The document discusses the endocrine system, describing the major glands including the hypothalamus, pituitary gland, thyroid gland, parathyroid glands, adrenal glands, pancreas, and gonads. It explains the hormones produced by each gland and their roles in regulating processes like growth and development, metabolism, fluid balance, and reproduction. Common endocrine disorders in children like diabetes are also mentioned.

1. Under the guidance of:
Dr. Sandeep Tandon
Professor and Head of Dept. of Pedodontics
Dr. Ambika Singh Rathore
Dr. Rinku Mathur
1
Dr .Shantanu Jain
Dr. Tripti Sharma Ra

2. CONTENT:
 Introduction
 Evolution of Endocrine system
 Chemical characteristics of Hormones
 Regulation of Hormone Release
 Hypothalamus & its Hormone
 Various glands and their importance
 Disorders of Endocrine system common in
Children
 References 2

3. INTRODUCTION:
 Constant internal environment
(i.e., homeostasis) should be maintained.
 Two systems help ensure communication:
NERVOUS HORMONAL
SYSTEM Neuroendocrine
Rapid transmission Long-lasting regulatory
action
 Both systems interact: Stimuli from the nervous
system can influence the release of certain
hormones and vice versa. 3

4. EVOLUTION OF ENDOCRINE SYSTEM
 The nervous system coordinates rapid and precise
responses to stimuli using action potentials.
 The endocrine system maintains homeostasis and long-
term control using chemical signals.
 The most primitive endocrine systems seem to be those of
the neurosecretory type, in which the nervous system
either secretes neurohormones directly into the circulation
or stores them in neurohemal organs (neurons whose
endings directly contact blood vessels, allowing
neurohormones to be secreted into the circulation), from
which they are released in large amounts as needed.
 True endocrine glands probably evolved later in the
evolutionary history of the animal kingdom as 4
separate, hormone-secreting structures.

5. CONVERGENT EVOLUTION:
Similarities among the endocrine systems of
crustaceans, arthropods, and vertebrates.
The vertebrate endocrine system consists
of glands (pituitary, thyroid, adrenal), and
diffuse cell groups scattered in epithelial tissues.
Endocrine glands arise during development for all three
embryologic tissue layers
(endoderm, mesoderm, ectoderm).
 The type of endocrine product is determined by which
tissue layer a gland originated in.
 Glands of ectodermal and endodermal origin: peptide
and amine hormones;
 Mesodermal-origin glands: hormones based on lipids. 5

6. WHAT ARE HORMONES?????
( “TO SPUR ON”)
 Hormones are molecules that
are produced by endocrine
glands:
i. The hypothalamus,
ii. Pituitary gland,
iii. Adrenal glands,
iv. Gonads, (i.e., testes and
ovaries),
v. Thyroid gland,
vi. Parathyroid glands, and
6
vii. Pancreas

7.  The term “endocrine” implies that in response to
specific stimuli, the products of those glands are
released into the bloodstream.
The hormones then are carried via the
blood to their target cells.
 The target cells for each hormone are
characterized by the presence of docking
molecules (i.e., receptors) for the hormone that are
located either on the cell surface or inside the cell.
 The interaction between the hormone and its
receptor triggers a cascade of biochemical
reactions in the target cell that eventually modify 7
the cell’s function or activity.

8. CHEMICAL CHARACTERISTICS
OF HORMONES
 Amines (from tyrosine)
I. hydroxylation - catecholamines
II. iodination - thyroid hormones
 Peptides/proteins
 Steroids (from cholesterol)
I. adrenocorticoids
II. sex hormones
III. active metabolites of vitamin D
 Their mechanisms of action (e.g., whether they
can enter their target cells and how they 8
modulate the activity of those cells) also differ.

9. MECHANISM OF ACTION:
STEROIDS: produced by gonads; structure
similar to cholesterol.
Enter their target cells and interact with the
cytoplasm or in the cell nucleus
Hormone-receptor complexes bind to certain
regions of the cell’s genetic material (i.e., the
DNA)
Regulating the activity of specific hormone- 9
responsive genes

10. MECHANISM OF ACTION:
10

11.  Amino acid derivatives:
are modified versions of building blocks of proteins.
thyroid gland & adrenal glands (i.e., the adrenal
medulla)
 Enter the cell, where they interact with receptor
proteins that are already associated with specific DNA
regions. The interaction modifies the activity of the
affected genes.
 Polypeptide and protein hormones:
found primarily in the hypothalamus, pituitary gland, and
pancreas
 Because of their chemical structure, the polypeptide
and protein hormones cannot enter cells. Instead, they
interact with receptors on the cell surface.
11

12. REGULATION OF HORMONE RELEASE
 Constant feedback from the target glands to
the hypothalamus and pituitary gland ensures
that the activity of the hormone system
involved remains within appropriate
boundaries.
To maintain the body’s homeostasis
 Negative feedback mechanism
 Short-loop feedback
 Positive-feedback mechanisms
12

13. Negative Feedback Loop
13

14. Positive Feedback Loop
14

15. THE HYPOTHALAMUS AND ITS HORMONES
Why is the Hypothalamus so Important?
 Eating and drinking,
 Sexual functions and behaviors,
 Blood pressure and heart rate,
 Body temperature maintenance,
 The sleep-wake cycle, and
 Emotional states (e.g., fear, pain, anger, and
pleasure)
15

16. Neurosecretory cells
16

17. THE HYPOTHALAMIC-HYPOPHYSEAL
PORTAL SYSTEM
17

18. hypothalamic nuclei
superior
hypophyseal
artery superficial
capillary plexus
trabecular artery
deep
long portal veins capillary plexus
inferior 18
hypophyseal
artery

19. hypothalamic nuclei
superior
hypophyseal
artery superficial
capillary plexus
trabecular artery
deep
long portal veins capillary plexus
short portal veins
inferior 19
hypophyseal
artery

20. hypothalamic nuclei
superior
hypophyseal
artery superficial
capillary plexus
trabecular artery
deep
long portal veins capillary plexus
short portal veins
adeno-
secondary
hypophyseal
capillary
plexus
capillary
plexus inferior 20
hypophyseal
artery

21. hypothalamic nuclei
superior
hypophyseal
artery superficial
capillary plexus
trabecular artery
deep
long portal veins capillary plexus
short portal veins
adeno-
hypophyseal
capillary
plexus inferior 21
hypophyseal
hypophyseal vein artery

22. HYPOTHALAMIC
HORMONES
RELEASING INHIBITING
 Corticotrophin (CRH) Somatostanin
 ACTH
 Gonadotropin (GnRH) Dopamine
 LH & FSH
 Thyrotropin (TRH)
 TSH
 Growth-Hormone (GHRH)
GH
22

23. 23

24. THE PITUITARY AND ITS MAJOR HORMONES
24

25. INTERMEDIATE LOBE
 There is also an intermediate lobe in
many animals,
but is rudimentary in humans.
 For instance, in fish, it is believed to control
physiological color change.
 In adult humans, it is just a thin layer of cells
between the anterior and posterior pituitary.
The intermediate lobe produces melanocyte-
stimulating hormone (MSH), although this
function is often (imprecisely) attributed to the 25
anterior pituitary.

26. GROWTH HORMONE
 Most abundant of the pituitary hormones
 Pivotal role in controlling the body’s growth
and development.
1. Stimulates the linear growth of the bones;
2. Promotes the growth of internal organs, fat
(i.e., adipose) tissue, connective tissue, endocrine
glands, and muscle; and
3. Controls the development of the reproductive
organs.
4. GH affects carbohydrate, protein, and fat
(i.e., lipid) metabolism.
 GH levels in the blood are highest during early 26
childhood and puberty and decline thereafter.

27. 27

28. INDIRECT ACTION OF GROWTH HORMONE
28

29.  Two hypothalamic hormones control GH release:
(1) GHRH: stimulates GH release,
(2) Somatostatin: inhibits GH release.
Short-loop feedback component:
GH acts on the hypothalamus to stimulate
somatostatin release.
In addition, GH release is enhanced by
 Stress, such as low blood sugar levels
(i.e., hypoglycemia) or severe exercise, and by the
onset of deep sleep.
 Acute and chronic alcohol consumption have been
shown to reduce the levels of GH and IGF-1 in the
blood. 29

30. PROLACTIN.
 Central role in the development of the female
breast and in the initiation and maintenance of
lactation after childbirth.
 Factors control Prolactin release:
1. Response to the rise in estrogen levels in the
blood that occurs during pregnancy.
2. In nursing women, Prolactin is released in
response to suckling by the infant.
3. Dopamine, which has an inhibitory effect.
4. Alcohol consumption by nursing women can
influence lactation both through its effects on
the release of prolactin and oxytocin. 30

31. POSTERIOR PITUITARY:
31

32. VASOPRESSIN
 Vasopressin (arginine vasopressin, AVP; anti-
diuretic hormone, ADH) is a peptide hormone
formed in the hypothalamus, then transported
via axons to, and released from, the posterior
pituitary.
 Two principles site of action:
KIDNEY & BLOOD VESSEL
32

33. MECHANISMS REGULATING THE RELEASE OF AVP
 Hypovolemia: decreased central venous
pressure, the decreased firing of atrial stretch
receptors leads to an increase in AVP release.
 Hypotension, which decreases arterial
baroreceptor firing and leads to enhanced
sympathetic activity, increases AVP release.
 Angiotensin II receptors located in a region of
the hypothalamus regulate AVP release – an
increase in angiotensin II simulates AVP release.
 Increased sympathetic activation stimulates
AVP release
33

34. OXYTOCIN HORMONE
I. Stimulates the contractions of the
uterus during childbirth.
I. In nursing women, the hormone activates
milk ejection in response to suckling by the
infant
(i.e., the so-called let-down reflex).
34

35. THE ADRENAL GLANDS AND THEIR HORMONES
35

36.  Action of Cortisol:
1. Cortisol increases glucose levels in the blood by
stimulating gluconeogenesis in the liver and
promotes the formation of glycogen in the liver.
2. Reduces glucose uptake into muscle and adipose
tissue,
3. Promotes protein and lipid breakdown into products
(i.e., amino acids and glycerol, respectively) that can
be used for gluconeogenesis.
4. Protect the body against the deleterious effects of
various stress factors.
5. Suppress tissue inflammation in response to injuries
and to reduce the immune response to foreign
molecules. 36

37. ACTION OF ALDOSTERONE:
 Regulate the body’s water and electrolyte balance.
 Conserve sodium and to excrete potassium from the
body.
 Reducing water excretion and increasing blood
volume.
 Decreases the ratio of sodium to potassium
concentrations in sweat and saliva, thereby
preventing sodium loss via those routes.
 Controlled primarily by another hormone system, the
reninangiotensin system, which also controls kidney
function. 37

38. THE THYROID AND ITS HORMONES
38

39. THYROID HORMONE PRODUCTION
39

40. THYROID HORMONE PRODUCTION
40

41. ACTION OF THYROID HORMONE
 Stimulates the production of certain proteins
involved in heat generation in the body, a
function that is essential for maintaining body
temperature in cold climates.
 Promotes other metabolic processes involving
carbohydrates, proteins, and lipids that help
generate the energy required for the body’s
functions.
 Plays an essential role in the development of the
central nervous system during late fetal and
early postnatal developmental stages.
 Required for the normal development of
teeth, skin, and hair follicles as well as for the
functioning of the nervous, cardiovascular, and 41
gastrointestinal systems

42.  Parafollicular C cells) in the thyroid gland
produce calcitonin, a hormone that helps
maintain normal calcium levels in the blood.
 Specifically, calcitonin lowers calcium levels
in the blood by reducing the release of calcium
from the bones; inhibiting the constant erosion
of bones (i.e., bone resorption), which also
releases calcium; and inhibiting the
reabsorption of calcium in the kidneys.
42

43. THE PARATHYROID GLANDS
AND THEIR HORMONES
43

44. ROLE OF PARATHYROID HORMONE
 Increases calcium levels in the blood, helping
to maintain bone quality and an adequate
supply of calcium.
 Causes re-absorption of calcium from and
excretion of phosphate in the urine.
 Promotes the release of stored calcium from
the bones as well as bone resorption.
 PTH stimulates the absorption of calcium from
the food in the gastrointestinal tract.
Functions facilitated by a substance called
1,25-dihydroxycholecalciferol, a derivative of
vitamin D. 44

45. CALCIUM HOMEOSTASIS
45

46. THE PANCREAS AND ITS HORMONES
46

47. TWO DISTINCTLY DIFFERENT FUNCTIONS
PANCREAS
EXOCRINE ENDOCRINE
GLUCAGON
Digestive Enzymes INSULIN
Islets of Langerhans 47

48. INSULIN & GLUCAGON
Beta cells of Islet Alpha cells of Islet
Blood sugar-lowering Increases blood glucose levels
hormone Actions opposite to insulin
Effect of Insulin:
1. Inhibits gluco-neogenesis
2. Insulin promotes the formation of storage forms
of energy (e.g., glycogen, proteins, and lipids)
and suppresses the breakdown of those stored
nutrients. 48

49. REGULATION OF BLOOD GLUCOSE
LEVELS
49

50. THE GONADS AND THEIR HORMONES
OVARIES AND TESTES
They produce the germ cells.
Synthesize steroid sex hormones that are
necessary for the development and function of
both female and male reproductive organs and
secondary sex characteristics.
Affect the metabolism of carbohydrates and
lipids, the cardiovascular system, and bone
growth and development.
50

51. 51

52. DIABETES
 ''Type 1 diabetes is growing by 5% per year among
pre-school children in India.
 It is estimated that 70,000 children, who are under
15 years, develop juvenile type 1 diabetes each year
(almost 200 children a day!).“
Symptoms of Diabetes in Children:
 Stomach pains,
 Headaches
 Behaviour problems
 Weight loss, thirst, tiredness and frequent urination.
 Detected through the presence of ketoacidosis
52

53. CAUSES:
 Type I (Juvenile Diabetes): body’s inability
to produce insulin
 Genetic factors; environmental factors
 Increased Type 2 Diabetes: linked
overwhelmingly to lifestyle changes that have
contributed to increased weight problems and
lack of activity in children. 53

54. TREATMENT:
 INSULIN: The advent of insulin pumps for
administration has allowed many children added
flexibility in their daily lives.
 Monitoring blood sugar levels
Crucial factor
 Diet: reduced consumption of fats and sugars,
intake fibers, vegetables and fruits.
 Exercise: helps in lowering blood glucose levels
of the body
54

55. COMPLICATIONS
 Sudden hypoglycemia & hyperglycemia
Immediately giving the child a glucose tablet or
glucose beverage
LONG-TERM COMPLICATIONS
 Problems of the kidney, heart, lungs, eyes, feet
and nerves.
 High blood sugar or high cholesterol levels
55

56. GIGANTISM
 Gigantism refers to abnormally
high linear growth due to
excessive action of insulin-like
growth factor-I (IGF-I) while the
epiphyseal growth plates are
open during childhood.
 Acromegaly is the same
disorder of IGF-I excess when it
occurs after the growth plate
cartilage fuses in adulthood.
 Robert Wadlow, called the Alton
giant, who stood 8 feet 11
inches tall at the time of his
death in his mid-20s 56

57. CAUSES
 Causes of excess IGF-I action may be
divided into 3 categories:
 Those originating from primary GH excess
released from the pituitary;
 Those caused by increased GH-releasing
hormone (GHRH) secretion or hypothalamic
dysregulation; and
 Hypothetically, those related to the excessive
production of IGF-binding protein, which
prolongs the half-life of circulating IGF-I. 57

58.  Most people with giantism have GH-secreting
pituitary adenomas or hyperplasia.
TREATMENT
 Medical Care
i. Surgery clearly fails to cure a notable number
of patients with IGF-I excess
ii. Long-acting somatostatin analogs and dopamine
agonists improve adherence and efficacy.
iii. Octreotide are the most effective medical
therapies for GH excess. Bromocriptine are
best used as adjuvant treatments.
58

59. PITUITARY DWARFISM
 The achondroplastic
dwarf has an
orthopedic reason for
having short limbs and
a short spinal
colum. The pituitary
dwarf lacks growth
hormone (an endocrine
reason).
 SYMPTOMS:
 GH Deficiency
 Low blood sugar
59

60. RISK FACTORS:
 Disease of the hypothalamus of the brain
 Disease of the front of the pituitary gland in the brain
 Newborns who had some type of serious medical event
(such as a lack of oxygen) happen in the perinatal
period, are at risk for the type of growth hormone
deficiency caused by damage to the hypothalamus.
TREATMENT:
Treatment with human growth hormone
theoretically corrects the deficiency, but is
most successful when the child is young. It must
be given by injection.
60

61. PRECOCIOUS PUBERTY
 Precocious puberty
describes puberty
occurring at an unusually
early age.
CAUSES:
Central:
 damage to the inhibitory
system of the brain
 hypothalamic hamartoma
produces pulsatile
gonadotropin-releasing
hormone (GnRH)
 Langerhans cell
histiocytosis 61

62. PERIPHERAL CAUSES
 Secondary sexual development induced by sex
steroids from other abnormal sources is
referred to as peripheral precocious puberty.
Causes can include:
 Endogenous sources
 gonadal tumors (such as arrhenoblastoma)
 adrenal tumors
 germ cell tumor
 congenital adrenal hyperplasia
 McCune–Albright syndrome
 Exogenous hormones
 Environmental
62
 As treatment for another condition

63. TREATMENT
 GnRH agonists stimulate the pituitary to release
Follicle Stimulating Hormone (FSH) and
Luteinizing Hormone (LH).
 One possible treatment is with anastrozole.
Histrelin acetate.
63

64. PEDIATRIC CUSHING’S SYNDROME
(CS)
 Rare in childhood and adolescence.
 Caused by prolonged exposure to excessive
glucocorticoids which can be secreted endogenously
or administered exogenously.
 Supra-physiological doses of exogenous gluco-
corticoids in the form of topical, inhaled or oral
corticosteroids.
 Eczema and asthma are common conditions in
childhood often requiring treatment with
corticosteroids.
64

65. 65

66. 66

67. TREATMENT
 Primary adrenal lesions
Surgical excision is the first-line therapy for a
cortical-secreting ACT.
Mitotane therapy appears to be the treatment
of choice
 Cushing’s disease
Medical therapies such as Metyrapone and
Ketoconazole to lower serum cortisol levels can
be used as a short-term measure, but cannot be
recommended as long-term therapy. 67

68. THYROID DISORDERS
 Thyroid disease occurs less
frequently in children than in adults, the signs
and symptoms can be similar.
Congenital hypothyroidism
 Affects infants at birth, and occurs in about 1 in
4000 live-born babies.
 Loss of thyroid function, due to the thyroid
gland failing to develop normally.
 Enzyme defect leading to deficient hormone
production, iodine deficiency and a brain
pituitary gland abnormality. 68

69.  Within the first week of life, a heelprick blood sample is
taken to assess an infant's thyroid hormone level.
 Infant is immediately given thyroid hormone replacement
therapy (T4 — thyroxine). Normal growth and
development should then continue, with no adverse
effects on the child's mental capacity.
Subtle symptoms: Severe:
1. Poor feeding Poor growth and development
2. Constipation Dry skin & hair
3. Low body temperature Slow tendon reflex
4. Slow pulse Enlarged tongue
5. Prolonged jaundice, Umbilical hernia
6. Increased sleepiness Puffiness & swelling
7. Decreased crying.
69

70. HYPERTHYROIDISM IN NEWBORNS
 Overactive thyroid gland: referred to as
NEONATAL HYPERTHYROIDISM.
If the mother has Graves' disease, the thyroid-
stimulating antibodies in her blood can cross the
placenta and stimulate the unborn child's thyroid
gland, thus producing too much thyroid hormone.
 Some newborns may hardly be affected if the levels
of antibodies are low.
 No treatment may be necessary as the mother's
antibodies will soon clear from the baby's
bloodstream, usually within 2 to 3 months.
70

71. NEWBORNS WITH ADVANCED HYPERTHYROIDISM
• EXTREMELY FAST
PULSE
IRRITABILITY
FLUSHED MOIST SKIN
• INFANT TENDS TO BE THIN &
LONG
TREATMENT
Anti-thyroid drugs is safe and effective, and will only be
needed for a short period of time, until the stimulating
antibodies pass from the baby's bloodstream.
If the mother is on a high dose of anti-thyroid
medication, the diagnosis can be delayed by about a
week until the infant clears the anti-thyroid medication. 71

72. HASHIMOTO'S THYROIDITIS
 The most common cause of
hypothyroidism in children
and adolescents is
Hashimoto's thyroiditis, an
autoimmune disease.
 As the thyroid gland
becomes increasingly
underactive, physical and
mental changes will
become more obvious.
 Symptoms of
hypothyroidism develop
very slowly 72

73. SIGNS AND SYMPTOMS
 The first sign is that the child's growth rate
decreases unexpectedly and skeletal
development is delayed.
Decreased
GOITRE Energy
Lethargy
Dry Itchy Skin
WEIGHT
&
GAIN
Constipation
Poor
73
Concentration

74. TREATMENT
 Thyroid hormone replacement is
taken daily for life.
 The dosage of thyroid hormone needs to be age-
appropriate, as the body's demands for thyroid
hormone vary with age.
SIDE-EFFECTS:
In children who have had long-standing
hypothyroidism, ultimate height potential may be
partly lost.
As the child regains normal thyroid
function, behavioural problems may arise as their 74
physical and mental processes speed up

75. GRAVES' DISEASE
 The most common
cause of
hyperthyroidism in
children and
adolescents is an
autoimmune condition
called Graves' disease.
 In Graves' disease the
body produces
antibodies that
stimulate the thyroid
gland uncontrollably, to
make too much thyroid
hormone.
75

76. SIGNS AND SYMPTOMS
Increased
Energy, hyperactive, restless,
Easily distracted
Enlarged Thyroid Gland, fast
pulse, nervousness, heat
intolerance, weight loss
Accelerated growth rate, Shaky
hands
Muscle weakness, diarrhoea, and
Sleep & behavioural disturbances. 76

77. TREATMENT
 Propylthiouracil (PTU) or Carbimazole.
 Period of 'block and replace therapy' (anti-thyroid
drugs as well as thyroxine) is useful.
 Throughout a child's treatment, thyroid hormone levels will
need to be monitored regularly, along with their clinical
symptoms.
SIDE EFFECTS
 Anti-thyroid drugs can, however, occasionally stop the
production of white blood cells or platelets.
 Sore throats, mouth ulcers, excessive bruising or skin
rashes can indicate this.
77
 The only safe action is to stop the medication until after
the result of the blood test.

78. REFERENCES:
 Susanne Hiller-Sturmhöfel and Andrzej Bartke. The Endocrine
Syste An Overview. Alcohol Health & Research World; Vol.
22(3):1998; 153-64
 Ashley B. Grossman, Martin O. Savage.Pediatric Cushing’s
Syndrome: Clinical Features, Diagnosis, and Treatment. Arq
Bras Endocrinol Metab 2007;51/8:1261-1271)
 Kim E. Barrett, Susan M. Barman. Ganong’s Review of Medical
Physiology;Vol.23:451-568
 Arthur C. Guyton. Textbook of Medical Physiology 10th edi;993-
1019
 K. Sembulingham. Essentials Of Medical Physiology;3rd
edi;667-714 78

79. Presented by:
Dr. Ruby Kharkwal
1st year postgraduate student
Department of Pedodontics 79