Chapter 22: Alteration of Hemostasis PDF
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This document discusses hemostasis, encompassing clotting mechanisms and related factors. It covers the various stages of the process and the intrinsic, extrinsic, and common pathways involved in clotting. It also touches upon disorders associated with abnormalities in blood clotting.
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CHAPTER 22: ALTERATION OF HEMOSTASIS Blood = plasma + formed elements (erythrocytes, leukocytes thrombocytes) emostasis is a term that refers to the cessation of blood flow, particularly through the action of coagulation (clotting) H mechanisms Hemorrhage refers to copious bleeding which c...
CHAPTER 22: ALTERATION OF HEMOSTASIS Blood = plasma + formed elements (erythrocytes, leukocytes thrombocytes) emostasis is a term that refers to the cessation of blood flow, particularly through the action of coagulation (clotting) H mechanisms Hemorrhage refers to copious bleeding which can be outside the skin (from laceration) or in the skin (ecchymoses) Disorders of hemostasis are related to excessive coagulation or excessive bleeding - disruption of homeostasis can occur at any point of coagulation 1. Vascular phase (initiation) a. Spasm of blood vessels (injury to blood vessel causes a reactive constriction of spasm of the blood vessels, and platelets are activated and travel to site) 2. Aggregation phase (amplification) a. Platelets form a plug (clump together) 3. Coagulation phase (propagation) a. Formation of fibrin (platelets release immune proteins+ forms film over platelet) Clotting is caused by intrinsic, extrinsic, and a common pathways Intrinsic Extrinsic Common Pathway ctivated by trauma A inside the vascular system Activated by platelets, exposed endothelium, chemicals, or collagen ctivated by A external trauma that causes blood to escape from the vascular system This pathway is much quicker F actor X is a vitamin K-dependent clotting factor and plays a central role in the coagulation cascade at the point of convergence of the intrinsic and extrinsic pathway Factors XII, IX, VII Factors VII, III ctivated factor X causes a set of reaction resulting in the inactive enzyme A prothrombin (factor II) being converted in the active form thrombin Thrombin then converts soluble fibrinogen (factor I) into insoluble fibrin strands The fibrin strands compromising the clots are then stabilized by factor XIII lotting cascade is similar to the complement system and each enzyme of the pathway is present in the plasm in an inactive form C The coagulation pathway is a series of + and - feedback loops that control the activation process with the end goal being to reduce thrombin Thrombin alters the structure of fibrinogen, transforming it into fibrin Fibrin provides a mesh like framework on which platelets can clump ofactors includecalcium, which serves to bind theclotting factors together for coagulation to occur while andvitamin Kis C essential for the functioning of several proteins involved in the regulation of blood clotting Both are required for the synthesis of protein c, an anticoagulant that prevents excessive coagulation after the coagulation cascade occurs. Deficiency of any of these clotting cofactors will cause an impaired ability for blood to coagulate and can contribute to excessive bleeding and hemorrhage reaking down clots involves primary fibrinolysis, the body’s normal process and secondary fibrinolysis, caused by medication or B disease process Plasmin is the main enzyme that cuts the fibrin mesh at various places Leads to the production of circulating fragments ○ Fibrin degradation produce ○ This number is reflected in the D-dimer D -dimer is a product of fibrin degradation that is present after blood clots are broken down. An elevated result may imply the presence of significant clotting propensity. Elevated levels can also be found in a number of other medical conditions and states. Plasminogen is the inactive from of plasmin produced in the liver ○ Required tissue plasminogen activator (T-PA) and urokinase to be converted to the active form of plasm ○ T-PA can be made in the lab and is known as recombinant r-PA Clot buster Various type of test for coagulation and bleeding D-dimer - fragment of fibrin degradation ○ D-dimer is a product of fibrin degradation that is present after blood clots are broken down. An elevated result may imply the presence of significant clotting propensity. Elevated levels can also be found in a number of other medical conditions and states. Activated partial thromboplastin time (aPTT) - same parameters as PTT, with clotting activator ○ Increased levels indicate prolonged bleeding. Particularly prolonged bleeding is associated with changes in the levels of select clotting factors, primarily factors II, V, IX, X, XI, and XII Fibrinogen - presence of soluble protein necessary for formation of fibrin Partial thromboplastin time (PTT) - functional ability of clotting pathway Vitamin k - vitamin essential to formation of several clotting factors Primary disorders Secondary disorders ssociated with abnormalities in number or function of A platelets ssociated with lack of, or reduction in, factors tied to A coagulation May occur as a result of genetic factors, liver dysfunction, dietary deficiency ON WILLEBRAND DISEASE V Most common genetic bleeding disorder involving partial or complete deficiency in clotting factors (in which a lack of a certain factor prevents platelets from adhering to the site of injury, preventing the formation of a blood clot) Type 1 - most frequent and least severe, often asymptomatic Type 2 - some bleeding issues Type 3 - significant blood loss, internal bleeding, similar to hemophilia Treatments for spontaneous bleeding episode include desmopressin and transfusion with plasma derived vWF products T HROMBOCYTOPENIA Most common cause of abnormal bleeding involving a decrease in number of circulating blood platelets auses not well understood, infection and other inflammatory C states. artifact, deficient production, increase destruction, consumption or both, abnormal distribution or pooling linical manifestation include purpura (easy or excessive C bruising), ecchymoses, epistaxis (bleeding from nose), serious hemorrhages, petechiae (superficial bleeding into the skin that appears as a rash or pinpoint sized reddish purple spots, usually on lower legs) Treatment include plasmapheresis (plasma exchange), TTP EMOPHILIA H Hereditary genetic bleeding disorder associated with the loss of select clotting factors and significant bleeding or soft tissues or joints Hemophilia A - factor VIII Hemophilia B - factor IX an also be acquired from autoimmune disease, cancer, C pregnancy linical manifestation C (infants) excessive bleeding after circumcision (adults) severe mucosal bleeding from tongue or hum injuries, permanent bruising over trunk and extremities L ab test would should prolong PTT, normal PT, platelet counts, bleeding time, platelet function assays, Diagnosis involves analysis of factor VIII and IX activity T reatment involves episodic or prophylactic administration of factor VII or XI concentrates therapy, infusion of fresh frozen plasma Issues of hypercoagulopathy in sickle cell disease Clinical manifestation include hypoxia and tissue ischemia Diagnosis involves increase concentration of thrombin with corresponding loss of anticoagulant proteins Treatment includes pharmacological treatments that reduce platelet binding and inhibit platelet activation isseminated intravascular coagulation (DIC) is a life threatening condition that involves protein that control clotting becoming D overreacting Causes include sepsis, shock, or damage to blood vessels ○ 3 can increase tissue factor and cause systemic activation of coagulation pathways Clinical manifestations - clots cause organ dysfunction, difficulty breathing, hemoptysis, tachycardia Diagnosis - low platelet and fibrinogen levels, prolongation of PT and aPTT results, with elevation in D-dimer values Treatment involves monitoring for blood loss and signs of organ failure due to ischemic damage or administration of platelet and other blood factors Patient education Patient who are at risk of excessive bleeding need to be educated about their condition and provided with instruction about preventing bleeding Bleeding precaution include using a soft toothbrush, wearing shoes at all times, avoiding contact sports, using stool softener to prevent straining
