Endocrine System Overview (Summary) PDF

Summary

This document provides a summary of the endocrine system, detailing various hormone types, their functions, and mechanisms of action. It covers topics such as hormone classification, water-soluble versus lipid-soluble hormones, and the roles of the hypothalamus, adrenal glands, and thyroid in regulating bodily functions.

Full Transcript

Endocrine system overview - Endocrine hormones travel in blood to local or distant receptors. - Response takes minutes to hours. - Each hormone fits exactly into receptor. Hormones - Peptides/proteins - Chains of amino acids - Cannot be given orally (broken down in GI trac...

Endocrine system overview - Endocrine hormones travel in blood to local or distant receptors. - Response takes minutes to hours. - Each hormone fits exactly into receptor. Hormones - Peptides/proteins - Chains of amino acids - Cannot be given orally (broken down in GI track) - **Examples**: oxytocin, insulin - Amino acid derivatives - Synthesised from tyrosine. - **Examples**: thyroid hormones, adrenaline, dopamine - Steroids - Derived from cholesterol. - **Examples**: testosterone, estrogen - Eicosanoids (paracrine) - Signalling molecules - Polyunsaturated fatty acid derivatives - **Examples**: PGE2 - Water soluble hormones travel freely through the blood, whereas lipid soluble hormones travel in the blood bound to transport proteins. - Hormones that are water soluble (peptides & proteins) generally have their hormone receptor located on the cells surface since it cannot easily cross the phospholipid bilayer. - Hormones that are lipid soluble (steroid & thyroid hormones) generally have their hormone receptor in the cytoplasm since they can easily cross the membrane. - **Examples of water-soluble hormones:** - Amines - Peptides/proteins - Noradrenaline - TSH - Growth hormone - Water soluble hormone binding 1. bind to membrane receptor. 2. Binding activates a G protein. 3. Activated G protein activates adenylyl cyclase. 4. Adenylyl cyclase catalyses the conversion of ATP to cAMP. 5. cAMP activates protein kinases. 6. Protein kinases phosphorylate proteins in the cytoplasm, this activates these proteins allowing them to alter cell activity. - **Examples of lipid-soluble hormones:** - Testosterone - Progesterone - Cortisol - Aldosterone - Lipid soluble hormone binding 1. Lipid soluble hormone diffuses through plasma membrane. 2. Hormone binds to receptor in cytoplasm forming receptor-hormone complex. 3. Receptor-hormone complex enters the nucleus and triggers gene transcription. 4. Transcribed mRNA is translated into proteins that alter cell activity. Hypothalamus - Links the brain to the endocrine system. - Produces hormones that help in regulating the body. - Controls the function of the pituitary gland via stimulating the release or inhibiting the release of hormones. - Posterior pituitary hormones released = ADH, oxytocin (releases hormones made in the hypothalamus) - Anterior pituitary hormones released = FSH, TSH, PRL, GH, ACTH (makes and releases hormones in response to signals from the hypothalamus) Adrenal glands - Cortex - Releases steroid hormones such as: - Mineralocorticoids (aldosterone) - Glucocorticoids (cortisol) - Androgens (DHEA, testosterone, estradiol) - Medulla - Makes and releases catecholamines: - Adrenaline (epinephrine) - Noradrenaline (norepinephrine) - Cortex is stimulated by positive regulation by ACTH. Pathways - Negative feedback loop - Stops the release to return levels to normal. - Positive feedback loop - Increases the release to return levels to normal. - diagnostic testing, if low levels of T3 and T4 observed there is a defect in either hypothalamus, pituitary, or thyroid gland. Thyroid - secretes thyroid hormone. - secretion is regulated by the HPT axis. 1. Hypothalamus 2. Anterior pituitary 3. Thyroid gland - TH synthesis, release and storage - Iodine and sodium enter follicular space. - Iodine exits into colloid space whilst chlorine enters follicular space. - Iodine becomes iodide, iodide undergoes oxidation by thyroid peroxidase. - This then becomes TG-mon and TG-di - These molecules couple with thyroid peroxidase, however it is easier to couple two di rather than one mono and one di, so more TG-T4 is made compared to TG-T3. - TG-T3/T4 undergo lysosomal degradation creating T3 and T4. - T4 is most common, however is the less active form so it goes through peripheral conversion to be made into T3 (the active form with a short half-life). - Effects on metabolism - T3 can increase metabolism of carbohydrates, fats and proteins, also increase demand for oxygen and also increase heat production. - Effects on cardiovascular - Increase heart rate and cardiac output. - Increase risk of irregular heartbeat. - Effects on growth/ development - Increase production of essential growth hormones. - Affect production of parathyroid hormone and calcitonin (skeletal) - Primary hyperthyroidism/ hypothyroidism is associated with the thyroid gland. - Secondary hyperthyroidism/ hypothyroidism is associated with either hypothalamus or anterior pituitary. - Cortical (compact/hard) bone - Trabecular (spongy) bone - Bone resorption - Mediated by osteoclast. - Breaking down of the bone matrix. - Bone formation - Mediated Osteoblast - Laying down new organic minerals. - Pathway - Calcium, phosphate, and vitamin D absorbed through diet, - vitamin D is converted into calcidiol in the liver. - In the kidney calcidiol becomes its active form calcitriol, whilst some absorbed material is excreted. - Calcitriol helps with the reabsorption of calcium. - Calcium is used to strengthen bones. - If excess calcium parathyroid gland supresses PTH secretion. (reduces calcium reabsorption) - If insufficient calcium stimulates PTH secretion. (increases calcium reabsorption) Diabetes - Unable to maintain normal blood glucose levels. - When glucose is ingested, it cannot be taken up into tissues therefore remains in the blood causing blood glucose levels to increase causing hyperglycaemia. - Type 1: - Insulin is not produced at all, often born with this disorder. - Autoimmune destruction of pancreatic **beta cells**. - Type 2: - Insufficient insulin production. - Cells fail to respond. - Often due to being overweight. - Glucose is a simple carbohydrate and is a major source of energy. - Hypoglycaemia = low BGLs, \>4mmol/L - Hyperglycaemia = high BGLs \ - Insulin resistance - Impaired pancreatic insulin secretion. - Excessive glucose production. - Symptoms: - Thirst - Urinary frequency - Tired - Slow healing cuts - Lured vision - Ketoacidosis is uncommon since some insulin is still being produced. Macrovascular consequences - Atherosclerosis: pro-coagulant effects -- plaque = thrombus formation - Glucose can stimulate platelet activation. Obesity - Chronic and metabolic disease - Energy intake exceeds energy expenditure.

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