Pathophysiology of Diabetic Foot Ulcer

Running header: RIGHT FOOT ULCER 1
Right foot ulcer
Student name
Student ID number
Specialty area

Schneider2
Pathophysiology of diabetic foot ulcer
Mrs. Gina has a history of type two diabetes, peripheral vascular disease and obesity which
led to a right foot ulcer. Her blood glucose level was 12.6mmol/L and surrounding skin was wet
from exudate, dark pink and painful to touch. Factors that caused the growth of diabetic foot
ulcer in diabetic patients are divided into two. This includes causative factors and contributing
factors. Causative factors include peripheral neuropathy, vasculopathy, and immunopathy.
Contributing factors include atherosclerosis, and diabetes (Obaid & Eljedi, 2014).
a. Neuropathy
Peripheral neuropathy also called loss sensation is the impairment of nerves throughout the
body. An increased hyperglycemic condition in the blood causes the secretion of sorbitol
dehydrogenase and aldolase reductase. This enzyme causes the conversion of glucose to fructose
and sorbitol. The accumulation of these sugar products leads to a decreased production of nerve
cell myoinositol hence affecting nerve conduction. This causes a decreased peripheral sensation,
vasomotor control of the pedal circulation and lastly, it damages the nerves of the little muscles
in the foot (Merza & Tesfaye, 2018). When the normal functioning of the nerves is impaired it
may expose an individual to minor injuries without recognizing it until it makes an ulcer. High
sugar levels in the blood cause dryness and fissuring of the skin predisposing it to infection. The
autonomic nervous system controls the microcirculation of the skin. Damage of the autonomic
nervous system lead to the enlargement of ulcers, gangrene and lastly limb loss.
b. Vasculopathy

Schneider3
Uncontrolled glucose level causes endothelial cell damage and smooth cell abnormalities.
Endothelial cells damage leads to rapid growth of endothelial cells, reduced production of nitric
oxide, increased blood viscosity, thickening of the basement membrane and reduced blood flow.
Endothelial cells synthesize nitric oxide which causes vasodilation of blood vessels. Reduced
nitric oxide production leads to a propensity for atherosclerosis, vasoconstriction of blood
vessels and finally leading to ischemia. Hyperglycemia cause overproduction of thromboxane A2
causing plasma hypercoagulability. Clients with this condition manifest with rest pain, absent
peripheral pulse and lastly thinning of the skin (Merza & Tesfaye, 2018).
c. Immunopathy
The immune system of a diabetic patient is much weaker than healthy people. The
hyperglycemic condition causes overproduction of pro-inflammatory cytokines and damage of
polymorphonuclear function like chemotaxis and phagocytosis. The immune system is weakened
due to decreased leukocyte activity, wrong inflammatory response and lastly disturbance of
cellular immunity (Merza & Tesfaye, 2018). Diminished chemotaxis of cytokines and growth
factors impended wound healing by extending the inflammatory state. The presence of an open
wound in a fasting state creates a catabolic state. Negative nitrogen balance results caused by
protein break down. This impairment of metabolic function affects the synthesis of proteins,
collagen, and fibroblast. Lack of these factors in the blood will result in prolonged healing of the
wound. High blood glucose creates a favorable condition for the growth of bacteria mainly the S.
Aureus and B- hemolytic streptococci (Robelledo, Soto, & Pena, 2015).
Causes of the patient post-operative wound status