Which two conditions are causes of secondary hyperaldosteronism?

Secondary hyperaldosteronism occurs as a result of increased stimulation of the adrenal cortex to produce aldosterone due to external factors affecting the renin-angiotensin-aldosterone system (RAAS). Conditions that lead to decreased renal perfusion can trigger this overproduction of aldosterone by increasing renin secretion.

Fibromuscular dysplasia and renal artery stenosis are directly involved in this process. Both conditions lead to reduced blood flow to the kidneys, which the body interprets as low blood volume or low blood pressure. This activates the RAAS cascade, resulting in increased renin release from the juxtaglomerular cells of the kidney. The increased renin levels convert angiotensinogen into angiotensin I, which is subsequently converted to angiotensin II. Angiotensin II stimulates the adrenal glands to produce more aldosterone, leading to the condition of secondary hyperaldosteronism.

The other choices involve conditions that either do not have a direct impact on the renin-angiotensin-aldosterone system or involve primary adrenal pathologies rather than secondary causes. For example, diabetes and hypertension may affect the overall health of the kidney but do not directly stimulate aldosterone production as a secondary response. Cirrhosis