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Syndrome of inappropriate antidiuretic hormone secretion (SIADH)



Endocrine system


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Syndrome of inappropriate antidiuretic hormone secretion (SIADH)


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High Yield Notes
13 pages

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

12 flashcards

USMLE® Step 1 style questions USMLE

3 questions

A 30 year-old woman comes to her primary care physician because of muscle cramps, nausea, and fatigue. The patient endorses a history of depression and seizure disorder, both of which are currently managed with medications. Family history is notable for Addison disease in her maternal uncle. Temperature is 36.9°C (98.4°F), pulse is 75/min, respirations are 14/min and blood pressure is 115/80 mmHg. Cardiac, pulmonary, and abdominal examinations are noncontributory. Additional laboratory results are as follows:  

Laboratory value  Result 
Sodium   122 mEq/L 
 Potassium   3.7 mEq/L 
 Creatinine  0.9 mg/dL 
 Glucose  102 mg/dL 
 Serum osmolality   240 mOsm/kg 
 Urine osmolality  445 mOsm/kg 

Which of the following is the most likely explanation of the patient’s symptoms?

Memory Anchors and Partner Content

Content Reviewers:

Rishi Desai, MD, MPH


Tanner Marshall, MS

How does your body know when to retain fluids and when to get rid of them?

It’s not like you just think to yourself “I’ve had too much water, better get rid of some.” (If you do, and it works, call us).

Your body uses chemicals called hormones to send widespread messages, kind of like how the P.A. system at school tells everyone to ignore the smoke billowing out of the science wing.

The antidiuretic hormone, abbreviated as ADH, is the hormone that controls water retention in the body.

It also constricts blood vessels, and incidentally the vasoconstrictor drug called vasopressin is just ADH. Cool! But that’s not what we’re talking about right now.

Anyways, the more ADH floating around in your blood, the more fluid you retain.

The less ADH in your blood, the more fluid you excrete.

The nephrons in the kidneys are the structures that physically control how much water is excreted from your body.

Nephrons are mostly a series of tubes attached end-to-end that type fluids and wastes towards the bladder.

These tubes though also allow fluids and electrolytes to move through the tube walls and back into the blood if needed.

ADH affects the last two-thirds of these tubes, called the distal convoluted tubule and the collecting ducts.

These tubes focus almost exclusively on reabsorbing water back into the blood.

The wall of these tubes are unsurprisingly made up of cells, a common trait of living things, but these cells have proteins called aquaporins.

Aquaporins allow water to move quickly in and out of the cells.

The more ADH floating around in the blood, the more aquaporins are available to... ahem...facilitate water movement through the cell (yo, wata, come over here for a sec).

So when ADH is low, most of the water flows through the distal convoluted tubule and the collecting duct, giving us diluted urine.

When ADH is high, aquaporins grab much of the water passing through the these tubes and throws them back into the blood.

When I drink a glass of water and that water is absorbed into my blood, my plasma osmolality drops, which means I’m diluting my blood with the water.

That means there’s more fluid for all those blood cells to bounce around in (wooo parrttayy).

The part of my brain called the hypothalamus sees this drop in plasma osmolality and tells the pituitary gland to slow down the release of ADH (that’s enough!).

Low ADH leads to lots of diluted urine (urine with low osmolality), which brings our plasma osmolality back to normal. What a nifty feedback loop.

Now suppose ADH continues to be released even though my plasma osmolality has dropped (stop it! STOP IT! pituitary gland whistling).

We’re going to continue retaining water, and as we drink more and more water, we might expect our plasma osmolality to continue dropping. However this isn’t exactly the case.

As more water is retained, it dilutes the other solutes floating around in our blood, like sodium.

The extra fluid also takes up more space in our blood vessels.

This taking up more space issue triggers another mechanism in our body that causes the hormone aldosterone to stop being released.

Less aldosterone floating around in the blood causes the body to start dumping sodium from the blood into the urine.

Concentration gradients cause water to follow sodium, so we end up with the excess water being excreted in the urine with the sodium, normalizing the fluid volume in the blood.

So now our body is removing sodium from blood that already has a lower concentration of sodium. Uh oh!

This means the plasma sodium osmolarity is dropping significantly.

This whole fiasco we’ve just talked about is called syndrome of inappropriate antidiuretic hormone, often abbreviated as SIADH.


Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by excessive release of antidiuretic hormone from the posterior pituitary gland or another source. The increase in fluid retention often results in dilutional hyponatremia in which the plasma sodium levels are lowered. SIADH may present with euvolemic hyponatremia with continued urinary sodium excretion. Urine osmolality is usually higher than serum osmolality. Very low serum sodium levels can lead to cerebral edema or seizures. Other symptoms of SIADH include fatigue, confusion, muscle weakness, nausea, vomiting, lack of appetite, and weight loss. Treatment usually involves fluid restriction, salt tablets, IV hypertonic saline, diuretics, and drugs like conivaptan, tolvaptan, or demeclocycline.