1. Endocrine System General Physiology Tony Serino, Ph.D.
Biology Department
College Misericordia

2. Endocrine System
Controls and modifies the internal environment by releasing chemicals (hormones) into the blood
Slower response time but longer duration of action compared to nervous system

3. Chemical Messengers (hormones)
Hormone –secreted by cell into blood and acts on another cell some distance away
Neurohormone –secreted by neuron into blood to affect a target cell some distance away
Local hormones –secreted by cell into interstitial fluid to affects cells nearby
Paracrines –affect neighboring cells
Autocrines –affect the secreting cell
Pheromones –secreted by cell onto body surface to affect cells of another individual

4. Hormones Chemical Classification
Amines –single or few amino acids, most water soluble
Epinephrine, Thyroxine (but water insoluble), Melatonin
Peptides –short to long chains of amino acids; water soluble, most hormones are of this type
GH, FSH, LH, Insulin, Glucagon, ADH, etc.
Steroids –derivatives of cholesterol; water insoluble
Estrogen, Testosterone, Progesterone, Cortisol, Aldosterone

5. Amine Hormones
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Tyrosine

6. Steroid Hormones

7. Typical Protein Pathway
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8. Steroid Hormone Synthesis Pathway
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PKA –phosphokinase A
StAR –steroidogenic acute regulating protein (facilitates transfer of cholesterol from outer to inner membrane)
PBR helps anchor StAR to inner membrane

9. Steroid Hormones of Adrenal Cortex
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10. Steroids of Gonads
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11. Characteristics Common to all Hormones
Must have target cell with appropriate receptor molecules
Receptor-hormone complex must trigger events in target cell that changes its physiology
Mechanisms for deactivating the hormone response must be present

12. Controlling Hormone Response
Half-life of the hormone
Physiological range
Modifying target cell response
Up and down regulation of receptors
Turning on/off secretion
Negative feedback
Control by other hormones, neurons and metabolites
Hormone Interactions

13. Control of Hormone Secretion
(Tropic hormones)

14. Hormone Interactions
Permissive-one hormone increase effect of another (usually by up-regulation)
Synergistic –2 or more hormones working together to create effect greater than the individual hormone
Antagonistic –hormone with opposite effects
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15. Mechanisms of Hormone Action
2nd messengers
Water Soluble
Water
Insoluble
Carrier protein

16. 2nd Messengers: cAMP

17. 2nd Messengers: IP3 and Ca++-Calmodulin

18. Steroid Hormone Transduction

19. Different Styles of Secretion
Prohormone –a hormone that is made as a larger (inactive form) that must be changed prior to secretion (allows for storage of hormone in secreting cell) (may be first made as larger precursor –a preprohormone) Ex.: proinsulin, pro-opiomelanocortin
Prehormone –a hormone that is secreted in an inactive form that must be changed near or in the target cell Ex.: Thyroxine, Angiotensinogen

20. Proinsulin

21. Types of Endocrine Disorders
Hypersecretion (primary and secondary)
Too much secretion of the hormone
Hyposecretion (primary and secondary)
Too little secretion of hormone
Hyporesponsiveness
Normal secretion, but little to no response by target cells
Hyperesponsiveness
Normal secretion, but increased sensitivity and response by target tissue

22. Endocrine Glands

23. Hypothalamus Control of Pituitary
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24. Posterior Pituitary

25. Hypophyseal Portal Blood Flow
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26. Anterior Pituitary

27. Releasing Hormones of Hypothalamus
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28. Long and Short Loop Feedback
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29. Control of Growth
Growth periods: prenatal and postnatal (consists of pre-puberal (especially the first 2 years –infancy) and puberty
Several factors influence growth: genetics, diet, health, and hormonal balance
Prenatal growth dominated by insulin secretion, post-natal dominated by GH, thyroxine, and sex hormones

30. GH secretion and effects
GH secretion stimulated by exercise, fasting, sleep (diurnal rhythm), stress, decreased plasma glucose, increased plasma AA (such as after a high protein meal)
Increase protein synthesis
Increase differentiation
(increase mitosis)

32. GH interactions with other Hormones
Thyroxine: essential and permissive for GH
Needed to maintain energy levels for growth
Increases sensitivity of target cells to GH effects
Insulin: essential for GH effects
Dominant hormone for pre-natal growth
Estrogen and Testosterone: surge at puberty stimulates GH release, synergistic with GH anabolism; also trigger epiphyseal closure
Cortisol: anti-growth effects; decrease GH secretion, cell division, and increase catabolism

33. GH pathologies Hypersecretion:
Gigantism –in children with responsive epiphyseal plates
Acromegaly –in adults, with closed epiphyseal plates

34. Gigantism
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Identical twins (one with GH secreting tumor)

35. GH pathologies Hypofunction: Dwarfism –in children
Pituitary –decreased GH secretion
Laron –decreased responsiveness due to lack of GH receptors
28 yo woman with pituitary dwarfism; 45” tall
Achondroplastic Dwarfism (genetic dwarf) due to failure of cartilage to form in epiphyseal plate

36. Thyroid Location

37. Thyroid Follicle Parafollicular cells  calcitonin
(follicular cells  thyroxine)
Parafollicular cells  calcitonin

38. T3 & T4 Formation and Secretion

39. T3 & T4 Actions: Increase metabolic rate
Increase carbohydrate absorption in SI
Increase fatty acid release from fat cells
Stimulate Na-K ATPases throughout body
Up-regulate ß-adrenergic recp. in many tissues, esp. heart and nervous tissue

40. Control of Thyroxine Secretion
Short loop
Long loop

41. Thyroid Malfunction
Hypothyroidism (cold intolerant, tend toward weight gain)
Endemic goiters –due to iodine deficiency
Hashimoto’s disease (autoimmune destruction of thyroid tissue)
Cretinism –i thyroxine in child results in igrowth (dwarf) and severe mental retardation
Myxedema –i thyroxine in adult, leads to swelling of facial tissues plus other symptoms

42. Cretinism -due to low Iodine in mother’s diet
-Rare in US where Iodized salt is used (1 NaI for every 10,000
NaCl molecules)

43. Thyroid Malfunction
Hyperthyroidism (Thyrotoxicosis, Graves Disease) (heat intolerant, weight loss, increased sympathetic activity)
Toxic goiters (Graves disease) –Ab may stimulate thyroid without negative feedback control
Exophthalmoses –symptom present in many hyperthyroid patients

44. Exophthalmoses before and after
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45. Parathyroid Location

46. Parathyroid

47. PTH Actions Stimulates resorption of bone  hCa+ and PO4- in blood
Stimulates Ca+ absorption in intestine (active Vit. D3 necessary for Ca+ absorption)
Stimulates Ca+ reabsorption and PO4- excretion in kidney
Stimulates Vit. D3 formation (skin) and activation (kidney)
Vital for life

48. Adrenal Location and Structure

49. Steroid Hormones of Adrenal Cortex
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51. GAS (General Adaptation Syndrome)

53. Adrenal Malfunction Hypersecretion
Cushing’s syndrome –increase in glucocorticoids
Usually due to over secretion of ACTH by pituitary or from adrenal cortex tumors stimulating an increase in glucocorticoids. Characteristic obesity of trunk only and development of “buffalo hump” (a fat pad behind the shoulders). Will develop hypertension, atherosclerosis, muscular weakness and fatigue.
Conn’s syndrome –excess amount of aldosterone
Salt imbalance, water retention, hBP, muscle weakness
Adrenogenital syndrome –too much androgen
Premature sexual development in children or masculinization in women

54. Cushings
(buffalo hump)
Obesity of trunk

55. Adrenogenital syndrome
A 15 yo girl, note typical masculine build, under developed breasts, and excessive body hair

56. Adrenal Cortex Malfunction
Hyposecretion –Addison’s disease
Due to decrease amounts of mineral and glucocorticoids
Can be due to over use of steroids or an autoimmune mechanism resulting in destruction of the gland
Dehydration, K+ loss, iBP, fatigue, pigmentation deepening (bronzing of skin) may be symptom of loss of negative feedback

57. Pineal Gland
Plays a major role in circadian rhythm control through its sympathetic connection to the hypothalamus
Melatonin increases at night and decreases during daylight
Implicated in the control of major life changes (such as the onset of puberty and adulthood

58. Thymus Gland
Bilobed organ that is largest in children, but begins to regress sharply at the onset of puberty (around age 11)
It is the site of T-cell lymphocyte production and produces hormones (such as, thymosin) that modifies their physiology