Diabetic Foot: Pathogenesis and clinical findings • Polyol Pathway - Excess glucose enters Polyol pathway -> reduced to sorbitol which accumulates in cells • Hexosamine Pathway - Excess glucose deflects GIs into the HP -> production of UDNAG which alter TFs essential for cell function • Glycosylation - AGE cause increasing cytogenetic dysfunction and inflammation • Increased PKC Activity -> Artery wall thickening as a result of WBC invasion and smooth muscle proliferation • Hypoinsulinemia - Decreased insulin in blood -> Impairment of peripheral nerve repair mechanisms -> Oxidative stress, Ischemia, Accelerated nerve deterioration -> Peripheral vascular disease and neuropathy => Diabetic foot - Foot affected by ulceration and deformity associated with neurovascular disease in a person with diabetes Charcot Arthropathy - Progressive and destructive arthropathy -> Localized inflammatory response and impaired vascular smooth muscle as a result of sensory, motor and autonomic neuropathies -> Collapse of Arch Foot Ulceration - Breakdown of skin and soft tissue -> Sensory and motor neuropathies result in inopportune loading of the foot, resulting in skin/soft tissue degradation. Healing is impaired due to the decreased blood supply as a result of microvascular damage -> Ulcer Formation Osteomyelitis - Infection of bone -> Contiguous spread of bacteria from superficial tissues results in inflammation, exudate formation, and bone necrosis -> Infection #DiabeticFoot #pathophysiology #complications #Diabetes
