Diabetes Insipidus Causes, Symptoms, Diagnosis, Treatment.

we are going to talk about diabetes insipidus and its type and causes all the investigations that you need to do and the treatment of diabetes insipidus,

First of all, what is diabetes insipidus?

Diabetes insipidus is a deficiency of the antidiuretic hormone, What antidiuretic hormone does is that it causes reabsorption of water in the kidneys antidiuretic hormone causes reabsorption of water from the distal convoluted tubule and the collecting ducts. whenever there is a deficiency of the antidiuretic hormone.

The water is not being reabsorbed and that water is lost in urine the loss of water in the urine causes an increase in urine volume and polyurea which is the major complaint with which the patient presents.

Now based on the cause of this diabetes insipidus it is divided into two types central diabetes insipidus in which the cause lies within the brain and nephrogenic diabetes insipidus in which there is resistance to the action of antidiuretic hormone in the kidneys in central diabetes insipidus.

 what happens is that adh(Administer Desmopressin hormones) is produced from the pituitary gland. Whenever there is some problem with the pituitary gland or there is inflammation of the brain the antidiuretic hormone is not produced and deficiency of antidiuretic hormone results in diabetes insipidus.

What are the things that can cause central  diabetes and separatists  the causes of central diabetes in sepidus are adenoma in the pituitary gland a non-functioning adenoma can cause central diabetes insipidus,

Encephalitis is a brain infection or head trauma and craniopharyngioma, and craniopharyngioma is a tumor of the pituitary gland and it can also be idiopathic in nephrogenic diabetes insipidus as we said that there is resistance to the action of adh.

In the kidneys, nephrogenic diabetes in sepidus is caused by drugs.

Drugs like macrocycline lithium, lithium is a very important drug that is used for the psychiatric disorder bipolar disorder and lithium blocks the ADH receptors in the kidneys resulting in diabetes insipidus and infiltrative diseases like amyloidosis sarcoidosis can cause nephrogenic diabetes insipidus hypercalcemia can result in nephrogenic diabetes insipidus hypokalemia and sickle cell disease can result in nephrogenic diabetes insipidus so these were all the causes that result in deficiency of adh hormone and loss of water in urine so whenever a patient presents to you with polydipsia increased thirst and polyuria increase urinary frequency and urinary volume the first thing that you need to do is you have to perform water deprivation test.

What do you do in a water deprivation test?

 Is that you stop the water intake for two to three hours before the test you stop water intake and expect is that whenever the patient stops taking water body will try to reabsorb more water from the kidneys and to reabsorb water from the kidneys body will secrete more anti-diuretic hormone than that anti-diuretic hormone will result in water absorption.

So whenever there is any problem with the production of the ADH hormone or whenever there is resistance to the adh action in the kidneys then the body will not be able to reabsorb. That water how will you know that body is not reabsorbing water

what do you do you basically measure urine volume and osmolality every hour and you also measure serum sodium and osmolality every two hours if the urine osmolality increases or if the urine osmolarity is greater than 600 milli or small per kg?

It means that the body has reabsorbed all the water when you have stopped the intake of water the body is now reabsorbing more water and the urine osmolality has increased urine osmolality increase shows that there is no deficiency of adh hormone and there is no diabetes insipidus it rules out the diagnosis of diabetes insipidus.

Then why was this patient having polyurea and polydipsia this patient was having polyurea and polydipsia because he was taking too much water because that person was drinking so much water and that increased intake of water resulted in polyurea and polydipsia this condition is called primary polydipsia it is a psychological problem in which person drinks more and more water and pees more. Water out if the urine osmolarity is not greater than 600 milli or small per kg, it means the urine is hypo or smaller and the body is still losing water.

Then you need to measure Uranus molarity for the next two to three hours and if the urine osmolarity stays low and if it is hypo or smaller and the body is keeping losing water despite the patient not taking any water from outside and plasma or molarity stays greater than 295 milli or moles per kg. It means that the body is dehydrated plasma is hyper or smaller and urine is hypo or smaller plasma is losing water and urine is having more water, therefore, it's more hypo osmolar in that case now it confirms that this patient is having some problem with the antidiuretic hormone is deficient either it's the central cause or it's the nephrogenic cause now you want to find out that whether it is the central cause which is not producing antidiuretic hormone or it is the nephrogenic cause, which is due to the resistance of antidiuretic hormone action.

You have to administer desmopressin is an adh analogue and it's called

it causes reabsorption of water from the kidneys and then you measure urine osmolality every 30 minutes for the next two hours if the urine osmolarity increases, it means that adh hormone was deficient it means that antidiuretic hormone was deficient, and when your give an antidiuretic hormone analog like desmopressin.

It started working and urine osmolality has finally started increasing body is reabsorbing more

Water, so it means that there was a deficiency from the brain adh was not being produced from the pituitary gland.

It was a central cause that was causing diabetes in Cepeda so it is central diabetes insipidus if Uranu's morality does not change if urine osmolarity stays hypo or a smaller body is losing water despite giving desmopressin despite giving adh analog it means, that their is some resistance in the kidneys to this adh hormone despite giving adh hormone desmopressin.

This patient is still not reabsorbing water from the kidneys and urine osmolality is still low it means that the problem is in the kidneys and we call it nephrogenic diabetes insipidus so that's how you differentiate between the central cause and the nephrogenic cause by giving adh analog treatment of diabetes insipidus depends upon that whether it is central or nephrogenic if it is central it means that anti-diuretic hormone is deficient and if you give antidiuretic hormone analogues like vasopressin decimal pressing.

It corrects the state it corrects diabetes insipidus and you can also give drugs that stimulate ADH secretion drugs like chlorpropamide and carbamazepine cause secretion of ADH hormone from the pituitary gland nephrogenic diabetes insipidus is treated by giving diuretics now you will be thinking that the body is already losing water in diabetes insipidus and we are giving diuretics as the treatment.

What happens is that these diuretics are these weak diuretics like hydrochlorothiazide and amyloid they act on the distal part of the tubule distal convoluted tubule and they cause loss of sodium in urine stimulating the proximal convoluted tibial to reabsorb more salt and water and proximal convoluted tubules start reabsorbing more water and more water is being reabsorbed from the proximal tubules so in response to the loss of sodium in the distal tubule body. starts reabsorbing more water from the proximal convoluted tubule, so that's how these weak diuretics cause a little loss of sodium and water but that little loss of sodium and water causes more water reabsorption from water from the proximal convoluted tibia.

 How nephrogenic diabetes in sepidus is treated in summary diabetes and sepitus can be central or nephrogenic and these are all the causes of diabetes and sepitus to see whether there is diabetes insipidus or not, you do water deprivation tests you stop water intake if you urinate molality increases. It means that the body has started reabsorbing water and it was primary polydipsia if you know molality stays low, it means the body is losing water you administer decimal pressing.

 If your urinate molality increases it means it was central diabetes insipidus in which ADH hormone is deficient and if urine osmolarity does not change it means it was nephrogenic diabetes insipidus and the body is still losing water despite giving them that desmopressin adh analog treatment depends upon the cause central diabetes insipidus is treated with adh analogues and adh secreting drugs and you also treat the underlying cause in nephrogenic diabetes insipidus is treated with diuretics like thiazides and amyloids that cause a little loss of sodium and that a little loss of sodium causes more reabsorption of water from the proximal convoluted tubule.

So this was diabetes insipidus.

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