplets in their cytiplasm.
– Cells are also called spongyocytes due to vacolization.
Zona-reticularis:
– This is the innermost layer of the adrenal cortex which secrets androgen but
in small quantities.
– Occupy 7% of the adrenal cortex.
– Smaller cells disposed in irregular cords forming anastomosing network.
– Presence of lipafuscin pigment granules –large and numerous.

77. Hormones of the Adrenal cortex
The adrenocortical hormones and their functions
in the body are classified into three groups:
1. Mineralocorticoids
2. Glococorticoids
3. Adrenal androgens.
Bio-synthesis of adrenal hormones:

78. Mineralocorticoids
Mineralocorticoidss:
– secreted from the adrenal cortex-zona glomerulosa.
– Main secreted hormone is aldosterone.
– It also secrets deoxy-corticosterone,9-alpha
fluorocortisol,cortisol,cortisone.
Functions:
– Maintain balance of electrolytes content of the body fluid.
– Increased tubular reabsorption of Na+ ions in the exchange
for K+ and H+ ions.

79. – Act mainly on the distal kidney tubles, salivary glands
and sweat glands.
– Increase blood volume and cardiac output.
– Increase blood pressure.
Regulations of aldosterone secretion :
– Increased of K+ ions.
– Decreased of Na+ ions.
– Undefined pituitary factors.
– ACTH

80. – Hypotension
– Increased renin angiotensin.
Glucocorticoids:
– Secreted from adrenal cortex-zona fasciculata.
– Main secreted hormones are:
• Cortisol
• Prednisone & mythyl prednisone
• Corticosterone
• Cortisone

81. Functions :
– Effects in the metabolism of carbohydrates,proteins and lipids.
• Stimulation of gluconeogenesis.
• Mobilization of amino acids from extra hepatic tissues.
• Inhibition of glucose uptake in muscles and adipose tissues.
• Stimulation of fat breakdown.
– Suppress immune response.
• Destroying circulating lymphocytes.
• Inhibiting mitotic activity.
• Controlling secretion of cytokines.
– Promotes maturation of lungs and production of surfactants in
fetal development.

82. Androgen :
– Secreted from the adrenal cortex-zona reticularis.
– Exhibit actions similar to testosterone.
Functions :
– Responsible for the development and maintenance of
reproductive functions.
– Stimulation of secondary sex characteristic.
– Stimulates the production of skeletal muscles and bones
and RBC.

83. Regulations of androgen:
– Controlled by lutenizing hormone (LH) and follicle
stimulating hormone(FHS).
– Prolactin shows an inhibitory effects on androgen secretion.
There are some types of adrenal glands disorders :
– Tumors including pheochromocylomas.
– infectionss
– Genetic mutations.

86. – Cushings syndrome.
– Addison’s disease.
– A problem in another gland, such as pituitary,
which helps to regulates the
A.G.
– Certain mediciness.
– Hyperaldosteronism etc.

87. Adrenal Medulla
• Structure
• Biosynthesis of hormones
• Functions and regulations
• Disorder of adrenal medulla

88. Introduction
• The adrenal medulla is part of the adrenal gland
it is located at the center of the gland. It is
surrounded by adrenal cortex. It is the innermost
part of the adrenal gland and it has such type of
cells that secrete epinephrine also known as
adrenaline and norepinephrine which is known
as nonadrenaline. It also secretes dopamine at a
small amount in response to stimulation by
sympathetic preganglionic neurons.
• In general adrenal medulla is a less common site
of chemically induced degenerative lesions.

89. Adrenal medulla

90. Structure of adrenal medula
• The adrenal medulla consists of irregularly shaped cells
grouped around blood vessels. These cells are intimately
connected with the sympathetic division of the autonomic
nervous system(ANS).
• The cells of the adrenal medulla are derived from the neural
crest in contrast to the mesodermal origin of the adrenal
cortex. The secretory cells of the adrenal medulla are called
chromaffin cells because of the formation of colored
polymers of catecholamines after exposure to oxidizing
agents such as chromate.
• In fact these adrenal medullary cells are modified
postganglionic neurons and preganglionic autonomic nerve
fibers lead to them directly from the central nervous system.

91. Structure of adrenal medulla

92. Structure of adrenal medulla
• Chromaffin cells are derived from the embryonic neural
crest and are simply modified neurons.
• They are modified postganglionic sympathetic neurons
of the autonomic nervous system that have lost their
axons and dendrites receiving innervation from
corresponding preganglionic fibers.
• The cells from clusters around fenestrated capillaries
where they release norepinephrine and epinephrine into
the blood.
• As a cluster of neuron cell bodies,the adrenal medulla is
considered a ganglion of the sympathetic nervous
system.

93. Structure of adrenal medulla

94. Functions of adrenal medulla
• Biosynthesis of hormones:
The adrenal medulla is the principal site of the conversion of
the amino acid tyrosine into the catecholamines, epinephrine,
norepinephrine and dopamine.
• Stimulation of the sympathetic nerves to the adrenal
medullae causes large quantities of epinephrine and
norepinephrine to be released into the circulating blood, and
these two hormones in turn are carried in the blood to all
tissues of the body. On average, about 80 percent of the
secretion is epinephrine and 20 percent is norepinephrine,
although the relative proportions can change considerably
under different physiological conditions.

95. Functions of adrenal medulla
• The circulating epinephrine and norepinephrine have almost
the same effects on the different organs as the effects caused
by direct sympathetic stimulation, except that the effects
last 5 to 10 times as long because both of these hormones
are removed from the blood slowly over a period of 2 to 4
minutes.
• The circulating norepinephrine causes constriction of most
of the blood vessels of the body; it also causes increased
activity of the heart, inhibition of the gastrointestinal tract,
dilation of the pupils of the eyes, and so forth.
• A third difference between the actions of epinephrine and
norepinephrine relates to their effects on tissue metabolism.

97. Functions of adrenal medulla
• Epinephrine has 5 to 10 times as great a metabolic effect as
norepinephrine. Indeed, the epinephrine secreted by the
adrenal medullae can increase the metabolic rate of the
whole body often to as much as 100 percent above normal,
in this way increasing the activity and excitability of the
body. It also increases the rates of other metabolic activities,
such as glycogenolysis in the liver and muscle and glucose
release into the blood.
• In summary, stimulation of the adrenal medullae causes
release of the hormones epinephrine and norepinephrine,
which together have almost the same effects throughout the
body as direct sympathetic stimulation, except that the
effects are prolonged, lasting 2 to 4 minutes after the
stimulation is over.

98. Structure of epinephrine

99. Regulatory activity of adrenal
medulla
• Adrenal medulla is the part of the sympathetic
system amd is important for the regulation of
blood pressure . Catecholamines released from the
adrenal medulla also have metabolic effects . The
following are the most important effects of
catecholamines:
• They increase blood pressure , skeletal muscle
blood flow,skeletal contractility, heart rate, blood
glucose, lipolysis.
• They decrease visceral blood flow
,gastrointestinal contractility ,urinary output.

100. Disorder of the adrenal medulla
• Pathology within the adrenal medulla and the
autonomic nervous system is primarily because of
neoplasms. The most common tumour, called
phaeochromocytoma when located in the adrenal
medulla, originates from chromaffin cells and excretes
catecholamines. Those tumours found in extra-adrenal
chromaffin cells are sometimes referred to as secreting
paragangliomas. Neoplasms may also be of neuronal
lineage, such as neuroblastomas and ganglioneuromas.
There have also been reports of neoplastic proliferation
of sustentacular cells . We will also briefly discuss the
catecholamine deficiency state.

101. Phaeochromocytoma
• Phaeochromocytoma is a chromaffin cell
neoplasm that typically causes symptoms and
signs from episodic catecholamine release,
including paroxysmal hypertension. The tumour
is an unusual cause of hypertension and accounts
for approx. 0.1–0.2% of hypertension cases. In
population-based cancer studies, its frequency is
approximately two cases per million of the
population. The diagnosis of phaeochromocytoma
is typically made in the fourth or fifth decade of
life without gender differences

103. Symptoms of phaeochromocytoma
• The classical sign of phaeochromocytoma is hypertension, often
labile or refractory to treatment. As phaeochromocytoma is a
potentially curable form of hypertension, which can be life
threatening, a high index of suspicion for the diagnosis is
imperative, given a suitable clinical presentation. In about 50% of
patients, the hypertension is sustained, but otherwise the
hypertension tends to be paroxysmal, with relatively normal blood
pressure between surges.
• Phaeochromocytomas may occasionally secrete other hormones,
such as calcitonin, ACTH, parathyroid hormone or somatostatin, and
patients may have symptoms related to their excess. Certain
reactions to medications may suggest phaeochromocytoma, such
that patients may report an increase in blood pressure after receiving
particular antihypertensive drugs.

104. Paragangliomas
• Extra-adrenal phaeochromocytomas can be referred to
as paragangliomas. They arise from paraganglionic
chromaffin cells in association with sympathetic nerves,
and are found in the organ of Zuckerkandl, urinary
bladder, chest, neck and at the base of the skull. They
are more common in children than in adults, and are
more frequently malignant. As discussed earlier,
mutations in the SDH family may predispose to head
and neck paragangliomas and phaeochromocytoma.
One series of 128 paragangliomas found that 40% were
hyperfunctioning with evidence of catecholamine
excess .

105. Paragangliomas

106. Neuroblastomas
• Neuroblastomas and ganglioneuromas are tumours of the
primitive neuroblast cells from the sympathetic nervous
system in ganglia and the adrenal medulla. They may
represent a continuum of neuronal maturation and are the
most common malignancy found in children, representing
7–10% of all childhood cancers. For neuroblastomas, the
median age of diagnosis is 18 months, with approx. 65%
found in the abdomen with the adrenal medulla as the most
common site.
• Because of their more mature ganglion cells which are
histologically benign, ganglioneuromas are often
metabolically inactive and asymptomatic. They are found
incidentally or with compressive symptoms mostly in the
posterior mediastinum or retroperitoneum.

107. Neuroblastoma

108. ANY QUESTIONS?
ANY SUGGESTIONS?

109. THANK YOU