Endocrine system

1. ENDOCRINE SYSTEM
SHAMA PRAVEEN
LECTURER
DEPARTMENT OF PHYSIOLOGY

2. ENDOCRINE SYSTEM
 The system which helps in regulating the function of whole body by releasing active
substances called hormones.
 Hormones circulate in blood.
 They distantly bind with specific receptors present on target site.
 Basic categories of hormones:-
• Amino acid hormones
• Peptide or protein hormones
• Steroid hormones

4. Mechanism of hormone action

5. Endocrine organs
 Hypothalamus
 Pituitary
 Pineal
 Thyroid
 Parathyroid
 Thymus
 Adrenal
 Kidney
 Pancreas
 Ovary and testis

6. Pituitary : sits in hypophyseal fossa
 Growth hormone(GH)
 Thyroid stimulating hormone (TSH)
 Follicle stimulating hormone (FSH)
 Luteinizing hormone (LH)
 Prolactin
 Adrenocorticotropic hormone(ACTH)
 Melanocyte stimulating hormone (MSH)
 Antidiuretic hormone (ADH)
 Oxytocin
Anterior pituitary
Posterior pituitary

7. Intermediate lobe of pituitary
 α and β melanocyte stimulating
hormone
NOTE:-
ADH and oxytocin synthesize by magnocellular
Neurosecretory cells present in supraoptic and
Paraventricular nuclei of hypothalamus.

8. Growth hormone
 Growth of bones, muscles and cartilages.
 Increases calcium retention, and strengthens and increases the mineralization of
bone
 Increases muscle mass through sarcomere hypertrophy
 Promotes lipolysis
 Increases protein synthesis
 Stimulates the growth of all internal organs excluding the brain
 Plays a role in homeostasis
 Reduces liver uptake of glucose
 Promotes gluconeogenesis in the liver[37]
 Contributes to the maintenance and function of pancreatic islets
 Stimulates the immune system
 Increases deiodination of T4 to T3.

10. Clinical aspects
 Gigantism- due to overproduction of GH during adolescence (before
epiphyseal closure)
• excessive growth of long bones (height grows as much as 8feet)
• bilateral gynaecomastia due to increase in estrogen and androgen ratio
• large hands and feet.
 Acromegaly- due to overproduction of GH during adulthood.
• it causes growth in those areas where cartilage persists.
• enlargement of peripheral region
• Prognathism
• prominent brow
• hypertrophy of some soft tissues
• osteoarthritis (additional)

11. Clinical aspects
 Dwarfism- due to deficiency of GH secretion
Sexual immaturity
hypothyroidism
adrenal insufficiency

12. Factor affecting growth factor
 Genetic factors
 Nutritional factors
 Environmental factors ( exercise, season, diseases, emotional disturbance)
 Hormonal factors

13. Prolactin
 Lactogenic
 Control of prolactin secretion
• Exercise
• Pregnancy
• Nursing and breast stimulation
• Dopamine antagonist
 Action of Prolactin
• Enhance milk secretion
• Amennorrhea (anovulation)

14. Oxytocin
 Synthesized by magnocellular neurosecretory cells of paraventricular nuclei
present in hypothalamus and stored in posterior pituitary. It is transported
bound to a carrier protein, Neurophysin I, from the hypothalamus to posterior
pituitary.
 Action
• Milk ejection
• Contraction of uterus
• Contraction of cervix during coitus
 Control
• Stimulation of cholinergic nerve fibers
• Milk Let Down Reflex

15. Milk Let Down Reflex
 Receptor- Tactile receptor present on areolar region of
Breast
 Stimulation- sucking by baby
 Neural tract- somatoasthetic neural tract
 Centre- paraventricular nuclei of hypothalamus
 Increases the release of oxytocin
 Contraction of myoepithelial cells which cover the stromal
surface of epithelium of the alveoli, ducts and cisternae of
mammary gland
 Expels their contained milk into the lactiferous ducts
 Milk ejection can be the result of stimulation of
limbic system without activation of tactile receptor.

16. Factors decreases oxytocin release
 Emotional stress and psychic factors
 Activation of sympathetic neurons
release of epinephrine and nor epinephrine
excitation of adrenergic fibers to hypothalamus
decreases oxytocin release
 Drugs eg. Ethanol and enkephalins

17. Antidiuretic Hormone (ADH)
 Synthesized in supraoptic nuclei of hypothalamus and transported by binding with
Neurophysin II from hypothalamus to posterior pituitary.
 Receptors- V1A, V1B and V2.
 Control of ADH
 Conditions in which secretion increases,
 hyperosmolality- concentration of solute increases
 hypovolemia – concentration of solvent decreases.it is more potent to ADH release
 conditions in which secretions decreases
 hypoosmolality
 hypervolemia
 hypertension

18. Function of ADH
 Increased membrane permeability to water permits back diffusion of
solute free water, resulting in increased urine osmolality.
 cAMP activates protein kinase that permits and activates aquaporin or
water channels in DCT and collecting ducts.
 Regulates blood pressure by constricting blood vessels that’s why it is
also known as vasopressin.

19. Clinical aspects:-
 Diabetes insipidus:- due to deficiency of ADH
ADH Secretion defect impairement of ADH response on
nephron
Neurogenic DI Nephrogenic DI

20. Thyroid Gland

21. Structure and function

22. Hormones synthesized by thyroid gland
 T4 Thyroxine production
 T3 tri-iodothronine
- growth and development
- metabolism (protein anabolic, fat catabolic in nature)
- body temperature by increasing basal metabolic rate (BMR)
- heart rate by increasing speed of cardiac contraction.
- Reaction time shorten by these hormones
 Calcitonin
- regulate blood calcium and phosphate levels
- effects long bones growth

23. Synthesis of thyroid hormones
 Collection of iodine
 Synthesis of thyroglobulin
 Release of hormone from thyroglobulin

25.  T3 has shorter life span than T4
 80µg/d of T4 secreted by follicular cells whereas 4µg/d of T3 secreted
 Plasma level of T4 is 8µg/dl whereas T3 is 0.15µg/dl.

26.  Daily average intake of iodine - 500µgm
 Daily requirement of iodine for thyroid functions- 100-200µgm
 Normal plasma iodide level- 0.15- 0.3µgm
 Transport of thyroid hormone is by thyroid binding globulins, transthyretin or
albumin.
 Total amount of iodide in ECF:
60µg/d result of metabolism of T3 & T4
40µg/d diffuses back to ECF
500µg/d daily intake
(500 + 60+ 40)µg/d= 600µg/d
 20% of this iodide enters the thyroid whereas 80% excreted in urine.

27. Regulation of secretion
 TSH (thyroid stimulating hormone)
 Thyroid autoregulation. (WOLFF CHAIKOFF EFFECT)
TRH from hypothalamus TSH from anterior pituitary thyroid gland
T3 T4
(-)

28. Clinical aspects
 Hyperthyroidism- Overactive thyroid gland
 Characterized by nervousness, weight loss, hyperphagia, Exophthalmos
(bulging of eye ball),heat intolerance, increased pulse pressure, tremors,
warm and soft skin and high BMR .
 Causes:-
- Graves disease- autoimmune disease in which antibodies to the TSH receptor
stimulate the receptor.
- TSH secreting pituitary tumor
- mutation causing constitutive activation of TSH receptor
- Hashimoto thyroiditis
- toxic multinodular goiter

29. Hypothyroidism
 In adults, it is generally called as myxedema.
 Causes:-
- dietary iodine intake falls below 50µg/d (goiter)
- drugs eg. Thioureylenes, propylthiouracil, methimazole etc.
- large dose of iodine inhibits binding of iodide itself (Wolff Chaikoff Effect)
 signs:- slow Mentation ,poor memory, low BMR, dry skin, poor cold tolerant,
enlargement of thyroid gland
 In children, it is generally called as cretinism
 Signs:- dwarfed, mental retarded

30. Calcitonin
 Secreted from parafollicular cells(C-cells)
 Not secreted until the plasma Ca2+ exceeds 9.5%
 Functions:-
- inhibits osteoclastic activity
- inhibits calcium permeability of osteoclasts and osteoblasts
- decreases renal formation of 1-25 DHCC which in turn decreases serum
calcium and phosphate level by inhibiting renal 1-α-hydroxylase activity.
- increases calcium excretion

31. Vitamin D
 Converted to a more important hormone, 1-25 DHCC
(dihydroxycholecalciferol)
 It increases serum calcium & phosphate by its action on GIT, bones and
Kidney.
 Reabsorption of calcium increases in the intestine.
 Causes proliferation of osteoclasts which mobilizes Ca2+ and PO4 from the
bones by increasing the active transport of these out of osteoblast into ECF.
Regulation
 low plasma Ca2+ increasing PTH secretion stimulates 1α
hydroxylase increases formation of 1-25 DHCC increases serum
Ca2+ in plasma.
 Low plasma phosphate

32. Parathyroid hormone
 It is secreted by parathyroid gland. It is divided into 4 parts.
 it has numerous chief cells which contain a prominent golgi apparatus,
endoplasmic reticulum and secretory granules, synthesize and secrete
parathyroid hormone(PTH).
 It also has less abundant Oxyphil cells contain oxyphil granules. (function is
unknown)
ACTIONS:-
 Increase bone resorptionand mobilizes calcium.
 Increases plasma calcium and phosphate excretion (phosphaturic action).
 Calcium excretion increases in hyperparathyroidism because the increase in
the load of filtered calcium overwhelms the effect on reabsorption.
 Increases the formation of 1-25, DHCC
 Stimulates both osteoblasts and osteoclasts.

33. THANK YOU