Transcript for:
Endocrine System Overview

all right hello everyone we are going to start the endocrine system Today Chapter 13 it is um going to be a long one um so we'll start out with some Roots prefixes and suffixes that you'll need to know um for the incron system some of them that you already know Indo means um inside um EXO means outside right um hyper means above hypo means below all right so all right so just some general characteristics of the endocrine system um basically the endocrine system and the nervous system are going to kind of work hand in hand to um perform the function um they're very very interrelated um in order to maintain homeostasis remember homeostasis is that body Zen um to maintain that um that natural internal um that constant state of um of well-being and also you know coordinate information um within the body um it is a unique system in that not all the organs are connected anatomically usually like with the cardiovascular system you know the heart and the blood vessels are connected together um the nervous system is connected together the respiratory system you know it's all connected together with the endocrine system um all the organs are kind of spread out you know you have your um adrenal glands that sit on top of your kidneys and your pancreas it's kind of like in the um underneath your left rib cage um you have glands in your brain um you can see some of the major endocrine glands you know your pituitary gland that's in your brain your thyroid gland parathyroid glands those are going to be kind of like um in your neck area adrenal glands I said were on your kidney um pineal gland is in your brain ovaries and teses those are your reproductive organs um down ovaries are um in your pelvic area testes um I hope by now you know where your testes are males um all right so here you can see where the the glands are um located um okay so more characteris so we have endocrine glands and exocrine glands that make up the endocrine system endocrine glands um endocrine just means internal secretion they um dump their Gunk or their their their substance into typically it says body fluid so typically that's going to be like a bloodstream um they are duct list so when they um dump whatever they're dumping um they're going to dump their stuff into a body fluid and then these these hormones um we'll talk about hormones later on these hormones are going to uh go in through these body fluids typically the bloodstream and they're going to act on these target cells that have receptors on them and a Target cell is just a cell that has a receptor for a specific hormone and receptors are just made from proteins or glycoprotein prots um exocrine glands um are glands that secrete through a duct or a tube to a free apical surface um like your sweat glands your sweat glands um secrete to the outside surface like to your skin um so they can secrete like externally um your gastric um some of your digestive uh enzymes or hormones secrete stuff to a um a specific area inside um inside a hollow space that's um inside your gut so that would be a free or apical surface um and we have these cells um that secrete these chemical Messengers internally we call them local hormones but they're not actually hor hormones um they're called paracrine cells and autocrine cells or paracrine secretions and autoc autocrine secretions and paracrine secretions are going to affect cells that are nearby so for example like white blood cells can secrete um histamine which would dilate nearby blood vessels um autocrine secretions are produced within one tissue and the regulated another tissue within the same organ so for example when there's damage to the liver some cells need to be produced and the liver can use this autocrine signaling process um special chemicals are secreted from the cells of the liver and they act on the same cell making cell division possible um or the base layer of cancer cells they have some genetic material that sends one chemical to the same cell cell um starting the replication process and that's how tumors form in the body so here are some different types of glands um that do um that kind of show the difference between endocrine and exocrine so the thyroid gland for example will secrete their um their hormones directly into the bloodstream so the thyroid gland is an endocrine gland whereas um sweat glands they will dump out their contents into these uh these ducts um or these this this this duct is kind of like a hollow area so that would be an exocrine gland and if you remember from am1 we had the mirrin the apocrine and the holocrine um different types of um exocrine secretions and it depending depending on how much um cellular debris came off um was uh how we categorized if it was a mirrin apocrine or holocrine um all right so characteristics between the nervous system and endocrine system right Mar said that they are very very much interrelated um that both system use um they both communicate with uh via chemicals that bind to receptor molecules um remember that the nervous system releases neurotransmitters into synapses we talked about acetylcholine norepinephrine um nervous system travels a very short distance remember um we have you know that synapse and that synaptic CLE and we had that the the pre um the one neuron connected to the other neuron or we had a pre pre ganglionic neuron and a a postganglionic neuron um or we had a the the the pre synaptic neuron and then we had that skeletal muscle um so those nervous system those those trans neurotransmitters um only travel a very short distance um the endocrine system can travel um a a short distance or um far away uh you know if it's if it's released uh from your thyroid gland and has to go all the way to your big toe or um to your kidneys or to wherever cell it needs to go it has to travel through your bloodstream so it can circulate um long distances um the nervous system is going to respond much quicker than the endocrine system um you know you say when you start walking your nervous system is going to contract your skeletal muscle um rather quickly you know it doesn't take any time at all but if you have to adjust your blood glucose level um your body doesn't like sudden changes in your body so it's going to take a while to um get your blood glucose leveled down to normal or if you have a temperature um of 103° and and if if the endocrine system has um a part to play in that then you know you're not going to go over 103° back down to 98.6 so um once the um remember like when we talked about a um skeletal muscle contraction we had acetycholine and then we had acetylcholine esterase that breaks up the acetylcholine um once that aceto Coline is gone the nervous system is done Contracting the skeletal muscle um so the effects of the nervous system are pretty much quick on quick off where whereas with the endocrine system those effects can last a lot longer than those of the nervous system and here's just like a a summary chart of um of kind of what we just what we just talked about um and when it says uh while it says that the duration of action may be brief or it may last for days even if secretion um ends typically hormones um typically hormones um only last a relatively short amount of time rarely do hormones take days to work what this slide is meaning by lasting for days even if secretion ceases is called Half-Life um you will need to know this comparison chart and how to interpret the differences between um the nervous system and endocrine system so speaking of halflife um halflife is just the interval of time required for one/ half of the hormone or medication or whatever we're talking about to be used up um so for example if we have um you know we'll be talking about a medication here so let's say we we can talk about a hormone um you can insert medication for hormone um but let's say we have 250 milligrams of a certain medication um that has a half life of 30 minutes so uh when we have a half life of 30 minutes um basically all we're going to do is come over here and um we're just going to do our our time of at time wh I was trying to get my pen there we go um Time Zero 30 minutes 60 Minutes 90 minutes 120 150 and 180 and then um so our percentage um we're just going to divide um we're just going to chop it in half every 30 minutes so we're going to start out with 100% of the drug and then after 30 minutes we're going to have 50% of the drug left after 60 minutes we're going to have 50 divid 2 is 25 after 90 minutes 25 / 2 is 12 1/2 um after 100 20 minutes 122 / 2 is 6.25 6.25 ID 2 is 3.125 divid 2 is 1.5625 um so that's the percentage of drug remaining after X number of time so when it comes to how many milligrams are are remaining we started out with 250 milligrams so we're going to start out with 250 milligrams and we just keep dividing by two 250 divid 2 is 125 divid two ID two ID two divided by two divided by two um so if I said you know what percentage of the drug is remaining after 150 minutes you can come and say oh at 150 minutes we only have 3.125% of the drug remaining okay if I said um how many milligrams are remaining after 120 minutes after 120 Minutes we have 15.625 millgram of the drug remaining and that's just kind of how you interpret um this chart um there will be one question like this on the exam um it's not going to be you know I can promise you you're not going to have to go down to the 39625 um your it's it's going to be um it's going to be one where you could kind of do it in your head so um I will say that if you have a hormone that where its effect does last for days um you can pretty much guess it's going to have a long halflife so if we're getting down into the you know we're only here you know 180 minutes um 180 minutes is 3 hours um that's really not a long half life of 30 minutes um but if we're talking if if we're going into like uh let's see what is you know 24 * 3 so 72 hours if we're going in at 72 hours which is three days um you know that's going to be a really long halflife Okay so this is um going back to the slide up here that or this slide and this slide that I was talking about um about the um more on the um traveling uh a very short distance um you can see that the um neurotransmitter you know this space is not a big space um so this would be acetylcholine because it looks like we're looking at maybe some skeletal muscle or um because we have some stations here um so this space here is not a big space whereas the um and the endocrine system has to travel through the bloodstream so it's going to be um a long a long way to go all right here are some different hormones that we'll be talking about um so sometimes you'll hear people talk about um corticotropin releasing hormones sometimes you'll hear it abbreviated as CR um sometimes you'll um so here prolactin releasing inhibiting hormones sometimes you'll hear it as Pi sometimes you'll hear it referred to as dopamine um I can tell you you I have never heard it as prolactin releasing inhibitory in inhibiting hormone I've never heard it abbreviated as Pi I've only known it as dopamine but just know that there are um different ways to saying different things um and depending on what field you are in you know if you're in um you know a genetic uh embryology research field you might call it something something different because that might pertain to your field whereas if you're in you know ANP class you might call it something different because that's what their field is going to typically call something um uh so for example um you know I know it as growth hormone and I abbreviate it as GH but other fields I've heard it called somatotropin um so it depends on where you work as to what you're going to call it but just know that a lot of different thing uh um that different hormones have different names for the exact same thing um now here I'll just point out it says prolactin releasing Factor prf um I just have this up here factors used because a specific prolactin releasing hormone has not yet been identified um so we're just call we're just going to call it prolactin releasing Factor even though we we really haven't um been able to isolate it or um kind of really identify it um so um just kind of start committing these to memory um you know where they are um the source is going to be you know these are going to be coming from the hypothalamus these are going to be coming from the anterior pituitary these are going to be coming from the posterior pituitary these are your thyroid hormones your parathyroid Adrenal medulla adrenal cortex and your pancreas hormones um so uh I will say you know antidiuretic hormone um I call it antidiuretic hormone I call it ADH and I call it vasopressin um so for you future nurses um you if you're working in a cardiac unit um you'll call it all three um if you're giving um if you're talking about a hormone you're going to be calling it anti- diic hormone or ADH um there is a medicine out there called vasopressin and basic and and you can give it an IV form and um basically it's just an IV form of ADH um so if you're giving it as a medication you're probably going to say vasopress and not um so thyroxine your thyroid hormones thyroxine and um uh triod thyronine um typically we just say T3 and T4 um parathyroid hormone or pth uh I would say most people do not say parathormone uh most people just say pth um you'll hear epinephrine and norepinephrine um you might hear epi um all that is all epinephrine is is just adrenaline so you drink a Red Bull um or you have an adrenaline rush um that's basically epinephrine and we'll talk about that later on um cortisol hydrocortisone you have hydrocortisone cream that you put on you know you get a beasting or something like that um hydrocortisone cream that's basically a synthetic version of cortisol okay so like I said just start committing those to memory and figuring out you know where where is everything uh released you're going to have to know um going to have to know those so hormones remember that hormones have an effect on another cell um and I should say has a Metabolic Effect on another cell um only because and I'll actually move this one up typically because they stimulate um stimulate growth reproduction and development and I'll correct my mistake there um and remember hormones are released into extracellular fluid um whether it be tissue fluid um the bloodstream um and uh we say that either hormones are water soluble or lipid soluble um remember that you know water and oil they don't don't mix so um if we have lipid soluble hormones then um in order for those to travel in bloodstream they have to be kind of packaged um in a different way and we'll talk about that later on um hormones very powerful in low concentrations it doesn't take a lot of um hormone in order to do the job um hormones can regulate water balance electrolyte balance uh blood pressure um hormones do a lot of things within our body um hormones they exert their effect like I said by altering the metabolic process and there's two ways that they can do that they can alter the enzyme activity of what's going on um and they can change the rate of membrane transport of a substance um and remember that they will um they have the these cells have the receptors on the target cell um and it says on slash in and we'll talk about the differ first messenger and a second messenger later on but um we have these receptors on and in a Target cell and um not all hormones are going to work on all cells um it says hormones are only going to affect those target cells that have those receptors that are unique for that specific hormone so if you know if we're talking about um let's find one here okay so if we're talking about um this growth hormone releasing hormone um this ghrh um that's actually going to work on the anterior pituitary um to actually release this thing called growth hormone um so that the anterior p is going to have receptor on it for this GH RH so you know if we're talking about a cell in the big toe it's not going to have receptors for this ghrh hormone um only the anterior pituitary will all right so hormones like I said um work in extremely low concentrations and they cause changes in target cells [Music] so we're going to talk about up regulation and down regulation so it says the number of receptors determine the strength of response so if we have um um a lot uh so I'll just read it says up regulation so it's basically an increase in number of receptors available for binding on a Target cell in response to a prolonged decrease decreased concentration of a hormone and down regulation would be the opposite a decrease in number of receptors available for binding On Target cell in response to a prolonged increase increased concentration of a hormone so basically what up regulation down regulation is is that if you have a prolonged uh High concentration of a hormone um that cell will say you know what I don't need so many receptors because I have a lot of drug available so the cell can actually get rid of some of those receptors um so if we have too much con or too much hormone the cell is going to get rid of some of those receptors on the cell and we say that that would be down regulation now on the flip side if we don't have enough hormone the cell only has you know let's say it's not going to be three receptors but let's say you know we have we need more receptors on the cell the cell will create more receptors on the cell to try and catch um that low concentration of hormone if the cell is creating more receptors we would say that that is up regulation because of the low concentration of hormone the cell's trying to to to the cell will create more receptors and hopes that it can it can bind more of that hormone and that's just upregulation all right so hormones are organic compounds remember organic compounds are carbon and hydrogen or organic compounds contain carbon and hydrogen we can break up um organic compounds into steroid or steroid like hormones and we can break them up in nonsteroid hormones so steroid hormones are lipid soluble they are are lipid likee and so um so therefore they're not water soluble or they're water insoluble um steroids are derived from cholesterol and and they are going to cause they're directly related to protein synthesis um we can see these in your sex hormones like your testosterone your estrogens um ADR your adrenal cortex hormones adrenal cortex um hormones cortisol aldosterone your nonsteroid hormones we have different categories of non-steroid hormones um amines um amines are going to be derived from tyrosine which is an amino acid hence the name amine um such as epinephrine norepinephrine um thyroxine um or it can be derived from tryptophan which is another amino acid such as melatonin um non-steroid hormones are can be classified as proteins remember proteins are just long chains of amino acids um so parathyroid hormone or growth hormone would be um classified as a prot protein glycoproteins um glycoproteins are just carbohydrates joined um together with with another protein um so like your TSH your thyroid stimulating hormone would be an example peptides uh peptides are just short chains of amino acids so your posterior pituitary gland hormones your uh ADH your anti-diuretic hormone oxytocin those are your two uh posterior gland hormon hormones um TR um and you're going to say well what's TR TR remember is your Oh wrong slide TR R up here thyrotropin releasing hormone um and we'll talk about uh we'll talk more about uh these these uh hormones later on all right and it says cause AC activation of adental Cycles we're going to hold off on that bullet point um later on uh I mentioned earlier we have first Messengers and second messengers um Iden toate cycl is um we'll talk about that when we talk about second messengers um here's just kind of like a summary chart of different amines peptides proteins glycoprotein steroids um so you're going to have to know um you know kind of what falls under what category um we'll talk a little bit more about um each of these hormones later on uh you know remember proteins are long chains of amino acids um peptides are short chains of amino acids um all right here um and this top left that's going to be quarters all um so you can see the um cortisol is going to be a steroid um that's remember steroids are derived from cholesterol and so it's going to be lipid soluble the um second one is um nor epinephrine um uh norepinephrine that's an amine so you can kind of see this little amine group here that's your amine um parathyroid hormone pth um remember those are that's a long chain of amino acids there's a there's a bunch of amino acids linked together so that's going to be a protein um and oxytocin uh Part D that's a short chain of amino acids so that's going to be a peptide um and the bottom picture is a prostag glandon um here you can see the terminal that terminal Co um there all right so steroid hormones um and um we we'll talk about thyroid hormones so even though um thyroid hormones are fall under the amine um group we we'll still classify them um well we'll still throw them under this the steroid like hormones um they're going to be soluble in lipids um so they have poor water solubility um remember I said that if you're lipid soluble you have to be packaged a little bit differently um in order to be in order to travel through the blood remember blood is water soluble so they're going to be bound to these plasma proteins these hydrophilic or water loving plasma proteins um they're going to kind of be packaged in inside of these plasma proteins so you're going to have like the water portion on the outside and then inside you're going to have your fat soluble um lipid hormone or your steroid hormone or your amine hormone and then on the outside you're going to have this plasma protein that's going to go around through the bloodstream and the good the good thing about this is that once it gets to the kidney um the kidney they're not going to filter out um large proteins so so um you know this protein won't get filtered out and it will still continue in the bloodstream and hopefully get to wherever it needs to get to um and then once it gets to wherever it needs to get to the good thing is is that you know it'll it'll kind of break up and then it'll it'll kind of leave that plasma protein and because that lipid by layer remember that cell that the cell is a the lipid bil layer it can actually because it's uh this hormone is lipid soluble it can actually penetrate or diffuse through the lipid B layer of um cell membranes um so some of the steroid hormones um testosterone um estradiol uh progesterone aldosterone you can see a lot of them are the ones that end in o NE um cortisol is another one so your um o ones um testosterone progesterone aldosterone and then estradi and then cortisol would be um some steroid hormones um so thyroid hormones and amines are kind of thought to enter the same the cell by the same method some of your thyroid hormones there's three of them um T3 T4 or if we wanted to call them something you know other than T3 T4 T3 is actually called triiodothyronine and T4 is called um Tetra iodo thyronine so T3 T4 and then the third one's called calcitonin and we'll talk about the thyroid hormones later um so both of these um um are going to both the um the steroids and the thyroid hormones are going to bind to this um this thing called an intra intercellular receptor and it's just basically a protein receptor that's usually in the nucleus and some things are going to happen um the first is that once we have this bound complex this hormone receptor complex it's um it's going to bind to the DNA sequence and it's either going to activate or repress um the Gene and if it activates the gene then we're going to cause this transcription process remember um DNA replication transcri translation transcription that we learned learned last semester um so it's going to cause this transcription process of converting you know mRNA and all that stuff and we're going to cause a change in gene expression and then that protein synthesis will actually lead to the action of the hormone so this hormone's going to come into the cell bind to the cell come in attach itself to the nucleus cause this um this uh mRNA uh translation process to happen this Gene is going to be expressed we're going to create a protein that protein's going to leave the nucleus going to leave the the cell and the hormone and then we're going to see the action of the hormone and this is just a um kind of a stepwise process of what we just uh mentioned um the endocrine gland is going to secrete that hormone the blood carries the molecule through the body um that hormone diffuses through the target membrane enters through the cytoplasm or the nucleus that combines with the um that receptor molecule the steroid hormone uh binds to the DNA um promotes transcription of mRNA mRNA causes the protein synthesis and that newly protein um that newly synthesized protein produces that hormones effects um and here you can just see the the stepwise process of what happens um all right so for nonsteroid hormones and this is going to be the rest of the amines your peptides and your protein hormones um because they are water Sol they cannot cross that cell membrane remember that cell membrane is a lipid bilayer it's lipid soluble um so that hormone is going to be bind to the receptor on those cell membranes um and this is where that first messenger and second messenger come into play that I was talking about earlier so that hormone binding um that hormone is considered that first messenger it's going to bind um to that cell membrane and it's going to activate this thing called a g protein and um then we have this chemical inducing change that's going to um cause the second messenger and the synthesis of the second messenger is how this non-steroidal hormone is going to affect the change in that Target cell um so the second messenger um this second the second messenger typically is going to be uh cyclic adinis monophosphate or cyclic or CM or Camp so the cyclic will say is the second messenger and I said you know we talked about it in Iden cycl earlier um and I said we'll hold off on that bullet point for a second so um what we're doing um with with adinal cycl is we're taking ATP remember adenis and tri phosphate and in the presence of adenylate cycl we'll take adate where we'll take ATP in the presence of AD denate cycl will create a MP ad denate mono phosphate and will get rid of two phosphate groups off of the ATP so um so we have um adinis phosphate phosphate phosphate and in the presence of um a denate cycl um what we're going to do is we're going to break it off right here and we're going to create a [Music] monop phosphate plus two phosphates that's all we're doing um we're taking adinis triphosphate and going to adinis Mono phosphate so that's just what an adenol cyclace does so now we've created this cyclic um and cyclic just means in a circle so so um so ad inocent um cyclic is is is what we call a second messenger um and the second messenger um so this entire process is called signal trans transduction how the hormone binds to The receptors on the cell tar on the cell membrane activates the protein uh the G protein comes in and um and kind of creates this cyclic that's all called signal transduction so um so this um so I'll kind of summarize so a hormone binds to its receptor and the resulting hormone receptor complex activates a protein called G protein G protein is an enzyme complex that is joined to the intracellular side of the hormone receptor and it is the link between that first messenger and the second messenger this activated G protein moves along the inside of the plasma membrane and binds to an enzyme called ad denate cyclas which is an intergral membrane protein with its active site facing inside the cell Aden activated adenol cycl removes two phosphates from ATP and forms am in a cyclic pattern cyclic activates another enzyme called protein kinases and these protein kinases transfers these phosphate groups from ATP to Mo um from the ATP molecules to protein substrate molecules in a process called phosphorilation and phosphorilation activates some proteins and renders other proteins inactive and the the phosphorated proteins after various cell cellular processes um brings about the effect of that particular hormone um so an example of this would be um epinephrine uses cyclic to activate the um to increase the uh activity of the enzyme that breaks down uh liver glycogen incre inreasing the number of glucose molecules to provide energy um we can have cyclicamp abnormalities so there's a disease out there condition syndrome out there called mune albite syndrome um basically it's a defect in this uh G protein that um that activates uh adinal cyclas converting converting ATP to cyclic amp um and this results in excess secretion of certain pituitary thyroid hormones gatal hormones or adrenal hormones and it can lead to um precocious puberty and that's basically where females can menstruate or males can produce a sperm as young as like six years old um and I mentioned that cyclic um acts as a second messenger we have different um other second messengers as well besides cylic um we can use um this D this diil glycerol um or um ip3 um I know um iosol triphosphate or um there's another compound called cyclic GMP um cyclic ginine monophosphate so we have different second messengers um um out there so um just know that cylic is just not the only one um all right and I realized that I um kind of forgot one bullet point um I never finished the slide so I just added in this um this sentence um how or this bullet that cyclic activates protein K Kinesis which leads to phosphorilation which leads to the hormone effect um and then just just remember that this entire process is called signal transduction all right so here is just a summary slide of kind of what we um just talked about and here is a picture version of um kind of what we just talked about you know the nonsteroidal reaches the um Target cell um Vines to the cell membrane activ Ates the G protein ad denate cycl um cyclicamp and then um we have that phosphorilation so and that leads to Cellular changes and um development of protein kinases um all right all right so um we talked several chapters ago about um abusing um certain drugs but um we haven't talked about you know steroids yet um so steroids can be used to increase you know muscular strength um it does have some harmful effects you know obviously we don't um want to abuse um any drug so um so um don't do it um but when you abuse steroids you can actually um stunt your growth um long-term use you can see breast development in males um you can see male characteristics in females you can actually damage your kidneys litter heart have issues with your cholesterol and obviously create psychiatric problems if you've heard of like Roid Rage um people do abuse um growth hormone or human growth hormone um it is used to enlarge muscles and decrease that um but it does not improve strength um so some people think that oh well I'll just take H uh this this this growth hormone um to improve strength it actually does not improve your strength um and some people so you know not to um advocate for abusing drugs but um you know people will often abuse or abuse um steroids in conjunction with growth hormone um because steroids will improve your strength um and and growth hormone will increase your muscle mass as well um but growth hormone does signal the release of um igf um from the liver um arthr proen um that's what the the the drug is or the hormone is that will increase the number of red blood cells so when we talk about anemia um which is basically a deficiency of red blood cells arthop potin will get produced um the hormone arthop potin will get produced and um will stimulate the bone marrow to produce red blood cells and we have this in medication form um medication there's different forms of medication but epogen is one of them and um you know people will take arthr potin to increase the number of red blood cells and hopefully um in turn will increase their oxygen delivery to muscles um which will um improve their athletic performance um one thing that you know obviously it's advised not to do that um it actually can lead to um heart attacks um and death all right prostaglandins um prostaglandins are paracrine substances remember paracrine substances they affect nearby cells so they're going to act locally um again they're very potent in small amounts just like hormones they are um uh lipid soluble they are synthesized from this thing called arachadonic acid um in the cell membrane they are not stored in cell cells but they are synthesized just before release um they're rapidly inactivated after use um and they can um activate or inhibit that cyclic amp that would talk or that adental cyclace to control that second messenger hormone cyclic am that we talked about a few slides ago um to change a cell's response to um a specific hormone um prostag glands have a lot of um effects you know we can contract smooth muscle like in your Airways of your lungs or blood vessels um so like uh menstrual cramps or um contractions for labor um um as well uh relax the smooth muscle so you can relax your lung Airway or your blood vessels stimulate or inhibit secretions um you know your adrenal cortex hormones um you could stimulate your adrenal cortex hormones um or inhibit your stomach acid hormones regulates blood pressure so it regulates blood pressure by um by sodium by influencing the sodium and water movement in the kidneys remember that wherever sodium goes water will will follow so if we hold on to sodium we're going to hold on to water if we um get rid of sodium in the urine we're going to pee out more water so wherever sodium goes water will follow so if we have high blood pressure and we what the body will want to do is get rid of sodium because water will follow and if we get rid of blood volume theoretically our blood pressure will decrease if we have low blood pressure your body will hold on to sodium and therefore conin water increasing your blood volume and uh your blood pressure will go grow up will go up not grow up um and I can get rid of this bullet point we've already said controlling movement sodium water all right promoting inflammation medical application so um ineds um so um aspirin Tylenol cortisone that can relieve you know Jo pain of rheumatoid arthritis by inhibiting the production of prostaglandins in the sovial fluid of affected joints um this is also why people take a lotos aspirin um to prevent heart attacks all right control of hormone secretions um it is precisely regulated remember acetylcholine and acetool esteras um you know that's on the neurotransmitter side so you know we're not talking about that but that's just an example of you know the the precise regulation um so just like acetylcholine acetool all of this is a negative feedback um actually I don't want to confuse you so I'll get rid of the aceto Coline aceto Coline esterase um so the secretion is is it's precisely regulated controlled by negative feedback mechanisms remember if something's too high we're going to lower it if something's too low we're going to raise it and remember back from that chart earlier on the chapter um the effects are shortlived however they may last for days um most of your hormones are excreted in the urine um and it can be broken down by your liver enzymes to stop the effects of hormones so I said negative feedback there are um negative feedback is going to be the main way of um controlling hormone secretion um there is you know a couple applications for positive feedback we'll get to that in a few slides but for for the main portion or main the 99 plus% of the time it's going to be negative feedback um and you know you by now you know the definition of negative feedback um and as and this is all going on um behind the scenes we don't know that's that it's going on so there's three ways that the body can perform this negative feedback um the first one is that the hypothalamus controls the release of anterior pituitary hormones and then the pit Ary hormones secrete the hormones that control the activity of other glands um so if we so all so we'll talk about um we'll talk about this one for a second so the hypothalamus controls the release of anterior pituitary hormones and then the pituitary hormones secrete hormones that control the activity of of other glands um and I say Tropic hormones Tropic hormones just means that hormones that stimulate other endocrine glands to secrete hormones so um so the hypothalamus controls the release of anterior pituitary hormones and then the then the pituitary hormone secrete hormones that control the activity of other glands so we're going to go back back to our chart up here okay so basically what bullet point one says the hypothalamus is going to control the anterior pituitary gland so here we can say uh or here we can see um growth hormone releasing hormone growth hormone so so GnRH will get released by the hypothalamus and it's going to come down to the anterior pituitary gland and it's going to stimulate the release of growth hormone um here we have prolactin releasing Factor so prolactin releasing Factor would come to the anterior pituitary to release prolactin all right thyrotropin releasing hormone will come and stimulate the anterior pituitary to release release TSH so that is the examp those are examples of how the hypothalamus will direct the anterior pituitary to release certain hormones now the anterior pituitary once the anterior pituitary releases these hormones um so these are Tropic hormones which means they cause a release of another um gland to release their hormon these hormones are going to act on um another gland so the thyroid stimulating hormone will act on the thyroid to release its um to release the thyroid hormones um the follicle stimulating hormone will act on the follicles um to release um what it needs to release all right so that is bullet point number one all right nervous system control the nervous system directly stimulates an endocrine gland to secrete hormones so here I want you to think of like the fight or flight or in stressful s stressful situations I said norepinephrine is the preganglionic neuros transmitter so if you remember from you know chapter 11 I believe um we had that slide that has the preganglionic and the postganglionic um neurons all right I pulled up the notes from chapter 11 if you remember this slide we had this um these autonomic neurotransmitters and I talked about um norepinephrine oops I talked about norep neine um being the neurotransmitter here um but up a couple slides there is the slide that we talked about so this is what I'm talking about um this this neur neurotransmitter the the the the nervous system um can actually uh Target the specific gland to secrete um certain hormones all right and then changes in the internal environment so changes in plasma levels um of a substance can stimulate or inhibit the gr gland directly so this is um you know your blood glucose change um then the pancreas either dumps out insulin or it doesn't um your sodium level is out of whack so then your then uh your body's going to either hold on to sodium or not uh or get rid of sodium um so these are three different ways that the um negative feedback Works in our body so here you can see um you know for example the hypothalamus is stimulating the anterior pituitary gland um which stimulates the peripheral endocrine gland that reaches the cell targets to act um and then the peripheral endocrine gland inhibits the hypothalamus and the pituitary gland so that's negative feedback in in the second example the nervous system is stimulating the endocrine gland secretions that reach the target cells to act and this action can inhibit the stimulation by the nervous system um in that third example the changing level as a substance and the plasma stimulates the endocrine gland secretion that reaches the target cell to act and that action can inhibit um the stimulation by the nervous system so all of these are negative Fe back Loops um here you can see the average concentration hormone is stable um so it actually fluctuates um it doesn't actually remain constant remember this negative feedback loop um so we're always you know your temperature doesn't hover at 98.6 constantly it's going to fluctuate um because the body is always trying to you know keep it at around 98.6 but it will um fluctuate so um here you know hormone levels are too high um it when hormone levels are too high hormone exerts its effects negative feedback inhibits the the system and the hormone secretion decreases then as the hormone levels in the blood decrease and the hormones affects Wayne um or stops inhibition of the system ceases and secretion of that hor hormone increases again as a result of negative feedback hormone levels in bloodstream remain relatively stable fluctuating slightly around an average value all right positive feedback um this is when we make the body worse worse worse and hope that we reset the system um such as in um with oxytocin um in labor contractions or in breast milk production um you will need to know specific examples of positive versus negative feedback and really outside of um labor contractions and milk production we're not going to go into other other um examples of positive feedback all right pituitary gland we can also call the pituitary gland the hypo ois um it's about 1 cm in diameter it lies at the base of the brain and this area called the celera it is part of the um in the sphenoid bone um it's controlled by the brain um and it's considered part of the nervous system so when we look at the structure of the pituitary gland you can see it um right here and um there's this thing called an infundibulum um that's like the stock of the um pituitary gland and um let's see all right yep um so it's attached to the um to it's it's attached to the hypothalamus and um it sits in this little thing called the the cell of Tura and um it has two different loes it has an anterior lobe and a posterior lobe which um the anterior lobe we also call it an adino hypothesis and the posterior lobe is called a neuro hypothesis um neuro the neuro hypo or the posterior lobe is is the portion that is actually part of the the nervous system um and the the secretion from the two loaves is actually controlled by two different methods from the hypothalamus um and the chemicals that are released from the tary gland they are considered hormones because these chemicals are released directly into the bloodstream um I will say that there is a third lobe even though it says um consists of two distinct PS portions the anterior lobe the posterior lobe um in fetal development we have this intermediate lobe called a pars intermedia um it's a small intermediate lobe called the pars intermedia develops in the fetus and it's um produces these uh it produces um it's called melanocyte stimulating hormone or msh which regulates the formation of melatonin but as you can see um in an adult it's it's not um defined at all but it would kind of sit right here um so um so in the adult we really only have um two loes and so I said that the hypothalamus has two different ways it can regulate the low for the anterior portion um we have these um hypothalamic releasing hormones or inhibiting hormones and they're transported to the the anterior lobe through this portal system it's called the hypo physial portal system and it stimulates that anterior lobe to release um other hormones and that's what we talked about oh up here um when I talk you know this hormone comes on hypothalamus and it stimulates here this stimulates this this stimulates this so that is what I'm talking about for the anterior lobe um so each of these releasing hormones act on a specific group of cells in the anterior pituitary um gland and they can inhibit or stimulate uh pituitary secretion all right so for the posterior lobe um we have uh remember it's part of the nervous system so we have nerve impulses from the hypothalamus that travel to the posterior lobe through the infundibulum and remember that infinum is that little stalk thing um and that those nerve impulses actually um kind of activate the posterior U pituitary to release the hormones so here um here is the anterior lobe and you can see that we have this hypophysial portal system that is going to release hormones um but here we have the nerve impulses you can see the little um synapses uh right here all right so um how do the hypothalmus control peripheral ocon glands remember we had that three step process um uh we have uh releasing or inhibiting hormones from hypothalamus um the anterior petuary um hormones act on cells and peripheral gland so we have the hypothalamus acting on the anterior pituitary then the anterior pituitary releases those thyroid hormones to act on the thyroid for example to stimulate the thyroid to secrete the hormones and the peripheral glands um secrete um its hormones um which it's exerted effects on um it cells so there's that that three-step pathway hypothalamus to anterior to pituitary anterior pituitary to um the hormone so if we go back up to you know this slide um this is step one this is what we're talking about for the anterior pituitary remember those are called Tropic hormones hormones um remember Tropic hormones are hormones that cause um or hormones that stimulate other endocrine glands to secrete hormones all right and again um negative feedback um is is the is is is um involved here um and typically that final hormone is that um inhibiting or final pathway for that um negative feedback loop um here's just kind of like a another um another way of showing it um hypothalamus goes to the anterior pituitary goes to peripheral gland and then once our um hormone levels Rises it's going to shut off that hypothalamus and that anterior pituitary from uh re releasing oops I didn't Advance your slide I'm sorry um once we have that hypothalamus to the anterior pituitary to the pereral endocrine gland that hormone is is going to shut off that um negative feedback loop because now we have enough hormone to do what we need to do hopefully if not it will continue secreting all right so some of your um anterior pituitary hormones remember it's this one is um not um released by hor uh nervous system I mean still released by the hypothalamus um but they are the the releasing or inhibiting hormones they are not directly stimulated by the nervous system um that's going to be the posterior side so some of your um anterior pituitary hormones um growth hormone prolactin thyroid stimulating hormone corticotropic hormone follicle stimulating hormone lutenizing hormone um dopamine um which is um actually released from the hypothalamus um actually inhibits the uh release of prolactin so dopamine would inhibit the release of prolactin all right so so if we go back up to this slide and oh what all does what um do some erasing okay so um so we have growth hormone we'll talk about growth hor hormone for a second so we have growth hormone we have um ghrh is going to um we have um ghr is going to stimulate growth hormone and somat Statin look here growth hormone releasing inhibiting hormone so somatostatin would be your inhibiting hormone so growth hormone is stimulated or is released by ghrh or is inhibited by somatostatin or g h r i h all right prolactin so um we'll do orange for prolactin all right prolactin prolactin is um you know we don't know but we're going to assume that prolactin is released by this prf this prolactin um releasing factor and we also have this thing called um e prolactin inhibiting or prolactin release inhibiting factor that would um inhibit the release of prolactin all right thyroid stimulating hormone thyroid stimulating hormone would be um really all it is is stimulated by TR we don't have an inhibiting aspect of TSH um if it's not there it's not going to be released if TR is not there it's not going to be released um let's see that's another one um act adrenocorticotropic releasing hormone it's going to be released by um prototropic releasing hormone um and again it doesn't have a an inhibiting um factor to it so once this CR stops act will stop as well all right so FSA H and LH so those are actually going to be working together by this gonadal tropen or gonad tropen releasing hormone um gonad G&R is um going to stimulate the release of both LH and FSH and there is no inhibiting hormones so once G&R stops um sh and LH will stop as well so there's your pretty colorcoded slide of what goes um what gets released when or inhibited so that is just kind of like a way of that's just a summary slide uh or a picture version of um what I did here with this slide um so we're not really going to talk about this slide because I colorcoded it for you on the other slide all right and this is just another picture version of what happens um so you know here it's kind of easy um GH RH is going to stimulate growth hormone somatostatin is going to inhibit Pi is going to stimulate and we don't have an inhibiting site if if Pi is shut off prolactin is going to um or I'm sorry uh if we don't prolactin is going to be released unless we have Pi I'm sorry I did that whole backwards um so thyrotrope and releasing hormone is going to stimulate TSH CR is act gonadotropin is going to stimulate both LH and FSH and you can see the glands um or the tissue that it's going to to work on um all right yeah so I actually should go back up here and kind of correct myself um prolactin releasing inhibitory hormone um oh yeah I did say it right I did say it right I'm sorry um yeah prf which we don't really know prf is going to be the stimulating and Pi is the inhibitory I did it right okay I'm sorry sorry for confusion all right okay so functions of your anterior pituitary um growth hormone or somat you know think of your body growing you know it stimulates cells to enlarge to divide um you know proteins are amino acids you know proteins is what makes your body grow stronger bigger you know bulkier um that is growth hormones so increasing your amino acid uptake enhancing amino acids uh moving amino acids inside the cell protein synthesis um um also um decrease rate of carbohydrate usage um remember um carbohydrate usage that is burning energy so burning energy would be the opposite of of growing um and then increase rate of fat usage if we are using fat we are getting rid of fat and hopefully creating muscle so carbohydrate usage is burning energy which is not growing um and then increasing rate of fat usage is getting rid of adapost tissue so growth hormone is basically to build up your body so taking in amino acids um prolactin um milk production females um thyroid stimulating hormone um is going to stimulate your thyroid hormone um typically we'll just say thyroid hormone and we mean T3 and T4 and we'll talk about T3 and T4 later on so stimulates your thyroid gland to secrete thyroid hormone Act adoc corticotropic hormone um that's going to secrete uh cortisol and other gluto corticoids from your adrenal cortex and we'll talk about where your adrenal cortex is it sits on top of your kidneys um later on cortisol is your stress hormone so when you're cramming for midterms or if you have a stressful situation in life um cortisol is going to be is going to be released um FSH follicle stimulating hormone that's what's going to uh regulate the menstrual cycles in in females or stimulate um ovulation in females um it's also going to produce uh sperm in males lutenizing hormone um that's what's also going to cause ovulation in females as well as um sex hormone production in both males and females all right pathway for oh I didn't Advance your slide all right pathway for thyrotropic our thyroid hormones so we have this thyrotropin releasing hormone that's secreted by the hypothalamus that thyrotropic releasing hormone is going to go to the anterior pituitary to secrete TSH remember those are called Tropic hormones TSH is going to go to the thyroid gland to secrete thyroid hormone um and that thyroid hormone is going to go to to the thyroid itself and um that thyroid hormone will cause a thyroid to secrete um the thyroid hormone um and then you know it's a negative negative feedback loop and basically the primary action of thyroid hormone is to enhance the rate at which proteins are synthesized um so TSH secretion is controlled by two methods in this pathway it's going to be a negative feedback loop um and it's still controlled by the same extent by the level of TR so the thyro thyrotropin releasing hormone from the hypothalamus as well as the amount of TSH in the body all right so here we can see uh you know the hypothalamus releases TR and stimulates the anterior pituitary gland to secrete tssh into the bloodstream TSH stimulates the secretion of certain um thyroid hormones by the thyroid gland the thyroid hormones stimulate target cells and the thyroid hormones inhibit TR from the hypothalamus and TSH from the anterior to gland um we do have um when we're talking about growth hormone um um we do have deficiencies or uh not uh I guess growth hormones ups and downs um too much growth hormone in two little growth hormone um hypopituitary dorismar hypopituitary dwarfism is caused by a deficiency of human growth hormone during childhood um that's when pretty much everything is short you are short statured but um all of your limbs are still proportionally correct um so your arms are still proportional to your legs um it just looks like everything has been shrunk down um your mental acuity is still there um with gigantism versus acral we talked about that um in chapter seven I believe um gigantism and acromegaly are are both um too much growth hormone um gigantism is too much growth hormone during childhood and acromegaly is too much growth hormone um during adulthood um they the the gigantism is usually caused by a pituitary tumor that causes um an over secretion of growth hormone so that all of your your long bones um kind of grow abnormally long and causes you to be really really tall sometimes over eight feet and usually you don't live um you know well into your 40s um with g G antism because um you do have a lot of metabolic problems with um gigantism acromegaly um doesn't show up until um adulthood and remember your bones completely aifi you know sometimes around somewhere around 23 to 25 years old and then you develop this condition called acromegaly where you have an over production of growth hormone um after um your bones have aifi so you don't have an increase in your height but your bones can still grow in width so a lot of these people will have you know very prominent thickened facial features um prominent thickened Fingers um enlargement of like some some of your endocrine glands um your hands feet Jaws stuff like that all right so moving on to the posterior pituitary hormones so remember these are really controlled by your nervous system itself um still coming from the hypothalamus but we say that um they have um that the posterior uh lobe has these nerve fibers or neuros secretory cells um whereas the anterior lobe has more glandular epithelium and we only have two hormones in in the posterior pituitary gland and they are stored and released in the posterior pituitary um and the two the two hormones are ADH and oxytocin for ADH we can say antidiuretic hormone or vasopressin um so antidiuretic hormone anti means opposite or against um diuretic kind of means to pee so um if you have an antidiuretic um anti-diuretic means so anti-p or to not PE so if I have an antidiuretic um that's going to be something that holds urine um so you have a decreased urine production um so this is where the kidneys are going to hold on to water um and also it causes basoc constriction rtion to increase blood pressure um and I mentioned before that you can give this um as a medication typically in the IU setting to increase blood pressure um so it causes basoc constriction so not only does it hold on to water um to increase your blood volume but it will also Vaso constrict to increase your blood pressure so it has a dual effect um um as a side note ADH um deficiency can cause a condition called diabetes insipidus um and alcohol um inhibits the secretion of ADH so that is why uh you have to urinate after just drinking a few beers um oxytocin um stimulates muscle contraction in the urin wall during childbirth so your body produces oxytocin naturally and um typically during a vaginal birth or a cerian we will give you um oxytocin as well to um kind of help you along um and also oxytocin will help cause milk ejection um during lactation um and that's responsible for so like if you hear um if a A lactating mom hears a baby's cry um even if it's not her own baby um she'll start to lactate um but um oxytocin hasn't really been studied a lot in males but um it can help with sperm movement or sexual response um and if you remember you know I told you about the anterior lobe and the posterior lobe but we have that um that intermediate lobe in fetal development called the pars intermedia so let's say you have a cyst that develops in that pars Media or pars intermedia um and that resulting um that's that cyst puts um pressure on the posterior lobe of the pituitary gland so you have a defective hormonal dysfunction or production secretion um you would see alterations in your oxytocin and ADH production so you um if you have a cyst in that area you could have over production of oxytocin and you might be at risk for going into pre-term labor so um we might opt to do a C-section instead of a vagil Nate uh a vaginal birth um you might have um you would be placed on high-risk labor um or have abnormal labor you might have a low response a low production of oxytocin um you might have weak uterine contractions so we would probably do opt for a C-section as opposed to a vaginal birth okay okay so here are some of your an or here are the anterior and posterior lobe um hormones with their actions and kind of their sources of control I'm not going to read those to you we kind of talked about most of these uh throughout the your thyroid gland um thyroid gland um kind of sits um about right here it's uh just below your larynx um anterior and lateral to the trachea has two loes um that is connected by this thing called an ismos there is your ismos right there can't do blue I like red um all right so there's your ismos right there um there's your there's your larynx and there's you know one lobe and two loes um so your th your thyroid is surrounded by these secretory cells called follicles or folicular cells so these are your um follicular cells right here that kind of just surround these um these things called uh poids and then we have extra folicular cells or outside the follicle cells um and this colloid builds these uh cavities so these are um kind of cavities right here uh you can see the the colloid right here with these folicular cells and then you have the out um extra folicular cells that are you know outside of this little circle right here so there's more extra folicular cells all right so the thyroid gland um its function is to basically remove iodine from the blood and it uses that iodine to produce the thyroid hormones um we have three thyroid hormones T3 T4 and calcitonin um T3 and T4 are produced by these follicular cells the ones that s around um that space and calcitonin is produced by these extra folicular cells so calcitonin extra folicular T3 and T4 follicular cells um and um T4 can be converted into T3 um in the peripheral tissues or T4 is converted into T3 um in the peripheral in the peripheral tissues um and then thyroid hormone uh basically increases the metabolic rate um meaning that it increases the rate at which cells release energy from carbohydrates um enhances the rate of protein synthesis and stimulates a breakdown and M ization of lipids and it also helps determine our BMR our basil metabolic rate we'll talk a little bit more about BMR in um in a future chapter I believe it's next chapter maybe um all right all right so here we have our T3 T4 and calcitonin um overall these three three hormones enhance the rate at which proteins are synthesized um we do have some diseases you know hyperthyroidism and hypo or H diseases that affect you know too much thyroid and too little thyroid hormones um you will need to know the symptoms of hyperthyroidism um and you will need to know the symptoms of graves disease um with infantile hypothyroidism um it's actually caused by a deficiency of thyroid hormones at Birth um here you can just see some um pictures that's infantile hypothyroidism um right here um uh here is Graves disease um here is a glater um you can see with both hyper and hypothyroidism you can see enlargement of the thyroid gland so just because you have a gler doesn't necessarily mean you have hyper thyroidism or hypothyroidism additional additional testing will be needed but you can see the presence of a goer um with hyper thyroidism or hypothyroidism now your parathyroid glands um they are located on the back side or the posterior side of your thyroid so here's looking um at the back of the thyroid gland um you can see there's one two three four um four four ah four parathyroid glands um and they secrete only one hormone called the parathyroid hormone or pth or parathormone I've never heard of called parathormone um basically pth regulates calcium and phosphorus concentrations in the blood um so typically they work in opposite directions you know if you have an increased blood level of calcium um you can see decreased phosphates but they act on the bones and kidneys and intestines to exert its effects um so we have um you can act on Bones to stimulate bone resorption um we have you know vitamin D metabolism so you know this is where sunlight comes into play you know vitamin D vitamin D is actually called um coloc calciferol vitamin D synthesis begins when the intestinal enzymes convert dietary cholesterol into the inactive inactive form of pro vitamin D or dehydrocholesterol and this provitamin is largely stored in the skin and exposure to ultraviolet light converts it to vitamin D and the liver changes the vitamin D into um hydroxy chol calciferol where it goes to the kidney to be converted to the active form of vitamin D dihydroxy coloc calciferol or calcitriol as long as pth is present and this enhances calcium absorption from the small intestine so if you have osteoporosis or something like that if you're on calcium supplements chances are you're going to be on Vitamin D supplements as well because vitamin D um once activated into um calcitriol or dihydroxy calciferol um you will um this is going to increase um this or vitamin D will enhance calcium absorption in the small intestine so if you're on calcium supplements you're going to be on Vitamin D supplements as well or you should be um and if you have a complete thyroid removal um so after a complete thyroid ectomy you're going to need to be on these coloc calciferol um supplements um as well now when you do a um a thyroid ectomy you can actually save your parathyroid glands um sometimes they will relocate your parathyroid glands um they can put them in either like your your forearm or they can put them in your abdomen um and your parathyroid glands will still work all right moving on so here's pth and calcium absorption so here you know intestinal enzymes convert the colesterol from the food to the inactive provitamin D ultraviolet light in the skin converts provitamin D to vitamin D which is called coloc calciferol it's also obtained directly from Foods um the liver changes the vitamin D to hydroxy calciferol uh which can be changed in the kidneys into the active form of vitamin D Di n Roxy coloc calciferol um and this step needs pth in order to do so and the active vitamin D controls absorption of calcium from the intestine um parathyroid glands on the posterior um of the thyroid um decreased blood calcium stimulates parathyroid hormone secretion in the [Music] bloodstream uh pth stimulates uh both bone to release calcium um ions and active vitamin D activates vitamin D the active uh vitamin D or vitamin D or D3 stimulates the intestines to absorb calcium ions and release the bloodstream um increased blood calcium inhibits pth secretion so the primary control for the secretion of pth is blood calcium levels and if you remember from um the skeletal system chapter if we have hypercalcemia or too much calcium in the blood the thyroid is going to sense that the calcium is too high the thyroid is going to essentially release calcitonin and the bones we're going to have um we're going to have this uh we're going to deposit calcium in the bones and the blood calcium levels are going to go down with hypocalcemia or too little calcium in the blood the parathyroid is going to sense that the calcium is too low the parathyroid releases pth and we're going to release calci calcium from the bones and that the blood calcium is going to go up now if your parathyroid has a if your parathyroid gland has a defect that prevents pth secretion you're going to remain hypocalcemic and therefore the amount of calcium ions and phosphate ions in the blood will remain low or decrease all right so hypoparathyroidism and Hyper parathyroidism um basically the most common cause of hyper parathyroidism is going to be a tumor um and you will need to know the symptoms of hypoparathyroidism you'll need to know the symptoms of those muscle cramps seizures um are going to be um the two symptoms that you'll need to know all right adrenal glands so adrenal glands we also call them suprarenal glands because they sit on top of the kidney they look like a little hat that sit on top of the kidney um we have a lot we have different hormones that are produced by the adrenal glands um basically they're going to be responsible for maintaining your sodium levels your stress levels and um your sex hormones and we have two different portions we have an A cortex and a medula um with the um the looking at the cortex we have three different um zones or areas that produce uh different hormones we have an outer zone called a Zona glosa um and that's going to produce aldosterone and uh mineral corticoids we have a middle Zone called a Zona fic ficula and that's going to produce cortisol and other glucocorticoids um that's going to be use for fat and protein metabolism and we have an inner Zone called a Zona reticularis um that's where your sex hormones uh male sex hormones or androgens are going to be produced um your adrenal glands um um you know we already said aldosterone cortisol androgens estrogens um that's going to be stimulated by act adreno corticotropic hormone so adrenal cortico cortex Tropic remember it's a Tropic hormone um so that's kind of like the breakdown of act um Adrenal medulla um that's the inside um that's a central portion of the gland so going back to this slide you know you have your um you know your cortex is is on the outside and the medulla is going to be kind of like the inner layer um right here so that's your medulla and this is your cortex so cortex [Music] and medulla all right so medulla um is going to secrete these amine hormones called catacol amine um and if we look at the pathway basically we're going to start with tyene we're going to go to dopa dopamine so tyene is going to get converted to dopamine and dopamine is going to get converted into norepinephrine and then to epinephrine um and um epinephrine and both both epinephrine and norepinephrine are going to act on these um Alpha and beta receptors if you heard like beta blockers that's kind of what I'm talking about but we have Alpha and beta receptors um and both epinephrine and norepinephrine work on Alpha and beta receptors however norepinephrine will have a greater affinity for Alpha receptors um and you can see that epinephine um is about 80% um in our body 20% is norepinephrine we can say epinephrine is the equivalent to Adrenaline um um so if you get an adrenaline rush that's epinephrine um norepinephrine we also call it nor adrenaline um I will go back to um you know the aldosterone cortisone stuff like that um aldosterone helps um regulate uh blood pressure by managing sodium pottassium in your blood and um and it impacts your blood volume cortisol I said earlier was your stress hormone it's basically going to increase sugar or glucose in the bloodstream um and it also enhances the brain's use of glucose um and it increases the availability of substances in the body that uh repair tissues um um epinephrine uh we'll see uh might be on the next slide um epinephrine is going to um induce increased uh vascular smooth muscle contraction uh pupilary dilator muscle contraction intestinal sphincter contraction so think of um and and norepinephrine increases heart rate blood ping from the heart so with epinephrine and norepinephrine kind of think of you know what happens when you meet the bear in the middle of the woods so here's a chart of you know what happens with epinephrine and norepinephrine so this is think of your sympathetic nervous system this is this is what happens when you meet the bear in the middle of the woods your heart rate increases um your heart starts pumping um your heart starts pumping um more vigorously your blood vessels they're going to vasodilate you have to get ready for fighter flight um your blood pressure is going to increase because you have now you now have this increased cardiac output well we'll talk about cardiac output in a couple chapters when we talk about the cardiovascular system um your Airways are going to dilate you're you're going to get ready to run away from the bear um or fight the bear you need that that increased lung volume to be able to uh get ready for that your reticular activating system is um or your reticular system is now activated you have to be able to process everything your liver is going to um is going to break up that glycogen into glucose so that you can have that energy to either run away or from from the bear or to fight the bear um your metabolic rate is going going to increase so like I said think of what's going to happen um when you meet the bear and um and that's your pretty much your sympathetic nervous system all right aldosterone um you know I said um I said that aldosterone helps regulate the blood pressure by managing sodium and pottassium in your blood and impacting the blood volume um but aldosterone it conserves energy or energy sorry conserves sodium and excretes potassium and remember that wherever sodium goes water will follow so because we are conserving energy water is going to be conserved as well so aldosterone kind of works the same way as antidiuretic hormone and that it retains uh retains fluid um I mean different mechanism of course but um you know aldosterone is going to retain sodium and therefore water um we have this thing called a renin Angiotensin system that's going to help with our blood pressure um we'll briefly look at it we're not going to go in depth into the renin Angiotensin or the ren renin Angiotensin aldosterone system um some people say the renin Angiotensin osone system um that's going to be more um more nursing school um um in depthness um we'll just kind of briefly um go over it um here you know you have a a decreasing blood blood pressure um Andor sodium ion concentration it's going to stimulate the secretion of this enzyme renin and um renin uh converts con s angiotensinogen to Angiotensin one which is converted to Angiotensin 2 by this enzyme called Ace or Angiotensin converting enzyme um and Angiotensin 2 stimulates the adrenal cortical cells to secrete aldosterone and aldosterone is going to then act on the kidney to conserve uh sodium ions and therefore water is going to follow sodium so we're going to hold on to hold on to sodium and hold on to water and now because we have that increased blood volume our blood pressure and sodium ion concentration is going to hopefully return to normal inhibiting further uh secretion of renin um so we have this enzyme called Ace Angiotensin converting enzyme Ander of Ace inhib ACE inhibitors um to treat hypertension um so they bind to the ace blocking um the formation of angiotensin 2 um and then Brady Kine and aasad dilator can now work to lower your blood pressure so um if you have an Ace inhibitor it's going to kind of block this step um right here and um um basically prevent the conversion of anot tensin one into Angiotensin 2 and hopefully lower your blood pressure all right so regulation of cortisol secretion um you know your higher brain cells signal the hypothalamus to secrete this um crh um cortisol releasing hormone and stimulates the anterior pituitary gland to secrete um adreno cortico Tropic hormone into the bloodstream and then a create the ACT stimulates the adreno uh adrenal cortex to release cortisol um and cortisol affects various target cells it can stimulate the production of glucose from non-c carbohydrates um it can promote fatty acid release it can inhibit protein synthesis and cortisol inhibits the secretion of CR and act remember it's a negative feedback loop um but cortisol can reduce inflammation um cortisol it can decrease the permeability of capillaries and prevent the leakage of fluids that surround or that swell the surrounding tissues um cortisol can stabilize the lysomal membranes that release uh preventing the release of their enzymes that would otherwise destroy tissues remember lomes are the garbage disposal of the cell and they dump out their contents and kind of eat up the cellular debris so cortisol would help stabilize those cell membranes and um cortisol inhibit cros gland and synthesis remember we talked about prostaglandins earlier on in the lecture all right summary slide of um aldosterone cortisol and adrenal androgens um so fight ORF flight what happens um you want to your body wants to protect itself cortisol is going to inhibit protein synthesis and various tissues um so it's going to increase the blood concentration of amino acids it's going to stimulate your liver cells to synthesize glucose that's called glucon neogenesis synthesize new glucose gluco neo genesis and it's going to promote fatty acid release to use as Body Energy so that the brain can use the glucose for the neurons energy source um remember from the neuros uh neuro chapters the brain cannot use anything but glucose as their energy source remember the body can use um the body is good about using carbs lipids and proteins and kind of convert everything into um into into energy source but um brain the brain can only use glucose so for this slide you will need to know the um the action of cortisol um and cortisol is useful in controlling inflammatory reaction because cortisol decreases the permeability to or permeability of capillaries all right um disorders of the adrenal cortex we have Addison's disease um and Cushing syndrome just a name two there's plenty of others um Addison's disease is a um hyposecretion or a um insufficient um hormone from the adrenal cortex it's usually going to be cortisol and aldosterone um um and that results from electrolyte glucose imbalances dehydration low blood pressure fatigue nausea increased skin pigmentation so over overall we're going to have decreased blood sodium levels um and this could be fatal because you know sodium is very vital um and we do have a electrolyte imbalance but basically um with Addison's disease um it's going to result in um um blood uh decreased sodium blood levels and if we go back back to what aldosterone does it conserves energy or I keep saying energy conserves sodium so if we have decreased aldosterone we're going to pee out more sodium and excrete more sodium so we're going to have a lower um sodium blood sodium content all right with Cushings syndrome it's usually a hyp secretion of cortisol um usually because of an adrenal tumor um or excess production of act by the anterior pituitary so we have too much cortisol or too much stress hormone so with your stress hormone you're going to see um muscle wasting uh bone loss um increased blood glucose levels sodium retention water retention because remember water follows sodium uh um because of the increased blood volume we're going to have increased blood pressure puffy skin um but one characteristic of Cushing syndrome is that you're going to have this abnormal deposit of adapost tissue um on the back of your um at the upper part of your back in your neck it's um usually called a hump um but you can see some increased adapost tissue in your face as well uh pancreas is um an elongated flat and posterior stomach so it's going to lie in your um like mid to left um rib cage um and basically it's going to uh transport digestive juices to your small intestine to the dadum um um and it has remember your pancreas falls under the digestive system and the endocrine system but actually has endocrine function and exocrine gland function um it stim it's an endocrine function because it's it secretes hormones directly into the body fluids or bloodstream um like uh like insulin and then also has exocrine gland functions because it's these digestive juices go through the pancreatic duct um down in into the um the digestive system so we have three hormones that we're going to talk about um and they are secreted from these cells called the pancreatic eyelets or the eyelets of longerons um glucagon insulin and somat so glucagon are secreted by these alpha cells and glucagon increases concentrations of blood glucose um glucagon is a protein that stimulates the liver to break down glycogen into glucose so remember the suffix to break down is Lis so if we're breaking down glycogen we would say glycogen ois so glycogen is a protein that stimulates the liver to break down glycogen into glucose so glycogen allyis and convert non-c carbohydrates and such as amino acids into glucose so now creating new glucose glucon neogenesis um insulin is another hormone so insulin is secreted by these beta cells and they're going to decrease blood glucose concentrations um and insulin is just a protein protein is just amino acids that stimulate the liver to form glycogen from glucose inh and inhibit the conversion of nonc carbohydrates into glucose and so Mast Statin is secreted by these Delta cells and they inhibit the secretion of insulin and glucagon so here you can see the pancreas um and it's going into the small intestine here you can see the the eyet cells um all right all right so hormones of the pancreatic eyelets we've already talked about the glucagon insulin and somatostatin um and by now you should know the action of glucagon and Insulin we've we've talked about that enough throughout amp1 that you should know um you should know these uh inside and out soasta we haven't talked about but helps regulate carbs um but it also shuts off both insulin and glucagon so here um you know after a meal blood glucose increases um in the pancreatic eyelets um insulin insulin secretion increases and glucagon uh secretion decreases you have cellular uptake of glucose and the formation of glycogen um and then in between meals blood glucose decreases and the pancreatic eyelets uh insulin secretion decreases and um glucagon secretion increases glycogen is now broken down into glucose and non-c carbohydrates are converted into glucose all right diabetes um it's a metabolic disease you know lack of insulin or the ability of the cells to recognize insulin um it's an immune system disorder um there are there is some research out there to suggest that it might be a viral disorder um but right now um immune system but basically you know elevated blood glucose can damage you know your eyes heart kidneys nerves um you know altered carbohydrate protein fat metabolism um a lot of us already know what this what what goes on with diabetes you know we have um glucose that um is poorly up up uptake by the cells um typically insulin will help that that glucose uptake into atopos and muscle cells but in diabetes those carbs or that um that glucose cannot enter cells um in normal quantities I'll just change that to glucose and that's going to result in hyperglycemia or high blood gluc glucose um and then because of that we have to look at other forms of energy usage um and in true diabetes if you see someone who's truly a diabetic um like a type one diabetic you're going to see um a really fast decline in weight um you're going to see um uh their hunger uh they're going to be hungry a lot uh tired their wounds aren't going to he heal well um their growth if they're a child their growth is going to stop um there's three signs that you're going to look for um polydipsia polyphasia polyuria um you're going to uh drink a lot eat a lot and pee a lot so glucose is going to spill into the urine um it's going to it's called glucose Uria and and then water is going to follow by Osmos so that's your polyurea um and that's going to lead to dehydration and thirst so that's your poly dipsia too much drinking and then urine is going to have a high um osmotic pressure and we'll talk about osmotic pressure um I believe it's next chap no in a couple chapters all right so we know that there's type one and type two diabetes type 1 diabetes is basically in insulin dependent Di diabetes usually we see this um at um before 20 years of age for onset um it is an autoimmune disease where the beta cells of the pancreas are destroyed um and that we uh typically have a lack of insulin production um type 2 diabetes it's not that we don't have insulin production it's usually um that the insulin that we do produce the cells don't um have a sensitivity to that insulin um and that's going to be the majority of the cases that we see as type two diabetes um is that the body is unable to recognize that insulin that we that we do produce so how do we treat it um type one diabetics are going to have to require insulin um remember that the pancreas does not produce insulin because the beta cells are destroyed um that insulin does come from can be obtained from pigs cattle um we we do have an inhaled form of insulin um we're looking at other ways to deliver insulin we have an insulin pump so that you don't have to you know inject yourself every time um you know you see the things on the back of people's arms that can measure your blood glucose reading so you don't have to prink your finger and test your blood sugar anymore um we are looking at um other countries are looking at uh doing pancreatic eyet transplantations we aren't uh doing that in the United States yet so for treating type 2 diabetes um basically you know carbs get broken down into sugar um so get rid of the sugar get rid of the carbs and eat more protein get exercise um take medicines that will decrease um glucose production ction and I thought it was interesting that the book said gastric bypass surgery um so gastric bypass surgery is typically only you know indicated for people over you know 400 um to 600 pounds and um so try and do um the exercise before you go for the gastric bypass surgery so you know with type one diabetics um without treatment um fatty acids and Ketone bodies will accumulate in the blood um if you've heard of diabetic keto acidosis um dka um that's when you have these Ketone bodies that are going to be building up um in your bloodstream all right um some other glands um the pineal gland it's going to be found in the brain um it's actually attached to the thalamus it's going to secrete melatonin uh Mel um Mel tone and helps regulates our circadian rhythms um you know our circadian rhythm lets us know if it's daylight or nighttime when we should be awake when we should be asleep um our thymus gland is kind of found in between our lungs kind of about right here um uh we looked at it in am1 um secretes these things called thymosins um it's actually uh good for um production differentiation of our white blood cells remember our lymphocytes our T lymphocytes um and uh for immunity and as we get older our thymus gland gets replaced by atopus tissue um and other glands in our reproductive organs the ovaries produce estrogen Pro progesterone testes produce testosterone um our digestive glands um our heart and our kidneys um we'll talk about um the ntic peptides and we talk about the cardiovascular system we've already talked about um arthropo to stimulate red blood cell formation um so stress so survival is going to be dependent on homeostasis you know we everything goes back to homeostasis um we have changes every millisecond in our internal and external environment that are potentially lifethreatening in um and we have to do what we can to minimize the effects of those changes um and we have sensory receptors that going to send those impulses to the hypothalamus the hypothalamus kind of oversees everything and determines from a nervous system perspective what needs to happen and that the hypothalamus is going to be the the the controller of the endocrine system to stimulate the endocrine gland and to do or not do something um and we have different types of stress um you know we have good stress and bad stress um but you know here we're going to talk about the bad stress and we can break it up into physical stress and psychological stress physical stress is you know temperature extremes infection injury oxygen deficiency psychological stress you know if you're in danger if you've just uh lost a loved one or if you're feeling um anger or if you're in fear of something um and how we respond to stress is based on the hypothalamus and we have this thing called a General Adaptation Syndrome or a general stress syndrome the first phase is going to be an alarm phase and that's kind of like our fight ORF flight response um that's pretty much immediate and it doesn't last very long we had that sympathetic nervous system and those are going to provide impulses that you know do uh pretty much everything that this chart says um we're going to increase our blood glucose increase thatty acids increase our heart rate increase our breathing rate increase our blood pressure dilate our air passages um shunt blood to skeletal muscles increase um epinephrine production um epinephrine is going to intensify and prolong these responses then we're going to fall into um the resistance stage so this is you know after the immediate threat is over if we still continue to experience stress so this would be you know more psychological stress or long-term abuse um long-term depression long-term whatever stress you're you're experiencing um your your CR act cortisol pathway you're going to have a prolonged um secretion of cortisol um and remember cortisol is your stress hormone so cortisol glucagon growth hormone are going to mobilize the energy sources um you're going to have ADH and water um that's going to cause uh or ADH and R that's going to cause um water retention um you know blood blood concentrations of epinephrine cortisol atth every a lot of these are going to increase um you can see here in the um alarm stage stress from changes in the internal or external environment um signals from sensory receptors stimulate the hypothalamus uh sympathetic impulse ules to the Adrenal medulla cause the release of epinephrine and norepinephrine sympathetic impulses I didn't change your slide um sympathetic impulses directly influence induce the release of norepinephrine short-term fight or flight um then we have the short-term fight or flight alarm stage um blood glucose increases uh blood glycerol and fatty acids increase your heart rate increases your blood pressure increases your air passage dilates your pubil dilate your blood flow um redistributes and then we have the um resistance stage where your stress signals from your sensory receptors um stimulate the hypothalamus to release uh this crh um and the anterior pituitary releases act which stimulates the adrenal cortex to release um uh to release cortisol and you can see um then we have this thing called the longterm adjustment or resistance stage where um your blood concentration of amino acids increase um release a fatty acids increase glucose formed from non-carbohydrate sources amino acids from proteins and glycerol from fatty acids are all going to increase and then if we still don't take care of ourselves we're going to go into the exhaust phase um the exhaustion phase is going to begin um you know months you know this is months of abuse months of depression months of being stressed out um months of act months of cortisol um we're going to see electrolyte imbalances immune system um suppression um uh wasting syndrome and it can result in death so take care of yourself only you can take care of yourself I'm very Advocate I'm a big advocate for uh mental health so here's just a summary of um uh major events in the general stress syndrome um so um basically remember that act is going to be the regulator of cortisol and and oh some lifespan changes um you know with everything endocrine glands are going to decrease in size um your muscle skeletal strengths are going to decrease your growth hormone levels are going to decline overall so you know after you're born you know we're going to go through growth spurts and then you know your growth hormone increases in puberty and then it's going to level off after adolesence and it's going to start to decline um after about 40 years old um your 80 pH levels or your anti-p levels are going to increase due to slower elimination by the liver and kidneys your calcium loow your calcitonin levels are going to decrease increasing the risk of osteoporosis um and we're going to have pth level changes um increasing the risk of osteoporosis especially in females and especially once we um females um are postmenopausal needing uh hence the need for hormonal replacement therapy um in insulin resistance May develop um uh changes in melatonin may affect the body clock and um aryos and production declines mainly because um AR thymus gets converted into or about 80% of our thymus gets converted into um adapost tissue all right so like I said that was a long chapter we are done with the um with the endocrine chapter uh let me know if you have any questions and uh I'll see you next time bye