Problems with ADH: SIADH and Diabetes Insipidus Video

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  • 0:07 Introduction & Background
  • 1:46 Diabetes Insipidus
  • 5:35 SIADH
  • 9:01 Lesson Summary
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Lesson Transcript
Instructor: Jennifer Szymanski

Jen has taught biology and related fields to students from Kindergarten to University. She has a Master's Degree in Physiology.

Humans can live about three weeks without food, but only about three days without water. Antidiuretic hormone (ADH) helps maintain our body's water balance. In this lesson we'll take a look at what happens when there's either too much or too little ADH in the body.

Introduction and Background

Water. It's a vital component of our bodies, making up about 70% of each cell's volume. Water homeostasis is key to survival - and our body has evolved complex biochemical systems to keep the right amount of water in our cells. One of these includes a hormone called antidiuretic hormone, or ADH. ADH's job is to act on the kidneys to promote water reabsorption. In this lesson, we'll compare and contrast diabetes insipidus, or DI, in which there is too little ADH, and syndrome of inappropriate antidiuretic hormone secretion , or SIADH, in which there is too much ADH.

Let's start by reviewing a little about ADH. ADH is also called arginine vasopressin, AVP, or just vasopressin. Made in the pituitary gland, ADH has a many functions, but for this lesson, we'll focus on its main place of action: the kidneys. ADH binds to receptors on the kidneys' nephrons, stimulating them to reabsorb water. The volume of urine made drops, and the amount of solute (salts and other solids) in it increases. This measure of amount of solute per kilogram of solvent is called osmolality. We'll see how DI and SIADH affect osmolality of both blood and urine later in the lesson.

Diabetes Insipidus

In diabetes insipidus, or DI, the body produces too little anti-diuretic hormone. Since diuresis means the production of urine, a shortage of ADH, which works against diuresis, results in polyuria, the production of a lot of urine. And indeed, polyuria is the primary symptom of diabetes insipidus. It's also because of polyuria that diabetes insipidus shares part of its name with diabetes mellitus, since both have polyuria as a symptom. However, these conditions are not related, because the etiologies behind them are very different. In diabetes mellitus, polyuria is caused by hyperglycemia, too much glucose in the blood. In DI, polyuria is not caused by hyperglycemia. Instead, it stems from something else, depending on how the disorder is generated. Notice that 3 of 4 of these terms have the root 'gen'.

  • Neurogenic - a problem with ADH production
  • Nephrogenic - a problem with the kidneys' nephrons not being able to respond to the ADH produced
  • Dipsogenic - a problem with the way that the body stimulates thirst, or
  • Gestational - DI caused by pregnancy. In some pregnant women, the placenta over-produces a chemical that breaks down ADH.

When we're talking about polyuria in a DI patient, we're talking about extreme fluid loss. On average, a DI patient makes over 3 L of urine daily, when compared to a normal person's output of about 1.5 L. The urine is also very dilute, with an osmolality of less than 200 mOsm/kg in DI, compared to a normal value of about 500-800 mOsm/kg.

Dangers of untreated diabetes insipidus are those caused by dehydration, especially

  • Hypotension (or, low blood pressure)
  • Fatigue and weight loss
  • High blood sodium (or, hypernatremia), and other symptoms of electrolyte imbalance, including,
  • Heart arrhythmia and palpitations, as sodium and potassium are important for nervous and muscular system function.

Diagnosis is designed to not only distinguish DI from diabetes mellitus, but also to determine what kind of DI is present. Common tests include urinalysis to determine the composition and dilution of urine, MRI to check for pituitary gland problems, and a water deprivation test. In this test, patients are deprived of fluids for a period of time to pinpoint how and why ADH isn't functioning properly.

Treatment for DI depends on etiology. For neurogenic DI, synthetic ADH (or, desmopressin) is usually prescribed to make up for ADH not being manufactured or released by the body. Low doses of desmopressin are also used in cases of gestational DI. In cases of nephrogenic DI, where the problem is with the kidneys not being able to respond to either natural or synthetic ADH, desmopressin would not be effective. Therefore, treatment usually consists of a low-salt, high-fluid diet, with additional medications (antidiuretics) to prevent too much water loss. There is no satisfactory treatment for dipsogenic DI.

Syndrome of Inappropriate Antidiuretic Hormone Secretion

In syndrome of inappropriate antidiuretic hormone secretion, sometimes called Schwartz-Bartter syndrome or SIADH, the body secretes too much ADH, and doesn't release as much water as it should. The main symptom of SIADH is hyponatremia, a low (hypo) concentration of sodium. Remember: Na is the chemical symbol for sodium, and '-emia' refers to blood. Notice this is the direct opposite of one of the symptoms of DI. Another symptom of SIADH is small amounts of highly concentrated urine that has a high osmolality, as opposed to the dilute urine produced in DI.

Most cases of SIADH stem from over-production of ADH from the pituitary due to tumors, injury, or degeneration of the nervous system. In other cases, the use of drugs such as MAO inhibitors or tricyclic antidepressants stimulate excess ADH secretion. Pulmonary disorders such as pneumonia and lung cancer can also cause SIADH.

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