Hello and welcome to the Zero to Finals podcast. My name is Tom and in this episode I'm going to be

talking to you about Diabetes Incipidus. And you can find written notes on this topic at

0.0tofinals.com slash diabetes insipidus or in the endocrinology section of the zero to finals medicine book.

So let's get straight into it.

Diabetes insipidus occurs due to either a lack of antidioretic hormone, which is called cranial diabetes

insipidus, or a lack of response to antidiarrotic hormone,

which is called nephrogenic diabetes insipidus.

Antidiarrotic hormone is produced in the hypothalamus

and secreted by the posterior pituitary gland.

It's also known as vasopressin.

Antidiarrotic hormone stimulates water reabsorption from the collecting ducks in the kidneys.

In patients with diabetes insipidus, the kidneys are unable to reabsorb water and concentrate the urine and this leads to

polyurea with excessive amounts of urine and polydipsia which is excessive thirst. Primary polydipsia

is a separate condition where the patient has a normally functioning antidioretic hormone system,

but drinks excessive amounts of water, which leads to excessive production of urine or polyurea.

This is not diabetes insipidus.

Let's talk in more detail about nephrogenic diabetes insipidus.

Nephrogenic diabetes insipidus is when the collecting ducks of the kidneys do not respond to

antidiarrotic hormone. This can be idiopathic without any clear cause.

It can be caused by medications, particularly lithium, which is used in

bipolar effective disorder, genetic mutations in the ADHD, which is found on the X-chromozoan,

which is found on the X-chromozoan and inherited in an X-linked recessive pattern.

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