What Schools Never Taught About Skin Injuries

As I pursue my Holistic Functional Medicine program, I have been studying a book titled Biochemical Pathways: An Atlas of Biochemistry and Molecular Biology by Gerhard Michal and Dietmar Schomburg. One of my tasks is to create a summary or essay on Blood Coagulation and Fibrinolysis.

Blood coagulation and fibrinolysis are two essential components of the process called hemostasis. Hemostasis is the mechanism that stops bleeding from an injured blood vessel to prevent excessive blood loss. It involves the controlled formation of a blood clot, primarily through coagulation and the formation of fibrin, to effectively seal and support the healing of the vessel.

In simple terms, hemostasis is just a fancy word for what happens when you get injured, whether on the skin or anywhere else in the body where blood vessels are damaged and bleeding occurs. The purpose of hemostasis is to stop the bleeding and initiate the healing of the wound.

In this blog, I’m going to share what I’ve learned from the book, using a few medical terms along the way, but don’t worry, I’ll explain everything in simple, layman’s language. I’ll also discuss the gaps I noticed in the book and what needs further study in the future biochemistry subject.

In Chapter 9 “Blood Coagulation and Fibrinolysis”, by Gerhard Michal, I learned about the hemostasis process, which stops bleeding from an injured blood vessel to prevent blood loss. This process involves the controlled formation of a blood clot and fibrin by specific cells to effectively seal and heal the vessel. It is important to understand this process, as both insufficient and excessive clotting can have life-threatening consequences for individuals.

When a blood vessel is injured, the hemostasis process must respond quickly and effectively in a controlled manner. Coagulation and fibrinolysis, which occur through a cascade of proteolytic enzyme activations involving amino acids, are key mechanisms that help seal leaks in blood vessels and promote wound healing.

In coagulation, two main pathways are involved: the extrinsic pathway and the intrinsic pathway. The extrinsic pathway begins when tissue factor (TF), also known as thromboplastin, Factor III, or CD142, is exposed to blood after vessel injury. TF is normally found on the surface of cells surrounding blood vessels, beneath the endothelial layer. When TF comes into contact with Factor VII in the blood, it activates the coagulation cascade, which helps start clot formation. The intrinsic pathway, also called the contact activation pathway, begins when certain proteins called prekallikrein (PK), kallikrein (KK), Factor XII, and high molecular weight kininogen (HK) that bind to the site of injury. This pathway mainly supports inflammation and the continued formation of the clot. Interestingly, people with deficiencies in Factor XII, HK, or PK usually do not experience abnormal bleeding; instead, some may have a higher risk of blood clots, suggesting that Factor XII also plays a role in breaking down clots (fibrinolysis). Both pathways depend on special binding surfaces made of phospholipids and proteins that appear when blood vessels are damaged. These surfaces help the coagulation reactions occur in a localized and controlled way, protecting them from being stopped too soon. The coagulation process involves several key factors, including VII, IX, X, prothrombin, and the regulatory factors PC (protein C) and PS (protein S). The final stage of coagulation is the production of thrombin, a crucial enzyme that converts fibrinogen into fibrin to form a stable blood clot. This step is strengthened by an additional pathway that activates Factor IX through Factor XIa.

The second key step in sealing an injured blood vessel is the generation of fibrin. Fibrin is formed from fibrinogen, a plasma protein composed of two sets of three polypeptide chains, symmetrically linked at the center by disulfide bonds. During coagulation, the enzyme thrombin cleaves four negatively charged peptides from fibrinogen. This process exposes binding sites (epitopes) at both ends of the fibrinogen molecule, allowing the molecules to self-assemble into fibrin polymers. These fibrin strands form a stable network that reinforces the platelet plug. Fibrin and fibrinogen also contain binding sites for other proteins, enabling crosslinking with platelets and cells—a crucial mechanism for rapidly stopping bleeding. The fibrinolytic system not only helps form the fibrin seal but also removes excess fibrin deposits and thromboembolic clots within blood vessels. This system maintains a dynamic balance with coagulation to prevent both excessive bleeding and unwanted clot formation. Tissue plasminogen activator (tPA), continuously released from endothelial cells, plays a central role in initiating fibrinolysis. Fibrin itself acts as both the target and a cofactor of fibrinolysis, helping to regulate where, when, and to what extent clot breakdown occurs.

In short, when a blood vessel is injured, the body forms a blood clot and produces fibrin, along with various cells, proteins playing the biggest role, to seal the damaged area and prevent blood loss. This whole process is carefully regulated to avoid both excessive bleeding and excessive clotting. That’s it.

This is what I’ve realized after reading the book:

Understanding the basic concepts of coagulation and fibrinolysis is essential. These processes are vital for maintaining the balance between stopping bleeding and preventing excessive clot formation. By understanding how they work, everyone can better recognize, manage, and prevent life-threatening conditions such as severe bleeding, thrombosis, and delayed wound healing. The information I learned about coagulation and fibrinolysis was very enlightening. However, I noticed that the book focuses mainly on these mechanisms at the genomic level, describing only how they function under normal physiological conditions. While this is important for understanding the basic science, it does not take into account other external and environmental factors that may influence these processes in real-life situations.

For instance, microbes and nutrients can have a significant impact on coagulation and fibrinolysis. Microorganisms that enter the bloodstream may alter immune responses, damage blood vessel linings, or produce toxins that affect clotting factors. A good example is pernicious anemia, a condition caused by a lack of vitamin B12, which is necessary for the production of healthy red blood cells. According to Dr. Hulda Clark in her book The Cure for All Diseases, most patients with pernicious anemia were found to be infected with Ascaris worms that absorb vitamin B12 from their host. This link between infection and nutrient deficiency shows how microbes can directly influence blood health and clotting function. Nutritional factors are also crucial. Chlorophyll, as mentioned by Dr. Rudy Davis, can support blood health and help reduce bleeding by promoting tissue repair and oxygen delivery. Likewise, vitamin C, highlighted by Dr. Thomas Levy, plays an essential role in controlling inflammation, strengthening blood vessels, and supporting overall immune function. These examples show that nutrients work together with the body’s natural coagulation system to maintain vascular integrity and promote healing.

In the future, I hope that biochemistry research and education will expand beyond the genomic level and include discussions on how microbes, nutrients, hormones, and medications affect coagulation and fibrinolysis. Understanding these interactions could lead to a more holistic approach to patient care, one that connects genes, molecular biology with nutrition, microbiology, and pharmacology. This broader perspective can ultimately improve disease prevention, treatment outcomes, and overall health management.