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Costanzo Physiology (Chapter 9B) Endocrine Physiology: Hypothalamus/Pituitary axis || Study This!
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hello and welcome to the second part of the endocrine physiology chapter of costanzo's physiology textbook in this video we are going to go over the hypothalamic pituitary axis which is essentially the mastermind that's able to control the majority of our endocrine systems it consists of the hypothalamus which is clearly up in the brain which we covered in the neurology portion and then also the pituitary gland that kind of sits just underneath it the pituitary gland is made up of two separate glands or two separate lobes the posterior lobe which is called also the neural hypothesis mainly because it's made out of neuron cells and secretes neuropeptides and then we have the anterior lobe which is also called the adeno hypothesis which is actually made out of endocrine cells themselves so you can see it over here figure 9.9 here where we have the posterior lobe made out of neurons and you can see that the cell body of the neuron is actually located within the hypothalamus and then also the anterior lobe made out of endocrine cells which is connected with the hypothalamus with a bloodstream its own hypothalamic hypophyseal portal vessels so this is essentially the venous system to the hypothalamus so then the anterior lobe of the pituitary gland receives high concentrations of the hormones from the hypothalamus that does not enter the systemic circulation and that directs which hormones should be released from the anterior pituitary gland once either the posterior or anterior pituitary gland is stimulated to release a certain type of hormone that just gets released into the systemic circulation now the posterior pituitary gland only secretes two neuropeptide hormones adh and oxytocin adh is primarily associated with the supraoptic nuclei within the hypothalamus whereas oxytocin is primarily associated with the paraventricular nuclei in the hypothalamus so how this works is that the hormone is actually synthesized in the cell body of the neuron within the hypothalamus and then actually gets transported to then sit in vesicles right at the end of the neuron and the dendrites waiting to be stimulated to be released when told so by the hypothalamus whether that's adh or oxytocin we'll go into more details about those two different hormones later on in this video and to start with we'll talk about the anterior pituitary gland hormones because we have six major hormones here and each are secreted by their own cell type ending in troph for example we have thyroid stimulating hormone or tsh released from thyrotropes we have acth released from corticotropes we've got growth hormone released from somatotropes prolactin from the lactotrophs and then lastly follicular stimulating hormone and luteinizing hormone fsh and lh secreted by gonadotrophs so these tropes a particular endocrine cells within the anterior pituitary gland that secretes its own endocrine hormone when stimulated too from the release of a releasing hormone from the hypothalamus so hypothalamus secretes a releasing hormone in response to a stimuli that releasing hormone tells the stimulating hormones from the pituitary gland to be released which then get released into the systemic circulation and then these stimulating hormones go to their target endocrine glands within the body to then stimulate the release of the hormone that they want to release so for instance when it comes to thyroid hormone which we'll go in in another video the hypothalamus releases thyroid releasing hormone which then tells the anterior pituitary gland to release thyroid stimulating hormone and the thyroid stimulating hormone tells the thyroid gland to release thyroid hormone so that's the basics behind the hypothalamic territory axis so going through some of the particular hormones released from the anterior pituitary gland specifically now just briefly tsh fsh and lh are all glycoproteins it goes into a little bit of detail about their actual molecular structure which i don't think is as important but essentially they are all a similar type of protein a glycoprotein tsh we will go into more details in the thyroid hormone video which will be coming up shortly and then fsh and lh will be in the reproductive tract is acth or adrenocorticotrophy hormone is released from the anterior pituitary gland to increase the secretion of our adrenal cortical hormones from the adrenal gland we will go into much more details about that actually in the adrenal video coming up i know this seems ridiculous that we're going to go over these in more detail later but these are the major hormones that we will be covering in much more detail in a later video so acth is slightly different to these other ones and how it is formed within the anterior pituitary gland you can see that ac th actually comes from originally this molecule called pomc or pro opio melanocortin the main point here is that although we get acth getting produced we do have these other and the fragments of acth that can also have a minor effect and more importantly if we have a high production of acth we will get increased of these other fragments and more important clinically is the production of the melanocytes stimulating hormones the msh hormones so these hormones will actually cause skin pigmentation so then that will cause clinical signs in the presence of excessive acth or end up with increased skin pigmentation so we'll go into growth hormone in more detail now so growth hormone is also released from the anterior pituitary remember from the somatotropes the growth hormone as the name implies is important for growth so it does that by altering our protein carbohydrate and fat metabolism it gets stimulated to be released from the anterior pituitary gland due to growth hormone releasing hormone from the hypothalamus and that occurs in a pulsatile way every roughly two hours and also has some other stimulatory factors as well all noted in table 9.4 here in addition to its inhibitory factors the best way to think about this is that anything that will be inhibiting growth so let's say you don't have enough nutrients then your growth hormone will be stimulated to increase those nutrients in your body so growth hormone is trying to provide an environment for you to grow so if you have decreased glucose decreased free fatty acids you're fasting or you're exercising you're under stress then you're going to release growth hormones to try and provide an environment for you to actually grow obviously when you're going through puberty you have higher growth hormone during those times as well growth hormone will then steadily decrease as you get older now our inhibitory factors are going to be the opposite of those so if we have high glucose high free fatty acids then we already kind of have an environment for growth so you don't need to release your growth hormone obesity reduces it some metastatin remember that's our stop hormone from our gi chapter somatostatin also plays a role with inhibiting our growth hormone effects as well growth hormone itself actually inhibits itself there are negative feedback mechanism and then circling back to somatostatin this is an example of a gi protein coupled receptor remember we talked about the gs protein receptors which cause an increase in cyclic amp gi proteins are inhibitory g proteins they reduce the level of cyclic amp by inhibiting the admiral cyclase enzyme so somatostatin the stopping hormone which inhibits growth hormone does so by interacting with a gi protein as a receptor so figure 9.11 here tells us how growth hormone has a negative feedback on itself the first thing to point out here is that when growth hormone actually has its effect on the target tissue it gets broken down into these somatometers or igf's these igfs then actually have an inhibitory role on the release of further growth hormone by having a direct effect on inhibiting our anterior pituitary gland but then also by having a stimulatory effect on the hypothalamus to release somatostatin remember somatostatin our stopping hormone inhibits also the anterior pituitary gland so that's one way the growth hormone has negative feedback on itself when it's broken down the byproducts have an inhibitory effect growth hormone itself also has an inhibitory effect on itself by increasing the release of somatostatin from the hypothalamus so increased growth hormone will actually self-regulate itself and the last mechanism out of the three is growth hormone releasing hormone actually having an inhibitory effect on the hypothalamus itself so although it's released from the hypothalamus as soon as that increases in concentration it's going to tell itself to stop secreting itself essentially so the growth hormone that negative feedback mechanism has these three different feedback systems somatometers growth hormone and growth hormone releasing hormone so how does growth hormone actually have an effect on the body we know it's used to promote growth but what is it actually doing well we have three main effects here to remember number one is being diabetogenic or having an insulin resistant effect it blocks the effects of insulin which is trying to reduce your glucose levels in your body or in your blood so by blocking or making insulin resistant you increase the amount of glucose in your bloodstream and then it also increases lipolysis and adipose tissues basically what this is doing is increasing our energy stores and our plasma so then our body has a lot of energy to be able to grow so we're increasing energy availability by antagonizing insulin in an effect for an easy way to think about that first effect our second effect is increasing growth by stimulating protein synthesis and organ growth so we're increasing the uptake of amino acids into our cells and we're increasing the stimulation of protein development this will increase lean body mass and organ size our third effect is an increased in linear growth so before puberty before your growth plates have used it will increase the production of bone within your growth plate so then you're able to grow you know this is why during your growth spurt your high growth hormone but then if you're already finished your growth it will actually increase our periosteal bone growth so kind of the edges of our bones so we have this influence on bone growth more dramatic obviously before puberty that brings us to when we have an issue with our growth hormone if we have deficiency then that's going to lead into dwarfism which is treated with growth hormone with excess what you're going to see depends on when this occurs if it's before puberty then you end up with gigantism because you're actually increasing your long bone growth after puberty when linear growth is complete then you end up with just larger features so larger facial features larger hands increased organ size insulin resistance glucose intolerance etc from that excessive growth hormone so that is growth hormone in a nutshell next up is prolactin now prolactin is responsible for milk production so producing milk not letting it down that's oxytocin but milk production and the development of the breasts so obviously we're going to have an increased secretion of prolactin during pregnancy and lactation now the thing with prolactin secretion from the anterior pituitary gland which works on the breasts is that on the day-to-day it's getting inhibited from dopamine release from the hypothalamus up until pregnancy or lactation that's when that gets overridden and we start to increase trh release trh stimulates the release of prolactin and prolactin nature has an inhibitory effect on itself for its own negative feedback by increasing the level of dopamine so the stimuli for prolactin release is suckling that's the main stimulation so obviously that's a need for lactation after pregnancy then you're going to increase milk production there is also another time for prolactin release which is that puberty for breast development but otherwise it only gets released during lactation in order to produce milk for the baby any pathophysiology of prolactin includes deficiency where obviously you fail to lactate and then excess which can occur due to some kind of prolactin producing tumor which can lead to infertility because prolactin does inhibit ovulation and also galactoria or excessive milk production so moving on to our posterior lobe hormones now remember we talked about adhd and oxytocin as our two posterior pituitary gland hormones produced and synthesized by the cells within the hypothalamus in the neuron but then that neuron extends all the way down into that posterior pituitary gland where it sits waiting to be stimulated to be released so adh is the first one that we'll focus on here this gets secreted whenever we have a depolarization of that nerve that the adh is sitting in that stimulates calcium and to enter the terminal and causes exocytosis of the adh and also the oxytocin when we get to talking about oxytocin now we've already talked about adh in our renal chapter remember adh is involved with controlling our oils predominantly and then also an influence on controlling our blood pressure now our hypothalamus will sense if our osmolarity will change if there is an increase in osmolarity then that stimulates increased adh secretion adh goes to the kidneys and then tells the kidneys to increase the reabsorption of water it's able to do that by actually interacting with a v2 receptor which is a gs protein to increase cyclic amp in the principal cell of the late distal tubule and cortical tubules that will ultimately end up with the phosphorylation of aquaporin two proteins that insert themselves into the membranes aquaporin ii results in increased permeability of those principal cells to water so now that terminal nephron can actually absorb water when it was previously impermeable so the absorbing of water from the nephron reduces the osmolarity in our plasma and helps to restore our osmolarity now if we also need to increase the water reabsorption from our kidneys because of hypotension then that will occur because our dairy receptors within our carotid artery and aortic arch will sense a low blood pressure that will transmit a signal via the vagus nerve to the hypothalamus and then that will tell the hypothalamus to stimulate the release of adh to increase water reabsorption to help to increase our blood volume again and blood pressure now adh also has another influence to help with blood pressure through contraction of our vascular smooth muscle via the v1 receptor so v1 for vascular smooth muscle contraction v2 for aquaporin 2 and increasing water reabsorption from the kidneys now interestingly the v1 receptor for the vascular smooth muscle actually utilizes the ip3 calcium secondary messenger system versus the v2 receptor which utilizes the cyclic amp secondary messenger system so when it comes to disorders of adh we have central diabetes insipidus and nephrogenic diabetes insipidus diabetes insipidus just means very watery urine or very dilute urine now that occurs because we have an inappropriate response to adh either because we don't have enough adh such as in central diabetes insipidus where there is no secretion of adh from the posterior pituitary gland at all which needs to be treated by giving an adh analogue like ddavp or nephrogenic diabetes insipidus where the principal cells are actually unresponsive to adh altogether now these will not respond to adh analogues and will actually require a different type of treatment like thiazide diuretics to help to reduce our sodium reabsorption to increase our osmolarity of our urine and also reduce the gfr to reduce the amount of water that's getting excreted so diabetes insipidus means dilute urine due to inappropriate adh either due to reduced secretion and low levels in central or not responding to adh in the kidneys which is nephrogenic diabetes insipidus we do have syndrome of inappropriate adh siadh which means adh is getting secreted from an anomalous site like a cancer within the lungs this will dilute our body fluids by actually hyper concentrating our urine because now adh is sucking all the water out of our nephrons and that gets treated by an adh antagonist the last hormone we'll talk about coming from the posterior pituitary gland is oxytocin which is the milk let down hormone so prolactin stimulates milk production oxytocin then tells that milk to be let down or ejected so the stimulus for that is obviously going to be suckling or we do have some other stimulatory factors like the sight sound or smell of an infant and it is also released with dilation of the cervix during pregnancy it actually helps with uterine contractions this is one of those positive feedback mechanisms during pregnancy it is inhibited from opioids but other than that that'll conclude our video for today in the next video we'll go over our thyroid hormones in our thyroid gland feel free to drop a comment otherwise we'll see in the next video
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