Test 1 Study Guide Glands 2 types o Exocrine ducts leading to external environment Merocrine cell secretes product Apocrine cell pinches off with secretory product inside Holocrine entire cell goes off with product and disentigrates o Endocrine ductless secrete hormones into blood Homeostasis balances autonomic branches of the nervous system parasymtpathetic and sympathetic Usually negative feedback o Sensor detects regulated variable sends to integrating center integrating center compares to set point error signal integrating center sends output to effectors to return back to set point o Positive feedback loop stimulus must end for response to end o Chemical Messenger Types o Autocrine local communication receptor on same cell o Paracrine local communication neighboring cell o Cytokines peptides or proteins for cell development differentiation and immune response o Neurotransmitter mostly amino acids hydrophilic o Neurohormone neuron secretes into blood o Hormone released into blood to target cell with receptor o Types of messenger Amino acid based amine amino acid with amine group peptide protein prepropeptide propeptide peptide Steroid hydrophobic made from cholesterol Uses direct gene activation Eicosanoids includes prostaglandins made from lipids o Hydrophobic messengers needs carrier in blood and cytosol either cytosolic or nuclear slower response for release can just diffuse out longer half life because it is bound o Hydrophilic can t pass membrane so need a surface receptor fast response for release it must be exoctyosed Hormone Interactions o Antagonism two hormones effects oppose each other like glucagon o Additive summation of two hormones use different receptors seen and insulin in GH o Synergism two hormones favor each other exceeds sum like glucagon and cortisol on blood glucose o Permissiveness need one hormone for another to work such as a steroid estrogen causing expression of a receptor oxytocin receptor so oxytocin can work in the uterus Hormone levels are controlled through secretion amount bound metabolism and half life The magnitude of response depends on the concentration of messenger number of receptors present on or in cell and receptor affinity for ligand When too much messenger the receptor can be down regulated when to little up regulation this is done by altering shape to change affinity or changing the number of receptors o Case study Androgen Insensitivity Syndrome AIS cant bind androgens so unresponsive to testosterone Pathologies in secretion o Primary problem with organ secreting hormone o Secondary pituitary tropic hormone problem o Tertiary problem with hypothalamic tropic hormone Signal transduction signal molecule receptor intracellular signal target protein response Membrane Receptor Types o Enzyme linked ex Tyrosine kinase and guanylate cyclase GTP to cGMP o G protein coupled Gas stimulatory stimulates adenlyate cyclase to make cAMP hormone binds receptor G protein binds receptor and GTP replaces GDP alpha subunit dissoaciates and activates adenylate cyclase cAMP activates PKA Epi glucagon LH PTH and ACTH use this pathway cAMP degraded by phosphodiesterase to stop response Gai inhibits adenylate cyclase lowering cAMP GHIH SST aka SMS Gaq activates PLC cause conversion of PIP2 to IP3 intracellular calcium release leading to electrical changes exocytosis muscle contraction ca calmodulin complex to activate protein kinase and DAG activation of PKC Vasopressin ADH TSH Angiotensin o Channel linked ligand gated G protein coupled You know it faster when receptor is on channel slower when o Exogenous agonists and antagonists can alter the feedback loop like if you take testosterone you re testes will shrink because they do not need as much testosterone side note made in class Hormonal release can be caused by hypothalamic stimulation pituitary stimulation a humoral response stuff in the blood such as low calcium or blood sugar or circadian rhythms which use melatonin ex Varying levels or cortisol and GH Hypothalamus and endocrine glands have different groups of cells that secrete different products so if you have a tumor different locations will have different pathological effects Hypothalamus o Uses releasing and inhibiting hormones and is the master control o Makes neurhormones that are stored at nerve endings released in pulses into portal veins hypothalamic hypophyseal o Receives short loop pituitary product and long loop feedback final product o Classes of hypothalamus hormones Neuropeptide hormones ADH Oxytocin Hormone releasing hormones GnRH Gq pathway TRH Thyrotropin Releasing Hormone GHRH CRH PRF PRH messenger system not well studied G protein Hormone release inhibiting hormones GHIH SST SMS blocks secretion of GH TSH and prolactin Gi pathway PIH PIF aka dopamine Gi Pituitary Gland figurehead o Anterior glandular Adenohypophysis TSH Thyrotropin Targets thyroid Glycoprotein Gs Pathologies o Hyperthyroidism increased thyroid hormone leading to hotness weight loss and irregular heart beat o Hypothyroidism weight gain intolerance to the ACTH targets adrenal cortex cold Gs GPCR cAMP stimulates mobilization of cortisol from lipid droplets to make steroid hormones like cortisol Derived from the poly protein propiomelanocortin POMC Pathologies o Hypersecretion o Hyposecretion Cushing s syndrome buffalo hump obesity muscle weakness Over suppression of the immune system High BP hyperglycemia weak bones depression Masuclanization from androgen hypersecretion Addison s syndrome can t adapt to stress well without cortisol Bronze skin tone weak muscles You get more progenitor hormone POMC because it is the ACTH precursor so you build up other compounds from more melanocyte stimulating hormone and gain fearlessness from endorphins FSH targets testes ovaries sperm and follicle development respectively glycoprotein that uses Gs LH targets testes ovaries testosterone production and ovulation respectively glycoprotein that uses Gs GH Targets entire body Gs pathway Growth of skeletal muscles and long bones stimulates IGF 1 in liver causing cell division tissue growth breakdown of fats and production of proteins Hypoglycemia increases GH hyper decreases GH deficiency causes increased insulin sensitivity because GH opposes insulin action hypoglycemia Too much GH can lead to diabetes from hyperglycemia Binds to JAK receptor dimerizes and self phosphorylates phosphorylates STAT kinase which dimerizes and translocates to the nucleus activating TFs Repressed by