2.27
Diabetic neuropathy is nerve damage caused by long-standing diabetes mellitus.
Excess glucose inside nerve cells activates the polyol pathway, leading to the conversion of glucose into sorbitol and fructose.
Build-up of sorbitol and fructose causes cell swelling and triggers oxidative stress, disrupts nerve signaling, and weakens structural proteins.
At the same time, advanced glycation end products accumulate, further damaging proteins and lipids and reducing the nerves' ability to repair themselves.
Alongside these metabolic disturbances, diabetes also affects the small blood vessels that supply nerves. Thickened basement membranes and narrowed vessels reduce oxygen and nutrient flow, creating ischemia that worsens nerve injury.
As a result, nerves undergo demyelination and axonal loss. Long sensory nerves are most vulnerable, leading to numbness and pain in the hands and feet, known as glove and stocking distribution.
Motor and autonomic nerves are also affected, causing weakness, gastrointestinal disturbances, and bladder dysfunction.
Definition
Diabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.
Pathophysiology
The pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.
Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve signaling, and damages structural proteins. Advanced glycation end products (AGEs) further modify proteins and lipids, which impairs repair mechanisms and speeds up degeneration.
Vascular injury: Diabetes also causes microvascular disease. Thickening of basement membranes and narrowing of small vessels reduce blood flow to the vasa nervorum. This deprives nerves of oxygen and nutrients. The resulting ischemia intensifies metabolic damage and worsens nerve dysfunction.
Diabetic neuropathy is nerve damage caused by long-standing diabetes mellitus.
Excess glucose inside nerve cells activates the polyol pathway, leading to the conversion of glucose into sorbitol and fructose.
Build-up of sorbitol and fructose causes cell swelling and triggers oxidative stress, disrupts nerve signaling, and weakens structural proteins.
At the same time, advanced glycation end products accumulate, further damaging proteins and lipids and reducing the nerves' ability to repair themselves.
Alongside these metabolic disturbances, diabetes also affects the small blood vessels that supply nerves. Thickened basement membranes and narrowed vessels reduce oxygen and nutrient flow, creating ischemia that worsens nerve injury.
As a result, nerves undergo demyelination and axonal loss. Long sensory nerves are most vulnerable, leading to numbness and pain in the hands and feet, known as glove and stocking distribution.
Motor and autonomic nerves are also affected, causing weakness, gastrointestinal disturbances, and bladder dysfunction.
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