Endocrine Physiology Lecture Notes PDF

Endocrine Physiology Lect. 2 Introduction II Dr. Majid H. Ahmed Hormone Receptors Location: – In or on the surface of the cell membrane –peptides, catecholamines – In the cell cytoplasm – steroid hormones – In the cell nucleus – Thyroid hormones Hormonal receptors are large...

Endocrine Physiology Lect. 2 Introduction II Dr. Majid H. Ahmed Hormone Receptors Location: – In or on the surface of the cell membrane –peptides, catecholamines – In the cell cytoplasm – steroid hormones – In the cell nucleus – Thyroid hormones Hormonal receptors are large proteins The number of receptors does not remain constant (from day to day, even from minute to minute). Each cell has 2,000 – 100,000 receptors Hormone Receptors Hormones determine the sensitivity of the target tissue by regulating the number or sensitivity of receptors. 1. Down-regulation of receptors A hormone decreases the number or affinity of receptors for itself or for another hormone. e.g. in the uterus, progesterone down-regulates its own receptors and the receptors for estrogen. 2. Up-regulation of receptors A hormone increases the number or affinity of receptors for itself or for another hormone. e.g. in the ovary, estrogen up-regulates its own receptors and the receptors for LH. Mechanism of Peptide Hormone Action  Mechanism of Hormone Action  cAMP is degraded to 5’-AMP by phosphodiesterase, which is inhibited by caffeine. Mechanism of Hormones Action Signal Amplification of the Hormone Sensitivity of the Hormone  Sensitivity is defined as the hormone concentration that produces 50% of the maximal response.  If more hormone is required to produce 50% of the maximal response, then there has been a decrease in sensitivity of the target tissue.  If less hormone is required, there has been an increase in sensitivity of the target tissue. Stimuli for Hormone Secretion A) Humoral Stimuli for Hormone Secretion B) Neural Stimuli for Hormone Secretion C) Hormonal  Control of Hormone Secretion 1. Negative feedback mechanism Prevents over activity of hormone system Depends mainly (directly or indirectly on biologic action of H., not on its level.  Control of Hormone Secretion 2. Positive feedback mechanism, which occurs when the biological action of the hormone causes additional secretion of the hormone  estrogen before ovulation  Secretion of LH more estrogen more LH until reach appropriate level then follow negative feedback loop.  Control of Hormone Secretion 3.Cyclical variation influenced by seasonal changes, stages of development and aging, circadian cycle, sleep etc. –Gonadal hormones - development and aging, seasonal changes, lunar cycles –ACTH, glucocorticoids etc. – circadian cycle 4. Reflex release influenced by stress and new situations – Stress hormones – prolactin, renin-angiotensin-aldosterone system 5. Feedforward control describes an anticipatory mechanism –Glucagon-like peptide-1 secretion from enteroendocrine cells in the small intestine is triggered by glucose in the gut lumen and acts as a feedforward signal to insulin secretion before the ingested glucose is absorbed into the blood. Hormone Interactions  Synergistic: 2 or more hormones work together to produce a particular result that is greater than each individual hormone. e.g.: FSH & testosterone on spermatogenesis  Permissive: Presence of 1 hormone in adequate amounts enhances the responsiveness of a target organ to a second hormone. e.g. Cortisol had permissive action on catecholamine and on glucagon.  Antagonistic: Actions of 1 hormone inhibit the effects of other hormone. e.g. Insulin and glucagon Endocrine Pathophysiology Underproduction.  Primary: defect in the gland. e.g. destruction of the adrenal cortex (↓ cortisol)  Secondary: defect in the stimulating H. of the gland. e.g. hypopituitirism (↓ ACTH → ↓ cortisol from adrenal cortex).  Apparent: defect in receptor, e.g. psuedohypoparathyroidism. Endocrine Pathophysiology Overproduction:  Primary: usually due to tumor in the gland e.g. adrenocortical adenoma (⇈ cortisol) even with absence of ACTH.  Secondary: due to excess input to the target gland e.g. tumor in pituitary ⇨ ⇈ ACTH ⇨ ⇈ cortisol from adrenal gland.  Apparent: due to activation of receptors or cellular components due to a mutation. Therefore, the function of the target gland is activated even in the absence of normal hormonal stimulation. e.g. Liddles syndrome (the renal epithelial Na+ channel is constitutively activated and mimics the effects of too much aldosterone, even though aldosterone is low.