coagulation-anticoagulation balance and imbalance of haemostatic system
DESCRIPTION
Coagulation-Anticoagulation Balance and Imbalance of Haemostatic System. Clinical Significances of Hemostasis. Bleeding Disorders. Hemophilia A. VIII. Deficiency in vitamin K. von Willebrand disease. Deficiencies in factor IX. Antithrombin deficiency. Thromboembolism. Role of Vitamin K. - PowerPoint PPT PresentationTRANSCRIPT
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Coagulation-Anticoagulation Balance and Imbalance of Haemostatic SystemCoagulation-Anticoagulation Balance and Imbalance of Haemostatic System
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Hemophilia A
Deficiencies in factor IX
Deficiency in vitamin K
von Willebrand disease
Antithrombin deficiency
VIII
Clinical Significances of HemostasisClinical Significances of Hemostasis
Bleeding Disorders
Thromboembolism
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Role of Vitamin KRole of Vitamin K
Inactive prozymogen
Carboxylated prozymogens
Vitamin K-dependentcarboxylase
(Clotting factors II, VII, IX, X, protein C and S)
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1. Concepts: Disseminated Intravascular Coagulation (DIC) , Shwartzman reaction
2. Conditions and predisposing factor
3. Mechanism of DIC
4. Clinical and laboratory findings
5. Prevention and treatment principle
ContentsContents
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Disseminated Intravascular Coagulation (DIC)
Disseminated Intravascular Coagulation (DIC)
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A disorder of widespread micro-vascular thrombosis caused by
activation of coagulation with or without bleeding caused by
secondary fibrinolytic activation.
DefinitionDefinition
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Meningococcemia on the calves
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Meningococcemia associated purpura
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A 23-year woman, induced abortion, delivered one dead fetus.
Case PresentationCase Presentation
14 hrs after parturition, convulsion and obnubilation developed.
Large ecchymosis on extremities and abdomen.
After parturition, profluvium sanguis from vagina constantly.
BP: undetectable; platelet: 7,000; BT: 1 min; CT: 1min; PT: 18 sec; Fib:1.1g/L; 3P test (+)
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Infections (most common): Acute DIC: Bacteria and their toxins, fungi, viruses, rickettsiae; Chronic DIC: Any chronic infection (eg, tuberculosis, abscesses, osteomyelitis)
Malignancy: Acute DIC: Acute promyelocytic leukemia, acute monocytic leukemia, disseminated prostatic carcinoma Chronic DIC: Lung, breast, gastrointestinal malignancy
Obstetrical complications: Acute DIC: Abruption placenta, abortions (especially therapeutic abortions), amniotic fluid embolism, hemorrhagic shock Chronic DIC: Dead fetus syndrome
Trauma: Acute DIC: Massive tissue destruction, brain damage
Vascular disease: Acute DIC: Brain infarction or hemorrhage Chronic DIC: Aortic aneurysm, giant hemangioma
Venoms: Acute DIC: Snake, spider (rare)
Others: Acute DIC: Heparin-induced thrombocytopenia with thrombosis (HITT), purpura in newborns (homozygous protein C deficiency)
Conditions Causing DIC SyndromesConditions Causing DIC Syndromes
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DIC Predisposing FactorsDIC Predisposing Factors
Impaired clearance system: Liver, mononuclear phagocyte Shwartzman reaction;
Hypercoagulable state: e.g., pregnancy;
Disorder of microcirculation: e.g., giant hemangioma.
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Excessive clotting
Infection
Cancer
Childbirth, dead fetus, or surgery
Severe head injuryPoisonous snake
Clotting factors and platelets are depleted
Excessive bleeding occurs
Endothelial damage; tissue damage; director activation of factor X, damage of blood cells
Hypercoagulable stage
Hypocoagulable stage
Secondary fibrinolytic stage
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Roel of Endothelial CellRoel of Endothelial Cell
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Scanning electron micrograph of moderately active plateletScanning electron micrograph of moderately active platelet
Pseudopods
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Intrinsic Extrinsic
The “Cascade” theory of
Coagulation
The “Cascade” theory of
Coagulation
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Anticoagulation SystemAnticoagulation System
Macrophage, endothelial cell, etc
Serine-containing enzyme inhibitors; Protein C system;
Tissue factor pathway inhibitor;Fibrinolytic system, etc
Molecules
Cells
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Antithrombin III is the most important
a2-macroglobulinheparin cofactor II a1-antitrypsin
Controls at Thromblin LevelControls at Thromblin Level
Others:
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Protein S
Activated Protein C
Degradation of Va, VIIIa
Protein C
Thrombin
Thrombomodulin
Resistance to activated protein C in patients with thromboembolism
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tPA: tissue plasminogen activator; PAI-1: plasminogen activator inhibitor; AP: antiplasmin
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VEC
Heparin+ATIII
TFPI
PC, PS, TM
FDPS
Plasmin
tPA,uPA
TFPI: tissue factor pathway inhibitor; PC: protein C; PS: protein S; TM: thrombodulin; ATIII: antithrombin III; tPA:tissue plasminogen activator; uPA:urokinase; FDPS: fibrin degradation products; plasminogen activator-inhibitors type 1 (PAI-1);VEC: vascular endothelial cell.
PAI
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1. Bleeding at multiple sites (Ecchymoses of skin, mucous membranes; Visceral hemorrhage)
2. Organ dysfunction (Waterhouse-Friderichsen syndrome;
Sheehan’s syndrome)
3. Shock
4. Hemolytic anemia (microangiopathic hemolytic anemia)
Clinical findings
Clinical and Laboratory Findings in DICClinical and Laboratory Findings in DIC
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Integumentary system: Widespread hemorrhage and vascular lesions, Oozing from puncture sites, incision, mucous membranes, irregular-shaped cyanotic patches
Central nervous system: Subarachnoid hemorrhage, altered state of consciousness
Gastrointestinal system: Occult bleeding to massive gastrointestinal bleeding; abdominal distention; malaise, weakness
Pulmanary system
Renal system: hematuria, oliguria, renal failure
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1. Coagulation abnormalities: prolonged prothromb
in time, activated partial thromboplastin time, thr
ombin time; decreased fibrinogen levels; increas
ed levels of FDP (eg, “3P” test, D-dimer)
2. Platelet count decreased as a rule but may be fall
ing from a higher level yet still be normal
3. Schistocyte
Laboratory abnormalities
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Plasma Protamin Paracoagulation Test (“3P”test)
ProtaminFDP+Fibrin
FDP+Protamin Fibrin Aggregation
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Schistocyte
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1. Avoid delay2. Treat vigorously
(eg, shock, sepsis, obstetrical problems)
Treat the underlying disease
Treatment PrinciplesTreatment Principles
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Blood components as needed
Fresh frozen plasma
Platelet transfusions
Anticoagulants after bleeding risk is corrected
Manage the DIC
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SummarySummary
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Thank youThank you