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Hemostasis is responsible for 3 important diseases Myocardial infarction (heart attack), Pulmonary embolism, and Cerebrovascular accident (stroke)
Hyperemia and Congestion results from what process? Local increased volume of blood w/in a tissue via dilation of small vessels
Hyperemia an ACTIVE process due to increased Arterial inflow and arises in conditions like inflammation, blushing, or exercise.
Congestion a PASSIVE process that arises from decreased Venous outflow and occurs in conditions like cardiac failure or obstructive venous disorder
Cyanosis bluish coloration due to accumulation of deoxygenated hemoglobin
Edema above normal amount of fluid in the intercellular (interstitial) tissue spaces or body cavities.
Anasarca generalized edema
Hydrothorax edema in chest cavity
Hydropericardium edema in heart cavity > pericardial sac
Hydroperitoneum (ASCITES) edema in the abdominal cavity
4 causes of NONinflammatory edema 1) Increase in intravascular hydrostatic pressure 2) fall in osmotic pressure of plasma proteins 3) impairment of lymphatic flow 4) removal or congenital malformation and renal retention of salt and water
Transudate edema fluid secondary to increased hydrostatic pressure that is protein-poor
Exudate inflammatory edema fluid that is protein-rich
Hemorrhage extravasation of blood due to rupture of blood vessel
Hemorrhagic Diathesis increased TENDENCY to hemorrhage
Hematoma a hemorrhage that accumulates within soft tissue
Petechiae minute hemorrhage (1-2mm) of the skin, mucous membranes or serosal surfaces
Purpura hemorrhage of 3-5mm in size
Ecchymosis hemorrhage over 1cm in size
Identify the changes in color when bruises resolve Hemoglobin (red-blood color) is converted to Bilirubin (blue-green) and then Hemosiderin (golden/yellow-brown) which account for color change in resolving bruise.
Hemothorax accumulation of blood in the chest cavity
Hemopericardium accumulation of blood in the pericardium
Hemoperitoneum accumulation of blood in the gut
Hemarthrosis accumulation of blood in join spaces
4 stages of HEMOSTASIS 1) arteriolar vasoconstriction 2) Injury to Endothelial cells begin coagulation cascade forming temporary hemostatic plus (Primary Hemostasis) 3) Coagulation is activated forming THROMBIN & FIBRIN (Secondary Hemostasis) 4) Anti-thrombotic Mechanism starts
Antiplatelet, Antithrombogenic, and Fibrinolytic properties of Endothelial Cells ADPase (adenosine diphosphatase), PGI2 (prostacyclin), NO (nitric oxide), Heparin-like molecules, Thrombomodulin, and Plasminogen activator.
PGI2 and NO inhibit platelet aggregation and prevent adhesion to uninjured endothelium.
ADPase degrades ADP, platelet aggregation
Heparin-like molecules bind to antithrombin
Thrombomodulin binds thrombin to activate Protein C to slow coagulation
Plasminogen activator promote fibrinolytic activity
Prothrombotic Properties Release of Tissue Factor and von Willebrand Factor
Tissue Factor Factors that enable cells to initiate the blood coagulation cascade.
von Willebrand Factor Endothelial cells that produce glycoprotein that facilitate platelet attachment to exposed collagen.
Damage to endothelium generate what three platelet reactions? Adhesion, Activation, and Aggregation
Platelet Adhesion Platelet adhere to exposed collagen with the help of von Willenbrand Factors to form a temporary plug
What products are released by Platelet Adhesion and its action? Calcium, ADP, and Thromboxane A2 (TXA2). Platelet adhesion leads to surface expression of Phospholipid Complex necessary for coagulation cascade with the help of these products.
Platelet Aggregation leads to what two types of plugs? Primary Hemostatic Plug and Secondary Hemostatic Plug.
Primary Hemostatic Plug initial mass of loosely packed platelets and is Temporary
Secondary Hemostatic Plug composed of Viscous Metamorphosis (initial gelatinous mass of platelets) that form into a Definitive hemostatic plug.
Clinical use of Aspirin Pts at risk for coronary thrombosis are given aspirin to inhibit TXA2, that create antithrombotic environment.
The Coagulation System is divided into what two pathways? Extrinsic and Intrinsic Pathways but interconnections exist between them.
Clinical testing for Hemostasis Clotting Time and Bleeding Time
Clotting Time length of time for specimen of blood to clot, it measures intrinsic system
Bleeding Time length of time for a puncture wound to stop bleeding, it measures platelet aggregation
Laboratory testing for Hemostasis Partial Thromboplastin Time (PTT), Prothrombin Time (PT), and Thrombin Time (TT)
Partial Thromboplastin Time (PTT) measures intrinsic (naturally occurring) system of clotting
Prothrombin Time (PT) Measures extrinsic (outside factors) system through mixture of Factor III and plasma
Thrombin Time (TT) Checks for fibrinogen deficiency by mixture of thrombin and plasma
Fibrinolytic System a process that prevents blood clots from growing, it is contained within the site of injury.
Fibrinolytic System is composed of what three groups of anticoagulants and pathway inhibitor? Antithrombics, Fibrinolytic, and Thrombolytics. Tissue Factor Pathway Inhibitor
Antithrombics Heparin-like molecules that reduce blood clot formation.
Fibrinolytic Plasminogen converted into PLASMIN which splits fibrin (clot) and inhibit coagulation. FIBRIN SPLIT PRODUCTS are formed from fragments of proteins released form dissolving clots.
Thrombolytic Thrombomodulin are present on endothelial cells that interact with thrombin and converts it to an anticoagulant. This activates Proteins C and S (vit K-dependent components) that inactivates coagulation factors.
Tissue Factor Pathway Inhibitor secreted by endothelium and inactivates active Factor X and activated tissue factor (Factor VIIa) = slowing of extrinsic pathway.
What is Thrombosis? the formation of blood clots inside a blood vessel or heart, typically obstructs blood flow in the circulatory system
The name of the blood clot mass? Thrombus
What is the term for 3 primary influences for predisposing thrombus formation and it's characteristics? Virchow's Triad. Endothelial injury, Alteration in blood flow, and Hypercoagulability
Endothelial Injury Primarily the cause of thrombogenesis and is the only condition that by itself, can lead to thrombus formation. Typically occur at traumatic of inflammatory injury, atherosclerotic or adjacent to MI or Injury.
Other Risks associated with Endothelial Injury subtle injury like Hypercholesterolemia, radiation, tabacco, dysfunction of endothelial cells leading to greater procoagulants and less anticoagulants.
Two main causes of Alteration in Normal Blood Flow Stasis and Turbulence (both promote thrombus formation through disruption of laminar blood flow)
Mechanism associated with stasis and turbulence Disruption of flow pattern allow platelets to contact endothelium which permit platelet aggregation, decreases dilution of activated coagulation factor, and decrease clotting inhibitors.
Typical areas for Stasis and Turbulence Stasis - problematic in veins. Turbulence - seen in arterial aneurysms (bulging of arterial walls) or adjacent to MI.
Common cause of Hypercoagulability Although not common, caused by primary (genetic) or secondary (acquired)
Genetic causes of Hypercoagulability mutation of prothrombin, mutation in Factor V, deficiency of Anticoagulants (antithrombin, protein C, protein S).
Clinical Significance of Hypercoagulability Inherited (Genetic) causes should be investigated with Pts under 50 w/ significant thrombosis, even if risk factors are present.
Leiden Mutation mutation on the Factor V gene resulting in prothrombotic state, homozygous carriers are at a higher risk for thrombosis.
Acquired Hypercoagulability Damage to endothelial cells (MI), increased estrogen (pregnancy or contraceptives), cancers, autoantibodies leading to arterial and venous thrombosis, smoking, and obesity.
Heparin-induced thrombocytopenia (HIT) development of thrombocytopenia (a low platelet count), HIT predisposes to thrombosis, HIT is caused by the formation of abnormal antibodies that activate platelets.
Antiphospholipid antibody syndrome (APS) occurs with Lupus pts, is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies, inhibit phospholipid complexes and inhibit coagulation
Arterial Thrombi typically arises at the site of endothelial damage or turbulence, they are either attached to the vascular wall (MURAL - aorta or seen in aneyrysm) or obstruct the lumen (OCCLUSIVE - small arteries)
Lines of Zahn a characteristic of thrombi[1] that appear particularly when formed in the heart or aorta, visible and microscopic alternating layers (laminations) of platelets mixed with fibrin.
White or Coaglutination thrombi because they are mostly platelets and fibrin
Venous thrombosis (phlebothrombosis) occurs in static (stasis) area 90% in leg veins, most being occlusive in nature. (aka Red, Coagulative, Stasis thrombi)
Characteristic of Red, Coagulative or Stasis Thrombi slow moving with rich erythrocyte accumulation
4 possible arises from vascular occlusion 1) Propagation (often until critical vessel is blocked) 2) Embolization 3) Dissolution 4) Organization and recanalization
Disseminated Intravascular coagulation (DIC) sudden or insidious onset of widespread thrombosis, can lead to consumption of platelets and coagulation factors. (aka Consumption Coagulopathy)
Embolous detached intravascular solid, liquid or gaseous mass carried in the blood away from origin.
Other Thromboemboli fat, atherosclerotic debris, gas bubbles, tumor fragments, bone marrow or foreign substances. can occur in arteries or veins
Pulmonary thromboembolism a blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body through the bloodstream (embolism). common among hospitalized pts
Clinical significance of Pulmonary thromboembolism 95% come from deep leg veings above the knee
Saddle Embolous Large pulmonary embolus, often fatal due to massive right side heart strain (ACUTE COR PULMONALE) or hypoxemia secondary to blockage of pulmonary vessel
Systemic Thromboembolism traveling thrombus through the Arterial system, originates from intracardiac mural thrombi(80%) or less frequently from aneurym or atherosclerotic plaque.
Paradoxical Embolism rare, systemic emboli appear to arise in veins but end up in arterial circulation due to interatrial or interventricular defect.
Fat Embolism rare, may arise from soft tissue trauma, burns, but typically from bone fractures. 90% skeletal injury but less than 10% develop signs or symptoms.
Amniotic Fluid Embolism occrs during birth 1/40,000 with 80% motality rate. emboli contains mixture of epithelial cells, hair, fat and mucus from amniotic fluid via tear in placentalmembrane or rupture of uterine veins.
Gas Embolism gas bubbles that act like a physical obstructiom or form frothy masses that occlude vessels, aka Decompression Disease - occurs in deep sea divers.
Caisson Disease persistent gas emboli in bones leading to multiple foci of ischemic necrosis, affects the head of long bones.
Infarction localized area of ischemic necrosis within a tissue or organ produced by occlusion of either arterial supply or venous drainage.
Characteristics of Infarction may either be red (Hemorrhagic) or white (Anemic). most common and dangerous infarction is myocardial, pulmonary and brain infarction. if pt survives, infarction is replaced by scar tissue.
Factors determining if an occlusion will produce infarction 1) alternative or collateral circulation will help maintain vitality 2) if it developes slowly, alternative pathways of flow 3) tissues vulnerable to ischemia (myocardium and cns) 4) low O2 increases extent of infarction (hypoxemia)
Shock systemic Hypoperfusion due to reduction in cardiac output or in the Effective circulatin blood volume. leads to hypotension, impaired tissue perfusion and cell hypoxia
3 major categories of Shock 1) Cardiogenic Shock 2) Hypovolemic Shock3) Septic Shock
Cardiogenic Schock pump failure from infarction, arrhythmias(irregular heartbeat/abnormal heart rythm), extrinsic compression, or decreased heart function.
Hypovolemic Shock arise through acute loss of critical fraction of the plasma volume, can be due to hemorrhage or exudation of plasma from large wounds or burns.
Septic Shock occurs most frequently from gram negative infection resulting in endotoxemia. toxins produce visceral pooling of blood which lower circulating volume. muuch more complicated in mechanism and can lead to multiple system failure.
Neurologic shock less common, may occur form anesthetic accident or spinal cord injury resulting in loss of vascular tone and peripheral pooling
Anaphylactic shock Generalized IgE mediated hypersensitivity, systemic vasodilation and increased vascular permeability = loss of circulatory volume.
3 progressive stages of Shock if untreated 1) Nonprogressive Stage 2) Progressive stage 3) Irreversible stage
Nonprogressive stage compensatory mechanism through tachycardia (fast heart rate), peripheral vasoconstriction, and renal retention of fluid.
Characteristic of Nonprogressive stage pts present with hypotension, skin is cool and pallor but dont get confused with septic shock which will produce warm and flushed appearance.
Progressive stage hypoperfusaion leading to widesapread tissue hypoxia and shift to anaerobic metabolism, release of lactic acid (decrease in blood pH, metabolic acidosis)
Characteristic of Progressive stage vital organ begin to fail, anoxic endothelial damage and lead to DIC
Irreversible stage organs become severely injured, myocardial damage leading to reduced cardiac output, intestinal necrosis allow GI flora to enter circulation and complete renal shutdown.
Coagulation Diagram Refer to pdf 1)endothelial injury & expose subendothelial collagen 2)platelet aggregation 3)coagulation pathway initiated 4) platelet aggregation progress 5)thrombin with fibrin formation 6)plasmin formation & antithrombin check 7)...
....Coagualtion Diagram 7)clot retraction and fibrinolysis reduces clot size 8)connective tissue repair begin 9)endothelial repair begins
Created by: ddde227