Hyponatraemia, diabetes insipidus Flashcards
What is vasopressin, where is it synthesised and how is it controlled?
Pituitary hormone which acts to promote the retention of water by the kidneys and increase blood pressure.
Synthesised in the paraventricular nucleus and supraoptic nucleus in the hypothalamus and released from the posterior pituitary into the blood stream.
It has a half life of 5-20 minutes so it quickly adapts to changes in plasma osmolality.
Controlled by osmoreceptors and baroreceptors.
When plasma osmolality decreases, what happens to vasopressin secretion?
Decreases.
How does vasopressin cause water retention?
- Vasopressin binds to V2 receptors on the renal collecting duct principle cells
- When bound, it is activated and causes the aquaporin molecule to embed into the basolateral membrane and this allows water to be reabsorbed from collecting duct urine to to blood, down the concentration gradient.
What is osmolality and what is a normal extracellular fluid osmolality?
Osmolality is an estimation of the osmolar concentration of plasma and is proportional to the number of particles per kilogram of solvent; it is expressed as mOsmol/kg
The normal osmolality of extracellular fluid is 280-295 mOsmol/kg.
In a normal person, what effect would an increased plasma osmolality cause?
In normal people, increased osmolality in the blood will stimulate secretion of antidiuretic hormone (ADH). This will result in increased water reabsorption, more concentrated urine and less concentrated blood plasma.
What occurs in nephrogenic diabetes insipidus with ADH levels?
Insensitivity to the effects of ADH due to a V2 receptor defect or aquaporin 2 defect.
What is happening with ADH in cranial diabetes insipidus?
There is a lack of ADH
What is happening with ADH in syndrome of anti-diuretic hormone secretion (SIADH)?
Too much ADH released when it should not be released - common.
Can be from ectopic tumour (lung usually) or from hypothalamus secreting too much ADH.
Signs or symptoms of cranial diabetes insipidus?
Polyuria Polydipsia No glycosuria Passing at least 3L a day of urine Serum osmolality >300 and urine osmolality <200 = urine is not being concentrated.
What does measurement of copeptin tell us?
Copeptin is a stable surrogate marker of AVP and provides a valuable and reliable diagnostic marker in the differential diagnosis of the polyuria-polydipsia syndrome. In patients with hypotonic polyuria, measurement of basal copeptin levels identifies nephrogenic DI.
How do we manage Cranial DI?
Treat any underlying condition
Desmopressin tablets/nasal spray/injection.
Management of nephrogenic DI?
Hard to treat as it involves avoiding any precipitating drugs (lithium, tetracycline)
What is hyponatraemia?
What is it usually cased by?
Low levels of sodium in the blood = (<135mmol/L mild , 125-129mmol/L moderate, severe = <125mmol/L)
- Usually caused by excess water, not low sodium (hypervolemic hyponatraemia)
What are the causes of hypervolemic hyponatraemia?
- Large increase in water, little increase in sodium
- Congestive heart failure
- Cirrhosis
- Nephrotic syndrome
- All of these cause oedema which decreases circulating volume (even though theres more overall water)
- Lower circulating volume → ADH release which retains water
- Lower circulating volume → Release of aldosterone retaining sodium (and therefore, water)
What are the causes of hypovolemic hyponatraemia?
- Small decrease in water, large decrease in sodium
- Diarrhoea, vomiting
- Duiretic use
- Cerebral salt wasting (meningitis disrupts SNS)
