Diabetic Foot: Pathogenesis and clinical findings

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 
Contributed by

The Calgary Guide to Understanding Disease
Account created for The Calgary Guide to Understanding Disease - Linking pathophysiology to clinical presentation - http://calgaryguide.ucalgary.ca/

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