Basic Principles of Wound Healing in the Skin, Pathophysiology of Atherosclerosis : Pharmaguideline

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Basic Principles of Wound Healing in the Skin, Pathophysiology of Atherosclerosis

Cellular structures and layers of tissues that are damaged and missing must be restored during wound healing.

Basic Principle of Wound Healing in the Skin

Cellular structures and layers of tissues that are damaged and missing must be restored during wound healing. The process in adults can be divided into three or four phases. Authors earlier referred to three phases of the process: inflammation, fibroblastic proliferation, and remodeling. Some maintain that there are three phases. Among the four phases outlined in the 4-phases concept are hemostasis, inflammation, proliferation, and remodeling. Hemostasis is included in the inflammatory phase of the 3-phase approach.

An individual's health changes with time, so the environment around a wound changes with it, making wound healing a complex process. Understanding wound healing requires understanding granulation, inflammation, hemostasis, and maturation, all of which occur during normal wound healing. An examination of the underlying causes is necessary when wounds do not heal as predicted. In order for wounds to heal, they must be treated holistically, collaboratively, cost-effectively, and based on evidence.

What causes wounds to heal?

Acute wounds heal in four phases according to animal models of wound healing. Chronic wounds are also thought to go through four phases of healing (although some authors combine the first two phases). Those phases include:

1. Hemostasis - A platelet acts as a utility worker sealing off a wound by sealing the damaged blood vessels. As a consequence of injury, blood vessels constrict, however this spasm eventually relaxes. Platelets secrete vasoconstrictor substances to help this process, but their primary function is to form a clot that seals the damaged vessel. The platelets attach to type 1 collagen exposed due to leaks of ADP (adenosine diphosphate). As they become activated, adhesive glycoproteins are secreted, causing platelets to aggregate. Thrombin is the initiator of the intrinsic clotting cascade, which invokes fibrin from fibrinogen. The clotting cascade is also triggered by these factors when they interact with them. It helps to stabilize the hemostatic plug by strengthening the fibrin mesh. Lastly, platelets secrete growth factors, which include platelet-derived growth factor. Initiating the healing process is one of the functions of this growth factor. By stimulating epithelial cells and recruiting fibroblasts (which initiate the following stage of wound healing), they promote wound healing. The hemostasis process occurs within minutes after an injury if clotting disorders are not present.

2. Inflammation - Inflammation is frequently associated with erythema, swelling, warmth, and pain during wound healing. This phase of the healing process remains predominant for the first few days following an injury. A response to inflammation releases neutrophils and plasma into the tissue. During neutrophil phagocytosis, the body is cleansed of microorganisms and debris. Upon death, neutrophils release intracellular enzymes into the surrounding tissue, digesting bacteria and debris. In turn, the tissue is further digested by these enzymes. The degradation products created by fibrin degradation attract fibroblasts and epithelial cells. Mast cells in the area also assist these cells.

3. Contraction (also called proliferation and granulation respectively) - Depending on the size of a wound and the patient's health, the proliferation phase usually begins approximately 4 days after wounding and lasts until day 21. The process of granulation tissue formation and wound contraction is marked by angiogenesis, collagen deposition, wound contraction, and epithelization. Wounds that undergo proliferative wound healing are usually characterized by red, pebbly tissue or collagen, and tissues under the dermis and subcutaneous layers of the skin are often replaced.

4. Remodeling (also called maturation) - A fibroblast is commonly referred to as the "framer" cell, which secretes the collagen framework upon which dermal regeneration can take place. Specifically, wound contraction is carried out by specialized fibroblasts. A plumbing cell is a pericyte, which regenerates the outer layer of a capillary, and an endothelial cell, which produces the lining. It is referred to as angiogenesis. Keratinocytes are responsible for epithelialization and are known as the "roofer" and "sider" cells respectively. Contractures occur when the keratinocytes form the stratum corneum, or protective outer layer, in the final phase of epithelialization. Growth factors cause the cells in a healing wound to divide so that they can produce new cells, which then migrate under the influence of cytokines to where they are needed. TIMPs and MMPs play an important role in the generation of new tissue.

Pathophysiology of atherosclerosis

Atherosclerosis is caused by plaque deposits (fatty deposits) that stack up in the arteries. cholesterol, fatty substances, calcium, and fibrin are the ingredients of plaques such as cholesterol, fatty substances, and waste products.

The incidence of atherosclerosis cannot be accurately estimated since it is primarily asymptomatic. Cardiovascular diseases are mostly caused by atherosclerosis. Coronary artery disease and ischemic stroke are the two main types of atherosclerotic cardiovascular disease. World-wide, coronary artery disease and stroke are among the top two causes of death.

Typically, atherosclerosis occurs as a result of chronic inflammation at vulnerable areas of the arteries due to the continuous process of arterial wall lesions caused by lipid retention by the intima, resulting from the trapping of lipids by a matrix (e.g., proteoglycans). As atherogenic progression unfolds, this plays a key role.

The aorta, coronary and carotid arteries exhibit similar systemic changes in atherosclerosis. It is usually understood that atherosclerosis is a continuous process that involves a series of histologic developments and lesions that can be seen unaided by the naked eye.
  1. The fatty streak - It has been found that children as young as 10 years of age can sometimes have this first stage of atherosclerosis. The aorta and carotid arteries, which are major arteries, appear with brown spots. Macrophages (types of white blood cells) and smooth muscle cells are present in this streak. Fibrotic plaques are a more harmful form of atherosclerosis that develops after the fatty streak phase.
  2. Fibrous plaque - Fibrous plaques form on the inner lining of vessels. Plaques like this are formed of macrophages, smooth muscle cells, and lymphocytes (more aggressive types of white blood cells). Cells with cholesterol are found in this plaque. Growing fibrous plaques begin to protrude into the vessels in which blood flows.
  3. Complicated lesion - The underlying cause of atherosclerosis is a series of risky events. When a fibrous plaque is broken up, cholesterol and connective tissue are exposed beneath it. Within seconds of an injury being detected, a blood-clotting cell is sent to the scene. Both the blockage and the clot make the situation particularly hazardous, as blood flow is now restricted. A ruptured plaque combined with a blood clot form a compound lesion.fibrin mesh
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