Endocrine Physiology

·         In the world of Hormone, GH is like Hermaphrodite.

In the world of Hormone, Thyroxine is the Foundation Hormone, having permissive action on all other Hormones to act.

·         Androgen decreases Binding protein of lipid hormone, whereas Estrogen increases it.

·         Glucagon & Cortisol has permissive relationship for action.

·         Catecolamine & Cortisol has  also permissive relationship for action.

·         Catecolamine & Thyroid has  also permissive relationship for action.

·         All Releasing Hormones: from ARCUARE & VM Nucleus BUT GnRH from PREOPTIC NUCLEUS

·         Nonpulsatile: TRH, TSH

Pulsatile: others

·         Zona Glomerulaosa is not under control of ACTH, but under Angiotensin & K+. Damage to it is an Endocrine Emergency.

·         Desmolase is activated by ACTH, AT II & K+.

·         In 21-OH def: AT II increases

In 17-OH def & 11-OH def: AT II decreases

·         In 17-OH def & 11-OH def: increase BP is due to 11-DEOXYCORTICOSTERONE and not ALDOSTERONE

·         Cortisol activates: Pyruvate Carboxylase (makes OAA) & PEPCK (makes PEP) INSULIN INHIBITS BOTH.

·         Cortisol promotes GLYCOGENOLYSIS in MUSCLE, but it promotes GLYCOGEN SYNTHESIS in LIVER.

·         CRH from Hypothalamus causes release of POMC from Ant Pitutary.

POMC: 1. ACTH

               2. beta lipoprotein-> beta MSH & Endorphin

Alpha MSH is subunit of ACTH.

·         ALDOSTERONE saves Na+ by creating concentration gradient.

ALDOSTERONE loses K+ & H+ by creating electrical gradient.

·         There is NO EDEMA in PRIMARY Hypo/Hyper ALDOSTERONISM.

·         EDEMA is present in SECONDARY HyperALDOSTERONISM.

·         In Space/Weightlessness: decrease ALDOSTERONE, ADH & increase ANP = increase URINE FLOW

·         Target cells of GLUCAGON are on the LIVER & the LIVER & the LIVER. (not muscle & adipose)

·         Remember Amino Acid causes increase in both GLUCAGON  & INSULIN.

·         GH has both Catabolic & Anabolic (increase uptake of AA like insulin) Action.

·         EPINEPHRiNE promotes CORI’s Cycle. (Glycogen-Lactate-Glucose) (anarebic)

·         EPINEPHRINE does not breakdown aminoacid.

·         Ca x PO4 > Solubility Product = Bone deposition

Ca x PO4 < Solubility Product = Bone resorption

·         Both deficiency & excess of VITAMIN D leads to bone loss.

·         Activity of Thyroid hormone depends on:

4.       Presence of 3 iodines

5.       5’ position must be empty

·         Hypothyroid Patient have RESTING BRADYCARDIA, but remember that thet may present eith Tachycardia due to the episode of Hypoglycemia.

·         GOITER is euthyroid Until Proved Otherwise.

·         The release of TSH from pituitary depends on T4 in blood (not on blood T3) & level of T3 in Pitutary. That’s why inspite of being Euthyroid Goiter patient, their gland continues to enlarge as they have less T4. (T3 remains normal)

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·         Because it lacks 3 beta-hydroxysteroid dehydrogenase, the enzyme that converts pregnenolone to progesterone (the initial step in both glucocorticoid and mineralocorticoid synthesis), the fetal cortex synthesizes primarily dehydroepiandrosterone.

·         Prolactin is the main hormone of lactation. Hormone levels increase early in pregnancy due to the influence of estrogens. However, lactation does not occur early in pregnancy because estrogens and progesterone inhibit the interaction of prolactin with receptors located on the alveolar cell membranes. At term, estrogen and progesterone levels decrease and milk production begins usually within three days of delivery.

·         Calcium deficiency evokes a synergistic sequence that increases PTH and 1,25-(OH)2-D secretion. The combined actions of these two hormones increase the inflow of calcium and restore plasma concentrations to normal. They simultaneously dispose of the inflow of extra phosphate by enhancing its renal excretion.

In contrast, phosphate deprivation evokes a synergistic sequence that increases 1,25-(OH)2-D secretion, but reduces PTH secretion. The result is to restore the plasma phosphate concentration toward normal while disposing of the inflow of extra calcium by increasing its renal excretion.

·         FSH acts directly on the Sertoli cells of the seminiferous tubules to initiate mitotic and meiotic activity of germ cells. LH effects are thought to be mediated via stimulation of testosterone secretion by the Leydig cells.

·         Because fetal cortex lacks 3β- hydroxysteroid dehydrogenase, the enzyme that converts pregnenolone to progesterone (the initial step in both glucocorticoid and mineralocorticoid synthesis), the fetal cortex synthesizes primarily dehydroepiandrosterone.

·         GH hormone exerts a wide variety of effects on body metabolism, including increased protein synthesis, decreased use of carbohydrate, and increased use of fat. The net effect is the accumulation of protein and conservation of carbohydrate at the expense of fat stores.

·         Synthesis and secretion of melatonin are increased in the dark via input from norepinephrine secreted by postganglionic sympathetic neurons. Melatonin is synthesized in the pineal gland from the amino acid tryptophan. Pinealomas (tumors of the pineal gland) that destroy the pineal gland and reduce secretion of melatonin and cause hypothalamic damage may cause precocious puberty by removing the inhibitory effect of melatonin on the pituitary response to gonadotropin-releasing hormone.

·         α-Glycerophosphate is produced in the course of normal use of glucose. In the absence of adequate quantities of a-glycerophosphate—a normal acceptor of free fatty acids in triglyceride synthesis—lipolysis will be the predominant process in adipose tissue. As a result, fatty acids will be released into the blood. The prevailing insulin level is decisive in the selection of substrate by a tissue for the production of energy. Insulin promotes use of carbohydrate, and a lack of the hormone causes use of fat mainly to the exclusion of uptake and use of glucose, except by brain tissue. Indirect depression of use of glucose by excess fatty acids is a result, and not a contributing cause, of increased use of fat.