Makindo Medical Notes.com

Many of the causes of ADH release are seen post op and with poor fluid management hyponatraemia and transient SIADH can occur

About

• ADH is a nonapeptide (9 peptide) hormone
• Produced by neurons of the supraoptic and paraventricular nuclei in the hypothalamus
• It is stored and released from the posterior pituitary
• It acts on the collecting ducts improving water permeability and hence water retention.

Stimuli to release

• Increase in osmolality in the plasma perfusing the hypothalamic osmoreceptors
• Low volume in atrial stretch receptors
• Low pressure in arterial baroreceptors
• Angiotensin II, Pain, stress and sleep, Morphine

Actions

• Sensation of thirst.
• Increases free water reabsorption in the collecting ducts of the kidney.
• Causes arteriolar contraction
• Raises Blood pressure (Vasopressor)
• Reduces Osmolality

Pathology SIADH (Excess ADH)

• Presents as hyponatraemia and reduced plasma osmolality
• Cell volume is very dependent on the Osmolality changes between ECF and ICF.
• Over release can lead to a fall in serum osmolality
• A fall in ECF osmolality results in cell swelling and e.g. brain swelling
• Cells can address this situation in the case of cell swelling by getting rid of intracellular solutes

Pathology of Diabetes Insipidus

• Polyuria and polydipsia
• Presents as hypernatraemia and increased plasma osmolality
• A loss of ADH release = Cranial DI
• Loss of renal response to ADH = Nephrogenic DI

Uses

• Vasopressin has also been used as an agent in cardiac arrest instead of Adrenaline [US Epinephrine] with mixed results
• In synthetic form may be administered as a nasal spray to treat enuresis
• In synthetic form may be administered as a nasal spray to treat Cranial diabetes insipidus