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Causes of Necrosis in Diabetes
Diabetes mellitus is a disease that results in the accumulation of glucose sugars within the vascular system. There are three basic types of diabetes and are classified as Type I, Type II and gestational. Type I diabetes, which is typically diagnosed in adolescence, is a disease that has a defect in specialized pancreatic cells that produce insulin, a protein that regulates blood sugar. Type II diabetes is classified as an insulin-resistant disease and is brought on later in life, whereas gestational diabetes only occurs during a woman's pregnancy. There are many long-term complications associated with diabetes including necrosis and gangrene.
Vascular Disease
One of the major complications associated with all types of diabetes is the potential development of vascular disease, also called peripheral arterial disease, or PAD 2. According to the MayoClinic.com, PAD describes the narrowing or blocking of the arteries in the extremities, primarily in the lower legs. PAD results in a restriction in the amount of normal blood flow required to supply the limbs with the proper nutrients. If this condition is not treated, eventually the cells within the tissue begin to die through a process called necrosis. During necrosis, cells swell and burst open spilling their components into the tissue, causing inflammation. If enough tissue dies because of necrosis, gangrene will develop and may lead to amputation.
- One of the major complications associated with all types of diabetes is the potential development of vascular disease, also called peripheral arterial disease, or PAD 2.
- If this condition is not treated, eventually the cells within the tissue begin to die through a process called necrosis.
Peripheral Neuropathy
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Due to the presence of vascular disease and a reduction in blood flow to the extremities, diabetes sufferers may also experience peripheral neuropathy 4. Neuropathy refers to nerve damage in the limbs causing a loss of sensation or feeling. Nerve damage reduces the ability to feel pain and may also cause motor sensory damage which can make movements difficult. Lack of pain sensation makes people vulnerable to injury and infection which can ultimately lead to conditions causing necrosis or gangrene.
- Due to the presence of vascular disease and a reduction in blood flow to the extremities, diabetes sufferers may also experience peripheral neuropathy 4.
- Lack of pain sensation makes people vulnerable to injury and infection which can ultimately lead to conditions causing necrosis or gangrene.
Free Radicals
Cells that line the blood vessel walls produce a compound called nitric oxide that is an important regulator of the expansion of blood vessels. In diabetes, nitric oxide levels are greatly reduced, thereby contributing to the narrowing of blood vessels and necrosis. When blood glucose is high, a condition called hyperglycemia, oxygen-free radicals are elevated. These free radicals react with nitric oxide to cause its degradation, according to the journal "Circulation." In addition, diabetes sufferers have much higher levels of free fatty acids, which also contribute to the production of oxygen-derived free radicals. Oxidative stress from oxygen free radicals can also directly induce cell necrosis.
- Cells that line the blood vessel walls produce a compound called nitric oxide that is an important regulator of the expansion of blood vessels.
- In addition, diabetes sufferers have much higher levels of free fatty acids, which also contribute to the production of oxygen-derived free radicals.
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References
- American Diabetes Association: Diabetes Basics
- MayoClinic.com: Peripheral Arterial Disease
- MedlinePlus: Necrosis
- American Diabetes Association: Neuropathy
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Writer Bio
Chris Bjorklund has been writing professionally since 2004 and has been primarily featured in peer-reviewed scientific journals such as "Nucleic Acids Research" and "Biochemistry." He has also been anonymously published as a content freelancer for several websites. He completed his doctoral degree in biochemistry at Washington State University in 2006.