Thrombosis – Disease Backgrounder
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Disseminated Intravascular Coagulation (DIC) and Thrombosis: the Critical Role of the Lab Paul Riley, Phd, MBA, Diagnostica Stago, Inc
Generate Knowledge Disseminated Intravascular Coagulation (DIC) and Thrombosis: The Critical Role of the Lab Paul Riley, PhD, MBA, Diagnostica Stago, Inc. Learning Objectives Describe the basic pathophysiology of DIC Demonstrate a diagnostic and management approach for DIC Compare markers of thrombin & plasmin generation in DIC, including D-Dimer, fibrin monomers (FM; aka soluble fibrin monomers, SFM), and fibrin degradation products (FDPs; aka fibrin split products, FSPs) Correlate DIC theory and testing to specific clinical cases DIC = Death is Coming What is Hemostasis? Blood Circulation Occurs through blood vessels ARTERIES The heart pumps the blood Arteries carry oxygenated blood away from the heart under high pressure VEINS Veins carry de-oxygenated blood back to the heart under low pressure Hemostasis The mechanism that maintains blood fluidity Keeps a balance between bleeding and clotting 2 major roles Stop bleeding by repairing holes in blood vessels Clean up the inside of blood vessels Removes temporary clot that stopped bleeding Sweeps off needless deposits that may cause blood flow blockages Two Major Diseases Linked to Hemostatic Abnormalities Bleeding = Hemorrhage Blood clot = Thrombosis Physiology of Hemostasis Wound Sealing break in vesselEFFRAC PRIMARY PLASMATIC HEMOSTASIS COAGULATION strong clot wound sealing blood FIBRINOLYSIS flow ± stopped clot destruction The Three Steps of Hemostasis Primary Hemostasis Interaction between vessel wall, platelets and adhesive proteins platelet clot Coagulation Consolidation -
Lower Extremity Deep Venous Thrombosis
SECTION 5 Vascular System CHAPTER 34 Lower Extremity Deep Venous Thrombosis Ariel L. Shiloh KEY POINTS • Providers can accurately detect lower extremity deep venous thrombosis with point-of- care ultrasound after limited training. • Compression ultrasound exams are as accurate as traditional duplex and triplex vascular ultrasound exams. • Compression ultrasound exam at only two sites, the common femoral vein and popliteal vein, permits rapid and accurate assessment of deep venous thrombosis. Background care providers can perform lower extremity compression ultrasonography exams rapidly Venous thromboembolic disease (VTE) is a and with high diagnostic accuracy to detect common cause of morbidity and mortality in DVT. 7–13 A meta-analysis of 16 studies showed hospitalized patients and is especially preva- that point-of-care ultrasound can accurately lent in critically ill patients.1–3 Approximately diagnose lower extremity DVTs with a pooled 70% to 90% of patients with an identified source sensitivity of 96% and specificity of 97%.14 of pulmonary embolism (PE) have a proxi- Traditional vascular studies, the duplex mal lower extremity deep venous thrombosis and triplex exams, use a combination of (DVT). Conversely, 40% to 50% of patients two-dimensional (2D) imaging with compres- with a proximal DVT have a concurrent pul- sion along with the use of color and/or spectral monary embolism at presentation, and simi- Doppler ultrasound. More recent studies have larly, in only 50% of patients presenting with a demonstrated that 2D compression ultrasound PE can a DVT be found.4–6 exams alone yield similar accuracy as tradi- Point-of-care ultrasound is readily available tional duplex or triplex vascular studies.9,11,15–17 as a diagnostic tool for VTE. -
Difference Between Vein and Venule Key Difference - Vein Vs Venule
Difference Between Vein and Venule www.differencebetween.com Key Difference - Vein vs Venule The veins are the blood vessels that carry blood towards the heart. It always has a low blood pressure. Except the pulmonary and the umbilical veins, all the remaining veins carry the deoxygenated blood. On the contrary, the arteries carry blood away from the heart. The veins have valves in them to prevent the black flow of blood and to maintain unidirectional blood flow. They are less muscular, larger and are located closer to the skin. Venules are very smaller veins. They are the ones that collect blood from the capillaries. The collected blood will be directed to the larger and medium veins where the blood is transported towards the heart again. Many venules unite to form larger veins. The key difference between Vein and Venule is, the vein is a larger blood vessel that carries blood towards the heart while, the venule is a smaller minute blood vessel that drains blood from capillaries to the veins. What is a Vein? The veins are larger blood vessels present in throughout the body. The main function of veins is to carry oxygen-poor blood back into the heart. Veins are classified into some categories such as, superficial veins, pulmonary veins, deep veins, perforator veins, communicating veins and systematic veins. The wall of the vein is thinner and less elastic than the wall of an artery. The walls of the veins consist three layers of tissues which are named as tunica externa, tunica media, and tunica intima. Veins also have larger and irregular lumen. -
Peripheral Vascular Disease (PVD) Fact Sheet
FACT SHEET FOR PATIENTS AND FAMILIES Peripheral Vascular Disease (PVD) What is peripheral vascular disease? Vascular disease is disease of the blood vessels (arteries and veins). Peripheral vascular disease (PVD) affects The heart receives blood, the areas that are “peripheral,” or outside your heart. sends it to The most common types of PVD are: the lungs to get oxygen, • Carotid artery disease affects the arteries and pumps that carry blood to your brain. It occurs when it back out. one or more arteries are narrowed or blocked by plaque, a fatty substance that builds up inside artery walls. Carotid artery disease can increase Veins carry Arteries carry your risk of stroke. It can also cause transient blood to your oxygen-rich [TRANZ-ee-ent] ischemic [iss-KEE-mik] attacks (TIAs). heart to pick blood from up oxygen. your heart TIAs are temporary changes in brain function to the rest of that are sometimes called “mini-strokes.” your body. • Peripheral arterial disease (PAD) often affects the arteries to your legs and feet. It is also caused by Healthy blood vessels provide oxygen plaque buildup, and can for every part of your body. cause pain that feels like a dull cramp or heavy tiredness in your hips or legs when • Venous insufficiency affects the veins, usually you exercise or climb stairs. in your legs or feet. Your veins have valves that This pain is sometimes Damaged Healthy keepvalve blood fromvalve flowing backward as it moves called claudication. If PAD toward your heart. If the valves stop working, blood worsens, it can cause cold Plaque can build backs up in your body, usually in your legs. -
Anatomy of the Large Blood Vessels-Veins
Anatomy of the large blood vessels-Veins Cardiovascular Block - Lecture 4 Color index: !"#$%&'(& !( "')*+, ,)-.*, $()/ Don’t forget to check the Editing File !( 0*"')*+, ,)-.*, $()/ 1$ ($&*, 23&%' -(0$%"'&-$(4 *3#)'('&-$( Objectives: ● Define veins, and understand the general principles of venous system. ● Describe the superior & inferior Vena Cava and their tributaries. ● List major veins and their tributaries in the body. ● Describe the Portal Vein. ● Describe the Portocaval Anastomosis Veins ◇ Veins are blood vessels that bring blood back to the heart. ◇ All veins carry deoxygenated blood. with the exception of the pulmonary veins(to the left atrium) and umbilical vein(umbilical vein during fetal development). Vein can be classified in two ways based on Location Circulation ◇ Superficial veins: close to the surface of the body ◇ Veins of the systemic circulation: NO corresponding arteries Superior and Inferior vena cava with their tributaries ◇ Deep veins: found deeper in the body ◇ Veins of the portal circulation: With corresponding arteries Portal vein Superior Vena Cava ◇Formed by the union of the right and left Brachiocephalic veins. ◇Brachiocephalic veins are formed by the union of internal jugular and subclavian veins. Drains venous blood from : ◇ Head & neck ◇ Thoracic wall ◇ Upper limbs It Passes downward and enter the right atrium. Receives azygos vein on its posterior aspect just before it enters the heart. Veins of Head & Neck Superficial veins Deep vein External jugular vein Anterior Jugular Vein Internal Jugular Vein Begins just behind the angle of mandible It begins in the upper part of the neck by - It descends in the neck along with the by union of posterior auricular vein the union of the submental veins. -
Heart – Thrombus
Heart – Thrombus Figure Legend: Figure 1 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study. A thrombus is present in the right atrium (arrow). Figure 2 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study (higher magnification of Figure 1). Multiple layers of fibrin, erythrocytes, and scattered inflammatory cells (arrows) comprise this right atrial thrombus. Figure 3 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study. A large thrombus with two foci of mineral fills the left atrium (arrow). Figure 4 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study (higher magnification of Figure 3). This thrombus in the left atrium (arrows) has two dark, basophilic areas of mineral (arrowheads). 1 Heart – Thrombus Comment: Although thrombi can be seen in the right (Figure 1 and Figure 2) or left (Figure 3 and Figure 4) atrium, the most common site of spontaneously occurring and chemically induced thrombi is the left atrium. In acute situations, the lumen is distended by a mass of laminated fibrin layers, leukocytes, and red blood cells. In more chronic cases, there is more organization of the thrombus (e.g., presence of vascularized fibrous connective tissue, inflammation, and/or cartilage metaplasia), with potential attachment to the atrial wall. Spontaneous rates of cardiac thrombi were determined for control Fischer 344 rats and B6C3F1 mice: in 90-day studies, 0% in rats and mice; in 2-year studies, 0.7% in both genders of mice, 4% in male rats, and 1% in female rats. -
Incidence of Deep Venous Thrombosis and Stratification of Risk Groups in A
ORIGINAL ARTICLE Incidence of deep venous thrombosis and stratification of risk groups in a university hospital vascular surgery unit Incidência de trombose venosa profunda e estratificação dos grupos de risco em serviço de cirurgia vascular de hospital universitário 1 1 1 2 Alberto Okuhara *, Túlio Pinho Navarro , Ricardo Jayme Procópio , José Oyama Moura de Leite Abstract Background: There is a knowledge gap with relation to the true incidence of deep vein thrombosis among patients undergoing vascular surgery procedures in Brazil. This study is designed to support the implementation of a surveillance system to control the quality of venous thromboembolism prophylaxis in our country. Investigations in specific institutions have determined the true incidence of deep vein thrombosis and identified risk groups, to enable measures to be taken to ensure adequate prophylaxis and treatment to prevent the condition. Objective: To study the incidence of deep venous thrombosis in patients admitted to hospital for non-venous vascular surgery procedures and stratify them into risk groups. Method: This was a cross-sectional observational study that evaluated 202 patients from a university hospital vascular surgery clinic between March 2011 and July 2012. The incidence of deep venous thrombosis was determined using vascular ultrasound examinations and the Caprini scale. Results: The mean incidence of deep venous thrombosis in vascular surgery patients was 8.5%. The frequency distribution of patients by venous thromboembolism risk groups was as follows: 8.4% were considered low risk, 17.3% moderate risk, 29.7% high risk and 44.6% were classified as very high risk. Conclusion: The incidence of deep venous thrombosis in vascular surgery patients was 8.5%, which is similar to figures reported in the international literature. -
Thrombotic Thrombocytopenic Purpura
Thrombotic thrombocytopenic Purpura Flora Peyvandi Angelo Bianchi Bonomi Hemophilia and Thrombosis Center IRCCS Ca’ Granda Ospedale Maggiore Policlinico University of Milan Milan, Italy Disclosures Research Support/P.I. No relevant conflicts of interest to declare Employee No relevant conflicts of interest to declare Consultant Kedrion, Octapharma Major Stockholder No relevant conflicts of interest to declare Speakers Bureau Shire, Alnylam Honoraria No relevant conflicts of interest to declare Scientific Advisory Ablynx, Shire, Roche Board Objectives • Advances in understanding the pathogenetic mechanisms and the resulting clinical implications in TTP • Which tests need to be done for diagnosis of congenital and acquired TTP • Standard and novel therapies for congenital and acquired TTP • Potential predictive markers of relapse and implications on patient management during remission Thrombotic Thrombocytopenic Purpura (TTP) First described in 1924 by Moschcowitz, TTP is a thrombotic microangiopathy characterized by: • Disseminated formation of platelet- rich thrombi in the microvasculature → Tissue ischemia with neurological, myocardial, renal signs & symptoms • Platelets consumption → Severe thrombocytopenia • Red blood cell fragmentation → Hemolytic anemia TTP epidemiology • Acute onset • Rare: 5-11 cases / million people / year • Two forms: congenital (<5%), acquired (>95%) • M:F ratio 1:3 • Peak of incidence: III-IV decades • Mortality reduced from 90% to 10-20% with appropriate therapy • Risk of recurrence: 30-35% Peyvandi et al, Haematologica 2010 TTP clinical features Bleeding 33 patients with ≥ 3 acute episodes + Thrombosis “Old” diagnostic pentad: • Microangiopathic hemolytic anemia • Thrombocytopenia • Fluctuating neurologic signs • Fever • Renal impairment ScullyLotta et et al, al, BJH BJH 20122010 TTP pathophysiology • Caused by ADAMTS13 deficiency (A Disintegrin And Metalloproteinase with ThromboSpondin type 1 motifs, member 13) • ADAMTS13 cleaves the VWF subunit at the Tyr1605–Met1606 peptide bond in the A2 domain Furlan M, et al. -
32 Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets Joan-Carles Reverter and Dolors Tàssies
32 Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets Joan-Carles Reverter and Dolors Tàssies Introduction Antiphospholipid antibodies (aPL) are related to thrombosis in the antiphospho- lipid syndrome (APS) [1, 2] and numerous pathophysiological mechanisms have been suggested involving cellular effects, plasma coagulation regulatory proteins, and fibrinolysis [3, 4]: aPL may act as blocking agents directly inhibiting antigen enzymatic or co-factor function of hemostasis; may bind fluid-phase antigens of hemostasis involved proteins and then decrease plasma antigen levels by clearance of immune complexes; may form immune complexes with their antigens that may be deposited in blood vessels causing inflammation and tissue injury; may cause dysregulation of antigen–phospholipid binding due to cross-linking of membrane bound antigens; and may trigger cell mediated events by cross-linking of antigen bound to cell surfaces or cell surface receptors [3, 4]. Moreover, several characteris- tics of the aPL, such as the concentration, class/subclass, affinity or charge, and several characteristics of the antigens, as the concentration, size, location or charge, may influence which of the theoretical autoantibody actions will occur in vivo [3]. Among the cellular mechanisms supposed to be involved, platelets have been considered as one of the most promising potential target for circulating aPL that may cause antibody mediated thrombosis as a part of the clinical spectrum of the autoimmune disorder of the APS. In the present chapter we will focus on the inter- actions that involve aPL binding to platelet membrane or platelet membrane bound antigens. Platelets as Target for aPL Platelets play a central role in primary hemostasis involving platelet adhesion to the injured blood vessel wall, followed by platelet activation, granule release, shape change, and rearrangement of the outer membrane phospholipids and proteins, transforming them into a highly efficient procoagulant surface [5]. -
What Is Dvt? Deep Vein Thrombosis (DVT) Occurs When an Abnormal Blood Clot Forms in a Large Vein
What is DVt? Deep vein thrombosis (DVT) occurs when an abnormal blood clot forms in a large vein. These clots usually develop in the lower leg, thigh, or pelvis, but can also occur in other large veins in the body. If you develop DVT and it is diagnosed correctly and quickly, it can be treated. However, many people do not know if they are at risk, don’t know the symptoms, and delay seeing a healthcare professional if they do have symptoms. CAn DVt hAppen to me? Anyone may be at risk for DVT but the more risk factors you have, the greater your chances are of developing DVT. Knowing your risk factors can help you prevent DVt: n Hospitalization for a medical illness n Recent major surgery or injury n Personal history of a clotting disorder or previous DVT n Increasing age this is serious n Cancer and cancer treatments n Pregnancy and the first 6 weeks after delivery n Hormone replacement therapy or birth control products n Family history of DVT n Extended bed rest n Obesity n Smoking n Prolonged sitting when traveling (longer than 6 to 8 hours) DVt symptoms AnD signs: the following are the most common and usually occur in the affected limb: n Recent swelling of the limb n Unexplained pain or tenderness n Skin that may be warm to the touch n Redness of the skin Since the symptoms of DVT can be similar to other conditions, like a pulled muscle, this often leads to a delay in diagnosis. Some people with DVT may have no symptoms at all. -
What You Need to Know About Deep Vein Thrombosis (DVT)
What You Need to Know About Deep Vein Thrombosis What is a Deep Vein Thrombosis? A deep vein thrombosis (DVT) is a blood clot that forms in the veins in the body (usually in the leg or pelvis). What causes a Deep Vein Thrombosis? Deep vein thrombosis (DVT) sometimes occurs for no apparent reason. However, certain factors can increase the chance of developing a DVT: • Inactivity • Hospital stays and surgery • Damage to your blood vessel from an injury or trauma • Medical and genetic conditions • Pregnancy • Taking estrogen-based medicine such as hormonal birth control or hormone replacement therapy • Overweight or obese • Family history of DVT • Older age What are the symptoms of DVT? Only about half of the people who have a DVT have signs and symptoms. These signs and symptoms of a deep vein clot include: • Pain or tenderness, often starting in the calf. • Swelling, including the ankle & foot. • Warmth and redness of the area or a noticeable discoloration Vascular Surgery -1- How is a DVT diagnosed? Your doctor will ask you questions about your symptoms and if your symptoms suggest that a blood clot is likely, you could have one or all of the following tests: • Blood test for a D-dimer: this test measures the level of a compound released when blood clots are dissolving. A high level may mean you have Deep Vein Thrombosis (DVT). • Imaging studies: o Ultrasound – This is the most common test for diagnosing deep vein blood clots. This test uses sound waves to create pictures of blood flowing through the arteries and veins in the affected leg. -
Acr–Aium–Spr–Sru Practice Parameter for the Performance of Peripheral Venous Ultrasound Examination
The American College of Radiology, with more than 30,000 members, is the principal organization of radiologists, radiation oncologists, and clinical medical physicists in the United States. The College is a nonprofit professional society whose primary purposes are to advance the science of radiology, improve radiologic services to the patient, study the socioeconomic aspects of the practice of radiology, and encourage continuing education for radiologists, radiation oncologists, medical physicists, and persons practicing in allied professional fields. The American College of Radiology will periodically define new practice parameters and technical standards for radiologic practice to help advance the science of radiology and to improve the quality of service to patients throughout the United States. Existing practice parameters and technical standards will be reviewed for revision or renewal, as appropriate, on their fifth anniversary or sooner, if indicated. Each practice parameter and technical standard, representing a policy statement by the College, has undergone a thorough consensus process in which it has been subjected to extensive review and approval. The practice parameters and technical standards recognize that the safe and effective use of diagnostic and therapeutic radiology requires specific training, skills, and techniques, as described in each document. Reproduction or modification of the published practice parameter and technical standard by those entities not providing these services is not authorized. Revised 2019 (Resolution 29)* ACR–AIUM–SPR–SRU PRACTICE PARAMETER FOR THE PERFORMANCE OF PERIPHERAL VENOUS ULTRASOUND EXAMINATION PREAMBLE This document is an educational tool designed to assist practitioners in providing appropriate radiologic care for patients. Practice Parameters and Technical Standards are not inflexible rules or requirements of practice and are not intended, nor should they be used, to establish a legal standard of care1.