Endocrine Glands 3 rd Year Medicine

1. Endocrine Glands3rd Year Medicine Dr. Zienab Al-Refaie Associate. Prof. Physiology

2. Endocrine Glands

3. Endocrine GlandsIntroduction Objectives: 1- intercellular communication 2-classification of hormones. 3-neuro endocrine inter-relation. 4-control of hormone secretion. 5-characters of hormone receptors. 6-mechanisms of hormone action.

4. Intercellular communication: cell to cell relation and its method • 1- Direct communication : it occurs between contiguous cells of the same type . e.g. myocardial cells • 2- Paracrine communication :the chemical messengers secreted by some cells may affect the nearby cells. • 3- Endocrine communication: some body cells release specific chemical substances, hormones, in blood to affect distant body cells . This method is slow because the blood velocity is slow (0.001-1m/sec). • 4- Neural communication: the cells of the nervous system communicate at their synaptic junctions with each other and with other body cells by releasing neurotransmitters.

6. Nervous &Endocrine Systems inter-relation • The nervous and the endocrine systems are inter-related in the hypothalamus through the: • The hypothalamo-hypophyseal tract . • The hypothalamo-hypopheseal –portal circulation .

7. Hypothalamo-hypophyseal Portal circulation

8. Note • The anterior pituitary receives portal blood • The posterior pituitary receives arterial blood.

10. Hypothalamo-hypophyseal Tract

11. Differences between steroid and peptide hormones

12. Forms of H. in the Blood 1- Free. * It is not carried on a plasma protein . * It can bind directly to the receptors : active . * It is small in size , so can be filtered in urine . 2- protein bound . * Carried on plasma protein . * It acts as a reservoir. * It increases the half life of the hormone. * It is more soluble in plasma ( the lipid steroids , when bound to plasma proteins they are transformed into water soluble. * It is large in size , and so is not filtered in urine .

13. Control of hormone secretion • I- Nervous control : through the hypothalamus. • 2- Freed back control : * -Ve feed back. * +Ve feed back.

14. What is Feed Back • When the endocrine gland senses that there is too much (or too little) of the regulated variable, it responds by decreasing (or increasing) the rate of hormone secretion.

15. -Ve Feed back control of Hormone secretion

16. +Ve feed back • During ovarian cycle in females High Estrogen Increase FSH More Estrogen Ovulation Increase LH

17. Quiz • H. that binds to cytoplasmic receptors and circulates mostly bound to plasma ptn. • Peptide H. that lacks hypothalamic pituitary control. • H. that shows late onset of action and acts through nuclear receptors. • Peptide H. which is formed in the post. Pituitary. A- thyroxin B- insulin C- cortisole D- vasopressin

18. Hormone Receptors • * Site • * Specificity • * Dynamic: • Down-regulation • Up-regulation

19. Adenyl Cyclase Pathway

20. Some hormones that act by adenyl cyclase pathway ACTH Angiotensin II Calcitonin Parathormone Catecholamines (β) LH FSH CRH ADH ( kidney) Glucagon TSH

21. Phospholipase C Pathway

22. Some hormones that act by phospholipase pathway Angiotensin II Oxytocin ADH (smooth muscles) Catecholamines (α receprors) GnRH GHRH

23. Second Messenger • Peptide hormone is the 1st messenger (outside the cell). • When it binds with its receptor, it leads to formation of a 2nd messenger (inside the cell). • The 2nd messenger performs the effects of the hormone.

24. Mechanism of Action of Steroid H.

25. Effects of Ant. Pituitary H.

26. Actions of Ant. Pituitary H.

27. Actions and Control of GH

29. Effect of sleep & exercise on GH secretion

30. Effect of GH injection on growth rate

31. Diabetogenic effects of GH Target Effect Muscle Decreased glucose uptake Fat Increased lipolysis. Liver Increased gluconeogenesis All of them Insulin resistance

33. GH and IGF

34. Effect of arginine infusion on GH and Insulin

35. Effect of protein deficiency and nutrient replacement on GH level

36. Acromegaly

37. Increased levels of GH Gigantism: increased before puberty before union of epiphysis growth of all bones and viscera Acromegaly: increased after puberty after union of epiphysis growth of flat bones

38. Major role of Prolactin

39. Antidiuretic hormone It is secreted from: * Supraoptic nucleus: mainly, to the posterior pituitary then into the blood. * Paraventricular nuclei: to lesser extent , to the anterior pituitary, stimulates ACTH

40. Actions of ADH On the V2 receptors of the late distal and the cortical collecting tubules, induces translocation of water channels, aquaporin 2 to the cell membrane. This allows passage of water from the lumen to the inside of the cell & then to the renal interstitium. On the V1 receptors in vascular smooth muscles, increases intracellular Ca2+ , which induces vasoconstriction in cases of hemorrhage. On the V3 receptors of the corticotropes, stimulates secretion of ACTH that in its turn causes cortisole secretion in stressful conditions.

41. Action of ADH on V2 receptors

42. Relationship between change in plasma osmolality and ADH

43. Relationship between plasma volume and ADH

44. Analysis of various types of diabetes insipidus

45. ADH level and Plasma osmolality in both types of diabetes insipidus

47. The adrenal cortex • It is the outer part of the adrenal gland and forms about 80 % of the gland. • It secretes steroid hormones . It is divided into three distinct zones: • Zona Glomerulose, the outermost layer,secretes mineralocorticoids, aldosterone, desoxycorticosterone and corticosterone . They maintain Na+ and K + balance and ECF volume • Zona Fasciculata : is the middle widest zone and secretes glucocorticoids : cortisol and corticosterone that have widespread effects on carbohydrate and protein metabolism . • Zona Reticularis : is the innermost layer and secretes mainly sex hormones, dehydroepiandrosterone ( DHEA ), androstenedione and small amounts of estrogen .

48. Actions of cortisole On carbohydrate metabolism : • 1- Stimulation of gluconeogenesis by the liver from amino acids. • 2- Increased gluconeogenesis leads to the build up of sufficient glycogen On protein metabolism: • 1- Cortisol reduces protein synthesis &increases protein catabolism in all body cells except liver cells. • 2- It increases plasma amino acid level. • 3- It inhibits amino acid transport to extrahepatic cells and stimulates amino acid transport into liver cells. On fat metabolism: • 1-Cortisol has a lipolytic action. • 2-It increases FFA in plasma.

49. Actions of cortisole Effect on vascular system: • Cortisole is required for the maintenance of normal arterial blood pressure in response to the vasoconstrictor effect of catecholamines (permissive action). Effect on Kidney: • Cortisole is essential for rapid excretion of a water load, as it inhibits ADH secretion and action. Functions of cortisole in stress: • Cortisole is required for catecholamines to exert their pressor and lipolytic actions. • It increases FFA that are important as emergency energy source, and raises blood glucose level together with catecholamines to protect against hypoglycemia.

50. Actions of cortisole Effect of cortisole on blood cells and immunity: • Cortisole decreases the number of circulating eosinphils and the number of lymphocytes (T lymphocytes) mainly. • It increases number of neutrophils (but inhibits their function). • It inhibits production of interleukin 2 (IL-2) by lymphocytes. • It antagonizes the synthesis, secretion and actions of interleukin 1. • High conctrations of glucocorticoids interfere with antibody production from B-lymphocytes. N.B. • * Large doses of glucocorticoids can lead to fulminating infection. • * On the other hand, this ability of glucocorticoids to suppress immunity makes them useful in prevention of immunological rejection of transplanted organs. Anti – Inflammatory Effects of Cortisole: • Cortisol stabilizes the membranes of lysosomes so prevents the release of their proteolytic enzymes. • It diminishes vasodilation. • It decreases migration of white blood cells into the inflammed area.