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Thrombosis and Its Mechanisms
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Thrombosis and Its Mechanisms

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Questions and Answers

What are the three predisposing factors for thrombus formation as described by Virchow's triad?

  • Embryonic development, hemodynamic stability, and vascular elasticity
  • Ventricular contraction, external compression, and platelet activation
  • Endothelial injury, blood hypercoagulability, and alteration in normal blood flow (correct)
  • Vascular injury, blood viscosity, and hypoxia

    • Which type of thrombus is usually occlusive and forms a solid mass with alternating layers of platelets and fibrin?

  • Microthrombus
  • Mixed thrombus
  • Arterial thrombus (correct)
  • Venous thrombus

    • What is a key mechanism by which stasis results in thrombus formation?

  • Disruption of laminar flow and interaction with endothelial cells (correct)
  • Enhancement of blood temperature and viscosity
  • Inhibition of platelet activation
  • Promotion of endothelial cell adhesion

    • Which primary genetic cause of hypercoagulability could lead to thrombus formation?

    <p>Antithrombin III deficiency</p> Signup and view all the answers

    What fate of a thrombus involves its dissolution back into the bloodstream?

    <p>Dissolution</p> Signup and view all the answers

    Which statement is true regarding venous thrombi compared to arterial thrombi?

    <p>Venous thrombi are usually less firmly attached and tend to be red</p> Signup and view all the answers

    What is one of the significant consequences of thrombi within vessels?

    <p>Source of obstruction in normal blood flow</p> Signup and view all the answers

    What is the most common cause of fat embolism?

    <p>Fractures of long bones</p> Signup and view all the answers

    What mechanism does endothelial injury trigger that leads to thrombus formation?

    <p>Exposure of subendothelial extracellular matrix and platelet adhesion</p> Signup and view all the answers

    What clinical feature is NOT typically associated with fat embolism?

    <p>Muscle and joint pain</p> Signup and view all the answers

    Which type of embolism is most likely to result from decompression sickness in divers?

    <p>Gas embolism</p> Signup and view all the answers

    What is the primary source of systemic thromboembolism?

    <p>Intra-cardiac mural thrombi</p> Signup and view all the answers

    What is a consequence of obstruction of small endarterioles during pulmonary embolism?

    <p>Infarction</p> Signup and view all the answers

    Which condition is characterized by sudden changes in atmospheric pressure leading to gas embolism?

    <p>Decompression sickness</p> Signup and view all the answers

    Which of the following sites is NOT commonly involved in systemic thromboembolism?

    <p>Heart</p> Signup and view all the answers

    What is the typical appearance of a pulmonary embolus in major pulmonary arteries?

    <p>RBC, platelets, and fibrin forming lines of Zahn</p> Signup and view all the answers

    What characteristic distinguishes post mortem clots from mural thrombi?

    <p>Post mortem clots are gelatinous and dark red.</p> Signup and view all the answers

    Which structure is identified by the presence of alternating bands consisting of platelets, fibrin, and red blood cells?

    <p>Lines of Zahn</p> Signup and view all the answers

    Which of the following is a complication associated with disseminated intravascular coagulation (DIC)?

    <p>Widespread activation of thrombin leading to bleeding</p> Signup and view all the answers

    What type of embolism originates from detached vascular masses, including thrombi?

    <p>Thrombo-emboli</p> Signup and view all the answers

    In pulmonary thromboembolism, which of these describes a large embolus that may occlude the main pulmonary artery?

    <p>Saddle embolus</p> Signup and view all the answers

    What is the primary cause for the sudden onset of disseminated intravascular coagulation (DIC)?

    <p>Release of thrombin due to massive tissue injury</p> Signup and view all the answers

    What is likely to cause a paradoxical embolism?

    <p>A thrombus transitioning from the venous to systemic circulation</p> Signup and view all the answers

    Which of the following best describes the composition of a complicated atheroma with thrombus?

    <p>A mixture of RBCs, platelets, and fibrin</p> Signup and view all the answers

    What is the primary mechanism responsible for ischemia in most cases?

    <p>Thrombotic or embolic mechanisms</p> Signup and view all the answers

    Which condition is most likely to cause red infarcts?

    <p>Venous occlusion</p> Signup and view all the answers

    Which of the following is NOT a common cause of infarction?

    <p>Sepsis</p> Signup and view all the answers

    What morphological feature distinguishes infarction?

    <p>Wedge shape with peripheral definition</p> Signup and view all the answers

    Which statement best describes the effects of ischemia with adequate collateral circulation?

    <p>It causes minimal or no functional disturbances.</p> Signup and view all the answers

    What is one potential clinical outcome if a patient survives amniotic fluid embolism?

    <p>Development of pulmonary edema and DIC</p> Signup and view all the answers

    Which factor is least likely to influence the development of an infarct?

    <p>Oxygen saturation in the blood</p> Signup and view all the answers

    In which situation would white infarcts typically occur?

    <p>Solid organs with end arterial circulation</p> Signup and view all the answers

    How does the anatomy of the vascular supply influence the outcome of blood vessel occlusion?

    <p>Dual blood supply can limit damage from occlusion.</p> Signup and view all the answers

    Which statement accurately describes the vulnerability to hypoxia of different cell types?

    <p>Fibroblasts in the myocardium can survive longer than myocardial cells during ischemia.</p> Signup and view all the answers

    What effect does low oxygen content in blood have on tissue infarction?

    <p>It increases both extent and vulnerability of infarction.</p> Signup and view all the answers

    In the stage of compensation during shock, which physiological response occurs?

    <p>Reflex sympathetic activation resulting in vasoconstriction.</p> Signup and view all the answers

    What characterizes the progressive stage of shock?

    <p>Impaired tissue perfusion leading to lactic acidosis.</p> Signup and view all the answers

    Which of the following correctly describes the function of the renal arterioles in shock?

    <p>They decrease pressure, leading to reduced urine output.</p> Signup and view all the answers

    What is a consequence of prolonged excessive vasoconstriction during shock?

    <p>Anaerobic glycolysis and subsequent cell necrosis.</p> Signup and view all the answers

    Which organ is most likely to show acute necrosis due to impaired perfusion during shock?

    <p>Kidney where acute tubular necrosis may occur.</p> Signup and view all the answers

    Most pulmonary emboli are symptomatic and lead to noticeable clinical manifestations.

    <p>False</p> Signup and view all the answers

    Thrombosis refers to the formation of a solid or semi-solid mass from blood constituents in the vascular system due to appropriate activation of hemostasis.

    <p>False</p> Signup and view all the answers

    Obstruction of small endarterioles during a pulmonary embolism can result in pulmonary hemorrhage.

    <p>False</p> Signup and view all the answers

    Fat embolism commonly arises from fractures of long bones.

    <p>True</p> Signup and view all the answers

    Endothelial injury can be caused by mechanical damage, atherosclerosis, and inflammation of heart valves.

    <p>True</p> Signup and view all the answers

    Gas embolism can occur due to rapid depressurization, causing nitrogen bubbles to form in the bloodstream.

    <p>True</p> Signup and view all the answers

    Turbulence of blood flow primarily leads to venous thrombosis.

    <p>False</p> Signup and view all the answers

    Chronic corpulmonale can result from multiple pulmonary emboli that occur over time.

    <p>True</p> Signup and view all the answers

    Hypercoagulability can be a result of both genetic conditions and acquired factors such as immobilization or smoking.

    <p>True</p> Signup and view all the answers

    Arterial thrombi are often red and not firmly attached to blood vessel walls.

    <p>False</p> Signup and view all the answers

    Aortic aneurysm is one of the least common sources of systemic thromboembolism.

    <p>False</p> Signup and view all the answers

    The most common sites of systemic thromboembolism include the brain and lower extremities.

    <p>True</p> Signup and view all the answers

    The fate of a thrombus can include propagation, dissolution, or calcification.

    <p>True</p> Signup and view all the answers

    Venous thrombi are typically characterized by their occlusive nature and a formation process that includes lines of Zahn.

    <p>False</p> Signup and view all the answers

    Clinical features of fat embolism can appear within 3 to 5 days after the inciting event.

    <p>False</p> Signup and view all the answers

    Stasis can prevent the dilution of activated clotting factors and promote the formation of thrombi.

    <p>True</p> Signup and view all the answers

    Post mortem clots are typically gelatinous, dark red, and usually attached to the wall.

    <p>False</p> Signup and view all the answers

    Mural thrombi are formed on the heart valves.

    <p>False</p> Signup and view all the answers

    Lines of Zahn are characteristic of post mortem clots.

    <p>False</p> Signup and view all the answers

    Disseminated intravascular coagulation (DIC) can lead to serious bleeding disorders.

    <p>True</p> Signup and view all the answers

    Embolism refers to a solid, liquid, or gaseous mass that remains stationary in the blood vessel.

    <p>False</p> Signup and view all the answers

    A saddle embolus may occlude the main pulmonary artery.

    <p>True</p> Signup and view all the answers

    Athero-emboli can consist of tumor fragments.

    <p>False</p> Signup and view all the answers

    Pulmonary thrombo-embolism is mainly caused by deep leg vein thrombi.

    <p>True</p> Signup and view all the answers

    Amniotic fluid embolism is a common complication of labor.

    <p>False</p> Signup and view all the answers

    Ischemia can occur due to compressive forces from a nearby tumor.

    <p>True</p> Signup and view all the answers

    Red infarcts only occur due to arterial occlusion.

    <p>False</p> Signup and view all the answers

    Anemia is the primary cause of white infarcts.

    <p>False</p> Signup and view all the answers

    All infarctions have a wedge shape morphology.

    <p>True</p> Signup and view all the answers

    The dominant histological characteristic of infarcts is ischemic coagulative necrosis.

    <p>True</p> Signup and view all the answers

    Pulmonary edema and DIC are guaranteed outcomes if a patient survives amniotic fluid embolism.

    <p>False</p> Signup and view all the answers

    Diminished collateral circulation can lead to cell death in ischemic tissues.

    <p>True</p> Signup and view all the answers

    The lungs have a singular blood supply from the pulmonary arteries.

    <p>False</p> Signup and view all the answers

    Neuronal cells can withstand hypoxia for up to 10 minutes before undergoing irreversible damage.

    <p>False</p> Signup and view all the answers

    Prolonged excessive vasoconstriction during shock leads to anaerobic glycolysis and lactic acidosis.

    <p>True</p> Signup and view all the answers

    In the stage of compensation, tachycardia and peripheral vasodilation are primary responses.

    <p>False</p> Signup and view all the answers

    Kidneys and spleen have a dual arterial supply, making them less susceptible to infarction.

    <p>False</p> Signup and view all the answers

    Severe shock is characterized by increased effective circulating blood volume.

    <p>False</p> Signup and view all the answers

    Fibroblasts within the myocardium can remain viable for hours after ischemia.

    <p>True</p> Signup and view all the answers

    Oxygen content of blood does not significantly affect the extent of tissue infarction.

    <p>False</p> Signup and view all the answers

    What role does endothelial injury play in the formation of a thrombus?

    <p>Endothelial injury exposes subendothelial extracellular matrix (ECM), leading to platelet adhesion and activation.</p> Signup and view all the answers

    Describe the significance of turbulence and stasis in thrombus formation.

    <p>Turbulence and stasis disrupt normal blood flow, bringing platelets into contact with the endothelium and preventing the dilution of activated clotting factors.</p> Signup and view all the answers

    Explain how blood hypercoagulability contributes to thrombus formation.

    <p>Blood hypercoagulability, due to genetic or acquired factors, leads to an increased tendency to form clots within the vascular system.</p> Signup and view all the answers

    What are the potential fates of a thrombus once formed?

    <p>The potential fates of a thrombus include propagation, embolization, dissolution, organization and recanalization, and calcification.</p> Signup and view all the answers

    How does the appearance of arterial thrombi differ from venous thrombi?

    <p>Arterial thrombi are usually gray-white, firmly attached to the wall, and occlusive, whereas venous thrombi are red, less firmly attached, and also typically occlusive.</p> Signup and view all the answers

    Identify and explain a primary genetic cause of blood hypercoagulability.

    <p>Antithrombin III deficiency is a primary genetic cause of hypercoagulability, which decreases the blood's ability to inhibit clot formation.</p> Signup and view all the answers

    What role do the lines of Zahn play in the morphological assessment of thrombi?

    <p>The lines of Zahn represent alternating layers of platelets and fibrin with red cells, indicating organized thrombus formation and helping to differentiate between thrombi types.</p> Signup and view all the answers

    Discuss how inflammatory processes contribute to endothelial injury.

    <p>Inflammatory processes, such as phlebitis and valvular inflammation, can damage endothelial cells, promoting thrombus formation by exposing the ECM.</p> Signup and view all the answers

    What mechanism commonly causes amniotic fluid embolism during labor?

    <p>The infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins.</p> Signup and view all the answers

    How does poor collateral circulation affect tissue ischemia?

    <p>Poor collateral circulation can lead to functional disturbances or cell death in the affected tissue.</p> Signup and view all the answers

    What is the primary histological characteristic observed in infarcts?

    <p>The dominant histological characteristic of infarcts is ischemic coagulative necrosis.</p> Signup and view all the answers

    In what condition do red infarcts typically occur?

    <p>Red infarcts occur due to venous occlusion or in tissues with dual circulation.</p> Signup and view all the answers

    Describe the primary mechanism leading to pulmonary hemorrhage in pulmonary embolism.

    <p>Obstruction of medium-size pulmonary arteries can lead to pulmonary hemorrhage by causing increased pressure and damage to the vessels.</p> Signup and view all the answers

    What are the clinical features commonly associated with fat embolism?

    <p>Pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia are commonly associated with fat embolism.</p> Signup and view all the answers

    What morphological feature distinguishes a white infarct?

    <p>A white infarct is characterized by the absence of blood, typically following arterial occlusion in solid organs with end arterial circulation.</p> Signup and view all the answers

    What could occur if a patient survives an amniotic fluid embolism?

    <p>If the patient survives, pulmonary edema and disseminated intravascular coagulation (DIC) may develop.</p> Signup and view all the answers

    What role does abrupt decompression play in gas embolism among divers?

    <p>Abrupt decompression causes dissolved nitrogen to bubble out of solution in the blood, forming gas emboli and leading to infarction.</p> Signup and view all the answers

    Explain the relationship between small endarterioles blockage and the resultant clinical consequence of infarction.

    <p>Obstruction of small endarterioles during pulmonary embolism can lead to infarction by cutting off blood supply, causing tissue death.</p> Signup and view all the answers

    What factors influence infarct development following vascular occlusion?

    <p>Factors influencing infarct development include the adequacy of collateral circulation and the location of the occlusion.</p> Signup and view all the answers

    Identify a major source of systemic thromboembolism and its potential consequences.

    <p>Intra-cardiac mural thrombi are a major source and can lead to obstruction in vital organs, resulting in organ ischemia or infarction.</p> Signup and view all the answers

    What is the typical appearance of an infarct over time?

    <p>Initially, an infarct has a wedge shape with a poorly defined edge, which becomes sharper and more defined due to hyperemia and inflammation over time.</p> Signup and view all the answers

    How does the presence of multiple pulmonary emboli over time contribute to chronic corpulmonale?

    <p>Multiple pulmonary emboli can lead to chronic corpulmonale due to continuous strain and remodeling of the pulmonary vascular system.</p> Signup and view all the answers

    What is a distinguishing feature in the composition of a pulmonary thromboembolus?

    <p>A pulmonary thromboembolus is characterized by lines of Zahn, consisting of alternating layers of red blood cells, platelets, and fibrin.</p> Signup and view all the answers

    List the two common clinical manifestations that a diver might suffer from due to gas embolism.

    <p>Muscle and joint pain, alongside respiratory distress, are common manifestations of gas embolism in divers.</p> Signup and view all the answers

    What are post mortem clots characterized by that distinguishes them from mural thrombi?

    <p>Post mortem clots are gelatinous, dark red, usually not attached to walls, and lack lines of Zahn.</p> Signup and view all the answers

    What is the significance of lines of Zahn in the identification of a true thrombus?

    <p>Lines of Zahn are alternating pale pink bands of platelets and fibrin with red bands of RBCs, indicating an organized thrombus.</p> Signup and view all the answers

    Describe the condition of Disseminated Intravascular Coagulation (DIC) and its main clinical consequence.

    <p>DIC is characterized by widespread fibrin thrombi formation and rapid consumption of platelets leading to serious bleeding disorders.</p> Signup and view all the answers

    What are the primary types of emboli that can occur in the bloodstream?

    <p>Types of emboli include thrombo-emboli, fat and bone marrow, gas, athero-emboli, tumor fragments, and foreign bodies.</p> Signup and view all the answers

    What is the potential impact of a saddle embolus during pulmonary thromboembolism?

    <p>A saddle embolus may occlude the bifurcation of the pulmonary artery, disrupting blood flow to both lungs.</p> Signup and view all the answers

    What distinguishes mural thrombi from vegetations on heart valves?

    <p>Mural thrombi are attached to the heart wall, while vegetations form on heart valves, often with lines of Zahn.</p> Signup and view all the answers

    How does the presence of thrombus in a narrowed atherosclerotic coronary artery affect blood flow?

    <p>A thrombus in a narrowed artery can significantly obstruct blood flow, potentially leading to ischemia or infarction.</p> Signup and view all the answers

    What role does endothelial injury play in the development of thrombosis?

    <p>Endothelial injury initiates the coagulation cascade, promoting platelet adhesion and thrombus formation.</p> Signup and view all the answers

    How does the presence of dual blood supply in the lungs impact the outcomes of pulmonary artery obstruction?

    <p>It allows for less severe damage because the bronchial artery can provide alternative blood supply until it is also blocked.</p> Signup and view all the answers

    What effect does the rate of development of an occlusion have on collateral circulation in coronary arteries?

    <p>A slowly developing occlusion allows time for collateral circulation to open, mitigating tissue damage.</p> Signup and view all the answers

    Why are neurons particularly vulnerable to hypoxia compared to myocardial cells?

    <p>Neurons can suffer irreversible damage after just 3-4 minutes without blood supply, while myocardial cells can endure ischemia for 20-30 minutes.</p> Signup and view all the answers

    What is the initial physiological response during the stage of compensation in shock?

    <p>Decreased cardiac output triggers reflex sympathetic stimulation, leading to tachycardia and peripheral vasoconstriction.</p> Signup and view all the answers

    What are the consequences of prolonged excessive vasoconstriction during shock?

    <p>It leads to impaired tissue perfusion, anaerobic glycolysis, and results in cell necrosis, especially in the kidneys.</p> Signup and view all the answers

    Describe a clinical outcome following sustained shock that leads to cellular hypoxia.

    <p>Sustained shock can lead to cell death after initial reversible injury as perfusion remains impaired.</p> Signup and view all the answers

    In what way does low oxygen content in blood exacerbate the extent and vulnerability of tissue infarction?

    <p>Low blood oxygen levels increase the likelihood of extensive infarction and heighten the vulnerability of tissues to damage.</p> Signup and view all the answers

    How does the anatomy of vascular supply contribute to the fate of infarction in organs like the kidney and spleen?

    <p>These organs have end-arterial circulation, so any arterial obstruction directly results in infarction.</p> Signup and view all the answers

    The solid or semi-solid mass formed from blood constituents within the vascular system is called a ______.

    <p>thrombus</p> Signup and view all the answers

    There are three predisposing factors for thrombus formation, known as Virchow’s ______.

    <p>triad</p> Signup and view all the answers

    Venous thrombi are almost invariably ______, meaning they block blood flow completely.

    <p>occlusive</p> Signup and view all the answers

    Endothelial injury can lead to the exposure of subendothelial ______, which promotes platelet adhesion.

    <p>ECM</p> Signup and view all the answers

    Turbulence in blood flow primarily leads to ______ thrombosis.

    <p>arterial</p> Signup and view all the answers

    The fate of a thrombus can include propagation, embolization, and ______.

    <p>dissolution</p> Signup and view all the answers

    Changes in blood composition can lead to blood ______, a key factor in thrombus formation.

    <p>hypercoagulability</p> Signup and view all the answers

    As thrombi develop, they feature apparent laminations known as the lines of ______.

    <p>Zahn</p> Signup and view all the answers

    Most pulmonary emboli are ______.

    <p>silent</p> Signup and view all the answers

    Amniotic fluid embolism is a grave but uncommon complication of ______.

    <p>labor</p> Signup and view all the answers

    Obstruction of medium-size arteries during pulmonary embolism can lead to ______.

    <p>pulmonary hemorrhage</p> Signup and view all the answers

    Fat embolism frequently arises from fractures of ______.

    <p>long bones</p> Signup and view all the answers

    Ischemia is defined as inadequate blood supply to an area of ______.

    <p>tissue</p> Signup and view all the answers

    Infraction is defined as ischemic necrosis due to occlusion of either an artery or a ______.

    <p>vein</p> Signup and view all the answers

    Gas embolism may occur when air enters the circulation during rapid changes in ______.

    <p>atmospheric pressure</p> Signup and view all the answers

    Red infarcts typically occur in tissues with ______ circulation.

    <p>dual</p> Signup and view all the answers

    Chronic corpulmonale can result from multiple pulmonary ______ over time.

    <p>emboli</p> Signup and view all the answers

    The clinical features of fat embolism may include pulmonary insufficiency and ______.

    <p>neurologic symptoms</p> Signup and view all the answers

    Thrombosis or embolism accounts for ______% of the causes of infarction.

    <p>99</p> Signup and view all the answers

    Paradoxical emboli occur when a thrombus crosses from the ______ to the arterial circulation.

    <p>venous system</p> Signup and view all the answers

    When collateral circulation is ______, ischemia can lead to severe functional disturbances or cell death.

    <p>poor</p> Signup and view all the answers

    The dominant histological characteristic of infarcts is ischemic ______ necrosis.

    <p>coagulative</p> Signup and view all the answers

    Obstruction of small endarterioles during pulmonary embolism can lead to ______.

    <p>infarction</p> Signup and view all the answers

    White infarcts typically occur following ______ occlusion in solid organs.

    <p>arterial</p> Signup and view all the answers

    Post mortem clots are gelatinous, dark red, usually not attached to the wall and lack lines of ______.

    <p>Zahn</p> Signup and view all the answers

    Mural thrombi are those ______ to the wall of the heart chambers or in the aortic lumen.

    <p>attached</p> Signup and view all the answers

    Vegetations are thrombi formed on heart ______.

    <p>valves</p> Signup and view all the answers

    DIC is characterized by widespread fibrin thrombi formation in the micro- circulation associated with rapid consumption of ______.

    <p>platelets</p> Signup and view all the answers

    An embolism is a detached intravascular solid, liquid, or gaseous mass, carried by blood to a ______ from its point of origin.

    <p>site distant</p> Signup and view all the answers

    In pulmonary thromboembolism, deep leg vein thrombi are the usual ______ of the embolus.

    <p>source</p> Signup and view all the answers

    A detached thrombus that travels through the bloodstream can result in a ______ embolism.

    <p>thrombo-</p> Signup and view all the answers

    Lines of Zahn represent alternating pale pink bands of platelets with fibrin and red bands of ______.

    <p>RBCs</p> Signup and view all the answers

    The anatomy of the vascular supply, such as the presence or absence of an alternative blood supply, can determine whether the occlusion of a blood vessel can cause ______.

    <p>damage</p> Signup and view all the answers

    Neurons undergo irreversible damage when deprived of their blood supply for ______ minutes.

    <p>3-4</p> Signup and view all the answers

    During shock, the stage of ______ is characterized by reflex sympathetic stimulation leading to an increased heart rate.

    <p>Compensation</p> Signup and view all the answers

    Prolonged excessive ______ during shock can impair tissue perfusion and lead to anaerobic glycolysis.

    <p>vasoconstriction</p> Signup and view all the answers

    Hypoperfusion results in ______ and cellular hypoxia due to diminished cardiac output.

    <p>shock</p> Signup and view all the answers

    Vulnerability to hypoxia varies among tissues; for instance, myocardial cells can withstand ischemia for ______ to ______ minutes.

    <p>20-30</p> Signup and view all the answers

    Low blood oxygen content increases the extent and vulnerability of ______.

    <p>infarction</p> Signup and view all the answers

    Acute renal tubular ______ can occur due to impaired tissue perfusion during shock.

    <p>necrosis</p> Signup and view all the answers

    Match the terms related to thrombus formation with their descriptions:

    <p>Endothelial injury = Exposure of subendothelial ECM leading to platelet adhesion Stasis = Reduced blood flow promoting thrombus formation Turbulence = Disruption of laminar flow enhancing thrombus formation Blood hypercoagulability = Altered blood composition leading to increased clotting tendency</p> Signup and view all the answers

    Match the type of thrombus or emboli with their characteristics:

    <p>Post mortem clots = Gelatinous, dark red, not attached to vessel walls Mural thrombi = Attached to heart chamber walls Vegetations = Formed on heart valves Complicated atheroma with thrombus = Contains numerous identifiable cholesterol clefts</p> Signup and view all the answers

    Match the types of thrombi with their characteristics:

    <p>Arterial thrombi = Gray-white, friable, and often occlusive Venous thrombi = Red, less firmly attached, and almost invariably occlusive Post-mortem clots = Smooth, gelatinous appearance and not attached to vessel walls Organization of thrombus = Reorganization involving new tissue formation in thrombus area</p> Signup and view all the answers

    Match the factors of Virchow's triad with their implications:

    <p>Endothelial injury = Initiation of thrombus formation through exposure of ECM Stasis of blood flow = Increased risk for venous thrombosis Blood flow turbulence = Often associated with arterial thrombosis Blood hypercoagulability = Increased risk from genetic and acquired factors</p> Signup and view all the answers

    Match the condition with its associated description:

    <p>Disseminated intravascular coagulation (DIC) = Widespread fibrin thrombi formation in micro-circulation Pulmonary thromboembolism = Typically arises from deep leg vein thrombi Thrombo-emboli = Solid masses carried by blood to distant sites Paradoxical embolism = Occurs when emboli enter systemic circulation</p> Signup and view all the answers

    Match the fates of a thrombus with their descriptions:

    <p>Propagation = Growth of the thrombus within the vessel Embolization = Release of a thrombus fragment into circulation Dissolution = Breakdown and disappearance of the thrombus Re-canalization = Formation of new channels through an organized thrombus</p> Signup and view all the answers

    Match the term with its definition:

    <p>Lines of Zahn = Alternating bands of platelets and fibrin Mural thrombus = Thrombus formed on the wall of the heart chambers Athero-emboli = Emboli formed from atherosclerotic plaques Fat embolism = Commonly results from long bone fractures</p> Signup and view all the answers

    Match the description of embolic phenomena with their consequences:

    <p>Saddle embolus = May occlude main pulmonary artery Gas embolism = Can occur due to decompression sickness Athero-emboli = Fragments of atherosclerotic plaques reaching systemic circulation Tumor fragments = Can cause blockage in distant organs</p> Signup and view all the answers

    Match the types of endothelial injury with their causes:

    <p>Mechanical injury = Pressure or rupture of a blood vessel Degeneration = Changes due to atherosclerosis or myocardial infarction Inflammatory processes = Phlebitis and inflammation of heart valves Aneurysm = Weakened vessel wall leading to potential rupture</p> Signup and view all the answers

    Match the conditions associated with blood hypercoagulability with their categorization:

    <p>Antithrombin III deficiency = Primary genetic cause Myocardial infarction = Secondary acquired cause Sickle cell anemia = Secondary acquired cause Protein C deficiency = Primary genetic cause</p> Signup and view all the answers

    Match the thrombus type with their formation attributes:

    <p>Coronary artery thrombus = Contains a pink red recent thrombus occluding artery Mural thrombus = Located inside heart ventricles over fibrous scar Post mortem clots = Not formed through active hemostatic processes Vegetations = Often contain lines of Zahn when formed on valves</p> Signup and view all the answers

    Match the morphology features of thrombi with their visual characteristics:

    <p>Lines of Zahn = Alternating pale and dark layers in thrombus Occlusive thrombus = Completely obstructs the vessel's lumen Gray-white appearance = Characteristic of arterial thrombi Red appearance = Common in venous thrombi</p> Signup and view all the answers

    Match the condition to its potential causes:

    <p>DIC = Complication of infections or massive tissue injury Pulmonary thromboembolism = Arises mostly from deep vein thrombosis Embolism = Can result from various solid or gaseous masses Coronary artery thrombus = Occurs in narrowed atherosclerotic arteries</p> Signup and view all the answers

    Match the type of thrombus with the following features:

    <p>Post mortem clots = Lack lines of Zahn Mural thrombi = Firmly attached to vessel walls Vegetations = Present on heart valves with potential for lines of Zahn Thrombo-emboli = Composed of detached vascular masses</p> Signup and view all the answers

    Match the consequences of thrombi with their effects on the vascular system:

    <p>Obstruction of vessels = Prevents normal blood flow Source of emboli = Potential movement to distal sites in circulation Dissolution of thrombus = Possible return to blood flow as liquid component Calcification = Hardening of chronic thrombus over time</p> Signup and view all the answers

    Match the features of thrombus or emboli to their classification:

    <p>Lines of Zahn = Characteristic of true thrombus formation Friable thrombi = Associated with advanced atherosclerosis Obstruction of small arterioles = Can lead to pulmonary hemorrhage Paradoxical embolism = Caused by emboli entering systemic circulation through defects</p> Signup and view all the answers

    Match the clinical consequence of pulmonary embolism with its description:

    <p>Most pulmonary emboli are silent = Present without symptoms Sudden death (acute corpulmonale) = Rapid onset of fatal cardiac failure Obstruction of small endarterioles = Leads to pulmonary infarction Multiple emboli over time = Causes chronic corpulmonale</p> Signup and view all the answers

    Match the source of systemic thromboembolism with its specific origin:

    <p>Intra-cardiac mural thrombi = Most common source of emboli Aortic aneurysm = Dilation of aortic wall leading to thrombus Fragmentation of valvular vegetations = Typically occurs in endocarditis Paradoxical emboli = Occurs through a right-to-left shunt</p> Signup and view all the answers

    Match the type of embolism with its common cause:

    <p>Fat embolism = Fracture of long bones Gas embolism = Rapid depressurization Thromboembolism = Fragments of atheromatous plaques Decompression sickness = Sudden ascent from deep waters</p> Signup and view all the answers

    Match the common clinical feature of fat embolism with its timeline:

    <p>Pulmonary insufficiency = Symptoms appear in 1-3 days Neurologic symptoms = Arises within days post-injury Thrombocytopenia = Occurs as platelet counts decline Anemia = Reflects reduced red blood cell production</p> Signup and view all the answers

    Match the complication of gas embolism with its clinical presentation:

    <p>Muscle and joint pain = Sensation of ache in limbs Respiratory distress = Difficulty in breathing Physical obstruction to vessels = Causes potential infarction Symptomatic air entry = Results from high-pressure exposure</p> Signup and view all the answers

    Match the site involved in systemic thromboembolism with its frequency:

    <p>Lower extremities = 75% of cases Brain = 10% risk of embolism Kidneys = Commonly affected by emboli Upper extremities = Less frequently involved</p> Signup and view all the answers

    Match the consequence of pulmonary embolism with its underlying mechanism:

    <p>Obstruction leading to infarction = Results from blockage of endarterioles Pulmonary hemorrhage = Occurs from obstruction of medium-size arteries Chronic corpulmonale = Develops from repeated embolic events Acute corpulmonale = Results in sudden cardiac failure</p> Signup and view all the answers

    Match the following causes of ischemia with their descriptions:

    <p>Thrombotic mechanism = 99% of ischemia cases Complicated atheroma = Atherosclerosis with subsequent hemorrhage Extrinsic compression = Tumor or hernia affecting blood vessels Venous obstruction = Can occur in a varicose vein</p> Signup and view all the answers

    Match the type of gas embolism with its scenario:

    <p>Decompression sickness = Rapid ascent from underwater Obstetric procedures = Air entry during childbirth Chest wall injury = Air leakage into vascular system High-pressure breathing = Dissolved gas causing emboli on ascent</p> Signup and view all the answers

    Match the types of infarcts with their characteristics:

    <p>Red infarcts = Occur due to venous occlusion or dual circulation White infarcts = Result from arterial occlusion in solid organs Septic infarcts = Associated with abscess formation Wedge-shaped infarcts = Morphological characteristic of infarcts</p> Signup and view all the answers

    Match the clinical effects of ischemia with their corresponding manifestations:

    <p>Chest pain (angina) = Ischemia in the heart Intermittent claudication = Pain in the calf muscle during exercise Pulmonary edema = Possible outcome if patient survives embolism Cyanosis = Clinical sign during amniotic fluid embolism</p> Signup and view all the answers

    Match the complications of infarction with their definitions:

    <p>Ischemic necrosis = Tissue death due to lack of blood supply Expansion of atheroma = Can lead to arterial occlusion Traumatic rupture = Vessel damage causing rapid bleeding Hyperemia = Narrow zone of inflammation around infarcts</p> Signup and view all the answers

    Match the phrases associated with amniotic fluid embolism with their implications:

    <p>Sudden severe dyspnea = Immediate respiratory distress symptom Hypotensive shock = Drop in blood pressure condition Seizures = Neurological manifestation during complication DIC (Disseminated Intravascular Coagulation) = Potential outcome after survival</p> Signup and view all the answers

    Match the factors influencing infarct development with their effects:

    <p>Adequate collateral circulation = Leads to minimal or no effect Poor collateral circulation = Results in cell death Vascular occlusion = Can range from no effect to tissue death Age of the patient = Can influence tissue viability after infarction</p> Signup and view all the answers

    Match the morphologies of infarcts with their descriptions:

    <p>Firm and brown infarct = Likely develops after prolonged ischemia Pale infarct = Widely defined structure on examination Hemorrhagic infarct = Resulting from compromised venous drainage Scar tissue = Final change after white infarct evolves</p> Signup and view all the answers

    Match the mechanisms leading to infarction with their examples:

    <p>Thrombosis = Major cause in nearly 99% of cases Local vasospasm = Can lead to temporary ischemia Extrinsic compression = Tumors creating pressure on blood vessels Traumatic rupture = Immediate blood vessel loss due to injury</p> Signup and view all the answers

    Match the following organs with their blood supply characteristics:

    <p>Lungs = Dual blood supply from pulmonary and bronchial arteries Kidney = End-arterial circulation Spleen = End-arterial circulation Heart = Dual blood supply via coronary arteries</p> Signup and view all the answers

    Match the stages of shock with their descriptions:

    <p>Stage of Compensation = Increased heart rate and peripheral vasoconstriction Stage of Impaired Tissue Perfusion = Prolonged excessive vasoconstriction Stage of Cellular Hypoxia = Diminished tissue perfusion leading to cell death Reversible Injury Stage = Initial cellular injury that can recover</p> Signup and view all the answers

    Match the following cell types with their vulnerability to hypoxia:

    <p>Neurons = 3-4 minutes before irreversible damage Myocardial cells = 20-30 minutes before ischemic damage Fibroblasts = Viable for hours after ischemia Liver cells = Highly resistant to hypoxia</p> Signup and view all the answers

    Match the following consequences with their related causes in shock:

    <p>Decreased urine output (oliguria) = Increased vasoconstriction in renal arterioles Lactic acidosis = Anaerobic glycolysis due to impaired tissue perfusion Acute renal tubular necrosis = Prolonged hypoperfusion of kidneys Shock lung (ARDS) = Hypoxia leading to pulmonary edema</p> Signup and view all the answers

    Match the following factors with their effects on tissue infarction:

    <p>Rate of occlusion development = Allows time for collateral circulation to open Oxygen content of blood = Low levels increase infarction vulnerability Collateral circulation = Mitigates damage in slowly developing occlusions Hypoperfusion = Leads to cellular hypoxia and potential cell death</p> Signup and view all the answers

    Match the following terms in shock with their meanings:

    <p>Hypotension = Low blood pressure due to decreased cardiac output Progressive stage = Prolonged excessive vasoconstriction and tissue impairment Compensation = Initial mechanisms to maintain vital organ perfusion Cellular necrosis = Unrecoverable damage following sustained shock</p> Signup and view all the answers

    Match the following pathophysiological changes with their related organs:

    <p>Kidney = Acute renal tubular necrosis from hypoperfusion Lung = Acute alveolar damage and edema Liver = Anoxic necrosis of hepatic lobules Brain = Irreversible damage after 3-4 minutes of ischemia</p> Signup and view all the answers

    Match the following statements with their corresponding physiological responses:

    <p>Tachycardia = Reflex sympathetic stimulation in response to shock Vasoconstriction = Maintains blood pressure in vital organs Oliguria = Reduced glomerular filtration rate due to renal vasoconstriction Anaerobic glycolysis = Leads to lactic acid production in impaired tissue perfusion</p> Signup and view all the answers

    Study Notes

    Thrombosis

    • Thrombosis is the formation of a solid or semi-solid mass from blood constituents within the vascular system during life due to inappropriate activation of hemostasis.
    • The mass is called a thrombus.
    • Thrombus formation is influenced by Virchow's triad:
      • Endothelial injury
      • Stasis or turbulence of blood flow
      • Blood hypercoagulability

    Endothelial Injury

    • Can be caused by mechanical injury, degeneration, or inflammatory processes.
    • Endothelial injury leads to exposure of subendothelial ECM which promotes platelet adhesion.

    Alteration in Normal Blood Flow

    • Turbulence: associated with arterial and cardiac thrombosis
    • Stasis: associated with venous thrombosis
    • Can lead to endothelial injury, disrupt laminar flow bringing platelets into contact with endothelium, prevent dilution of activated clotting factors, retard inflow of clotting factors inhibitors, and promote endothelial cell activation leading to local thrombosis and leukocyte adhesion.

    Blood Hypercoagulability

    • Primary causes (genetic): Antithrombin III deficiency, Protein C deficiency
    • Secondary causes (acquired): Immobility, MI, HF, tissue damage, burns, OCCP (oral contraceptive pills), sickle cell anemia, leukemia, smoking

    Fate of Thrombus

    • Propagation
    • Embolization
    • Dissolution
    • Organization and re-canalization
    • Calcification
    • Thrombi can cause vessel obstruction and are potential sources of emboli.

    Morphology of Thrombus

    • Grossly and microscopically, thrombi have apparent laminations (lines of Zahn), produced by alternating pale layers of platelets with fibrin and darker layers of red blood cells.
    • Arterial thrombi are typically occlusive, firmly attached to the wall, and are gray-white and friable.
    • Venous thrombi are almost invariably occlusive, less firmly attached to the wall, and are red.
    • Post-mortem clots are gelatinous, dark red, usually not attached to the wall, and lack lines of Zahn.
    • Mural thrombi are attached to the wall of the heart chambers or in the aortic lumen.
    • Vegetations are thrombi formed on heart valves.

    Disseminated Intravascular Coagulation (DIC)

    • Is the sudden or insidious onset of widespread fibrin thrombi formation in the microcirculation associated with rapid consumption of platelets and coagulation proteins (consumption coagulopathy).
    • Results in activation of fibrinolytic mechanisms leading to serious bleeding disorders.
    • DIC is not a primary disease but rather a complication of many conditions, all having in common the widespread activation of thrombin (obstetrical complications, infections, massive tissue injury).

    Embolism

    • A detached intravascular solid, liquid, or gaseous mass, carried by the blood to a site distant from its point of origin.

    Types of Embolism

    • Thromboemboli
    • Fat and bone marrow
    • Gas (air, nitrogen)
    • Ateroemboli
    • Tumor fragments
    • Foreign body

    Pulmonary Thromboembolism

    • Most commonly originates from deep leg vein thrombi.
    • Can occlude the main pulmonary artery, impact across the bifurcation (saddle embolus), pass into smaller arterioles, or enter the systemic circulation (paradoxical embolism).

    Clinical Consequences of Pulmonary Embolism

    • Most pulmonary emboli are silent.
    • Sudden death (acute corpulmonale)
    • Obstruction of medium-size arteries: pulmonary hemorrhage
    • Obstruction of small endarterioles: infarction
    • Multiple emboli over time: chronic corpulmonale

    Systemic Thromboemboli

    • Can originate from intracardiac mural thrombi (89% of emboli), aortic aneurysm, thrombi on ulcerated atherosclerotic plaques, fragmentation of valvular vegetations, paradoxical emboli, or be of unknown origin (15%).
    • Main sites involved in embolism: lower extremities (75%), brain (10%), intestines, kidneys, spleen, upper extremities.

    Fat Embolism

    • Can result from fractures of long bones (most common), soft tissue trauma, and burns (rare).
    • Clinical features: pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia.
    • Symptoms typically appear within 1 to 3 days.

    Gas Embolism

    • Air may enter the circulation during obstetric procedures, chest wall injury, or deep sea diving.
    • More than 100 cc is required to have a clinical effect.
    • Bubbles produce physical obstruction to vessels leading to infarction.
    • Decompression sickness occurs when a diver ascends (depressurizes) too rapidly, causing nitrogen to expand in tissues and form gas emboli.
    • Clinical features of decompression sickness: muscle and joint pain, respiratory distress, infarctions in various tissues.

    Amniotic Fluid Embolism

    • A grave but uncommon complication of labor.
    • Caused by the infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins.
    • Clinical features: sudden severe dyspnea, cyanosis, hypotensive shock, seizures, and coma. Long-term effects include pulmonary edema and DIC.

    Ischemia

    • Inadequate blood supply to an area of tissue.

    Causes of Ischemia

    • Thrombotic or embolic mechanism (99%)
    • Complicated atheroma
    • Twisting of a blood vessel
    • Compression from outside by a tumor or entrapment in a hernial sac
    • Venous obstruction in a varicose vein

    Effects of Ischemia

    • Variable depending on the adequacy of collateral circulation.
    • Good circulation: little or no effect.
    • Poor circulation: Functional disturbances or even cell death.
    • Ischemia in the heart: chest pain (angina)
    • Ischemia in the lower limbs: intermittent claudication (pain in the calf muscle during exercise)

    ### Infarction

    • Ischemic necrosis due to occlusion of either an artery or vein.

    Causes of Infarction

    • Thrombosis or embolism (99%)
    • Local vasospasm
    • Expansion of an atheroma
    • Extrinsic compression of a vessel (tumor, twisting, edema, hernia)
    • Traumatic rupture of a vessel

    Morphology of Infarction

    • Wedge shape, with the apex at the site of the occluded blood vessel and the periphery of the organ forming the base, which is poorly defined.
    • Dominant histological characteristic: ischemic coagulative necrosis.
    • With time, the edge becomes more defined by a narrow zone of hyperemia due to inflammation.
    • Pale infarcts become paler and sharply defined, while red infarcts become more firm and brown.
    • Septic infarcts result in abscess formation.

    Red Infarcts

    • Occur in the following situations:
      • Venous occlusion (testis, ovaries)
      • Loose tissue
      • Tissue with dual circulation
      • Previously congested tissue
      • Re-established blood flow

    White Infarcts

    • Occur following arterial occlusion in solid organs with end-arterial circulation.
    • Change to scar tissue over time.

    Factors That Influence Infarct Development

    • The consequences of vascular occlusion can range from no effect to death of tissue or even the individual.
    • Factors that influence the outcome include:
      • Anatomy of the vascular supply (for example, the presence or absence of alternative blood supply)
      • Rate of development of occlusion
      • Vulnerability to hypoxia
      • Oxygen content of blood

    Shock

    • A pathological state of life-threatening hypoperfusion of vital organs and cellular hypoxia, due to diminished cardiac output or reduced effective circulating blood volume, resulting in hypotension, impaired tissue perfusion, and cellular hypoxia.
    • Initially, cellular injury is reversible; but if shock is sustained, it leads to cell death.

    Stages of Shock

    • Stage of Compensation (initial nonprogressive stage): decreased cardiac output causes reflex sympathetic stimulation leading to tachycardia and peripheral vasoconstriction, maintaining blood pressure in vital organs. Decreased urine output.
    • Stage of Impaired Tissue Perfusion (progressive stage): prolonged excessive vasoconstriction impairs tissue perfusion and oxygenation. This leads to anaerobic glycolysis, lactic acid production, lactic acidosis, cellular necrosis (especially in kidneys, lungs, and liver).

    Thrombosis

    • Thrombosis is the formation of a solid or semi-solid mass in the blood vessels during life due to inappropriate activation of hemostasis.
    • This mass is called a thrombus.
    • Virchow's Triad describes three contributing factors to thrombus formation:
      • Endothelial Injury: Mechanical injury, degeneration of vascular endothelium (atherosclerosis, aneurysm, myocardial infarction), inflammation (phlebitis, arteries, heart valves).
      • Alteration in Blood Flow: Turbulence (arterial and cardiac thrombosis), Stasis (venous thrombosis).
      • Blood Hypercoagulability: Primary causes (genetic) include antithrombin III deficiency, protein C deficiency. Secondary causes (acquired) include immobilization, myocardial infarction, heart failure, tissue damage, burns, oral contraceptive pill use, sickle cell anemia, leukemia, smoking.

    Fate of Thrombus

    • Propagation: The thrombus grows in size.
    • Embolization: Thrombus breaks off and travels to another location.
    • Dissolution: Thrombus is dissolved by the body.
    • Organization and Re-canalization: Formation of new blood vessels within the thrombus.
    • Calcification: Thrombus becomes hardened with calcium deposits.

    Morphology of Thrombus

    • Grossly and microscopically: Thrombi have distinct laminations (lines of Zahn) due to alternating pale layers of platelets and fibrin, and darker layers of red blood cells.
    • Arterial thrombi: Firmly attached to the wall, gray-white, friable.
    • Venous thrombi: Less firmly attached to the wall, red.
    • Post mortem clots: Gelatinous, dark red, not attached to the wall, lack lines of Zahn.
    • Mural thrombi: Found on the wall of heart chambers or in the aortic lumen.
    • Vegetations: Thrombi formed on heart valves.

    Disseminated Intravascular Coagulation (DIC)

    • DIC is a widespread fibrin thrombi formation in the micro-circulation, associated with platelet and coagulation protein consumption.
    • It is a complication of various conditions leading to widespread thrombin activation, including obstetrical complications, infections, and massive tissue injury.

    Embolism

    • An embolus is a detached solid, liquid, or gaseous mass carried by blood to a site distant from its origin.
    • Types of emboli: thromboemboli, fat and bone marrow, gas (air, nitrogen), atheroemboli, tumor fragments, foreign bodies.

    Pulmonary Thromboembolism

    • Deep leg vein thrombi are the most common source.
    • Size of the embolus determines impact: occlusion of main pulmonary artery, saddle embolus, passage into smaller arterioles, entry into systemic circulation (paradoxical embolism).
    • Clinical consequences: Most emboli are silent, sudden death (acute corpulmonale), obstruction of medium-size arteries (pulmonary hemorrhage), obstruction of small endarterioles (infarction), multiple emboli (chronic corpulmonale).

    Systemic Thromboemboli

    • Originate from: intra-cardiac mural thrombi, aortic aneurysm, thrombi on ulcerated atherosclerotic plaques, fragmentation of valvular vegetations, paradoxical emboli.
    • Main sites involved: lower extremities, brain, intestines, kidneys, spleen, upper extremities.

    Fat Embolism

    • Result from: fractures of long bones, soft tissue trauma and burns.
    • Clinical features: pulmonary insufficiency, neurological symptoms, anemia, thrombocytopenia.

    Gas Embolism

    • Air enters the circulation during: obstetric procedures, chest wall injury.
    • More than 100 cc of air is required for clinical effect.
    • Bubbles obstruct vessels, leading to infarction.

    Decompression Sickness

    • Gas embolism occurring in those exposed to sudden changes in atmospheric pressure.
    • High pressure breathing causes nitrogen to dissolve in blood and tissues.
    • Rapid depressurization leads to nitrogen expansion and bubble formation.
    • Clinical features: muscle and joint pain, respiratory distress, infarctions.

    Amniotic Fluid Embolism

    • Rare but grave complication of labor.
    • Infusion of amniotic fluid or fetal tissue into maternal circulation.
    • Clinical features: sudden severe dyspnea, cyanosis, hypotensive shock, seizure, coma.

    Ischemia

    • Inadequate blood supply to an area of tissue.
    • Causes: thrombotic or embolic mechanism, complicated atheroma, twisting of blood vessel, extrinsic compression, venous obstruction.
    • Effects: Variable depending on collateral circulation, functional disturbances, cell death.

    Infarction

    • Ischemic necrosis due to occlusion of an artery or vein.
    • Causes: thrombosis, embolism, vasospasm, atheroma expansion, extrinsic compression, traumatic rupture.
    • Morphology: Wedge-shaped, apex at occlusion site, base poorly defined, ischemic coagulative necrosis.
    • Red infarcts (hemorrhagic): venous occlusion, loose tissue, dual circulation.
    • White infarcts (anemic): arterial occlusion in solid organs with end-arterial circulation.

    Factors Influencing Infarct Development

    • Vascular supply: presence of alternative blood supply.
    • Rate of occlusion development: allows time for collateral circulation.
    • Vulnerability to hypoxia: neurons, myocardial cells have different tolerance to hypoxia.
    • Oxygen content of blood: low oxygen increases infarction extent.

    Shock

    • Pathological hypoperfusion of vital organs due to decreased cardiac output or reduced blood volume.
    • Causes: decreased cardiac output, reduced circulating blood volume.
    • Stages:
      • Compensation: Reflex sympathetic stimulation, tachycardia, vasoconstriction.
      • Impaired Tissue Perfusion: Prolonged vasoconstriction, impaired tissue perfusion and oxygenation, anaerobic glycolysis, lactic acidosis, cell necrosis, acute renal failure, shock lung (ARDS).

    Thrombosis

    • The pathological counterpart of Hemostasis is Thrombosis: The formation of a mass (thrombus) within the vascular system due to inappropriate activation of hemostasis.
    • Virchow's Triad (three predisposing factors for thrombus formation):
      • Endothelial Injury:
        • Mechanical - pressure, rupture, torsion of vessel
        • Degeneration - atherosclerosis, aneurysm, myocardial infarction
        • Inflammatory - phlebitis, arteries, heart valves
      • Alteration in Normal Blood Flow:
        • Turbulence - Arterial and cardiac thrombosis
        • Stasis - Venous thrombosis
        • Effects: endothelial injury, platelets contact w/ endothelium, prevents dilution of clotting factors, retards clotting factor inhibitors, promotes endothelial cell activation
      • Blood Hypercoagulability:
        • Primary (Genetic): antithrombin III deficiency, protein C deficiency
        • Secondary (Acquired): immobilization, MI, HF, tissue damage, burns, cancer, sickle cell anemia, leukemia, smoking

    Fate of Thrombus

    • Propagation: thrombus grows
    • Embolization: thrombus detaches
    • Dissolution: thrombus breaks down
    • Organization and re-canalization: new tissue replaces thrombus
    • Calcification: thrombus hardens

    Morphology of Thrombus

    • Grossly and Microscopically: Laminations (Lines of Zahn) - alternating pale layers of platelets w/ fibrin and darker layers of red cells.
    • Arterial Thrombi: usually occlusive, firmly attached, gray-white, friable.
    • Venous Thrombi: almost always occlusive, less firmly attached, red.
    • Post mortem Clots: gelatinous, dark red, not attached, lack lines of Zahn.
    • Mural Thrombi: attached to the wall of the heart chambers (in the aortic lumen).
    • Vegetations: thrombi formed on heart valves.

    Disseminated Intravascular Coagulation (DIC)

    • Sudden or insidious onset of widespread fibrin thrombi formation in microcirculation.
    • Rapid consumption of platelets and coagulation proteins (consumption coagulopathy).
    • Activation of fibrinolytic mechanisms ---> serious bleeding disorders.
    • Not a primary disease, but a complication of many conditions that activate thrombin: obstetrical complications, infections, massive tissue injury.

    Embolism

    • Detached intravascular solid, liquid, or gaseous mass, carried to a site distant from its origin.
    • Types of Embolism:
      • Thrombo-emboli
      • Fat and bone marrow
      • Gas (air, nitrogen)
      • Athero-emboli
      • Tumor fragments
      • Foreign body (bullet)

    Pulmonary Thrombo-Embolism

    • Most frequently originates from deep leg vein thrombi.
    • Size determines impact: occludes pulmonary artery, impacts bifurcation (saddle embolus), travels into smaller arterioles, or enters systemic circulation (paradoxical embolus).
    • Clinical consequences:
      • Most are silent (asymptomatic)
      • Sudden death (acute corpulmonale)
      • Obstruction of medium-size arteries ---> pulmonary hemorrhage
      • Obstruction of small endarterioles ---> infarction
      • Multiple emboli over time ---> chronic corpulmonale

    Systemic Thrombo-Embolism

    • Origin:
      • Intra-cardiac mural thrombi (89%)
      • Aortic aneurysm
      • Thrombi on ulcerated atherosclerotic plaques
      • Fragmentation of valvular vegetations
      • Paradoxical emboli
      • 15% unknown origin
    • Main sites:
      • Lower extremities (75%)
      • Brain (10%)
      • Intestines
      • Kidneys
      • Spleen
      • Upper extremities

    Fat Embolism

    • Results from:
      • Fractures of long bones (most common)
      • Soft tissue trauma and burns (rare)
    • Clinical features:
      • Pulmonary insufficiency
      • Neurologic symptoms
      • Anemia
      • Thrombocytopenia
      • Symptoms appear within 1 to 3 days

    Gas Embolism (Decompression Sickness)

    • Air enters circulation during:
      • Obstetric procedures
      • Chest wall injury
      • More than 100 cc to cause clinical effect.
      • Bubbles physically obstruct vessels ---> infarction
    • Cause: Exposure to sudden changes in atmospheric pressure (deep sea divers)
    • High pressure breathing dissolves nitrogen in blood and tissues.
    • Rapid ascent (depressurization) causes nitrogen to expand, forming gas emboli.
    • Clinical symptoms:
      • Muscle and joint pain
      • Respiratory distress
      • Infarctions in various tissues

    Amniotic Fluid Embolism

    • Grave, uncommon complication of labor.
    • Amniotic fluid or fetal tissue enters maternal circulation through a tear in placental membranes or rupture of uterine veins.
    • Clinical manifestations:
      • Sudden severe dyspnea
      • Cyanosis
      • Hypotensive shock
      • Seizures
      • Coma
      • Pulmonary edema and DIC if patient survives.

    Ischemia

    • Inadequate blood supply to an area of tissue.
    • Causes:
      • Thrombotic or embolic mechanism (99%)
      • Complicated atheroma (hemorrhage)
      • Twisting of blood vessel
      • Compression from outside (tumor, entrapment in hernia)
      • Venous obstruction (varicose vein)

    Effects of Ischemia

    • Depend on collateral circulation:
      • Good collateral: minimal or no effect
      • Poor collateral: Functional disturbances or cell death
    • Ischemia in the heart leads to (Angina) chest pain
    • Ischemia in lower limbs leads to (Intermittent claudication) pain in calf during exercise

    Infarction

    • Ischemic necrosis due to occlusion of an artery or vein.
    • Causes:
      • Thrombosis or embolism (99%)
      • Local vasospasm
      • Expansion of atheroma
      • Extrinsic compression of vessel (tumor, twisting, edema, hernia)
      • Traumatic rupture of vessel

    Morphology of Infarcts

    • Wedge shape:
      • Apex at occluded blood vessel
      • Base at organ periphery
    • Histological hallmark: Ischemic coagulative necrosis.
    • Edge: narrow zone of hyperemia due to inflammation.
    • Pale infarction: pales and sharply defined over time.
    • Red infarction: becomes firmer and brown over time.
    • Septic infarcts: abscess formation.

    Red Infarct (Hemorrhagic)

    • Occur when:
      • Venous occlusion (testis, ovaries)
      • Loose tissue
      • Tissue with dual circulation
      • Previously congested tissue
      • Re-established blood flow

    White Infarct (Anemic)

    • Occur due to arterial occlusion in solid organs with end arterial circulation.
    • Change into scar tissue with time.

    Factors Influencing Infarct development

    • Anatomy of Vascular Supply:
      • Dual blood supply (lungs): obstruction less damaging until bronchial artery also blocked.
      • End-arterial circulation (kidney, spleen): arterial obstruction ---> infarction.
    • Rate of Development of Occlusion:
      • Slow development allows time for collateral circulation (e.g., coronary artery anastomosis).
    • Vulnerability to Hypoxia:
      • Neurons: Irreversible damage after 3-4 minutes.
      • Myocardial cells: withstand ischemia for 20-30 minutes.
      • Fibroblasts: remain viable for hours after ischemia.
    • Oxygen Content of Blood:
      • Low blood oxygen increases infarct extent and vulnerability.

    Shock

    • Life-threatening state of hypoperfusion and cellular hypoxia.
    • Causes:
      • Diminished cardiac output or reduced effective circulating blood volume.
    • Leads to:
      • Hypotension
      • Impaired tissue perfusion
      • Cellular hypoxia
    • Initial cellular injury is reversible, but sustained shock leads to cell death.

    Stages of Shock

    • Stage of Compensation (Initial Nonprogressive Stage)
      • Reflex sympathetic stimulation from decreased cardiac output.
      • Tachycardia (increased heart rate)
      • Peripheral vasoconstriction maintaining blood pressure in vital organs (brain, myocardium).
      • Vasoconstriction in renal arterioles decreases glomerular filtration rate ---> oliguria.
    • Stage of Impaired Tissue Perfusion (Progressive Stage)
      • Prolonged vasoconstriction impairs tissue perfusion and oxygenation.
      • Anaerobic glycolysis ---> lactic acid production and lactic acidosis.
      • Cell necrosis most apparent in the kidneys:
        • Acute renal tubular necrosis
        • Acute renal failure
      • In the lungs:
        • Hypoxia ---> acute alveolar damage with intraalveolar edema, hemorrhage, and hyaline membranes (Shock lung or adult respiratory distress syndrome)
      • In the liver:
        • Anoxic necrosis of central regions of hepatic lobules.

    Thrombosis

    • Formation of a solid or semi-solid mass from blood constituents within the vascular system
    • Inappropriate activation of hemostasis
    • Thrombus is the name given to the mass
    • Three predisposing factors for thrombus formation: Virchow's triad
      • Endothelial injury
      • Stasis or turbulence of blood flow
      • Blood hypercoagulability
    • Endothelial injury:
      • Mechanical injury: pressure, rupture, torsion
      • Degeneration of vascular endothelium: atherosclerosis, aneurysms, myocardial infarction
      • Inflammatory processes: phlebitis, arteries, heart valves
    • Alteration in normal blood flow:
      • Turbulence: arterial and cardiac thrombosis
      • Stasis: venous thrombosis
      • Disrupts laminar flow, brings platelets into contact with endothelium
      • Prevents dilution of activated clotting factors
      • Retards inflow of clotting factor inhibitors
      • Promotes endothelial cell activation
    • Blood hypercoagulability:
      • Primary causes (genetic): antithrombin III deficiency, protein C deficiency
      • Secondary causes (acquired): immobilization, MI, HF, tissue damage, burns, OCCP, sickle cell anemia, leukemia, smoking

    Fate of Thrombus

    • Propagation
    • Embolization
    • Dissolution
    • Organization and recanalization
    • Calcification

    Morphology of Thrombus

    • Grossly and microscopically: apparent laminations (lines of Zahn)
      • Alternating pale layers of platelets with fibrin
      • Darker layers of red cells
    • Arterial thrombi:
      • Usually occlusive, firmly attached to the wall
      • Gray-white and friable
    • Venous thrombi:
      • Almost invariably occlusive, less firmly attached to the wall
      • Red
    • Post-mortem clots:
      • Gelatinous, dark red, usually not attached to the wall
      • Lack lines of Zahn
    • Mural thrombi:
      • Attached to the wall of the heart chambers or in the aortic lumen
    • Vegetations:
      • Thrombi formed on heart valves

    Disseminated Intravascular Coagulation (DIC)

    • Sudden or insidious onset of widespread fibrin thrombi formation in the microcirculation
    • Associated with rapid consumption of platelets and coagulation proteins (consumption coagulopathy)
    • Activation of fibrinolytic mechanisms leads to serious bleeding disorders
    • Not a primary disease, but a complication of many conditions
    • Common underlying cause: widespread activation of thrombin
    • Examples: obstetrical complications, infections, massive tissue injury

    Embolism

    • Detached intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin
    • Types:
      • Thromboembolism
      • Fat and bone marrow
      • Gas (air, nitrogen)
      • Atheroembolism
      • Tumor fragments
      • Foreign body

    Pulmonary Thromboembolism

    • Deep leg vein thrombi are usually the source
    • Size of embolus determines the impact:
      • Occlusion of main pulmonary artery
      • Impact across the bifurcation (saddle embolus)
      • Pass into smaller arterioles
      • Enter the systemic circulation (paradoxical embolism)
    • Clinical consequences:
      • Most pulmonary emboli are silent
      • Sudden death (acute corpulmonale)
      • Obstruction of medium-size arteries: pulmonary hemorrhage
      • Obstruction of small endarterioles: infarction
      • Multiple emboli over time: chronic corpulmonale

    Systemic Thromboembolism

    • Origin:
      • Intra-cardiac mural thrombi (89% of emboli)
      • Aortic aneurysm
      • Thrombi on ulcerated atherosclerotic plaques
      • Fragmentation of valvular vegetations
      • Paradoxical emboli
      • 15% of unknown origin
    • Main sites involved:
      • Lower extremities (75%)
      • Brain (10%)
      • Intestines
      • Kidneys
      • Spleen
      • Upper extremities

    Fat Embolism

    • Causes:
      • Fractures of long bones (most common)
      • Soft tissue trauma and burns (rare)
    • Clinical features:
      • Pulmonary insufficiency
      • Neurologic symptoms
      • Anemia
      • Thrombocytopenia
    • Symptoms appear within 1 to 3 days

    Gas Embolism

    • Air may enter the circulation during:
      • Obstetric procedures
      • Chest wall injury
    • More than 100 cc air is required to have clinical effect
    • Bubbles physically obstruct vessels, leading to infarction
    • Cause of decompression sickness in deep sea divers

    Amniotic Fluid Embolism

    • Grave but uncommon complication of labor
    • Infusion of amniotic fluid or fetal tissue into the maternal circulation
    • Occurs via tear in the placental membranes or rupture of uterine veins
    • Clinical features:
      • Sudden severe dyspnea
      • Cyanosis
      • Hypotensive shock
      • Seizure and coma
    • If the patient survives, pulmonary edema and DIC develop

    Ischemia

    • Inadequate blood supply to an area of tissue
    • Causes:
      • Thrombotic or embolic mechanism (99%)
      • Complicated atheroma
      • Twisting of blood vessels
      • Compression by tumor or entrapment in a hernial sac
      • Venous obstruction
    • Effect of ischemia:
      • Variable depending on collateral circulation
      • Good collateral circulation: minimal effect
      • Poor collateral circulation: functional disturbances, cell death
      • Heart ischemia: chest pain (angina)
      • Lower limb ischemia: intermittent claudication

    Infarction

    • Ischemic necrosis due to occlusion of either artery or vein
    • Causes:
      • Thrombosis or embolism (99%)
      • Local vasospasm
      • Expansion of atheroma
      • Extrinsic compression of a vessel
      • Traumatic rupture of vessel
    • Morphology:
      • Wedge shape: apex at the site of occlusion, base at the periphery
      • Dominant histological characteristic: ischemic coagulative necrosis
      • Time progression:
        • Edge becomes more defined by hyperemia
        • Pale infarcts become paler and sharply defined
        • Red infarcts become firmer and brown
      • Septic infarcts: abscess formation

    Morphology of Infarcts

    • Red infarcts (hemorrhagic):
      • Venous occlusion (testis, ovaries)
      • Loose tissue
      • Tissue with dual circulation
      • Previously congested tissue
      • Re-established blood flow
    • White infarcts (anemic):
      • Arterial occlusion in solid organs with end-arterial circulation
      • Change into scar tissue over time

    Factors that Influence Infarct Development

    • Anatomy of vascular supply:
      • Presence or absence of alternative blood supply determines damage
      • Lungs have dual supply, obstruction of pulmonary artery won't cause severe damage until the bronchial artery is also blocked
      • Kidney and spleen have end-arterial circulation, any arterial obstruction leads to infarction
    • Rate of development of occlusion:
      • Slowly developing occlusion allows time for collateral circulation to open (e.g., coronary artery anastomosis)
    • Vulnerability to hypoxia:
      • Neurons undergo irreversible damage after 3-4 minutes of deprivation
      • Myocardial cells can withstand ischemia for 20-30 minutes
      • Fibroblasts within the myocardium can remain viable for hours
    • Oxygen content of blood:
      • Low blood oxygen increases extent and vulnerability of infarction

    Shock

    • Pathological state of life-threatening hypoperfusion of vital organs and cellular hypoxia
    • Due to diminished cardiac output or reduced effective circulating blood volume
    • Results in: hypotension, impaired tissue perfusion, cellular hypoxia
    • Initially, cellular injury is reversible, but sustained shock leads to cell death

    Stages of Shock

    • Stage of Compensation (initial nonprogressive stage):
      • Decreased cardiac output causes reflex sympathetic stimulation
      • Increased heart rate (tachycardia)
      • Peripheral vasoconstriction to maintain blood pressure in vital organs
      • Decreased urine output (oliguria) due to vasoconstriction in renal arterioles
    • Stage of Impaired Tissue Perfusion (progressive stage):
      • Prolonged vasoconstriction impairs tissue perfusion and oxygenation
      • Impaired tissue perfusion leads to:
        • Anaerobic glycolysis, lactic acid production, lactic acidosis
        • Cell necrosis:
          • Kidney: acute renal tubular necrosis, acute renal failure
          • Lung: acute alveolar damage, intraalveolar edema, hemorrhage, hyaline fibrin membranes (shock lung, ARDS)
          • Liver: anoxic necrosis of the central region of hepatic lobules

    Thrombosis

    • Thrombosis is a pathological process where a solid or semi-solid mass (thrombus) forms within the vascular system during life. It’s caused by inappropriate activation of hemostasis.
    • Virchow’s Triad outlines the three key factors contributing to thrombus formation:
      • Endothelial injury: Mechanical injury, degeneration from atherosclerosis, aneurysms, or inflammation. This exposes subendothelial ECM, promoting platelet adhesion.
      • Altered blood flow: Turbulence (arterial & cardiac thrombosis) and stasis (venous thrombosis) disrupt normal blood flow, causing endothelial injury, platelet contact, and reduced dilution of clotting factors.
      • Blood hypercoagulability: This can be primary (genetic) or secondary (acquired). Primary causes include antithrombin III, protein C, or protein S deficiencies. Secondary causes include immobilization, myocardial infarction, heart failure, tissue damage, burns, cancer, sickle cell anemia, leukemia, and smoking.

    Fate of a Thrombus

    • Propagation: The thrombus can grow in size.
    • Embolization: The thrombus can break off and travel through the bloodstream.
    • Dissolution: The thrombus can be dissolved by fibrinolysis.
    • Organization and recanalization: The thrombus can be replaced by fibrous tissue and may develop new channels for blood flow.
    • Calcification: The thrombus can become hardened by calcium deposits.

    Morphology of a Thrombus

    • Grossly and microscopically: Thrombi have apparent laminations (lines of Zahn) formed by alternating pale layers (platelets with fibrin) and darker layers (red blood cells).
    • Arterial Thrombi: Usually occlusive, firmly attached to the wall, gray-white, and friable.
    • Venous Thrombi: Almost invariably occlusive, less firmly attached to the wall, and red.
    • Post Mortem Clots: Gelatinous, dark red, not attached to the wall, and lack lines of Zahn.
    • Mural Thrombi: Attached to the wall of heart chambers or aortic lumen.
    • Vegetations: Thrombi formed on heart valves.

    Disseminated Intravascular Coagulation (DIC)

    • DIC is a complication of numerous conditions characterized by widespread fibrin thrombi formation in the microcirculation.
    • The underlying pathology is the rapid consumption of platelets and coagulation proteins (consumption coagulopathy), leading to activation of fibrinolytic mechanisms and a bleeding tendency.
    • DIC is not a disease but rather a complication, often triggered by widespread activation of thrombin, seen with conditions like obstetrical complications, infections, and massive tissue injury.

    Embolism

    • An embolus is a detached intravascular mass (solid, liquid, or gaseous) carried by blood to a location distant from its origin.
    • Types of emboli include:
      • Thromboemboli: Mostly originating from deep leg veins, they can occlude major arteries, impact at bifurcations (saddle emboli), pass into smaller arterioles, or even enter systemic circulation (paradoxical embolism).
      • Fat and bone marrow emboli: Often associated with fractures of long bones.
      • Gas emboli: Air or nitrogen bubbles entering circulation, particularly associated with decompression sickness, obstetric procedures, and chest wall injury.
      • Atheroemboli: Fragments of atherosclerotic plaque.
      • Tumor fragments: Portions of malignant tumors.
      • Foreign body emboli: Objects like bullets.

    Pulmonary Thromboembolism (PTE )

    • Deep leg vein thrombi are frequently the source of PTE. The size of the embolus determines the severity of the impact.
    • Clinical consequences of PTE depend on the size of the embolus:
      • Most pulmonary emboli are silent.
      • Sudden death (acute corpulmonale)
      • Obstruction of medium-size arteries leads to pulmonary hemorrhage.
      • Obstruction of small endarterioles leads to infarction.
      • Multiple emboli over time lead to chronic corpulmonale.

    Systemic Thromboemboli

    • Systemic thromboemboli can originate from:
      • Intracardiac mural thrombi (89% of emboli).
      • Aortic aneurysm.
      • Thrombi on ulcerated atherosclerotic plaques.
      • Fragmentation of valvular vegetations.
      • Paradoxical emboli.
      • 15% are of unknown origin.
    • Main sites involved in embolism:
      • Lower extremities (75%)
      • Brain (10%)
      • Intestines
      • Kidneys
      • Spleen
      • Upper extremities.

    Fat Embolism

    • Fat embolism can result from:
      • Fractures of long bones (most common).
      • Soft tissue trauma and burns (rare).
    • Clinical features:
      • Pulmonary insufficiency
      • Neurological symptoms
      • Anemia
      • Thrombocytopenia
      • Symptoms typically appear within 1 to 3 days.

    Gas Embolism (Decompression Sickness)

    • Air can enter the circulation during:
      • Obstetric procedures
      • Chest wall injury
    • If air is breathed at high pressure, a large amount of gas (nitrogen) dissolves in the blood and tissues.
    • If the diver ascends (depressurizes) too rapidly, nitrogen expands in tissues and bubbles out of solution, forming emboli.
    • This causes:
      • Muscle and joint pain
      • Respiratory distress
      • Infarctions in various tissues

    Amniotic Fluid Embolism

    • A rare but serious complication of labor.
    • Caused by amniotic fluid or fetal tissue entering the maternal circulation via a tear in the placental membranes or rupture of uterine veins.
    • Clinical features:
      • Sudden severe dyspnea
      • Cyanosis
      • Hypotensive shock
      • Seizures
      • Coma
    • If the patient survives, they may develop pulmonary edema and DIC.

    Ischemia

    • Insufficient blood supply to a tissue area.
    • Causes of ischemia:
      • Thrombosis or embolism (99%).
      • Complicated atheroma (with subsequent hemorrhage).
      • Twisting of blood vessels.
      • Extrinsic compression (tumor, entrapment).
      • Venous obstruction (varicose veins).
    • Effects of ischemia:
      • Varies depending on collateral circulation. Adequate collateral flow minimizes damage, while poor collateral flow can lead to functional disturbances or cell death.
      • Ischemia in the heart can cause chest pain (angina), while in the lower limb, it can cause intermittent claudication (calf pain during exercise).

    Infarction

    • Infarction is ischemic necrosis (cell death due to lack of blood supply). It occurs when the occlusion of an artery or vein deprives tissue of blood flow.
    • Causes of Infarction:
      • Thrombosis or embolism (99%).
      • Vasospasm (narrowing of blood vessels).
      • Atherosclerotic plaque expansion.
      • Extrinsic compression of a vessel (tumor, twisting, edema, hernia).
      • Traumatic rupture of a vessel.

    Morphology of Infarcts

    • Infarcts typically have a wedge shape, with the apex at the point of the blocked vessel and the base forming the periphery of the organ.
    • The primary histological feature is ischemic coagulative necrosis.
    • Changes over time:
      • The edge becomes more defined by a zone of hyperemia (excess blood flow) due to inflammation.
      • Pale infarcts become paler and sharply defined.
      • Red infarcts become more firm and brown.
      • Septic infarcts can develop into abscesses.

    Red vs. White Infarcts

    • Red infarcts (hemorrhagic): Occur in:

      • Venous occlusion (testis, ovaries).
      • Loose tissues.
      • Tissues with dual circulation.
      • Previously congested tissue.
      • If blood flow is re-established.

    • White infarcts (anemic): Occur in:

      • Arterial occlusion in solid organs with end-arterial circulation.
      • Eventually turn into scar tissue.

    Factors Influencing Infarct Development

    • The consequence of vascular occlusion can range from no significant effect to tissue death, even fatality.
    • Key influencing factors:
      • Vascular supply anatomy: Presence or absence of alternative blood supply determines a vessel's occlusion impact (lungs with dual supply are more resilient).
      • Rate of occlusion development: Slow occlusion allows for collateral circulation.
      • Tissue vulnerability to hypoxia: Neurons and myocardial cells have short tolerance to ischemia, while fibroblasts have greater tolerance.
      • Blood oxygen content: Low oxygen levels increase infarction vulnerability and extent.

    Shock

    • Shock is a life-threatening state of hypoperfusion (inadequate blood flow) to vital organs and cellular hypoxia.
    • Causes of shock:
      • Reduced cardiac output (heart's pumping ability).
      • Decreased effective circulating blood volume (hypovolemia).
    • Shock leads to hypotension (low blood pressure), impaired tissue perfusion, and cellular hypoxia.
    • Initial cellular injury can be reversible, but if shock persists, cell death occurs.

    Stages of Shock

    • Stage of Compensation (initial nonprogressive stage):

      • Decreased cardiac output triggers reflex sympathetic stimulation.
      • This increases heart rate (tachycardia) and vasoconstriction, maintaining blood pressure in vital organs (brain, heart).
      • Vasoconstriction in renal arterioles reduces glomerular filtration rate, resulting in decreased urine output (oliguria).

    • Stage of Impaired Tissue Perfusion (progressive stage):

      • Prolonged excessive vasoconstriction impairs tissue perfusion and oxygenation.
      • Impaired perfusion leads to anaerobic glycolysis, producing lactic acid and acidosis.
      • Cell necrosis occurs, particularly in the kidneys (acute tubular necrosis and renal failure).
      • In the lungs, hypoxia causes damage, leading to alveolar edema, hemorrhage, and hyaline membrane formation (shock lung or ARDS).
      • In the liver, anoxic necrosis of central hepatic lobules can occur.

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    Description

    Explore the critical factors involved in thrombosis formation, including endothelial injury and altered blood flow. Understand how Virchow's triad influences the development of thrombi and the implications for vascular health. This quiz will test your understanding of crucial concepts and mechanisms related to thrombosis.

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