Patients with SIADH are typically euvolemic or hypervolaemic (i.e.Hypervolaemia: pulmonary oedema, peripheral oedema, raised jugular venous pressure and ascites.Īssess the patient’s fluid status to identify clinical and/or biochemical dehydration:.Brain stem herniation (severe acute hyponatraemia) resulting in coma and respiratory arrest.
Cognitive impairment: short-term memory loss, disorientation and confusion.The clinical signs of SIADH can also vary significantly, depending on the rate of serum sodium concentration change. Cerebral adaptation can only take place if the change in sodium concentration is gradual, explaining the more severe symptoms associated with acute hyponatraemia and the potentially less severe symptoms associated with chronic hyponatraemia. This is thought to be due to a compensatory process known as cerebral adaptation, in which brain cells adapt their metabolism to cope with abnormal sodium levels. Mild hyponatraemia may cause significant symptoms if the drop in sodium is acute, whereas chronically hyponatraemic patients may have very low serum sodium concentrations and yet be completely asymptomatic. Symptoms of SIADH vary depending on the rate at which hyponatraemia develops. Severe hyponatraemia: drowsiness, seizures and coma.Moderate hyponatraemia: muscle cramps, weakness, confusion and ataxia.Mild hyponatraemia: nausea, vomiting, headache, anorexia and lethargy.Symptoms of SIADH vary depending upon both the severity of the hyponatraemia and the rate at which it develops: There are lots of potential causes of SIADH including: Ultimately this leads to abnormally low levels of serum sodium and relatively high levels of urinary sodium, giving rise to the characteristic clinical features associated with SIADH. This results in continual ADH production, independent of serum osmolality. The important difference between normal physiology and what occurs in SIADH is the lack of an effective negative feedback mechanism. An illustration of how serum osmolality is regulated in healthy individuals. This results in both a decrease in volume and an increase in osmolality (concentration) of the urine excreted.Ħ. The extra water that has been reabsorbed re-enters the circulatory system, reducing the serum osmolality.ħ. This reduction in serum osmolality is detected by the hypothalamus and results in decreased production of ADH. These aquaporin-2 channels allow water to be reabsorbed out of the collecting ducts and back into the bloodstream. The binding of ADH to these receptors causes aquaporin-2 channels to move from the cytoplasm, into the apical membrane of the tubules. ADH then travels to the kidneys, where it binds to ADH receptors on the distal convoluted tubules.ĥ. ADH is released into the circulatory system via the posterior pituitary gland.Ĥ. ADH is transported from the hypothalamus to the posterior pituitary gland.ģ. ADH (also known as vasopressin) is produced by the hypothalamus in response to increased serum osmolality.Ģ. You might also be interested in our medical flashcard collection which contains over 1000 flashcards that cover key medical topics.ġ.
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