9.10.2 Clotting System

(Grabe 35). E-coli remains the most prevalent microorganism. (Grave 35). A pro-inflammatory response, involving neutrophils and macrophages, is produced by the activation of the complement system and the cellular immune responses by the urogenital tract bacteria. (Wagenlehner 964). Stimulation of hematopoietic growth factors lead to the formation of new neutrophils and the release of store neutrophils which are activated causing the production of bactericidal substances. (Wagenlehner 964). B-lymphocytes and T-lymphocytes are stimulated for antibody synthesis; however, cytokines and secondary mediators caused endothelial cells to become damaged due to hypotension caused by the platelet activating factor and nitric oxide being produced. (Wagenlehner 964). This process causes the formation of edema in the tissues. (Wagenlehner

Immune chemicals cause widespread inflammation, leading to blood clots and reduced blood flow 2• 1

noniceptors to reduce inflammation. They also have some effect on the nervous system to act on

Researchers have theorized about the many mechanisms CLA have an effect on. Some proposed mechanisms such as reduction of proliferation and differentiation of preadipocytes, decreased esterification

Tumour necrosis factor (TNF) is responsible for the disruption of the tight junction between endothelial cells which results in an increased permeability to plasma proteins and fluid, which worsens fluid accumulation in the alveoli further impairing gas exchanged (Bersten & Soni, 2009:709). TNF comprises of two different molecules, firstly TNFa which leads to programmed cell death in target cells, and when combined with IL-1 which acts on the central nervous system causing lethargy (Marieb, 2004). TNFB stimulates granulocyte activity and B cell proliferation which shows an increase in neutrophil count (Jean- Baptise, 2007:63).

Correct answer: c. is increased whenever fibrinogen and immunoglobulins cause the RBCs to clump together, stack up, and

It inhibits thrombosis by inactivating co-factors Va, and VIIIa (Neyrinck, 2009). When deficient, Factor V can cause excessive blood clotting and Factor VIII, being an essential clotting factor, can cause blood to profusely move out of tissues once cut or damaged (Faust, 2001 and Yan, 2001). Thrombin may become limited, one reason being the decrease of plasma D-dimer, which again stimulates fibrinolysis (Bernard, 2001).

Also Cytokines an be secreted by a variety of cells including neutrophils, activated macrophages, fibroblasts, endothelial cells and damaged muscle cells. The physiological response to tissue injury is inflammation, which involves the production of cytokines. .These soluble molecules will enhance the arrival of neutrophils, monocytes and lymphocytes to the damaged muscle tissue. Cytokine ruesponse depends on type of exercise, intensity, duration, recovery between exercise bouts and training status. cytokines is playing a significant role in both destruction and repair processes on damaged tissues. Some data reported that when IL-6 is secreted by muscle, it has been shown that it increases anti-inflammatory cytokines such as IL-10 and IL-1ra (Powers, 2012, Calle, M.,& Luz, F.,

The complement system is a part of the immune system that is established in the blood and functions to keep the body healthy. The complement system consists of more than thirty proteins that flow throughout the blood and attack bacteria, viruses, and any foreign invader found throughout the body. More specifically, the complement system helps pathogen cells commit apoptosis, have inflammation, lyse, and opsonization. There are nine major complement proteins, which are C1-C9, that act a little different in each of the three pathways: the alternative, classical, and the lectin complement pathway. The difference between the lectin and the classical pathway is that in the lectin pathway, C1q is not involved but instead a mannan binding protein

While inflammation is often viewed in a negative connotation, inflammation is actually an essential component of the healing process. Inflammation is commonly associated with pain, swelling, and redness; however, these effects are the body’s natural response to injury as blood and white blood cells move into the tissue and stimulate the repair process.2, 29 Therefore it is important to understand that even though certain molecular signals are traditionally identified as pro-inflammatory molecules, they are also critical molecules to support tissue regeneration through stimulation of reparative cells. Only when inflammation persists, as in chronic wounds, can it lead to tissue damage and prevent progression through the healing process. Therefore,

Blood is composed of three types of elements such as red blood cells (erythrocytes) which carry oxygen; white blood cells (leukocytes), defenders against infections; and platelets which are for clotting. There are five types of leukocytes, some with granules (granulocytes), and some without granules (agranulocytes). There are three types of white blood cell with granulocytes: Neutrophils, Eosinophils, and Basophils. Neutrophils engulf bacteria and fungi. Eosinophils target parasites and play an important role in allergy and asthma. Basophils release histamine in response to inflammation. Agranulocytes include lymphocytes and

In classical inflammation, macrophages follow the neutrophils to the site of the injury. The absence of mononuclear phagocytes at the site of the injury following irradiation in the present study could be associated with irradiation-induced structural modifications within these cells that could weaken the defence response. It is possible that mononuclear phagocytes lose their normal defence functions after irradiation and that they become unable to increase in number. Furthermore, the post-irradiation releases of the inflammatory mediators that recruit mononuclear phagocytes may not reach the threshold levels that are required to mobilise the macrophages, and inflammatory mediators regulate leukocyte production in the bone marrow. Irradiation may also alter the levels of gene expression associated with the inflammatory mediators and adhesion molecules that are required for macrophage transmigration, thereby preventing its occurrence. A previous study that

“Qualitative or quantitative abnormalities interfere with or prevent enzymatic reactions that transform clotting factors, circulating as plasma proteins into a stable fibrin clot” (Huether and McCance 544). Some defects are caused by a single factor, these would be hemophilias and von Willebrand disease and some are acquired and result from “deficient synthesis of clotting factors by the liver” which is caused by liver disease and vitamin K deficiency (Huether and McCance 544). Other abnormalities in coagulation disorders are caused by “pathologic conditions” such as a cardiovascular abnormality that alters blood flow. An example of this is thromboembolic disease where blood clots block vessels (Huether and McCance 544). Vasculitis and damage to vessels activates platelets which activates coagulation (Huether and McCance 544). Prolonged vasculitis leads to clogging of the

Collagen and von Willebrand factor can initiate coagulation by causing platelet activation which triggers coagulation.

There are three types of Hemophilia, Hemophilia A, B, and C. The process of blood clotting has a series of complex mechanisms that are 13 different proteins, ranging from factors Ι to ΧΙΙΙ in roman numerals. If the blood vessels are damaged, the platelets are supposed to form a plug in the injured