Alex's Endocrinology

Page 54

LCRS

Alexandra Burke-Smith

LUTEAL PHASE 

After the gonadotrophin surges, there is an increase in the production of steroids 17-BETA-OESTRADIOL and PROESTERONE o If fertilization does not occur, progesterone, oestradiol and inhibin exert a negative feedback on LH and FSH release, leading to LUTEOLYSIS and MENSTRUATION The steroid concentrations then start to decrease towards the end of the cycle

Clinical Correlates Amenorrhoea    

Definition: absence of menstrual cycles Primary – never had periods Secondary – did happen but have stopped OLIGOMENORRHOEA – infrequent cycles o Causes: various  Absence of LH surge e.g. due to insufficient oestrogenic effect at the end of follicular phase etc

Infertility  

Means unable to get pregnant o Men – unable to IMPREGNATE Various causes: o Physical o Psychological o Emotional o Endocrine problems Excess prolactin (e.g. from a PROLACTINOMA) can be a cause of infertility

The parathyroids and the endocrine control of calcium metabolism Endo 12 - Professor John Laycock (j.laycock@imperial.ac.uk)

1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

List the functions of calcium in the body. Identify the principal organs involved in calcium metabolism. Identify the bone cells and their functions. List the principal hormones which regulate blood calcium ion concentration, and their sites of synthesis. Briefly describe how parathormone, 1,25-dihydroxycholecaciferol (calcitriol) and calcitonin are synthesized. Describe the principal effects of parathormone, 1,25-dihydroxycholecaciferol and calcitonin on bone, the kidneys and the intestinal tract. Describe the mechanisms of action of parathormone, 1,25-dihydroxycholecaciferol and calcitonin. Explain how parathormone, 1,25-dihydroxycholecaciferol and calcitonin production are controlled, identifying the principal stimulus in each case. List the principal causes of hypocalcaemia. List the principal causes of hypercalcaemia. 54


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