Hemostasis Revision PDF

Revision PV TF neral -iCong t Br pla A Activ & constr Y HEAL Major pur b Fibri...

Revision PV TF neral -iCong t Br pla A Activ & constr Y HEAL Major pur b Fibri - pateintrmbe = stabe  Neural Brinjury +issue HEMOSTASIS BV - factor BV Injury & Neural · Tissue Factor BN - constriction - playeactivate - Blood Vessel - - - Platelet Coagulation - Constriction Activation Activation - - - (Thromboxane A2 ) & # Primary hemostatic plug - Reduced - 8 Plt-Fusion - Thrombin, Blood flow - Fibrin Stable Hemostatic Plug  HEMOSTASIS Stoppage of bleeding from the blood vessels Mechanisms - I Vasoconstriction of blood vessels - I primary II Platelet plug formation III Blood coagulation (fibrinogen fibrin) E seconding IV Clot - retraction V Fibrinolysis to dissolve the clot - S  PRIMARY HEMOSTASIS- VASCULAR PHASE Vascular constriction – first reaction of a severed blood vessel in nature - - - hours) ▪ [Stable clot 3– S (PRIMARY +SECONDARY HEMOSTASIS) - - - STABLE PLATELET PLUG  BLOOD COAGULATION EXTRINSIC PATHWAY INTRINSIC PATHWAY imitated Tissue trauma Contact activation 12 12 activate pathway Factor XII - XIIa 11 1 & Tissue thromboplastin , Ca++ Test :aPTT Factor XI - XIa 9 I = Test : PROTHROMBIN TIME Factor IX - IXa - A Factor VII - VIIa Factor VIII - VIIIa 7 - 7 Ptl.phospholipid, Ca++ COMMON Gactivation of clotting factor prothrom-thr Factor X 1 Ptl. PL, Ca++ - Factor V 5 ↳ platlet Fiborbran phospho... Prothrombin Thrombin 13 Factor XIII Fibrinogen FIBRIN ROLE OF THROMBIN IN = Fibmuge - HEMOSTASIS · · Fibro ou e fi · enhance platter aggregation - enhance prothrombin b thrombin > - Fibrinogen => 80  ROLE OF CALCIUM IONS IN CLOTTING Citrate ↳ Deionization o Laz No Ca++ → No Clotting - - Blood samples are prevented from clotting by adding: – Citrate ions → Deionization of Ca++ Deionization – Oxalate ions → ppt the Ca++ citration - cast of ↳ ① - precipitating ② oxalate ions y citrate oxalate i I i Ppk Deionization the cast of Ca2t Pa  INHIBITORS OF COAGULATION EXTRINSIC PATHWAY INTRINSIC PATHWAY Tissue thromboplastin, Ca++ Factor XII - XIIa Factor XI - XIa (TFPI) Factor IX - IXa Tissue factor pathway inhibitor Factor VIII -VIIIa Factor VII - VIIa Ptl. phospholipid, Ca++ COMMON Factor X PC, PS Ptl. phospholipid protein ( + protiens Ca++ Factor V Antithrombin Prothrombin Thrombin AT + Factor XIII heparin Fibrinogen FIBRIN Heparm INHIBITORS OF FIBRINOLYSIS =  INVESTIGATION OF A BLEEDING DISORDER SCREENING [ TESTS3 SPECIFIC TESTS Bleeding E u time Platelet count and morphology ~ - - O Prothrombin time (PT) & & Activated partial thromboplastin time (aPTT) - Thrombin time ⑧ - (TT) FXIII screening test 0 =  BLEEDING TIME (BT) Time taken for a standardized puncture to stop bleeding. - Prolonged : ▪ Abnormal blood vessels ▪ Thrombocytopenia's ▪ Thrombocytopathias ▪ von Willebrand disease ~ Normal bleeding time (Ivy method) – 1 – 6 minutes  LABORATORY DIAGNOSIS OF BLEEDING [50750x103/91] DISORDERS - 2 [150 450x183/9) - PLATELET COUNT thrombocytopenia - - ▪ Normal count is 150 – 450 x O - 103/µl ▪ Decreased count – [Thrombocytopenia3  Laboratory Test [A] (Thromboplastin) 5 ⑭  International Normalized ratio(INR) - evaluate doses Therapeutic Evaluate therapeutic doses of Warfarin - - of warfarin - Identify patients at higherG - - risk for bleeding - Identify patient Identify cause of: - Bleeding Deficiencies - Barn Vit k b Increased Levels of International Normalized - > - liver disease Ratio seen in Disseminated Intravascular Coagulation (DIC) ~ Liver disease => VitaminO - K deficiency Warfarin = INR of 1 is normal INR ofJ2-3 should be maintained in patients on warfarin => therapy  PATHOGENESIS OF BLEEDING DISORDERS ▪ Vascular defects ▪ Quantitative platelet defects - Thrombocytopenia ▪ Qualitative platelet defects – Thrombocytopathias ▪ Coagulation defects ▪ Excessive fibrinolysis  VASCULAR/PLT COAGULATION DEFECT DEFECT Nature of bleeding Petechiae and purpura Hematomas History of prolonged hemarthrosis, epistaxis bleeding History of prolonged bleeding Sites Skin and mucous Deeper tissues, organs, membranes joints Bleeding tests Bleeding time is Bleeding time & plt. prolonged, plt – normal/↓ count normal Coagulation tests Coagulation tests normal Coagulation tests abnormal  PETECHIAE & PURPURA Vascular disorder Platelet disorder Petechiae – small 1- 2 mm bleeding spots Purpura – confluent petechiae – 0.3 – 1 cm. in diameter  HEMATOMA ECCHYMOSES Coagulation disorders Hematoma – hemorrhage leading to extravasation of blood outside the blood vessels – collection of blood within tissues Ecchymoses – bruise – spread of blood under the skin  VASCULAR DISORDERS Causes:. 6 chronic Vitamin C deficiency (scurvy) Glucocorticod use Infectious and hypersensitivity vasculitis = - - - E Systemic amyloidosis 3 systemic = amyloidosis [ Chronic glucocorticoid use,J - rare ① - inherited conditions affecting the connective tissues  VASCULAR DISORDERS CLINICAL FEATURES & LABS - ▪Do not cause serious bleeding defects - - 00 ▪Small hemorrhages (petechiae and purpura) in skin - and mucous membranes - LABORATORY INVESTIGATIONS: Bleeding time - prolonged Platelet count, and coagulation tests - normal  QUANTITATIVE DISORDER - THROMBOCYTOPENIA Defined as reduced in the platelet count< 150, 000/µL that characterized by & spontaneous bleeding, a prolonged bleeding time, and a normal PT and PTT. Prombin partiat thrombo ▪ The risk of bleeding depends on the level of the platelet count: plasten time = O Mild J Moderate Severe & thrombocytopenia thrombocytopenia thrombocytopenia (platelet -