How does diabetes mellitus impair wound healing?
Uncontrolled diabetes results in reduced inflammation, angiogenesis, and collagen synthesis. Additionally, the large and small vessel disease that is the hallmark of advanced diabetes contributes to local hypoxemia. Defects in granulocyte function, capillary ingrowth, and fibroblast proliferation all have been described in diabetes. Obesity, insulin resistance, hyperglycemia, and diabetic renal failure contribute significantly and independently to the impaired wound healing observed in diabetics.
Supplementation of which of the following micronutrients improves wound healing in patients without micronutrient deficiency?
The vitamins most closely involved with wound healing are vitamin C and vitamin A. There is no evidence that excess vitamin C is toxic; however, there is no evidence that supertherapeutic doses of vitamin C are of any benefit. Vitamin A deficiency impairs wound healing, while supplemental vitamin A benefits wound healing in nondeficient humans and animals.
Vitamin A increases the inflammatory response in wound healing, probably by increasing the lability oflysosomal membranes. There is an increased influx of macrophages, with an increase in their activation and increased collagen synthesis. Vitamin A directly increases collagen production and epidermal growth factor receptors when it is added in vitro to cultured fibroblasts. As mentioned before, supplemental vitamin A can reverse the inhibitory effects of corticosteroids on wound healing. Vitamin A also can restore wound healing that has been impaired by diabetes, tumor formation, cyclophosphamide, and radiation. Serious injury or stress leads to increased vitamin A requirements. In the severely injured patient, supplemental doses of vitamin A have been recommended. Doses ranging from 25,000 to 100,000 IU/day have been advocated.
Zinc is the most well-known element in wound healing and has been used empirically in dermatologic conditions for centuries. To date, no study has shown improved wound healing with zinc supplementation in patients who are not zinc deficient.
Which type of collagen is most important in wound healing?
Although there are at least 18 types of collagen described, the main ones of interest to wound repair are types I and III. Type I collagen is the major component of extracellular matrix in skin. Type III, which is also normally present in skin, becomes more prominent and important during the repair process.
What is FALSE regarding healing of cartilage?
Cartilage consists of cells (chondrocytes) surrounded by an extracellular matrix made up of several proteoglycans, collagen fibers, and water. Unlike bone, cartilage is very avascular and depends on diffusion for transmittal of nutrients across the matrix. Additionally, the hypervascular perichondrium contributes substantially to the nutrition of the cartilage. Therefore, injuries to cartilage may be associated with permanent defects due to the meager and tenuous blood supply. The healing response of cartilage depends on the depth of injury. In a superficial injury, there is disruption of the pro-teoglycan matrix and injury to the chondrocytes. There is no inflammatory response, but an increase in synthesis of pro-teoglycan and collagen dependent entirely on the chondrocyte. Unfortunately, the healing power of cartilage is often inadequate and overall regeneration is incomplete. Therefore, superficial cartilage injuries are slow to heal and often result in persistent structural defects.
Signs of malignant transformation in a chronic wound include:
Malignant transformation of chronic ulcers can occur in any long-standing wound (Marjolin ulcer). Any wound that does not heal for a prolonged period of time is prone to malignant transformation. Malignant wounds are differentiated clinically from nonmalignant wounds by the presence of overturned wound edges. In patients with suspected malignant transformations, biopsy of the wound edges must be performed to rule out malignancy. Cancers arising de novo in chronic wounds include both squamous and basal cell carcinomas.
Click to expand