Hemodynamics. Objectives. Filtration across the endothelium 1/17/2017. K[(P cap - P int )-σ(π cap π int )]
|
|
- Roderick Strickland
- 5 years ago
- Views:
Transcription
1 Hemodynamics Amir Kol DVM, Ph.D, Dip ACVP (Clinical Pathology) UC Davis, School of Veterinary Medicine Objectives Understand the mechanisms that promote extravascular fluid accumulation Edema (tissues) Effusion (cavities) Hyperemia vs congestion Hemostasis - understand the cascade of events that lead to blood clotting Primary hemostasis Secondary hemostasis Tertiary hemostasis Cell based vs. cascade models Define hemorrhagic and thrombotic disorders Disseminated intravascular coagulopathy (DIC) Shock definition and pathogenesis Filtration across the endothelium K[(P cap - P int )-σ(π cap π int )] Robins & Cotran. Pathologic Basis of Disease. Fig 4.1, 9 th edition. 1
2 Filtration across the endothelium K[(P cap - P int )-σ(π cap π int )] Cleaver & Melton. Nature Medicine Filtration across the endothelium Increased microvascular permeability Inflammation Histamine, bradykinin, leukotrienes, substance P IL1, TNFα, IFNγ Inflammatory exudate Infectious agents Immune mediated Toxins Filtration across the endothelium Increased hydrostatic pressure Usually passive (i.e. congestion) Systemic Heart (right or left side) failure, fluid overload Local Hepatic fibrosis Venous obstruction Thrombosis, organ volvulus and torsion, compressive mass 2
3 Filtration across the endothelium Decreased osmotic pressure Protein losing nephropathy Protein loosing enteropathy Decreased hepatic synthesis Severe burns Malnutrition Water intoxication Hemostasis Arteriolar vasoconstriction Primary hemostasis Secondary hemostasis Clot stabilization and resorption Robins & Cotran. Pathologic Basis of Disease. Fig 4.4, 9 th edition. 3
4 Hemostasis Arteriolar vasoconstriction Primary hemostasis Secondary hemostasis Clot stabilization and resorption Robins & Cotran. Pathologic Basis of Disease. Fig 4.4, 9 th edition. Contributions of Vessels Vessels are anticoagulant in health Anticoagulant activities of normal endothelium. NO, nitric oxide; PGI2, prostacyclin; t-pa, tissue plasminogen activator; vwf, von Willebrand factor. The thrombin receptor is also called a protease-activated receptor (PAR). Robins & Cotran. Pathologic Basis of Disease. Fig 4.10, 9 th edition. Vessel response to injury Neuromechanical transient vasoconstriction Biochemical endothelial cells synthesize and metabolize many factors involved in hemostasis (pro- and anti-coagulant) and inflammation (See Box 2-1 in Zachary & McGavin, 5 th edition page 63) subendothelial collagen plays a key role in activating platelets and the coagulation system 4
5 Pro-coagulant Endothelial Function Endothelial Injury Endothelial Injury Endothelial Injury Russell JA. N Engl J Med, Primary hemostasis The final outcome of primary hemostasis is a platelet plug Platelet adhesion Rapid shape change Secretion Recruitment Platelet aggregation Primary hemostasis 5
6 Primary hemostasis Robins & Cotran. Pathologic Basis of Disease. Fig 4.5, 9 th edition. Primary hemostasis Video 2dry Hemostasis - Coagulation Multiple component backup systems fail safe (redundancy) Amplification coagulation systems anticoagulation systems Checks and balances positive amplification negative feedback loops 6
7 Key Aspects of Coagulation (Con t) Localized on a surface, does not occur in solution Occurs on phospholipid membranes (mostly platelet surfaces) Confines reactions to selected sites/wounds Requires Calcium Coagulation Factors Small Mostly produced by the liver Activity requires Vitamin K (II, VII, IX, X, protein C) Inactive precursors are made functional by vitamin K-dependent post-translational carboxylation of glutamic acid residues on the molecules Circulate as inactive pro-enzymes until activated Complexed with inhibitors prior to clearance by the liver Most are proteases (think of coagulation as a series of protein cleavages to make inactive enzymes into active enzymes) Primary exception is tissue factor (aka thromboplastin, factor III) Factors V and VIII and fibrinogen are also not proteases Coagulation Overview An amplification system to rapidly form a fibrin clot Rapid production of thrombin, which converts fibrinogen to fibrin: fibrinogen fibrin (soluble) thrombin (insoluble) Thrombin also has other important functions 7
8 2 schemes to classify coagulation pathways: 1 st Scheme Cascade (waterfall) 2 nd Scheme Cell-Based Model Coagulation System Cascade View Comprised of 3 inter-related pathways Intrinsic Pathway Extrinsic Pathway Common Pathway Common Pathway This scheme is a simplification for ease of understanding and clarification of laboratory testing Intrinsic Pathway Numerous substances XII XIIa XI IIa XIa IX IXa IIa VIII VIIIa Coagulation Cascade (IXa + PF-3 + VIIIa + Ca +2 ) VIIa Extrinsic Pathway Tissue factor (III) and other substances VII (VIIa + Tissue factor + Ca +2 + PF-3 ) Platelet phospholipid (PF-3) is a cofactor for several reactions Common Pathway X IIa V Va Prothrombin (II) Xa (Xa + Va + PF-3 + Ca +2 ) Fibrinogen Thrombin (IIa) Fibrin Cross linked fibrin Calcium (Ca +2 ) is a vital cofactor for several reactions IIa XIIIa XIII 8
9 Cascade scheme Implies 2 pathways of activation Exposure to tissue factor (TF) Tissue factor is found on exposed fibroblasts, activated endothelial cells, other cells Contact with basement membrane Sees coagulation as sequential activation Limits the role of the surface as passive In fact, cells (endothelial cells, platelets and leukocytes) provide a dynamic and regulatory function in coagulation Represents well how we measure coagulation in the laboratory, less adequate for definition of process in vivo Cell-Based Model of Coagulation Acknowledges central role of platelet surface, tissue factor and Thrombin Suggests that most coagulation is activated by TF which generates a small amount of thrombin which is followed and amplified by loop activation of intrinsic, extrinsic and common pathways Lessens role of contact activation and implies that the intrinsic pathway is secondary after initial activation through TF and thrombin. The intrinsic pathway is essentially amplification after extrinsic pathway generates a small amount thrombin via TF More real, less reflective of how we measure coagulation And now, A video Cell Based Model of Coagulation: 9
10 Cell-Based Model of Coagulation Initiation: plasma in contact with TF bearing cells due to break in vessel wall, small thrombin signal Amplification: small thrombin signal binds platelets that have adhered to collagen via vwf, enhances platelet activation activates the tenase complex Propagation: assembly of the prothrombinase complex and generation of lots of thrombin Hoffman & Monroe. Thromb Haemost, Cell-Based Model of Coagulation Initiation: plasma in contact with TF bearing cells due to break in vessel wall, small thrombin signal Amplification: small thrombin signal binds platelets that have adhered to collagen via vwf, enhances platelet activation activates the tenase complex Propagation: assembly of the prothrombinase complex and generation of lots of thrombin James W. Wisler & Richard C. Becker. Nature Reviews Cardiology, Functions of Thrombin Promotes coagulation Converts fibrinogen to fibrin Activates Factors V, VIII, XI, positive feedback (amplification) Activates Factor XIII strengthens clot by cross-linking fibrin Potent platelet agonist (via PAR receptors) 10
11 Functions of Thrombin Regulates coagulation: Converts plasminogen to plasmin, which breaks down fibrin clot. Activates Protein C (APC), an inhibitor of Va and VIIIa Stimulates the production of prostacyclin (PGI 2 ) a platelet inhibitor by endothelial cells J. Borrisoff et al. Cardiovascular Research, Clot Stabilization So, we have platelets Adhesion, aggregation, granule release Coagulation proteins Series of proteolytic cleavages with the end result of cleaving fibrinogen to fibrin Clot stabilization Fibrin monomers are polymerized into long, crosslinked chains through the action of factor XIIIa. 11
12 Regulators of Hemostasis Inhibitors of Coagulation - Natural Anticoagulants Antithrombin III (ATIII) Protein C TFPI Thrombomodulin Robins & Cotran. Pathologic Basis of Disease. Fig 4.10, 9 th edition. Regulators of Hemostasis ATIII Produced by hepatocytes Inactivates most coagulation enzymes, especially thrombin, IXa, Xa Loss is associated with thrombosis. Loss most commonly occurs through glomerular disease or consumption in DIC Acts at endothelial surface, needs heparin, binds thrombin, inactivates thrombin Heparin and heparan sulfate ENHANCE ATIII activity This is why heparin is used as an anticoagulant! Regulators of Hemostasis Protein C/ Protein S Produced by hepatocytes Vitamin K dependent Along with factors II, VII, IX, X Protein C is activated by thrombin and Protein S to activated protein C (APC) Part of Protein C / Protein S / Thrombomodulin complex Complex inactivates VIIIa and Va Thrombomodulin + thrombin markedly enhances activation of Protein S 12
13 Protein C and Protein S anticoagulant System: Vitamin K dependent proteins The Protein C Anticoagulant Pathway: Thrombin leaves a site of vascular injury binds to its receptor thrombomodulin (TM) on the intact cell surface. As a result, thrombin loses its procoagulant properties and instead becomes a potent activator of protein C. Activated protein C (APC) functions as a circulating anticoagulant, which specifically degrades and inactivates the phospholipid-bound factors Va and VIIIa. This effectively down-regulates the coagulation cascade and limits clot formation to sites of vascular injury. Regulators of Hemostasis Tissue Factor Pathway Inhibitor (TFPI) Produced by endothelial cells, monocytes, macrophages, hepatocytes and platelets Requires Ca +2 TFPI inhibits TF-factor VIIa complex. Therefore inhibits generation of IXa and Xa via TF-VIIa Regulators of Hemostasis Hepatocytes eliminate activated clotting factors and factor / inhibitor complexes Macrophage Phagocytic System removes factors Endothelium degrades activated factors Blood Flow removes factors 13
14 Major Regulators of Hemostasis XIIa + XIa AT III + Heparin VIIa + Tissue Factor IXa VIIIa Tissue Factor Pathway Inhibitor IIa APC-Protein S Protein C Xa Va IIa (Thrombin) Fibrin AT III + Heparin AT III + Heparin Where we are going Primary hemostasis: formation of platelet plug Secondary hemostasis: stabilization of the platelet plug with cross-linked fibrin Coagulation proteins Inhibitors of Coagulation Tertiary hemostasis: resorption of the clot by fibrinolysis Fibrinolysis Occurs within the developing clots where plasminogen activators and plasminogen bind to fibrin Factor XII and Tissueplasminogen activator 14
15 Control of fibrinolysis There are also checks & balances on fibrinolysis Robins & Cotran. Pathologic Basis of Disease. Fig 4.9, 9 th edition. Hemorrhagic disorders - Vasculitides Petechial and ecchymotic pattern Underlying etiologies (see Box 10-7 in Zachary & McGavin, 5 th edition pp.562): Viral Bacterial Mycotic Parasitic Immune mediated Hemorrhagic disorders Primary hemostasis Petechial and ecchymotic pattern Thrombocytopenia Decreased production Consumption Destruction Sequestration Thrombocytopathy Primary (vwd, Glanzmann Throbasthenia, Thrombopathy) Secondary (NSAIDs, uremia, E. canis) 15
16 Hemorrhagic disorders Secondary hemostasis Hereditary Coagulopathies Hemophilia A factor VIII deficiency Hemophilia B factor IX deficiency Other specific factor deficiencies less common and variable bleeding (See Box 2-5 in Zachary & McGavin, 5th edition page 77) Acquired Coagulopathies Rodenticides (Vitamin K antagonism) Liver Dz. PLN and PLE Drugs and toxins Acquired Coagulopathies Vitamin K antagonists (and, rarely, decreased vitamin K availability) In the absence of vitamin K, coagulation factors are secreted without sufficient carboxylation and have inadequate function Rodenticides, coumarin (moldy sweet clover) Malabsorption, others Drugs Liver disease Decreased production of coagulation factors Liver also responsible for removal of activated factors Envenomation Thrombosis Virchow s Triad THROMBOSIS Hypercoagulability 16
17 Endothelial Injury Viruses CAD1, equine Morbilivirus, herpes virus and Arterivirus, ovine orbivirus, bovine and procine pestvirus Bacteria Salmonella typhimurium, Manhemia haemolytica, Eryspelothrix rhusiopathiae, Haemophilus somnus Fungi Aspergilus, Mucor, Absidia, Rhizopus Nematodes Strongylus vulgaris, Dirofilaria, Spirocerca, Aelorostrongylus, Angiostrongylosis Endothelial Injury Immune mediated vasculitis FIP, Ehrlichia canis, Leismania Toxins Endotoxin, Claviceps Vitamin E/selenium deficiency Faulty intravenous injection Alterations in Blood Flow Local stasis GDV, intestinal torsion and volvulus, varicocele Cardiac disease DCM, HCM etc. Aneurysm Spirocerca lupi, Strongyulus vulgaris, Copper deficiency in pigs Hypovolemia Shock, diarrhea, burns 17
18 Hypercoagulability Inflammation Platelets hyper-reactivity Diabetes mellitus, nephrotic syndrome, malignant neoplasia, heartworm disease, uremia Antithrombin deficiency PLN, PLE, hepatic disease Metabolic abnormalities Hyperadrenocorticism Infarction Area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage. Zachary and McGavin. Pathologic Basis of Veterinary Disease. Infarction Factors That Influence Development of an Infarct: Anatomy of the vascular supply Rate of occlusion Tissue vulnerability to hypoxia Hypoxemia 18
19 Fate of the Thrombus Zachary and McGavin. Pathologic Basis of Veterinary Disease. Disseminated Intravascular Coagulation - DIC When things go out-of-control Disseminated Intravascular Coagulation - DIC Excessive activation of coagulation, diffuse thrombosis in microcirculation results in consumption of coagulation factors and platelets leads to bleeding Secondary to other diseases Widespread tissue damage, IMHA, pancreatitis, gram negative sepsis, heat stroke, neoplasia, infections (Heartworm, Rickettsia) 19
20 Shock A state of reduced effective circulating blood volume which results in cellular hypoxia Cardiogenic Hypovolemic Septic (inflammatory) Anaphylactic Neurogenic Pathogenesis of Septic Shock Inflammatory and counter-inflammatory responses Endothelial activation and injury Induction of a procoagulant state Metabolic abnormalities Organ dysfunction Pathogenesis of Septic Shock Robins & Cotran. Pathologic Basis of Disease. Fig 4.20, 9 th edition. 20
21 Stages of Shock Non-progressive phase Reflex compensation (baroreceptor reflex, catecholamine release, RAS activation, ADH release and sympatheic stimulation Progressive phase Cellular hypoxia Lactic acidosis Blood pooling Irreversible stage Wide spread cellular necrosis Shock Zachary and McGavin. Pathologic Basis of Veterinary Disease. Questions??? 21
Part IV Antithrombotics, Anticoagulants and Fibrinolytics
Part IV Antithrombotics, Anticoagulants and Fibrinolytics "The meaning of good and bad, of better and worse, is simply helping or hurting" Emerson Chapter 16: Blood Coagulation and Fibrinolytic System
More informationBlood coagulation and fibrinolysis. Blood clotting (HAP unit 5 th )
Blood coagulation and fibrinolysis Blood clotting (HAP unit 5 th ) Vessel injury Antithrombogenic (Favors fluid blood) Thrombogenic (Favors clotting) 3 Major systems involved Vessel wall Endothelium ECM
More informationPrimary Exam Physiology lecture 5. Haemostasis
Primary Exam Physiology lecture 5 Haemostasis Haemostasis Body s response for the prevention and cessation of bleeding. Broadly consists of: Primary Haemostasis - vascular spasm and platlet plug formation
More informationCh. 45 Blood Plasma proteins, Coagulation and Fibrinolysis Student Learning Outcomes: Describe basic components of plasma
Chapt. 45 Ch. 45 Blood Plasma proteins, Coagulation and Fibrinolysis Student Learning Outcomes: Describe basic components of plasma Inheritance of X-linked gene for Factor VIII hemophilia A Explain the
More informationBlood clotting. Subsequent covalent cross-linking of fibrin by a transglutaminase (factor XIII) further stabilizes the thrombus.
Blood clotting It is the conversion, catalyzed by thrombin, of the soluble plasma protein fibrinogen (factor I) into polymeric fibrin, which is deposited as a fibrous network in the primary thrombus. Thrombin
More informationHemodynamic Disorders, Thromboembolic Disease, and Shock
Hemodynamic Disorders, Thromboembolic Disease, and Shock Kumar et al: Robbins & Cotran Pathologic Basis of Disease 7E Figure 4-1 Factors affecting fluid balance across capillary walls. Capillary hydrostatic
More informationHemodynamic Disorders, Thrombosis, and Shock. Richard A. McPherson, M.D.
Hemodynamic Disorders, Thrombosis, and Shock Richard A. McPherson, M.D. Edema The accumulation of abnormal amounts of fluid in intercellular spaces of body cavities. Inflammation and release of mediators
More informationHemostasis. Learning objectives Dr. Mária Dux. Components: blood vessel wall thrombocytes (platelets) plasma proteins
Hemostasis Learning objectives 14-16 Dr. Mária Dux Components: blood vessel wall thrombocytes (platelets) plasma proteins Hemostatic balance! procoagulating activity anticoagulating activity 1 Thrombocytes
More informationThis slide belongs to iron lecture and it is to clarify the iron cycle in the body and the effect of hypoxia on erythropoitein secretion
This slide belongs to iron lecture and it is to clarify the iron cycle in the body and the effect of hypoxia on erythropoitein secretion Topics of today lectures: Hemostasis Meaning of hemostasis Mechanisms
More informationUNIT VI. Chapter 37: Platelets Hemostasis and Blood Coagulation Presented by Dr. Diksha Yadav. Copyright 2011 by Saunders, an imprint of Elsevier Inc.
UNIT VI Chapter 37: Platelets Hemostasis and Blood Coagulation Presented by Dr. Diksha Yadav Hemostasis: Prevention of Blood Loss Vascular constriction Formation of a platelet plug Formation of a blood
More informationHemostasis and Thrombosis
Hemostasis Hemostasis and Thrombosis Normal hemostasis is a consequence of tightly regulated processes that maintain blood in a fluid state in normal vessels, yet also permit the rapid formation of a hemostatic
More informationTopics of today lectures: Hemostasis
Topics of today lectures: Hemostasis Meaning of hemostasis Mechanisms of hemostasis - Vascular contraction - Platelets plug - Blood coagulation (clotting) - Structure and functions of platelets - Blood
More informationChapter 1 Introduction
Chapter 1 Introduction There are several disorders which carry an increased risk of thrombosis, clots that interfere with normal circulation, including: venous thromboembolism (VTE), comprising both deep
More informationChapter 19. Hemostasis
Chapter 19 Hemostasis Hemostasis Hemostasis is the cessation of bleeding stopping potentially fatal leaks important in small blood vessels not effective in hemorrhage excessive bleeding from large blood
More informationCirculatory Disturbances 5: Thrombosis, Embolism, Infarction, Shock
Circulatory Disturbances 5: Thrombosis, Embolism, Infarction, Shock Shannon Martinson, Feb 2016 http://people.upei.ca/smartinson/ VPM 152 General Pathology Thrombosis, Embolism, Infarction, Shock Learning
More informationHemostasis. Clo)ng factors and Coagula4on NORMAL COAGULATION. Overview of blood coagula4on. The Cascade Theory 5/1/12. Clot
Hemostasis Clo)ng factors and Coagula4on Dr Badri Paudel www.badripaudel.com Hemostasis is defined as a property of circula4on whereby blood is maintained within a vessel and the ability of the system
More informationThrombosis. Jeffrey Jhang, M.D.
Thrombosis Jeffrey Jhang, M.D. Introduction The human hemostatic system has evolved to maintain blood flow under normal physiologic conditions while remaining primed to rapidly respond to vascular injury
More informationHEME 10 Bleeding Disorders
HEME 10 Bleeding Disorders When injury occurs, three mechanisms occur Blood vessels Primary hemostasis Secondary hemostasis Diseases of the blood vessels Platelet disorders Thrombocytopenia Functional
More informationWhat are blood clots?
What are blood clots? Dr Matthew Fay GP Principal The Willows Medical Practice- Queensbury GPwSI and Co-Founder Westcliffe Cardiology Service GP Partner Westcliffe Medical Group Created 5/31/18 Dr. Matthew
More informationBleeding and Haemostasis. Saman W.Boskani HDD, FIBMS Maxillofacial Surgeon
Bleeding and Haemostasis Saman W.Boskani HDD, FIBMS Maxillofacial Surgeon 1 Beeding Its escaping or extravasation of blood contents from blood vessels Types: - Arterial - Venous - Capillary Differences
More informationChapter 1. General introduction
Chapter 1 General introduction 8 Haemostasis All organs and tissues of higher organisms are provided with nutrients and oxygen through the bloodstream. The bloodstream is an extensive vascular system that
More informationDiagnosis of hypercoagulability is by. Molecular markers
Agenda limitations of clinical laboratories to evaluate hypercoagulability and the underlying cause for thrombosis what is the INR the lupus anticoagulant and the antiphospholipid antibody syndrome hassouna
More informationACQUIRED COAGULATION ABNORMALITIES
ACQUIRED COAGULATION ABNORMALITIES ACQUIRED COAGULATION ABNORMALITIES - causes 1. Liver disease 2. Vitamin K deficiency 3. Increased consumption of the clotting factors (disseminated intravascular coagulation
More informationShock, Hemorrhage and Thrombosis
Shock, Hemorrhage and Thrombosis 1 Shock Systemic hypoperfusion due to: Reduction in cardiac output Reduction in effective circulating blood volume Hypotension Impaired tissue perfusion Cellular hypoxia
More informationOutline Anti-coagulant and anti-thrombotic drugs Haemostasis and Thrombosis Year 3 Dentistry
Outline Anti-coagulant and anti-thrombotic drugs Year 3 Dentistry Professor Yotis Senis Cellular Haemostasis y.senis@bham.ac.uk I. Haemostasis and II. Coagulation and anti-coagulants III. Platelets and
More information-Hashim ahmed is the one who wrote this sheet. I just edited it according to our record.
* Subjects of this lecture : - Hemostasis - Platelets, general information, their ultrastructure and role in hemostasis. - Definitions: Thrombus, Embolus, Arteriosclerosis and Atherosclerosis. *NOTE: Prof
More informationCoagulation Disorders. Dr. Muhammad Shamim Assistant Professor, BMU
Coagulation Disorders Dr. Muhammad Shamim Assistant Professor, BMU 1 Introduction Local Vs. General Hematoma & Joint bleed Coagulation Skin/Mucosal Petechiae & Purpura PLT wound / surgical bleeding Immediate
More informationWHITE PAPERS PRESENTATION VIDEO DOCUMENTATION EXPERIMENT WO NDCLOT. The WoundClot Principals for Effective Bleeding Control PRESENTATION
WHITE PAPERS PRESENTATION VIDEO DOCUMENTATION EXPERIMENT ARTICLES OUR STUDY BLEEDING CONTROL 5 POINT MODEL WO NDCLOT The WoundClot Principals for Effective Bleeding Control PRESENTATION Harnessing SCIENCE
More informationIntroduction to coagulation and laboratory tests
Introduction to coagulation and laboratory tests Marc Jacquemin Special Haemostasis Laboratory Center for Molecular and Vascular Biology University of Leuven Coagulation in a blood vessel: fibrin stabilises
More informationHemostasis and. Blood Coagulation
Hemostasis and Blood Coagulation Events in Hemostasis The term hemostasis means prevention of blood loss. Whenever a vessel is severed or ruptured, hemostasis is achieved by several mechanisms: (1) vascular
More informationThursday, February 26, :00 am. Regulation of Coagulation/Disseminated Intravascular Coagulation HEMOSTASIS/THROMBOSIS III
REGULATION OF COAGULATION Introduction HEMOSTASIS/THROMBOSIS III Regulation of Coagulation/Disseminated Coagulation necessary for maintenance of vascular integrity Enough fibrinogen to clot all vessels
More informationPhysiology of. The Blood hemostasis. By prof. Israa f. jaafar
Physiology of The Blood hemostasis By prof. Israa f. jaafar Learning objectives Understand the Platelet structure and function Explane the Platelet production Understand the phases of hemostasis: vascular
More informationHemodynamic Disorders Thrombosis and Shock. 1. Interstitial, between the cells, but outside of the vascular system. - water making up the blood and
Hemodynamic Disorders Thrombosis and Shock I. Body water, where is it and what keeps it there? A. Intracellular B. Extracellular (intercellular) 1. Interstitial, between the cells, but outside of the vascular
More informationChapter 19 Blood Lecture Outline
Chapter 19 Blood Lecture Outline Cardiovascular system Circulatory system Blood 1. distribution 2. regulation 3. protection Characteristics: ph 7.4 38 C 4-6 L Composition: Plasma Formed elements Erythrocytes
More informationChapter 4: Haemodynamic disorders, shock
Chapter 4: Haemodynamic disorders, shock 1. Regarding platelets (2006) (a) They are the main source of thrombin (b) they number 150-300 x10 3 per microlitre (c) They contain a nucleus (d) They are biconcave
More informationDisseminated Intravascular Coagulation. M.Bahmanpour MD Assistant professor IUMS
به نام خدا Disseminated Intravascular Coagulation M.Bahmanpour MD Assistant professor IUMS Algorithm for Diagnosis of DIC DIC Score factor score Presence of known underlying disorder No= 0 yes=2 Coagolation
More informationChapter 3. Haemostatic abnormalities in patients with liver disease
Chapter 3 Haemostatic abnormalities in patients with liver disease Ton Lisman, Frank W.G. Leebeek 1, and Philip G. de Groot Thrombosis and Haemostasis Laboratory, Department of Haematology, University
More informationAnatomy and Physiology
Anatomy and Physiology For The First Class 2 nd Semester Thrombocytes = Platelets Thrombocytes = Platelets Blood platelets are non-nucleated disc like cell fragments 2-4 µm in diameter. Platelets are not
More informationPHM142 Lecture 4: Platelets + Endothelial Cells
PHM142 Lecture 4: Platelets + Endothelial Cells 1 Hematopoiesis 2 Platelets Critical in clotting - activated by subendothelial matrix proteins (e.g. collagen, fibronectin, von Willebrand factor) and thrombin
More informationBLEEDING DISORDERS Simple complement:
BLEEDING DISORDERS Simple complement: 1. Select the statement that describe the thrombocytopenia definition: A. Marked decrease of the Von Willebrandt factor B. Absence of antihemophilic factor A C. Disorder
More informationVol. 25, No. 9 September Angell Memorial Animal Hospital Boston, Massachusetts Lillian I. Good, DVM Ann Marie Manning, DVM, DACVECC
CE 650 V Vol. 25, No. 9 September 2003 Article #1 (1.5 contact hours) Refereed Peer Review Comments? Questions? Email: compendium@medimedia.com Web: VetLearn.com Fax: 800-556-3288 KEY FACTS Hemostasis
More informationAgent Dose MoA/PK/Admin Adverse events Disadvantages Protamine Heparin: 1mg neutralizes ~ 100 units Heparin neutralization in ~ 5 min
Nanik (Nayri) Hatsakorzian Pharm.D/MPH candidate 2014 Touro University College of Pharmacy CA Bleeding Reversal Agents Agent Dose MoA/PK/Admin Adverse events Disadvantages Protamine Heparin: 1mg neutralizes
More informationBiochemical Reaction Networks and Blood Clotting
Biochemical Reaction Networks and Blood Clotting Yasmeen Hussain, Aaron Fogelson Abstract Following an injury to the walls of a blood vessel, platelet aggregation and blood coagulation are induced. Through
More informationOral Anticoagulant Drugs
Oral Anticoagulant Drugs Spoiled sweet clover caused hemorrhage in cattle(1930s). Substance identified as bishydroxycoumarin. Initially used as rodenticides, still very effective, more than strychnine.
More informationProceedings of the World Small Animal Veterinary Association Sydney, Australia 2007
Proceedings of the World Small Animal Veterinary Association Sydney, Australia 2007 Hosted by: Australian Small Animal Veterinary Association (ASAVA) Australian Small Animal Veterinary Association (ASAVA)
More informationPHASES OF HAEMOSTASIS
HAEMOSTASIS Maintains the integrity of a closed, highpressure circulatory system after vascular damage Vessel Wall Injury events in the vessel wall and in the blood which seal breach Delicate balance exists
More informationTHROMBOTIC DISORDERS: The Final Frontier
THROMBOTIC DISORDERS: The Final Frontier Jeffrey I. Weitz, MD, FRCP(C), FACP Professor of Medicine and Biochemistry McMaster University Canada Research Chair in Thrombosis Heart & Stroke Foundation/ J.F.
More informationHemostasis Haemostasis means prevention of blood loss from blood vessels.
١ Hemostasis Haemostasis means prevention of blood loss from blood vessels. Bleeding is stopped by several mechanisms, which are: 1. Local vasoconstriction 2. Formation of platelet plug 3. Blood coagulation
More information4/23/2009. September 15, 2008
The Current Treatment of Deep Venous Thrombosis: Are We Doing Enough? George H. Meier, MD Professor and Chief Division of Vascular Surgery University of Cincinnati College of Medicine Cincinnati, Ohio
More informationHYPEREMIA AND CONGESTION
HYPEREMIA AND CONGESTION Learning Objectives Define congestion and hyperemia Differentiate between the two with regard to: Mechanisms / underlying causes Appearance (gross and histologic) Effects Differentiate
More informationBachelor of Chinese Medicine Shock
BCM Year 2 Dr. Irene Ng Jan 28, 2003 9:30 am 1:00 pm Rm 004 UPB Bachelor of Chinese Medicine 2002 2003 Shock Learning objectives Be able to: know the definition of shock know the classification and causes
More informationL iter diagnostico di laboratorio nelle coagulopatie congenite emorragiche
L iter diagnostico di laboratorio nelle coagulopatie congenite emorragiche Armando Tripodi Angelo Bianchi Bonomi Hemophilia and Thrombosis Center Dept. of Clinical Sciences and Community Health University
More informationHaemostasis & Coagulation disorders Objectives:
Haematology Lec. 1 د.ميسم مؤيد علوش Haemostasis & Coagulation disorders Objectives: - Define haemostasis and what are the major components involved in haemostasis? - How to assess the coagulation status?
More informationReprinted in the IVIS website with the permission of the ACVP and ASVCP
Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology - Tucson, Arizona 2006 - Reprinted in the IVIS website with the
More informationJohn Davidson Consultant in Intensive Care Medicine Freeman Hospital, Newcastle upon Tyne
John Davidson Consultant in Intensive Care Medicine Freeman Hospital, Newcastle upon Tyne Overview of coagulation Testing coagulation Coagulopathy in ICU Incidence Causes Evaluation Management Coagulation
More informationDisturbance of Circulation Hemodynamic Disorder
Disturbance of Circulation Hemodynamic Disorder 2/17/2017 By Dr. Hemn Hassan Othman PhD, Pathology Fall 2016 1 Thrombosis Definition: Thrombosis is the formation of solid or semisolid blood clot within
More informationMoath Darweesh. Omar Sami. Saleem Khreisha. 1 P a g e
7 Moath Darweesh Omar Sami Saleem Khreisha 1 P a g e -First of all, I want to give a quick revision to simplify the whole hemostasis mechanism, it will be much easier here with me. Enjoy (you can skip
More informationHemostasis Haemostasis means prevention of blood loss from blood vessels.
1 Hemostasis Haemostasis means prevention of blood loss from blood vessels. Bleeding is stopped by several mechanisms, which are: 1. Local vasoconstriction 2. Formation of platelet plug 3. Blood coagulation
More informationDr. MUBARAK ABDELRAHMAN MD PEDIATRICS AND CHILD HEALTH Assistant Professor FACULTY OF MEDICINE -JAZAN
Dr. MUBARAK ABDELRAHMAN MD PEDIATRICS AND CHILD HEALTH Assistant Professor FACULTY OF MEDICINE -JAZAN The student should be able:» To identify the mechanism of homeostasis and the role of vessels, platelets
More informationThrombosis. Dr. László Terézia
Thrombosis Dr. László Terézia HYPERCOAGULABILITY THROMBOSIS BLOODFLOW ENDOTHEL VIRCHOW ENDOTHEL INJURY L. ventricle: Arteries: surgery infection prosthetic valve hypertension irradiation chemical: cigarette
More informationCoagulation Pathway and Physiology
Chapter 1 Coagulation Pathway and Physiology Russell A. Higgins, M Introduction Our understanding of blood clotting is intimately tied to the history of civilization. With the advent of writing 5000 years
More informationDisseminated Intravascular Coagulation (DIC) Seminar. Ron Kopilov 4 th year Medical Student, Tel Aviv University Internal Medicine A 8.3.
Disseminated Intravascular Coagulation (DIC) Seminar Ron Kopilov 4 th year Medical Student, Tel Aviv University Internal Medicine A 8.3.2012 1 Our plan: Understand the pathophysiology Identify risk factors
More informationPathophysiology of Catheter-Related Infection. All sources of infection are potential targets for prevention. Infusates/ drugs. hub/lines Dressing
Pathophysiology of Catheter-Related Infection All sources of infection are potential targets for prevention catheter hematogeneous Infusates/ drugs hub/lines Dressing skin Critically ill patient: 2-4 vascular
More informationHAEMORRHAGIA Bleeding
HAEMORRHAGIA Bleeding Cassification Size Location pathomechanism Hematoma: external or may be enclosed within a tissue petechiae : 1-2 mm hemorrhages into skin, mucous membranes, or serosal surfaces increased
More informationPage 1 of 6 THROMBOCYTES
Page 1 of 6 THROMBOCYTES Platelets are not cells in the strict sense. About one-fourth the diameter of a lymphocyte, they are cytoplasmic fragments of extraordinarily large cells (up to 60 µm in diameter)
More informationInflammation. (4 of 5)
Inflammation (4 of 5) What will we discuss today? Plasma protein derived mediators Anti-inflammatory mediators Morphologic patterns of acute inflammation Plasma protein derived mediators 3 systems: -Complement
More informationAnticoagulants. Pathological formation of a haemostatic plug Arterial associated with atherosclerosis Venous blood stasis e.g. DVT
Haemostasis Thrombosis Phases Endogenous anticoagulants Stopping blood loss Pathological formation of a haemostatic plug Arterial associated with atherosclerosis Venous blood stasis e.g. DVT Vascular Platelet
More informationDIC. Bert Vandewiele Fellow Critical Care 23 May 2011
DIC Bert Vandewiele Fellow Critical Care 23 May 2011 Dissiminated Intravascular Coagulopathie 11/3/2011 Dr. Bert Vandewiele 2 Dissiminated Intravascular Coagulopathie = Consumption coagulopathie = Defibrination
More informationThrombosis. By Dr. Sara Mohamed Abuelgasim
Thrombosis By Dr. Sara Mohamed Abuelgasim 1 Thrombosis Unchecked, blood coagulation would lead to dangerous occlusion of blood vessels if the protective mechanisms of coagulation factor inhibitors, blood
More informationCoagulation Pathway and Physiology
CHAPTER 1 Coagulation Pathway and Physiology Jerry B. Lefkowitz, M Introduction Our understanding of blood clotting is intimately tied to the history of civilization. With the advent of writing 5000 years
More informationCover Page. The handle holds various files of this Leiden University dissertation.
Cover Page The handle http://hdl.handle.net/1887/28736 holds various files of this Leiden University dissertation. Author: Debeij, Jan Title: The effect of thyroid hormone on haemostasis and thrombosis
More informationApproach to bleeding disorders &treatment. by RAJESH.N General medicine post graduate
Approach to bleeding disorders &treatment by RAJESH.N General medicine post graduate 2 Approach to a patient of bleeding diathesis 1. Clinical evaluation: History, Clinical features 2. Laboratory approach:
More informationHematology Review. CCRN exam. The Coagulation Cascade. The Coagulation Cascade. Components include: Intrinsic pathway Extrinsic pathway Common pathway
CCRN exam Hematology Review CCRN Review October 2013 Department of Critical Care Nursing Hematology is 2% of the exam Focus on coagulation cascade, DIC, and HIT Anatomy of the hematologic system Bone marrow
More informationBleeding Disorders: (Hemorrhagic Diatheses) Tests used to evaluate different aspects of hemostasis are the following:
Bleeding Disorders: (Hemorrhagic Diatheses) Excessive bleeding can result from: 1. Increased fragility of vessels. 2. Platelet deficiency or dysfunction. 3. Derangement of coagulation. 4. Combinations
More informationInherited Thrombophilia Testing. George Rodgers, MD, PhD Kristi Smock MD
Inherited Thrombophilia Testing George Rodgers, MD, PhD Kristi Smock MD Prevalence and risk associated with inherited thrombotic disorders Inherited Risk Factor % General Population % Patients w/ Thrombosis
More informationChapter 19 Cardiovascular System Blood: Functions. Plasma
Chapter 19 Cardiovascular System Blood: Functions 19-1 Plasma Liquid part of blood. Colloid: liquid containing suspended substances that don t settle out of solution 91% water. Remainder proteins, ions,
More informationBlood Lecture Test Questions Set 2 Summer 2012
Blood Lecture Test Questions Set 2 Summer 2012 1. Leukocytes are attracted to a site of injury or disease by: a. diapedesis b. chemotaxis c. leukocytosis d. heparin e. leukomotosis 2. Leukocytes leave
More informationPathology note 8 BLEEDING DISORDER
Pathology note 8 BLEEDING DISORDER Slide75 ( Types of clotting factors deficiency): Today we will talk about public public factor deficiency it could be acquired or inherited, acquired diseases are more
More informationDVT Pathophysiology and Prophylaxis in Medically Hospitalized Patients. David Liff MD Oklahoma Heart Institute Vascular Center
DVT Pathophysiology and Prophylaxis in Medically Hospitalized Patients David Liff MD Oklahoma Heart Institute Vascular Center Overview Pathophysiology of DVT Epidemiology and risk factors for DVT in the
More informationApproach To A Bleeding Patient
ABDUL MAJEED, RAHUL RAJEEV REVIEW ARTICLE INTRODUCTION Hemostasis is the process of forming clots in the walls of damaged blood vessels and preventing blood loss while maintaining blood in a fluid state
More informationCoagulation an Overview Dr.Abdolreza Abdolr Afrasiabi Thal assem a & Heamophili hilia G ene i tic R esearc C en er Shiraz Medical Medic University
In The Name God Coagulation an Overview Dr.Abdolreza Afrasiabi Thalassemia & Heamophilia Genetic Research hcenter Shiraz Medical University Bleeding Clotting Hemostasis Review of platelet function Platelets
More informationPathophysiology. Tutorial 3 Hemodynamic Disorders
Pathophysiology Tutorial 3 Hemodynamic Disorders ILOs Recall different causes of thrombosis. Explain different types of embolism and their predisposing factors. Differentiate between hemorrhage types.
More informationTrue/False: Idarucizumab can be utilized for the management of bleeding associated with dabigatran.
Discuss the role of idarucizumab for the management of bleeding associated with dabigatran Understand dosing, preparation and administration of idarucizumab I have no financial interest/arrangement or
More informationDiscuss the role of idarucizumab for the management of bleeding associated with dabigatran
Discuss the role of idarucizumab for the management of bleeding associated with dabigatran Understand dosing, preparation and administration of idarucizumab I have no financial interest/arrangement or
More informationINFLAMMATION & REPAIR
INFLAMMATION & REPAIR Lecture 7 Chemical Mediators of Inflammation Winter 2013 Chelsea Martin Special thanks to Drs. Hanna and Forzan Course Outline i. Inflammation: Introduction and generalities (lecture
More informationDISSEMINATED INTRAVASCULAR COAGULATION (DIC) Pichika Chantrathammachart MD Division of Hematology, Department of Medicine Ramathibodi Hospital
DISSEMINATED INTRAVASCULAR COAGULATION (DIC) Pichika Chantrathammachart MD Division of Hematology, Department of Medicine Ramathibodi Hospital Disseminated intravascular coagulation (DIC) Disseminated
More informationBleeding and Thrombotic Disorders. Kristine Krafts, M.D.
Bleeding and Thrombotic Disorders Kristine Krafts, M.D. Bleeding and Thrombotic Disorders Bleeding disorders von Willebrand disease Hemophilia A and B DIC TTP/HUS ITP Thrombotic disorders Factor V Leiden
More informationProthrombin Complex Concentrate- Octaplex. Octaplex
Prothrombin Complex Concentrate- Concentrated Factors Prothrombin Complex Concentrate (PCC) 3- factor (factor II, IX, X) 4-factor (factors II, VII, IX, X) Activated 4-factor (factors II, VIIa, IX, X) Coagulation
More informationBleeding Disorders. Dr. Mazen Fawzi Done by Saja M. Al-Neaumy Noor A Mohammad Noor A Joseph Joseph
Bleeding Disorders Dr. Mazen Fawzi Done by Saja M. Al-Neaumy Noor A Mohammad Noor A Joseph Joseph Normal hemostasis The normal hemostatic response involves interactions among: The blood vessel wall (endothelium)
More informationBlood platelets play important role in coagulation.
B.N. Bandodkar College of Science, Thane T.Y. B.Sc Paper II Haematology Blood Coagulation / Blood clotting By Dr N.N. Patil Introduction: When blood is shed, it looses its fluidity within few minutes and
More informationBranch of medicine that deals with blood, its formation and disorders is called. Three main functions of cardiovascular system are,, and.
Chapter 19 The Blood Human body must maintain a balance called. Body fluid inside the cells is called fluid; that outside is called or fluid. Two major fluid networks that help in connecting cells are
More informationBlood (II) Huawei Liang, PhD
Blood (II) Huawei Liang, PhD E-mail: hwliang@zju.edu.cn Physiological hemostasis 生理止血 The arrest of bleeding from a broken blood vessel -- that is, the stoppage of hemorrhage ( 出血 ) Three major events:
More informationHaemorrhagic Disorders. Dr. Bashar Department of Pathology Mosul Medical College
Haemorrhagic Disorders Dr. Bashar Department of Pathology Mosul Medical College Hemorrhagic Disorders These include Disorders of platelets. Disorders of blood vessels. Disorders of coagulation & fibrinolysis.
More information10. Which of the following immune cell is unable to phagocytose (a) neutrophils (b) eosinophils (c) macrophages (d) T-cells (e) monocytes
Chapter 2. Acute and chronic inflammation(6): 1. In acute inflammation, which events occur in the correct chronological order? (Remembered from 2000, 2004 exam.) p50 (a) transient vasoconstriction, stasis
More informationCIRCULATORY DISTURBANCES
CIRCULATORY DISTURBANCES Shannon Martinson, January 2017 Office: 418N Email: smartinson@upei.ca All lecture notes and slide shows are available online: http://people.upei.ca/smartinson REFERENCE TEXTS:
More informationHemostasis and fibrinolysis the hemostatic balance
Hemostasis and fibrinolysis the hemostatic balance Bleeding Clotting The hemostatic balance Reference: Boron & Boulpaep Medical Physiology, 3 rd Ed, Chapter 18 Dr. Ana-Maria Zagrean Carol Davila University
More informationHemodynamic Disorders Thrombosis and Shock
Hemodynamic Disorders Thrombosis and Shock SCPA 202 Basic Pathology Somphong Narkpinit, M.D. Department of Pathobiology, Faculty of Science, Mahidol University Email : somphong.nar@mahidol.ac.th Hemodynamic
More informationDisseminated intravascular coagulation (DIC) Dr. Klara Vezendi Szeged University Transfusiology Department
Disseminated intravascular coagulation (DIC) Dr. Klara Vezendi Szeged University Transfusiology Department Disseminated intravascular coagulation (DIC, consumptive coagulopathy) is a clinicopathologic
More informationINFLAMMATION. 5. Which are the main phases of inflammation in their "sequence": 1. Initiation, promotion, progression.
INFLAMMATION 1. What is inflammation: 1. Selective anti-infective pathological reaction. 2. Pathological process, typical for vascularized tissues. 3. Self-sustained pathological condition. 4. Disease
More informationThrombosis and emboli. Peter Nagy
Thrombosis and emboli Peter Nagy 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:
More information