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End organ damage

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Pathophysiology

End organ damage typically occurs where systemic disease causes cell death in most or all organs.

Hypertensive

When blood pressures are critically high (>180/120 mm Hg) or the rate of rise in blood pressure is rapid, a large volume of blood circulating in a small space creates turbulence and can damage the inner lining of blood vessels. The body’s repair systems are activated by damage and circulating blood components, like platelets, work on repair. The deposition of platelets can clutter the vessel space and impair the body’s natural ability to produce nitrous oxide, which would dilate blood vessels and help lower blood pressure. When high pressure is pushing on the walls of narrowed blood vessels, fluid leaves the inside of blood vessels and moves to the space just outside. This impairs necessary blood flow and cuts off circulating oxygen, which can lead to tissue death and permanent damage to the brain, heart, arteries, and kidneys. This may occur as a result of chronic or poorly controlled hypertension, illicit drug use, or as a complication of pregnancy. Recent studies have shown that activation of the immune system may also be closely involved with the development of end organ damage in hypertensive states.

Shock

Shock is when the body does not have adequate circulation to provide oxygen to body tissues. Hypovolemic shock occurs due to low circulating volume of fluids in the blood vessels. Distributive shock, which can occur due to anaphylaxis or sepsis, results in widespread dilation of blood vessels in the body resulting in lower blood pressure. In cases of extremely low circulating volume or inability to maintain an adequate blood pressure, body tissues do not receive enough oxygen and nutrients. When tissues lack oxygen and adequate circulation, organs can fail.

Diabetes

In diabetes, the dysregulation of insulin and blood glucose levels damages end organ cells and as the body compensates through regulating fluid volume to adjust glucose concentration, it also incurs collateral damage to organs. Microvascular and macrovascular complications include nephropathy, retinopathy, neuropathy, and ASCVD events. In diabetic neuropathy, glucose promotes oxidative stress leading to nerve damage. Chronically high insulin levels are also associated with early development of atherosclerotic plaques inside blood vessel walls.

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