Cushing’s Syndrome: Pathophysiology


Regardless of the etiology of Cushing’s disease or Cushing’s syndrome, the clinical manifestations are caused almost entirely by excessive cortisol production in the zona fasciculata of the adrenal gland. Cortisol is a catabolic steroid and causes profound muscle weakness if allowed to persist. Adipose tissue redistribution is prominent. Central obesity is easily observed, with a thinning of the extremities. Supraclavicular and posterior cervical (“buffalo hump”) fat pads are frequently encountered. Cortisol has negative effects on the connective tissue of the skin, leading to a decrease in collagen. This, in turn, leads to an increase in capillary fragility, easy bruising, ecchymoses, and a thin or translucent appearance to the skin. Prominent purple to red striae are seen as a result of the loss of normal connective tissue function within the skin. The striae are most prominent in areas of obesity and are made more noticeable by the central fat redistribution. Facial plethora is frequently seen and is likely caused by thinning of the skin and an underlying polycythemia. Excessive cortisol leads to increased blood glucose levels; this in turn can lead to poor wound healing and an increase in infections. Hyperglycemia can lead to polyuria and polydipsia.


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Aug 11, 2016 | Posted by in Dermatology | Comments Off on Cushing’s Syndrome: Pathophysiology

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