with diabetes insipidus diabetes means an increased passing of urine and insipidus means tasteless so diabetes insipidus is a condition characterized by the production of large quantities of dilute and tasteless urine the tasteless urine of diabetes insipidus distinguishes it from diabetes mellitus which describes sweet-tasting urine and to answer your question yes urine was really tasted at one point in time to make that distinction now in the brain there's a region called the hypothalamus inside the hypothalamus are osmoreceptors which can sense the osmolality of the blood or basically how concentrated it is osmolality is the concentration of
dissolved particles in the blood plasma or the liquid portion of blood there are a number of dissolved particles in the blood plasma but the major ones are glucose sodium and blood urea nitrogen and the normal osmolality is between 285 and 295 ml osmols per kilogram during periods of dehydration there's an increase in concentration of these particles in the blood and so osmolality increases the osmoreceptors and the hypothalamus detect that increased osmolality and that triggers the sensation of thirst which tells us to drink more water the water then gets absorbed and dilutes the blood bringing the
osmolality back to normal in addition to osmoreceptors the hypothalamus has a cluster of neurons that are found in a specific spot called the supraoptic nucleus these neurons produce a hormone called antidiuretic hormone or adh adh is also called vasopressin because it causes smooth muscle around the blood vessels to contract which increases blood resistance and raises the blood pressure when the osmoreceptors detect high osmolality they signal the superoptic nucleus to send adh down the supraoptico hypophyseal tract which runs through the infundibulum or pituitary stock and into the posterior pituitary gland where it's then released into the
blood adh travels to the kidneys specifically to the distal convoluted tubule and the collecting ducts of the nephrons and binds to a receptor called vasopressin receptor 2 or avpr2 when avpr2 is bound proteins called aquaporins which usually sit in vesicles inside the cells of the distal convoluted tubule and collecting ducts start to embed themselves in the apical surface of the cells which is the side that faces the lumen of the tubule these aquaporins ultimately allow water and only water to travel out of the lumen of the tubule and into the cells lining the nephron and
ultimately back into the blood just like drinking more water this dilutes the blood and returns plasma osmolality to a normal level this reabsorption process though also decides how much water leaves the body as urine and how concentrated that urine is which is one of the things that keeps a normal urine osmolality between 300 and 900 ml osmols per kilogram diabetes insipidus is when the kidneys reabsorb too little water from the lumen of the tubule and this causes the body to produce unusually large quantities of urine which is called polyuria since there's less water in the
blood plasma osmolality increases and that triggers thirst and causes an individual to drink a lot which is called polydipsia there are four types of diabetes insipidus each with its own underlying cause the first type is central diabetes insipidus which is when there's a problem in the hypothalamus or pituitary gland preventing adh production or release as a result there's insufficient adh in the blood and that means that there's less vasoconstriction and that there aren't enough aquaporins in the kidneys central diabetes insipidus is often caused by damage to the hypothalamus osmoreceptors the supraoptic nucleus or the supraoptical
hypophyseal tract but in other cases the exact cause is hard to identify the second type is nephrogenic diabetes insipidus which is when there's a problem with the kidneys themselves which makes them unresponsive to adh that can happen due to a genetic defect which can lead to abnormal vasopressin receptors or aquaporin proteins that are unresponsive to adh in addition there are medications like lithium that can decrease the production of aquaporin proteins in the collecting duct finally there are kidney disorders like polycystic kidney disease that can cause diabetes insipidus the third type is gestational diabetes insipidus which
happens when the placenta of a pregnant woman releases an enzyme called vasopressonase that breaks down vasopressin or adh as a result adh might still be produced and released as normal but it doesn't get to exert its full effect on the blood vessels or kidneys in women with gestational diabetes insipidus vasopressinase is produced starting in week 8 of pregnancy and peaks in the third trimester as a result the symptoms typically worsen during the course of the pregnancy right up until birth when the placenta is removed but can continue for up to two months after birth due
to residual vasopressinase the fourth type is dipsogenic diabetes insipidus or psychogenic polydipsia which is caused by drinking way too much water dipsogenic diabetes insipidus is often psychological in nature like in individuals with schizophrenia who might compulsively drink water in contrast to the other three types of diabetes insipidus dipsogenic diabetes insipidus leads to a decrease in blood osmolality the hypothalamus decreases the release of adh as a normal physiological response and the kidneys try to excrete water which leads to polyuria or excess urination the symptoms of diabetes insipidus are polyuria and polydipsia a person with diabetes insipidus
typically makes over three liters of dilute urine each day diabetes insipidus can quickly lead to dehydration and low blood pressure the increase in plasma osmolality can result in fatigue nausea poor concentration or confusion the diagnosis of diabetes insipidus might start with a blood osmolality test which would show an increased blood osmolality of above 295 milliosmoles per kilogram in central gestational and nephrogenic diabetes insipidus if blood osmolality is in the usual range but an individual is still experiencing both polyuria and polydipsia then it might be due to dipsygenic diabetes insipidus which would be confirmed by finding
out if the person is drinking massive amounts of water in addition a water deprivation test can be done this is where an individual doesn't drink water for a few hours then hourly measurements of urine volume and osmolality are done in a person with diabetes insipidus urine osmolality will usually stay below 300 ml osmols per kilogram despite having no fluid intake after taking an adh analog like desmopressin which is the medication that works like adh the urine osmolality might return to a normal level between 300 and 900 ml osmols per kilogram suggesting that the cause is
a low level of adh this would be evidence for both central and gestational diabetes insipidus which can be distinguished by looking at whether the person's pregnant or not if the adh analog causes urine osmolality to increase only slightly then the kidneys aren't responding to the adh meaning that it's nephrogenic diabetes insipidus treating central and gestational diabetes insipidus relies on desmopressin to make up for the lack of adh in the blood for nephrogenic diabetes insipidus drugs like thiazide diuretics can be given to increase urine excretion of sodium since sodium contributes to blood osmolality getting rid of
sodium reduces blood osmolality and stops the hypothalamus from stimulating thirst in the case of dipsogenic diabetes insipidus behavioral therapy can help reduce fluid consumption all right as a quick recap diabetes insipidus is caused by excessive water loss through urine central diabetes insipidus is due to adh not being produced or released and nephrogenic diabetes insipidus is the result of the kidneys not being able to respond to adh gestational diabetes insipidus is caused by vasopressinase which breaks down adh and is produced in the placenta of some pregnant women and dipsogenic diabetes insipidus is caused by excessive water
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