Embolism (THROMBOEMBOLISM)
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This document discusses different types of embolism. An embolism occurs when a mass carried by the bloodstream partially or completely obstructs part of the cardiovascular system. Emboli can be solid, liquid, or gas. They can be infected or sterile. Sources of emboli include the heart, veins, arteries, capillaries and lymphatics. Common types discussed are thromboembolism, fat embolism, air embolism, and amniotic fluid embolism. The document outlines the causes, pathophysiology and potential effects of each type.
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Thrombosis
Thrombosis is the formation of a blood clot or thrombus within a blood vessel. It occurs through the interaction of platelets, clotting factors, and altered blood flow. Predisposing factors include injury to blood vessels, stasis or turbulence of blood flow, and hypercoagulability. The clotting process involves platelet adhesion and aggregation at the site of injury, activation of clotting factors, and conversion of fibrinogen to fibrin. Thrombi can cause downstream effects such as ischemia, infarction, embolism, or disseminated intravascular coagulation depending on their location within arteries or veins.
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Thrombosis is the formation of a solid blood clot or thrombus within a blood vessel. Virchow's triad describes the three main factors that predispose to thrombosis: endothelial injury, alterations in blood flow, and hypercoagulability. Thrombi can form in arteries or veins and may cause ischemia or embolism, respectively. The predisposing factors for thrombosis include both genetic deficiencies that increase coagulation as well as acquired conditions like prolonged immobilization, oral contraceptive use, and cancer.
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Thrombosis
Thrombosis is the formation of a blood clot or thrombus in the circulatory system. A thrombus forms when the normal balance between coagulation and fibrinolysis is disrupted, such as after an injury to the blood vessel wall. Virchow's triad describes the three main factors that contribute to thrombosis: endothelial injury, changes in blood flow, and hypercoagulability. Thrombi can form in the heart, arteries, veins, or microcirculation and may cause complications like ischemic injury, thromboembolism, or organ infarction if left untreated. The fate of a thrombus depends on whether it is resolved by fibrinolysis, organized by the body, continues to grow, or embol
Thrombosis
Thrombosis is the formation of a blood clot within blood vessels. A thrombus is a blood clot that forms at the site of endothelial injury or abnormal blood flow and can cause vascular obstruction. Virchow's triad describes the three main factors that contribute to thrombus formation: endothelial injury, abnormal blood flow, and hypercoagulability. Thrombi form in different locations depending on the underlying cause, and can propagate and embolize, becoming potentially life-threatening.
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Thrombosis is the formation of a blood clot within blood vessels. A thrombus is a blood clot that forms at the site of endothelial injury or abnormal blood flow and can cause vascular obstruction. Virchow's triad describes the three main factors that contribute to thrombus formation: endothelial injury, abnormal blood flow, and hypercoagulability. Thrombi form in different locations depending on the underlying cause, and can propagate and embolize, becoming potentially life-threatening.
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The document discusses thrombosis and thrombus formation. It defines thrombosis as the formation of a solid blood clot within the circulatory system. A thrombus is the blood clot itself. The key points covered include:
- Virchow's triad predisposes to clotting via endothelial injury, altered blood flow, and hypercoagulability.
- Platelets play a central role by adhering to injuries, releasing activation factors, and aggregating.
- The coagulation cascade is activated via intrinsic and extrinsic pathways ultimately forming fibrin.
- Stasis and turbulence promote clotting by slowing blood flow and pushing platelets to vessel walls.
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Approach to thrombosis_gow_edit (1)
Thrombosis is the formation of a blood clot inside a blood vessel. It can occur in veins or arteries. Venous thrombosis leads to congestion while arterial thrombosis affects blood supply. Treatment depends on the location and severity, and may include antiplatelets like aspirin, anticoagulants like warfarin, and fibrinolytic drugs to dissolve clots. Investigation involves tests like Doppler ultrasound, CT scans, and MRI to locate clots and determine treatment approach.
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The document discusses coagulation, the process by which blood clots. More than 30 cells and substances affect clotting, which is initiated by platelets and involves a complex series of reactions converting fibrinogen into fibrin to form a clot. Thrombosis occurs when a blood clot forms inside a blood vessel or heart, partially or completely blocking blood flow. Causes of clotting include the blood composition, vessel wall injuries, and blood flow issues. Clots are classified as venous, such as deep vein thrombosis, or arterial, like those causing strokes and myocardial infarctions when coronary arteries suddenly clog.
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The blood coagulation cascade involves three pathways that ultimately lead to the formation of a fibrin clot. The intrinsic pathway is activated by disturbances in blood and platelet phospholipids and involves multiple coagulation factors leading to the activation of factor X. The extrinsic pathway is initiated when tissue factor is released from injured endothelium, also activating factor X. The common pathway follows, where factor Xa converts prothrombin to thrombin which then cleaves fibrinogen to form fibrin, an essential component of a clot.
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Hemostasis and thrombosis involve the regulation of blood clotting. Normal hemostasis maintains blood fluidity but allows clotting at sites of injury. Thrombosis is pathological clotting in uninjured or minimally injured vessels. It involves platelet adhesion and activation, coagulation cascade activation, and fibrin clot formation. Counter-regulatory mechanisms normally limit clotting to the injury site. Abnormalities in blood components, vessel walls, or flow can cause hypercoagulability and thrombosis.
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17. A 64-year-old woman has had several episodes of transient ischemic attacks (TIAs).
Aspirin would be a preferred treatment, but she has a history of severe “aspirin
sensitivity” manifest as intense bronchoconstriction. Which group aspirin belongs to?
Side effects of aspirin. What would be a suitable alternative to the aspirin? Mechanism
of action of this drug, indications, routes of administration.
19. A 42-year-old man with an acute MI is treated with alteplase. What is the
mechanism of main desired effect? Which group drug belongs to? Routes of alteplase
administration. Mechanism of action and major indications. Which group and what
drugs may counteract effects of alteplase?
20. A 60-year-old woman with deep-vein thrombosis (DVT) is given a bolus of heparin,
and a heparin drip is also started. 30 min later, she is bleeding profusely from the
intravenous site. The heparin is stopped, but the bleeding continues. Which drug may
reverse the adverse effect of heparin? What is mechanism of heparin action? Side
effects of heparin and routes of administration. Which group heparin belongs to?
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The document discusses thrombosis and thrombus formation. It defines thrombosis as the formation of a solid blood clot within the circulatory system. A thrombus is the blood clot itself. The key points covered include:
- Virchow's triad predisposes to clotting via endothelial injury, altered blood flow, and hypercoagulability.
- Platelets play a central role by adhering to injuries, releasing activation factors, and aggregating.
- The coagulation cascade is activated via intrinsic and extrinsic pathways ultimately forming fibrin.
- Stasis and turbulence promote clotting by slowing blood flow and pushing platelets to vessel walls.
- Hypercoag
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Thrombosis is the formation of a blood clot inside a blood vessel. It can occur in veins or arteries. Venous thrombosis leads to congestion while arterial thrombosis affects blood supply. Treatment depends on the location and severity, and may include antiplatelets like aspirin, anticoagulants like warfarin, and fibrinolytic drugs to dissolve clots. Investigation involves tests like Doppler ultrasound, CT scans, and MRI to locate clots and determine treatment approach.
Thrombosis
Thrombosis occurs when an imbalance in the blood coagulation system causes a blood clot or thrombus to form, blocking blood flow through a vein or artery and posing health risks. A thrombus can detach and lodge in the lungs, causing a life-threatening pulmonary embolism. The normal response that prevents significant blood loss after an injury is called hemostasis, involving platelets, cells, and activation of coagulation factors to form a blood clot.
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Thrombosis is a condition where a blood clot forms inside a blood vessel, restricting or stopping blood flow. It has two main categories: venous thrombosis, where a clot forms in a vein, and arterial thrombosis, where a clot forms in an artery. Thrombosis can be caused by abnormalities in blood coagulation, injuries to blood vessels, or slowed blood flow. Risk factors include inherited blood disorders, prolonged bed rest, obesity, smoking, cancer, and pregnancy. Symptoms vary depending on the location and severity of the clot. Treatment involves anticoagulant medications, compression stockings, filters, endovascular procedures, or surgery.
Fondaparinux persent
The blood coagulation cascade involves three pathways that ultimately lead to the formation of a fibrin clot. The intrinsic pathway is activated by disturbances in blood and platelet phospholipids and involves multiple coagulation factors leading to the activation of factor X. The extrinsic pathway is initiated when tissue factor is released from injured endothelium, also activating factor X. The common pathway follows, where factor Xa converts prothrombin to thrombin which then cleaves fibrinogen to form fibrin, an essential component of a clot.
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Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel, obstructing blood flow. It can cause serious complications in organs like the brain and lungs. A thrombus forms through platelet adhesion and aggregation at the site of injury, followed by coagulation and fibrin formation around the platelet plug. Virchow's triad outlines the factors of abnormal blood flow, endothelial dysfunction, and hypercoagulability that contribute to thrombosis. Venous thrombosis typically occurs in the leg veins, while arterial thrombosis is often associated with atherosclerosis and causes such events as myocardial infarction.
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Atherosclerosis is a preventable and treatable condition where plaque builds up inside arteries. It is caused by damage to artery walls from factors like high blood pressure, high cholesterol, smoking, or diseases like diabetes. Plaque forms as an inflammatory response where modified lipoproteins and immune cells like macrophages accumulate in the artery wall. Over time, plaques can restrict blood flow or burst, causing blood clots. The response-to-injury hypothesis describes this process as chronic endothelial injury leading to lipoprotein accumulation and proliferation of smooth muscle cells and extracellular matrix in the artery wall. Atherosclerosis is diagnosed through medical tests and can be prevented through a healthy diet and lifestyle.
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Hemostasis and thrombosis involve the regulation of blood clotting. Normal hemostasis maintains blood fluidity but allows clotting at sites of injury. Thrombosis is pathological clotting in uninjured or minimally injured vessels. It involves platelet adhesion and activation, coagulation cascade activation, and fibrin clot formation. Counter-regulatory mechanisms normally limit clotting to the injury site. Abnormalities in blood components, vessel walls, or flow can cause hypercoagulability and thrombosis.
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This document discusses various hemodynamic disorders including edema, hyperemia, congestion, hemorrhage, hemostasis, thrombosis, embolism, infarction, and shock. Embolism can involve solid materials like thrombi, liquids like amniotic fluid, or gases like air. Embolisms are classified as systemic arterial, pulmonary, or venous and can cause vascular obstruction and infarction. Infarction results from ischemia and leads to coagulative necrosis, appearing as either red or white lesions. Septic shock is a type of shock caused by gram-positive bacteria through endotoxins like LPS, and can involve multiple organ failure.
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CIRCULATORY DISTURBANCES OF OBSTRUCTIVE NATURE - THROMBOSIS
Similar to Embolism (THROMBOEMBOLISM)
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This document summarizes different types of thrombosis and embolism. It discusses thrombosis, thrombus formation, and the coagulation cascade. It also covers different causes of endothelial injury that can lead to thrombosis, including atherosclerosis, hypertension, diabetes, and smoking. Alterations in blood flow that can promote thrombosis are turbulence, stasis, and hypercoagulability. The document outlines various types of embolism including thromboembolism, fat embolism, gas embolism, and amniotic fluid embolism. It provides details on the pathogenesis, clinical manifestations, and consequences of pulmonary thromboembolism and systemic arterial embolism.
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Aspirin would be a preferred treatment, but she has a history of severe “aspirin
sensitivity” manifest as intense bronchoconstriction. Which group aspirin belongs to?
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of action of this drug, indications, routes of administration.
19. A 42-year-old man with an acute MI is treated with alteplase. What is the
mechanism of main desired effect? Which group drug belongs to? Routes of alteplase
administration. Mechanism of action and major indications. Which group and what
drugs may counteract effects of alteplase?
20. A 60-year-old woman with deep-vein thrombosis (DVT) is given a bolus of heparin,
and a heparin drip is also started. 30 min later, she is bleeding profusely from the
intravenous site. The heparin is stopped, but the bleeding continues. Which drug may
reverse the adverse effect of heparin? What is mechanism of heparin action? Side
effects of heparin and routes of administration. Which group heparin belongs to?
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- 1. Presented by Dr. YOGITA CHANDRAKAR B.A.M.S., M.D. Assist. Professor Department of Rog Nidan Avum Vikriti Vigyan
- 2. Embolism is a process of partial or complete obstruction of some part of cardiovascular system by any mass carried in the circulation. The mass is detached from its site of origin known as Embolus. 4/22/2020 2DR.YOGITA CHANDRAKAR
- 3. Matter of Emboli – Solid, liquid, Gas Infection – Septic, Sterile Source – Cardiac, Venous, Arterial, Capillary, Lymphatic Flow of blood – Paradoxical and Retrograde 4/22/2020 3DR.YOGITA CHANDRAKAR
- 4. Solid – detached atheromatous plug, tumor cell, detach thrombi Liquid – fat globules, amniotic fluid, bone marrow embolism Gas – Air embolism Septic – Infected emboli Sterile – if not infected Cardiac – detached mural emboli Venous – comes from vein i.e. varicose vein Arterial – atheromatous plug Capillary – SCA Lymphatic – Filaria Paradoxical – venous to arterial and vice versa Retrogade – Against to flow of blood eg : prostate cancer to spine cancer 4/22/2020 4DR.YOGITA CHANDRAKAR
- 5. Detached thrombus These may arise in the arterial and venous circulation 2. Arterial thromboembolism – causes within the heart and artery Cardiomyopathy Detached mural thrombi ( Lt. atrium and ventricle) Haberdon’s nodule (distal phalanges) in OA Rheumatoid nodules in middle phalanges RHD 4/22/2020 5DR.YOGITA CHANDRAKAR
- 6. Ill effects – Infarction, Gangrene, Sudden death, MI, 2. Pulmonary / Venous thromboembolism - Obstruction of pulmonary arterial tree Deep and large vein of leg (DVT) Varicose vein Pathogenesis – Paradoxical (venous to artery) And Saddle embolism 4/22/2020 6DR.YOGITA CHANDRAKAR
- 7. Caused by fat lobules Etiology – 1. Traumatic - Bone fracture, Trauma of soft tissue 2. Nontraumatic – Extensive burn, DM, Fatty liver, Pancreatitis, SCA, Inflammation of bone and soft tissue 4/22/2020 7DR.YOGITA CHANDRAKAR
- 8. Pathogenesis – Mechanical theory (injury) Emulsion – instability theory (lipid fat emulsification inhibited) Intravascular coagulation theory (DIC) Toxic injury theory (free fatty acid increased in plasma ) Consequences – Pulmonary fat embolism Systemic fat embolism (Cerebral and Renal) Skin tensed (Marble skin) Conjunctival hemorrhage 4/22/2020 8DR.YOGITA CHANDRAKAR
- 9. Air, Nitrogen, and other gases bubbles produced in blood circulation and obstruct the flowing material and produce ischemic injury and death Air embolism – Artery and vein Venous air embolism – Surgical procedure of head, neck and trauma case and obstetrical surgery (CS delivery – its fatal) I/V infusion of blood and fluid Angiography (during entering of dyes) 4/22/2020 9DR.YOGITA CHANDRAKAR
- 10. Effects – Depends upon the amount of air bubbles (100-150ml) Rapidity of entry Position of air Patient’s condition Arterial air embolism – cardiothoracic surgery, decompression air sickness, paradoxical Amniotic fluid embolism – drain is not properly performed and goes in mother circulation 4/22/2020 10DR.YOGITA CHANDRAKAR