Syndrome of inappropriate antidiuretic hormone Flashcards

1
Q

what is the definition of SIADH?

A

The syndrome of inappropriate antidiuretic hormone (SIADH) is characterised by hypotonic hyponatraemia, concentrated urine, and a euvolemic state. The impairment of free water excretion is caused by increased arginine vasopressin (antidiuretic hormone or AVP) release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the epidemiology of SIADH?

A

SIADH was the most common cause of hyponatraemia in patients with cancer, accounting for around 30% of the total hyponatraemia cases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the aetiology of SIADH?

A
Drugs 
Pulmonary process
Malignancy
CNS disorders
Other stimuli for AVP release
Nephrogenic syndrome of inappropriate antidiuresis or pseudo-SIADH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the risk factors for SIADH?

A
Aged >50
Pulmonary conditions
Nursing home resilience
 Malignancy 
Medicine associated with SIADH induction
CNS disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the pathophysiology of SIADH?

A

Inappropriate release of AVP can occur with malignancy, pulmonary processes, central nervous system disorders, and certain drugs. Often there is a concomitant resetting of the osmostat that also contributes to AVP effect and hyponatraemia. AVP exerts its effect by stimulating the AVP V2 receptor, located on the basolateral side of the principal cell. These receptors may also be activated by other, currently undiscovered antidiuretic substances.[3]
AVP V2 is a G-protein-coupled receptor that, when stimulated, initiates adenylate cyclase and leads to increased intracellular cAMP.[11] Elevated cAMP signals placement of vesicle-encased aquaporin-2 channels in the principal cell apical membrane, facilitating free water absorption in the collecting tubule.
Resulting concentrated urine, coupled with free water intake in excess of what can be excreted, leads to hyponatraemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the key presentations of SIADH?

A
Presence of risk factors
Asence of hypo/ hypervolaemia
Nausea 
Vomiting
Altered mental state, headache, coma, seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the signs of SIADH?

A

Presence of risk factors

Asence of hypo/ hypervolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the symptoms of SIADH?

A

Nausea
Vomiting
Altered mental state, headache, coma, seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the first line and gold standard investigations for SIADH?

A
Serum sodium - low
Serum osmolality - low
Serum urea - low
Urine osmolality - high 
Urine sodium - high (with euvolemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the differential diagnoses for SIADH?

A

Pseudohyponatremia
Hypovolaemia
Cerebral salt-wasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how is SIADH managed?

A

Severe:
IV hypertonic saline, treat underlying cause, furosemide, vasopressin receptor antagonist
Mild:
Treat underlying cause, vasopressin receptor antagonist, fluid restriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is SIADH monitored?

A

It may be necessary to continue free fluid restriction (1-1.5 L/day) after hypertonic saline therapy and to monitor serum sodium daily until it stabilises.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the complications of SIADH?

A

Central pontine myelinolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the prognosis of SIADH?

A

If the underlying cause is found and treated successfully, SIADH typically resolves. If the underlying condition persists, SIADH is difficult to manage, secondary to difficulty complying with necessary fluid restriction or medicines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly