Endocrine System: Study Notes

1. What regulates hypothalamic releasing factors hormone secretion from the anterior pituitary? 2. What are the hor- - TRH mones of the an- - CRF terior pituitary? - GnRH - MSH releasing factor (melanocyte-stimulating hormone) - prolactin-releasing factor - growth hormone releasing factor 3. What does - stimulates MSH the MSH-releas- - targets melanocytes ing factor stimu- - effects melanin synthesis late? What does it target + what are its effect? 4. Describe the endocrine control of thyroid hormone secretion: - hypothalamus releases TRH (+ feedback) - enters the anterior pituitary which releases TSH (+ feedback) - enters the thyroid gland which produces thyroxine (+feedback) - thyroxine negatively feeds back into the anterior pituitary which negatively feeds back to the hypothalamus to stop the production of thyroxine 5. TRH stand for: thyrotrophin releasing hormone 6. What is the differ- - T3 has 3 iodines + is the active form ence between T3 - T4 has 4 iodines + is the inactive form + T4? 7. Describe the process of thyroid hormone biosynthesis: 1) TSH binds to TSH receptor on the follicular cells of thyroid 2) this increases production of thyroglobulin which is then released into colloid 3) TSH stimulates the uptake of iodine from blood into 1/8 follicular cells using Na+/I- symporter 4) TSH increases the activity of TPO 5) TPO converts iodide to iodine (oxidation) 6) TPO facilitates the incorporation of iodine onto the tyrosine's of thyroglobulin 7) TPO also couples MIT with DIT (T3)/ DIT + DIT (T4) 8) T3 + T4 enter the follicular cell via endocytosis 9) proteases separate the thyroglobulin from T3 + T4 10) thyroxine-binding globulin (TBG) transports T4 + T3 into peripheral tissues 8. What is the process called when T4 is changed to T3? deiodination 9. Why is T4 converted to T3? T3 is more biologically active 10. Where is T4 - there is more T4 extracellularly more concentrat- - more T3 intracellularly ed compared to T3? 11. What converts T4 2-deiodinase (D2) which is located on the ER to T3? 12. Describe the steps for the HPA axis (stress response system): 1) ACTH stimulates synthesis + release of glucocorticoids (hydrocortisol) from the adrenal cortex (zona fasciculata) 2) CRF from the hypothalamus regulates ACTH release 3) mineralocorticoid (aldosterone) is released from the adrenal cortex (zona glomerulosa) + is controlled by the renin-angiotensin system 4) CRF is regulated by neural factors + negative feedback from the plasma glucocorticoids 13. Describe the steps of the renin-an- 1) renin catalyses the conversion of angiotensin into angiotensin I 2) angiotensin-converting enzyme (ACE) converts angiotensin I to II 2/8 giotensin system: 3) angiotensin II acts on receptors in the adrenal glands to stimulate the secretion of aldosterone which increases BP 14. What happens to insulin once it leaves pancreatic beta cells? 1) insulin enters the bloodstream 2) insulin binds to insulin receptors on insulin-responsive tissue (muscle, liver + fat) 3) this facilitates the uptake of glucose into insulin responsive tissue 4) blood glucose levels are lowered 15. What is the insulin receptor made of? a complex of 2 alpha + 2 beta subunits (transmembrane spanning proteins) held together by disulphide bridges 16. What do the al- insulin binding site pha-subunits in the insulin receptor form? 17. What do the B-units of the insulin receptor possess? the intracellular portion of the B units possess intrinsic tyrosine kinase activity 18. What does insulin binding promote? auto-phosphorylation of tyrosine residues on the intracellular domains 19. What do phosdocking sites which relay message from the activated phorylates tyro- receptor to the cell sine residues act as? 20. How does down- occupied receptors aggregate into clusters which are subregulation ocsequently internalised into vesicles cur? 21. What are the short-term ac- 1) recruits glucose transport channels (GLUT4) 2) increases glucose uptake into cells 3/8 tions of the cellular events triggered by activated insulin receptors? 3) increases glycogen synthesis (insulin converts glucose to glycogen) 4) decrease in both gluconeogenesis + glycogen breakdown 22. Insulin receptor nucleus to promote gene expression activation also signals to the ... 23. How does insulin resistance occur? (type 2 diabetes) 1) diet high in sugars + carbs can cause high insulin levels 2) the tissues that insulin exerts its effects become unresponsive 3) down-regulation of the insulin receptor (loss of insulin receptors from cell surface) 4) impaired signalling mechanisms 5) insulin-sensitive tissues are unresponsive + resistant to effects of insulin 6) glucose can no longer enter the cell leading to a further rise in blood glucose 7) pancreatic B cells produce more insulin resulting in hyperinsulinemia 8) pancreatic B cells become depleted of insulin (supply cannot keep up with demand) so impaired insulin secretion ensues 24. How does promote the development of small groups of follicles, each the follicle-stim- of which contains an ovum ulating hormone + LH act on the ovaries? 25. What is the Graafian follicle (GF)? produced when 1 follicle developed faster than + secreted oestrogen 26. What happens to - 1 becomes the Graafian follicle the follicles pro- - the others degenerate duces in the follicular phases? 4/8 27. What is the prolif- endometrium regeneration (days 5,6 to mid-cycle) erative phase? 28. What happens endometrium increases in thickness + vascularity during proliferative phase? 29. What happens at there is prolific cervical secretion of mucus (pH 8-9), which peak oestrogen is rich in protein + carbohydrates + facilitates the entry of levels? (prolifera- sperm tive phase) 30. What does high endogenous oestrogen secretion do? (proliferative phase) - just before mid-cycle, it sensitises LH-releasing cells of the anterior pituitary to the action of GnRH to cause surge in LH secretion 31. What happens in the Luteal phase? ruptured follicle proliferates + develops into the corpus luteum which secretes progesterone which acts on the oestrogen-primed endometrium to render the endometrium suitable for implantation of the fertilised ovum - this then causes rapid swelling + rupture of the Graafian follicle, resulting in ovulation 32. How does the lev- progesterone exerts negative feedback on the hypothalaels of LH demus + pituitary crease during the luteal phase? 33. What happens if - progesterone secretion stops fertilisation + im- - triggering menstruation plantation does - corpus luteum degenerates not occur? 34. What happens corpus luteum continues to secrete progesterone which if fertilisation + negatively feeds back to the hypothalamus + pituitary to implantation oc- prevent ovulation curs? 5/8 35. What is the ovari- - follicular phase an cycle? - ovulation - luteal phase 36. What is ovulation? The release of an egg from the ovary 37. What is menopause? - the end of female reproductive life - where the woman has no menstruation for 12 months 38. List 4 physi- itchy cal symptoms of - hot flashes menopause: - bloating/weight gain - fatigue 39. List 4 psycholog- - dizzy ical symptoms of - poor memory menopause: - irritability - depressive moods 40. What is perimenopause? stage immediately before menopause where physical changes begin to occur 41. What hormonal changes occurs during perimenopause? - uterine lining thickness - oestrogen decreases as ovaries run out of eggs - ovulation + periods become irregular - progesterone not produced if no ovulation occurs 42. What is The time after menopause post-menopause? 43. What hormonal - very little oestrogen released change occur - uterine lining does not thicken during - ovulation + periods does not occur post-menopause?- progesterone is not produced 44. What hormones - FSH increase signif- - LH icantly during menopause? 6/8 45. Where does progesterone come from? corpus luteum, which is formed after ovulation 46. What is oestrogen breakthrough bleeding? ovulation doesn't occur + endometrial lining breaks down 47. What does oebone mass + density by reducing activity of osteoclasts strogen protect + how? 48. Why does the amount of bone fractures increase after menopause? oestrogen stops being released causing an increase in bone resorption, causing increased age-related loss of bone density 49. What is the link it is though that oestrogen reduces levels of LDL cholesbetween oestro- terol + raises HDL cholesterol gen + cholesterol? 50. When is parathy- when plasma Ca2+ conc rises roid hormone secretion inhibited? 51. When does when there is a reduced conc of Ca2+ in the plasma parathyroid hormone secretion happen? 52. How do parathy- via the parathyroid chief cells roid hormones secrete Ca2+? 53. 7/8 How does bone resorption occur? osteoclasts break down the tissue in bones + release minerals, causing transfer of Ca from bone tissue to the blood 54. What is bone re- loss of bone tissue sorption? 55. How does 1) Ca2+ levels drop in the blood, causing PTH secretion parathyroid hor- which stimulates the synthesis of biologically active Vitamone (PTH) + cal- min D (calcitriol) in the kidney cium homeosta- 2) enhances reabsorption of Ca2+ from kidney distal sis occur? (4) tubules + causes urinary phosphate excretion 3) increases reabsorption of Ca2+ + PO4- in the gut 4) increased mobilisation of Ca2+ in bone via stimulation of osteoclasts (which increases bone resorption) 56. How does 98% of Ca is in the form of crystals calcium provide mechanical strength? 57. What happens parathyroid glands compensate by producing too much PTH (hyperparathyroidism) if there's not enough calcitriol (D3)/calcium? 58. What are 2 symp- - osteoporosis (bone weakening) toms of hyper- increased risk fracture parathyroidism? 8/8