riority medical diagnosis: Peripheral Vascular Disease
Peripheral vascular disease includes all vascular disorders of the blood vessel system outside of the heart.
Acute and chronic vascular diseases may develop progressively from atherosclerotic plaque formation. Atherosclerosis is defined as the process of fatty substances, cholesterol, cellular waste products, calcium, and fibrin building up in the intimal and medial layers of vessel wall, resulting in plaque building up and narrowing of the lumen of the artery. The intima is the innermost layer composed of endothelial cells within a matrix of collagen and elastin fibers. The media is the thick middle layer of smooth muscle. The adventitia is the outermost layer layer composed of collagen and elastin, which is the key element in providing strength for the arterial wall. Peripheral arterial disease is a subcategory of peripheral vascular disease. It is caused primary by embolic and pathophysiological processes that alter the aorta, its visceral arterial branches, and the arteries of the lower extremities (Osborn, 2014 p1069). The presence of PAD may indicate cardiovascular disease.
Atherosclerotic plaque formation occurs in three stages. The first or early stage is the development of fatty streaks beginning from childhood. The fatty streaks are formed from foam cells, which are lipid laden macrophages. Low-density lipoprotein cholesterol is the main lipid component that makes up thes fatty streaks. The second stge is the appearance of fibrous plaque later on in life from the progression of the fatty streaks made from foam cells to a more permant fibrous plaque. These plaques often will occur at areas of bifurcation of the arterial vessels. The last stage occurs when the fibrous plaque develops into a complicated lesion with necrosis and ulceration of the plaque surface with exposure, leading to thrombogenesis through platelet aggregation and formation of a thrombus. As the lipids are collected under the inner lining of damaged artery walls, it eventually narrows or blocks the artery and obstructs blood flow. The fatty tissue breaks down the artery wall over time and causes it to diminish its elasticity. Plaque deposits can also rupture, causing debris to migrate with an artery. Most patients with PAD will present with lower extremity pain, either as classic intermittent claudication or atypical leg pain. Although the supply of blood may be adequate to meet the demands of the inactive muscle, a mismatch will occur between the supply of blood and increased demand due to activity. The mismatch is what causes the atypical lower extremity pain. Patient started with small lesion on L foot. Eventually led to necrosis of the 2nd and 3rd toe.
Autonomic neuropathy occurs when blood is shunted away from peripheral