Thrombosis and Emboli Lecture 12 PDF

Thrombosis and emboli processthat Peter Nagy thrombusforms thrombus Blooddotinsidebloodvessel  MECHANISMS OF THROMBUS PRODUCTION. ARTERIAL THROMBI Th A thrombus is any solid object developing from the blood in vivo within the vascular...

Thrombosis and emboli processthat Peter Nagy thrombusforms thrombus Blooddotinsidebloodvessel  MECHANISMS OF THROMBUS PRODUCTION. ARTERIAL THROMBI Th A thrombus is any solid object developing from the blood in vivo within the vascular system or heart. Thrombosis is hemostasis in the wrong place. Major components, forms: Tu platelet aggregates platelet/white thrombus a clotmostly clotted blood wecallit red thrombus mposedof fibrin fibrin thrombus lesscommonform pinkisheosinophilicmaterialundermicroscope  thrombusformation isverycommon Pathogenesis of thrombosis problemin there life are majorfactorswhichc ( triad) for contribute theformationofmom whichcalledvirchowstriad im Changes in the vascular wall (endothelial damage) e s Changes in flow (slow or turbulent flow) if onefactorpresentisnot enoughfor w.mg 3factorincreasethechanceofthrombusformation Changes in the blood (hypercoagulability) g it'llhappen highrisk grayzone high chance composition roofThrombosismay occur even if the triad is not complete, just two of the conditions suffice. slow or turbulent flow  damage Changes in the vascular wall I b mostImp t p Atherosclerotic plaques changeflowofblood Inflamed tissues, immunological reactions Necrotic tissues 8 ortumortissue inneighborhood ofbloodvessels ofthrombus Moechance Surgical interventions insertin or if aus after vascular sutures surgery vessels remove e ndothelia Special conditions (TTP) etnromboti.si insmallbloodvessels thebody throughout incaseofmyocardialinfarctionover theinfarctedmyocardium wefrequentlyseeanadditionalthrombusformation  undernormalconditionflowinbloodvessel laminar thrombusformation is hashighspeed ifitchanges frequent mayhappen in lowerextremities How Changes in flow I patient who is unable to leaave their bed a Sluggish flow (veins, bedridden patients, pregnancy) Turbulent flow atherosclerosisalso change theflows Laminar flows are smooth and streamlined, whereas turbulent flows are irregular and chaotic. A low Reynolds number indicates laminar flow while a high number indicates turbulent flow. The flow behavior drastically changes if it is laminar vs. turbulent.  Changes in blood changesin compositionofblood Antiphospholipid syndrome (APS), also known as Hughes syndrome, is an autoimmune disorder in which the immune system mistakenly produces antibodies that target certain proteins and fats found in the blood. These antibodies are collectively known as antiphospholipid antibodies. Antiphospholipid antibodies can cause abnormal blood clotting in arteries and veins, leading to a variety of health issues. autoimmunediseases e inthe Acquired changes (cancer, pregnancy, antiphospholipid syndrome) patients Inherited conditions (Leiden mutation etc.) Leiden mutation" refers to a specific genetic mutation known as Factor V Leiden. Factor V Leiden is a mutation in one of the clotting factors in the blood, known as Factor V. This genetic mutation is cancer associated with an increased risk of developing abnormal blood clots in veins, a condition known as venous thromboembolism (VTE). with people cancersuffer.ae uentywiththrombus.Bctumorceks canproducedifferentmaterial usually acinrichadenocarcinoma iftingproducemucine a tumors of iisomehowfind glandular awayto organs circulation promote thrombus formation regnang offemalehormonescausechanges increaselevel bloodcomposition of ompressionotvenacava sothrombus formationcanbefrequent guterusinlatepregnancy inpregnancy coronation slows down utoimmune disease alsopromotethrombusformation  Lines of Zahn are a characteristic microscopic feature of thrombi, speci cally arterial or cardiac thrombi, formed under conditions of blood ow. They appear as alternating layers or laminations within the thrombus and are indicative of its formation in a owing typical blood environment (as opposed to postmortem clots). Here's a detailed explanation: or Components of the Lines of Zahn: Steps of thrombus formation Pale Layers: Composed mainly of platelets and brin. These form during periods of higher blood ow when red blood cells are less likely to be trapped. Dark Layers: Rich in red blood cells (RBCs) and brin. These layers form during slower blood ow, allowing RBCs to become incorporated into the thrombus. Importance: Diagnostic Value: The presence of Lines of Zahn con rms that the thrombus formed in a living organism, as they result from the interaction of owing blood with the clotting process. It helps di erentiate between ante-mortem thrombi (formed before death) and post-mortem clots (which lack these layers and hav a "chicken fat" appearance). Pathophysiological Insight: Indicates the cyclical nature of clot formation, with alternating deposition of platelets and brin during phases of varying blood ow Platelet aggregation, activation Fibrin formation with entrapped red blood cells Platelet aggregation B D F Fey of formation layersin thrombus RIE Try Lines of Zahn The clotting stops at the level of the nearest branch, where flow dilutes the clotting factors.  Fates of a thrombus µ athrombussi joie coagulativecascade H Dissolves disappear by fibrinolyticcascade i I Propagation thrombuscanspread callitemboli we p blood Breakes off and forms embolus travel in Organizes Recanalization Calcification (phlebolith) v that ifthrombusnotdissolve e staysatlocation fibroblaste inflamatory it forms cellsmigrate tothrombus from thrombus transformstofibrotic of wall vessel tissue wecallit organization recanalization calcification stoneinreins forms  Types of thrombus.aspirin can decrease the risk of thrombus aggregation and is used in myocardial formmostlyinarteriescorona areresultof g infraction. aspirinisrecomendedtoprenen O Arterial thrombi ( white thrombi, mostlyTplatelet aggregation) aggregation soasprinisImpforprevention paotingof blood Venous thrombi (red thrombi, coagulation) wegiveheparintopreventclottingmyocardialinfarctionm fifthrombusisformedonayoe.uauaweisTaeduegea p Vegetations (thrombus on a cardiac valve) usuallyassociatedwithendocarditis infection promotes thrombus formation pthrombusformsymicrobiainfectionespreadinboy 0 Infected thrombi (spreading of infection) snows thrombus i ndifferent.ca er oninapersons.itsusaaiyasymptomoe.Ean s'paraneoplastiosyndroing e o Migrating thrombophlebitis (paraneoplasia) when sb has repeated thrombosis in different parts of body as the disease progress(first in leg and then arm then knee for example Tumor thrombus exinking tumors canspreadinbloodressei that c anspreadinuenacara O Fibrin thrombi (DIC) in microcirculation  weusuallyseethrombusinmicro circulation netinvena cavaheart fDisseminated intravascular coagulation (DIC) Acute chronic (haemorrhagic microthrombosis) oiaoi.pl i Acut (Gram negative sepsis, trauma, complications of birth, snake bite cess Chronic (Paraneoplasia) 1.Generalized activation of the clotting cascade canberesultofsepsisoranytypeofshock jated ferO2.g Fibrinolysis j i coagocativefactors 4 In DIC, brinolysis becomes excessively activated in response to the widespread formation of microvascular clots. This leads to the following complications: 1. Overactivation of Fibrinolysis: that'swhywe Consumptive coagulopathy get In DIC, massive clot formation in microcirculation activates the brinolytic system as the body attempts to dissolve these clots. hemorrhagicdiaptesis Excessive plasmin generation results in rapid breakdown of brin into brin degradation products (FDPs) and D- a dimers. I go f 2. Fibrinolytic Imbalance: WITH The balance between clot formation and clot breakdown is disrupted: The coagulation cascade continuously forms new clots. Fibrinolysis works overtime to dissolve these clots, but the clotting process overwhelms it. it www.piu.io This results in a vicious cycle of clot formation and dissolution. 3. Depletion of Clotting Factors: I in we Both clotting factors and platelets are consumed in this process, leading to: Consumptive Coagulopathy: Depletion of resources needed for clot formation. Bleeding: Excessive brinolysis increases bleeding risk as clots cannot stabilize e ectively. 4. Hemorrhagic Complications: High levels of plasmin cause: Degradation of brin clots needed to prevent bleeding. Inhibition of coagulation factors (like brinogen), further contributing to uncontrolled bleeding. Hemorrhagic diathesis (severe bleeding from multiple sites). 5. Fibrin Degradation Products (FDPs) and D-dimers: FDPs and D-dimers are by-products of brinolysis, commonly elevated in DIC and are used as diagnostic markers for the condition. Elevated levels indicate extensive clot breakdown and brinolytic activity. Conseqences of DIC cause I. Microvascular thrombosis (multifocal brain necroses, coma; superficial ulceration, gangrene of skin, mucous membranes; oliguria; ARDS) Blockmicrocirculation wecanseeerosioninskin II. Hemorrhagic diathesis (intracerebral bleeding; petechiae; Hemorrhagic diathesis, also known simply as bleeding diathesis, hematuria; epistaxis; GI bleeding)is a medical term used to describe a tendency or predisposition to bleed excessively or abnormally. People with hemorrhagic diathesis are more prone to spontaneous bleeding III. Microangiopathic hemolytic anemia microthrombi insmallvessels notcompleteblockage isverydifficultforrisatopass Most important clinical aspects of thrombosis e Acute myocardial infarction p Arterial occlusion (AMI, stroke) o Deep vein thrombosis (pulmonary emboli) E th Thrombophlebitis whenthrombuscombinedwithinflamation thrombuscanbeinfected inflamedatthe sametime Pylethrombosis (thrombus in vena portae) DIC consequence of deep vein thrombosis  Emboli havedifferenttypesofemboli e we EMBOLI are solid, liquid or gaseousi objects carried by the i blood that can not mix with the blood and that are large enough to become impacted in the arterial or capillary lumen. (Embolism can not occur in veins (except the portal vein) because venous blood flows from small to ever larger vessels) emboliwillstopsomewhere usuallywherewehavebifurcation soonly inarteriesBctheygetsmaller III  Routes of embolization stemicembolization Emboli arising in the left heart or in the aorta (systemic embolization) can end up anywhere in the body except the lung. asembolization Emboli coming from the peripheral veins or from the right heart end up in the lungs Paradoxical embolization: they come from the systemic veins but (instead of the lung) they embolize in systemic arteries. Patent foramen ovale IN 20% OF THE INDIVIDULES THIS OPENING REMAINS OPEN! Arteriovenous shunts of the lung D foramen inreallife Ovale wecannot recognizeit Types of emboli Thromboemboli Fat or bone marrow emboli Gas emboli Amniotic fluid emboli Atheroma emboli Brain emboli Therapeutic emboli  A thromboembolus, often referred to as a thromboemboli (plural), is a type of embolus composed of a blood clot (thrombus) that has formed in one part of the circulatory system and subsequently becomes dislodged, traveling through Thromboemboli the bloodstream until it becomes lodged in a narrower blood vessel. Thromboemboli are a common cause of vascular obstruction and can have serious medical consequences. ifwehavedeepveinthrombus stockin my pulmonaryembolization Pulmonary emboli (most of them are silent) most important complication/don't have that many symptoms(mostly Massive sudden death silent) Medium - Small branch - - pulmonary haemorrhage/infarction Repeated pulmonary hypertension Systemic emboli canblockcirculation Infarction/gangrene frequentlyin kidney spleen  CPR Fat/bone marrow emboli Cardiopulmonary resuscitation lesscommon CAUSES Etiology: bone fraction, liposuccion, CPR Complications: asymptomatic islifethreateninglunginjury ARDS acuterespiratorydistresssyndrome thatallowsfluidtoleakintothelungs breathingbecomedifficult Brain microinfarction eoxygen cannot getintothebody Petechiae thrombocytopenia  Gas emboli ifgasbubblesform inblood Etiology: neck trauma, during labor, Caisson syndrome Complications: ARDS Focal brain ischaemia Chronic form ischaemic bone necrosis champain gasdissolvewithhighpressure alotofbubble wedecreasepressure op a.m a s t ate e wit exdivingwhenwecometowatersurface v Kia if b ng wi embolism so go a ios  Amniotic fluid emboli Rare complication of child birth if amnioticfluid find awaytovain akin ARDS, DIC  Other obstacles of blood flow otherthan thrombus embolus related to OBSTRUCTION of small vessels in position of laying down for a long time and pressure from the weight of the body will compress the body and blood will be obstruction Arterial spasma cause implications Coronary spasm (Prinzmetal angina) Cerebral arterial spasm (TIA) phenomenon infemale Gcauses Booe blood decreased flow blood spasms the to f ingersin in casesitcauses some less flowto b lood ears toes nose nipples knees whionnappens vessels t hose areas spasm in to h appens response stresse motional upset vesselscan obstructfrom Obstruction by external compression outsidepressure canhappenintestineinintestine 7 Torsion twistingaroundaxis Increased pressure (pressure sores) can cause hemoragic infraction venus outflow is bloked ulcer inskin in bloodflowto pressure tagloss