Download Free Medical Haemostasis and Coagulation PowerPoint Presentation

Haemostasis and Coagulation PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Haemostasis & Coagulation”.

This medical PowerPoint presentation is about haemostasis, the process of stopping bleeding from damaged blood vessels. It involves a complex interplay between platelets, blood vessels, and coagulation factors.

When a blood vessel is damaged, the bodys first response is to constrict the vessel to reduce blood flow to the area. This is followed by the formation of a platelet plug at the site of injury. Platelets are small cell fragments that circulate in the blood and are essential for haemostasis. They adhere to the damaged vessel wall and to each other, forming a temporary seal to prevent further bleeding.

The platelet plug is reinforced by the coagulation cascade, a series of enzymatic reactions that ultimately leads to the formation of a fibrin clot. Coagulation factors, which are present in the blood, are activated in a specific sequence to produce fibrin, a fibrous protein that forms a mesh-like structure around the platelet plug. This fibrin mesh consolidates the platelet plug and forms a stable clot that seals the damaged vessel.

Once the clot has formed, the body begins the process of fibrinolysis, which is the breakdown of the fibrin clot. This is important to prevent the formation of unwanted blood clots in the circulatory system.

Disorders of haemostasis and coagulation can lead to bleeding or thrombotic disorders. Bleeding disorders such as haemophilia are caused by deficiencies in coagulation factors, while thrombotic disorders such as deep vein thrombosis (DVT) are caused by an excessive formation of blood clots.

Tags : Haemostasis, Coagulation, blood vessels, platelets, blood vessels, coagulation factors, Hematology, Hematology PowerPoint presentation

Published on : May 29, 2023 | Views : 1930 | Downloads : 5

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Haemostasis & Coagulation
Slide 2-

ppt slide no 2 content not found
Slide 3-

ppt slide no 3 content not found
Slide 4-

‘THE DOCTOR WAS IN SUCH A HURRY TO OPERATE ON MY FATHER, LIKE A CHILD WANTING A LOLLYPOP’
Slide 5-

When an incision is made , the blood clots
Slide 6-

A 68 year old woman with a history of a 12 kg weight loss over the past six months presents to the emergency room with a history of passing bright red blood per rectum. Her pulse is 95, her blood pressure 120/70. She has not seen a physician in 40 years. Study Questions: What history and physical exam information would you gather to assess this patient's coagulation system? If there is a problem present, what would be the most likely? What laboratory tests would you order to assess this patient's coagulation system?
Slide 7-

A 24 year old man is in the operating room for a massive liver injury sustained when his motorcycle hit a truck. After one hour of surgery he has received 15 units of packed cells and has developed diffuse oozing from the surface of his liver. Clots are no longer forming. His body temperature is 34oC. Study Question: What are the most common coagulation difficulties associated with massive transfusion? What is the management of each?
Slide 8-

HAEMOSTASIS
Slide 9-

OBJECTIVES Mechanism of coagulation Tests Abnormal thrombosis Abnormal bleeding
Slide 10-

HAEMOSTASIS Keeps blood in fluid state & in circulation Prevents blood loss
Slide 11-

Haemostasis Four interconnected mechanisms form the basis of hemostasis: (a) blood vessel contraction (b) platelet plug formation (primary hemostasis) (c) clot stabilization with fibrin cross-linking (secondary hemostasis) (d) endogenous fibrinolysis.
Slide 12-

What is involved in Haemostasis? Blood vessels Platelets Plasma coagulation factors Inhibitors Fibrinolytics
Slide 13-

Events in Haemostasis Vascular spasm Formation of platelet plug Formation of fibrin plug - Blood clot Re-establishment of endothelium
Slide 14-

Haemostasis Vasoconstriction Clean cut vessels > crushed vessels Partially transected > completely cut Veins are easily compressed Danger areas of bleed
Slide 15-

Haemostasis Platelet plug - White bodies or microthrombi Contact with subendothelial collagen swell irregular with pseudopods release ADP, thromboxane A2 , phospholipids , HMWK sticky & aggregate
Slide 16-

Haemostasis Fibrin clot: Severe trauma - 15-20 secs Minor trauma - 1-2 mts Retraction - 20-60 mts
Slide 17-

Haemostasis COAGULATION 3 steps: Prothrombin activator Prothrombin Thrombin Fibrinogen Fibrin
Slide 18-

Haemostasis Pathways Intrinsic - XII = slow Extrinsic - VII = fast Common pathway factor V Xa Prothrombin activator phospholipid, calcium
Slide 19-

Haemostasis Extrinsic Tissue extract factor VII factor X Intrinsic surface contact VII XII XII a XI a IX a X HMWK phospholipid calcium BOTH ARE ESSENTIAL
Slide 20-

COAGULATION FACTORS
Slide 21-

HAEMOSTASIS ACTIVATED PLATELETS Prothrombin activator {rate limiting factor} {THROMBOPLASTIN} CALCIUM PROTHROMBIN THROMBIN FIBRINOGEN FIBRIN MONOMERS CALCIUM XIII FIBRIN POLYMERS STABLE CLOT
Slide 22-

Haemostasis Clotting of 1 ml of blood: 3 mg of fibrinogen 100 microgram of prothrombin 10 microgram of factor X 0.1 microgram of factor VIII
Slide 23-

HAEMOSTASIS PRODUCTION OF CLOTTING FACTORS Fibrinogen liver II, VII, IX, X liver with vit K VIII, V, XII endothelium XIII platelets
Slide 24-

HAEMOSTASIS THROMBIN Intensely proteolytic Activates factor V ,VIII, XIII Releases phospholipid from endothelium & platelet Activates protein C
Slide 25-

HAEMOSTASIS Clot retraction serum plasma [fibrinogen + consumed clotting factors] Platelets
Slide 26-

ppt slide no 26 content not found
Slide 27-

ppt slide no 27 content not found
Slide 28-

ppt slide no 28 content not found
Slide 29-

ppt slide no 29 content not found
Slide 30-

HAEMOSTASIS CONTROL Fibrinolysin or Plasmin Plasminogen activator DIGESTS ACTIVATES fibrin factor XII fibrinogen kinin factor VII complement factor V,XII prothrombin Inhibited by- alpha 2 plasmin inhibitor .
Slide 31-

HAEMOSTASIS Why does not blood clot normally ? Endothelium Fibrin & Antithrombin smooth thrombin fibrin [85-90%] glycocalyx antithrombin thrombomodulin prostacyclin heparin sulfate tissue plasminogen activator ADP ase
Slide 32-

HAEMOSTASIS Why does not blood clot normally? Heparin Thrombin Alpha 2 macroglobulin Thrombin C 1 inhibitor XII a, Kallikrein Alpha 1 antitrypsin XI a, Elastase Protein C Va, VIIIa
Slide 33-

Tests of blood coagulation 1. Bleeding time: 2.Clotting time: {modified Ivy’s method} {Lee & White method} N = 1-6 mts N = 6-10 mts in glass platelet plug N = 20-60 mts in Prolonged in: siliconized tubes Thrombocytopenia Measures intrinsic & Thrombasthenia common pathway Von-Willebrand’s disease
Slide 34-

Tests of blood coagulation Prothrombin time: { Quick’s one stage test } calcium oxalated blood from patient clot tissue thromboplastin N = 12 secs extrinsic & common pathway
Slide 35-

Prothrombin time contd... Prolonged in: 1. Oral anticoagulant drugs 2. Liver disease, obstructive jaundice 3. Vit K deficiency 4. D I C 5. Deficiency of factor VII , X, V, II SPECIFIC FOR FACTOR VII [ With X & V APTT is also prolonged]
Slide 36-

PARTIAL THROMBOPLASTIN TIME[ activated ] Contact activation KAOLIN + of factor XII + pt’s = Clot CEPHALIN blood phospholipid Intrinsic & Common pathway
Slide 37-

Partial thromboplastin time[activated ] contd….. Prolonged in: 1. D I C 2. Liver disease 3. Massive transfusion of stored blood 4. Heparin 5. Circulating anticoagulants 6. Deficiency of clotting factors other than VII 7. Haemophilia
Slide 38-

THROMBIN TIME PLASMA + THROMBIN CLOT Assesses fibrinogen Prolonged in : 1. Hypofibrinogenemia DIC CONGENITAL 2. FDP 3. Heparin [ assess with REPTILASE test ] 4. Dysfibrinogenaemia
Slide 39-

PLATELET COUNT N = 150 - 300 x 10 9 / L 80 x 10 9 / L Bleeding may follow trauma < 40 x 10 9 / L Spontaneous haemorrhage < 10 x 10 9 / L Lethal haemorrhage
Slide 40-

PRIMARY SCREENING TESTS Bleeding time Platelet count P T A P T T Specific tests- Factor VIII, XIII, fibrinogen Tests for fibrinolysis
Slide 41-

ABNORMAL HAEMOSTASIS Normal haemostasis Disorder of platelet function. Mild coagulation disorder Factor VII deficiency Early oral Anticoagulation 12-36 hrs Factor VIII, IX, XI, XII deficiency Prekallikrein, HMWK Deficiency, vWD, circulating anticoagulant
Slide 42-

ABNORMAL HAEMOSTASIS Vit K deficiency Oral anticoagulants Heparin, Fibrinogen Deficiency, Liver disease, Fibrinolysis Thrombocytopenia Massive transfusion Liver disease DIC
Slide 43-

SURGICAL SCREENING
Slide 44-

HAEMOSTASIS In a patient who bleeds: LIVER IMMUNOLOGIC RENAL COMPLETE CARDIAC WORK UP SEVERE INFECTION DRUGS Best screening test - HISTORY
Slide 45-

NATURAL ANTICOAGULANTS Antithrombin III Protein C and protein S
Slide 46-

NATURAL ANTICOAGULANTS Antithrombin III This is an inhibitor of thrombin, its action being potentiated by heparin. Congenital antithrombin III deficiency is inherited as an autosomal dominant. Heterozygotes may suffer from recurrent DVT, pulmonary embolism, and mesenteric thrombosis. Homozygotes present in childhood with severe arterial and venous thrombosis.
Slide 47-

NATURAL ANTICOAGULANTS Protein C and protein S These are synthesised in the liver and are dependant on vitamin K. Protein C degrades factors Va and VIIIa and promotes fibrinolysis by inactivating plasminogen-activator inhibitor I. Protein S is a cofactor for protein C and enhances its activity. Hereditary protein C defciency may occur, patients being more susceptible to DVT, PE, superficial thrombophlebitis, and cerebral venous thrombosis
Slide 48-

ANTICOAGULANT DRUGS Warfarin Warfarin is a coumarin derivative which is administered orally. It is a vitamin K antagonist and in effect induces a state analogous to vitamin K deficiency. It interferes with the activity of factors II, VII, IX and X. It delays thrombin generation, thus preventing the formation of thrombi. Warfarin is usually administered for 3–6 months following DVT or PE Lifelong warfarin is required for recurrent venous thromboembolic disease,some prosthetic heart valves, congenital deficiency of antithrombin III, deficiency of protein C or protein S,
Slide 49-

ANTICOAGULANT DRUGS Heparin Heparin potentiates the action of antithrombin III. Standard unfractionated heparin is administered i.v. or s.c. and has a half life of about 1 h. Low molecular weight heparin is used subcutaneously and has a longer biological half life.. Heparin does not cross the placenta and is, therefore, the drug of choice when anticoagulation is required during pregnancy. Bleeding due to overdose is managed by stopping the heparin and administering protamine sulphate intravenously. Side effects of heparin include thrombocytopaenia,hypersensitivity reactions, alopecia, and osteoporoi
Slide 50-

DISORDERS OF HAEMOSTASIS AND COAGULATION
Slide 51-

CONGENITAL HAEMOPHILIA A and B. Von WILLEBRAND’S disease. Defencies of factorXI and XII,prekallikrien,HMWkininogen. Defencies of factorVII,V and thrombin. Disorders of fibrinogen like a or hypofibrinogenemia or dysfibrinogenemia. Factor XIII defeciency.
Slide 52-

ACQUIRED VITAMIN K DEFECIENCY. ANTICOAGULANT DRUGS. HEPATIC FAILURE. RENAL FAILURE. THROMBOCYTOPENIA. THROMBOCYTOPATHY. HYPOTHERMIA. DIC.
Slide 53-

APPROACH
Slide 54-

HISTORY H\O bleeding,easybruising. Frequent or unusual mucosal bleeding. Metromenorrahgia. Haematuria. Epistaxis. Previous h\o prolonged bleeding asso with invasive procedures. Positive family history. Drug history like intake of NSAIDS,aspirin,etc.
Slide 55-

EXAMINATION Ecchymotic patches or petechiae on skin. Joint deformities. Adenopathy. Hepatospleenomegaly. Hypermobility of joints. Increased elaticity of skin.
Slide 56-

SCREENING TESTS CBC. Platelet count. PT. aPTT. Bleeding time. Fibrinogen level. Thrombin time. Platelet function tests. Specific factor assays.
Slide 57-

PROTHROMBIN TIME Measures function of factor VII,X, prothrombin and thrombin,fibrinogen and fibrin. Prolongation occurs when levels of factor V,VII or X fall. Seen in warfarin therapy and vit.k defeciency.
Slide 58-

aPTT Detects decreased levels ofHMWkininogen,prekallikrien,XII,XI,IX,VIII,V,X. Increased in heparin therapy.
Slide 59-

CONGENITAL DISORDERS HAEMOPHILIA A
Slide 60-

HAEMOPHILIA A Deficiency of factor VIII. X linked recessive disorder with males being affected exclusively. Severe bleeding if factor level<2%.Moderate bleeding with levels b\w 2%-5%.Mild bleeding with factor levels b\w 5%-30%. Patient has large haematomas and haemarthroses. Bleeding is prolonged for hours or days after injury. Lab tests show a prolonged Aptt with decreased factor VIII level,normal PT,bleeding time and vWF levels.
Slide 61-

HAEMOPHILIA A Desmopressin may temporarily raise factor VIII levels in mild disease. Can be given intranasally or iv and is ineffective in treating severe disease. Antifibrinolytic therapy with EACA and tranexemic acid with or without desmopressin is also effective in dental extarctions or paediatric patients. CRYOPRECIPITATE is a good source of factorVIII. One bag contains 80 units of factor VIII and 1U\kg increases levels by2%. Specific factor VIII concentrates are more popular now. Give 50U\kg stat then 30U\kg every 8 hrs for the first 2 days after surgery or injury.
Slide 62-

CONGENITAL DISORDERS HAEMOPHILIA B
Slide 63-

HAEMOPHILIA B Xlinked bleeding disorder with a deficiency of factor IX. Patient presents with deep bleeding and haemarthroses. Lab tests show increased Aptt with decreased factor IX levels, normal PT, BT,platelet count and factor VIII. Tt is by prothrombin complex concentrate which contains factor IX and all of the vit k dependent factors. HighPurity factor IX concentrate is also available.
Slide 64-

CONGENITAL DISORDERS Von WILLEBRAND’S DISEASE
Slide 65-

Von WILLEBRAND’S DISEASE Most common congenital bleeding disorder. vWF is an important stimulus for platelet aggregation and carrier protien for factor VIII. Type 1 is inherited as autosomal dominant and is characterized by quantitative defect in vWF. Type 2 has variable inheritance and there is qualitative defect in vWF. Type3 is autosomal recessive disease with absent levels of vWF. Patients present with mucosal bleeding,petechiae,epistaxis and menorrhagia. Tt is by desmopressin or cryoprecipitate.
Slide 66-

ACQUIRED DISORDERS VITAMIN K DEFECIENCY
Slide 67-

Platelet disorders Thrombocytopaenia This may be due to a failure of platelet production or increased destruction or sequestration of platelets, and abnormal platelet function. Abnormal platelet function may cause bleeding despite a normal platelet count. Abnormal platelet function may occur with: drugs, e.g. aspirin, non-steroidal antiinflammatory drugs carbenicillin, and ticarcillin; uraemia;septicaemia; and von Willebrand’s disease.
Slide 68-

Blood vessel wall abnormalities Blood vessel wall abnormalities These are rare and may be due to scurvy, steroids, Cushing’s syndrome, or Henoch-Schonlein purpura.
Slide 69-

VITAMIN K DEFICIENCY Vit k is required for the reaction that attaches a carboxyl gp to glutamic acid. Causes of def are inadequate dietary intake, Malabsorption,obstructive jaundice,biliaryfistula, Oral antibiotics and TPN. Tt is parenteral administration of vit k if there is no active bleeding. Administration of FFP rapidly corrects the coagulation deficit and is given in patients with ongoing bleeding. Correction of the etiology.
Slide 70-

ACQUIRED DISORDERS HEPATIC INSUFFICIENCY
Slide 71-

HEPATIC INSUFFICIENCY Liver is the site of synthesis of all clotting factors except factorVIII,vWF. Hepatic failure will result in coagulopathy. Asso with platelet dysfunction. Tt is by giving vitk,FFP,cryoprecipitate and platelets.
Slide 72-

ACQUIRED DISORDERS HYPOTHERMIA
Slide 73-

HYPOTHERMIA Usually seen in a lengthy open surgery on the abdomen or thorax. The coagulopathy is because of defect in platelet function,fibrinolytic activity,coagulation cascade enzyme. Intraoperatively all efforts should be made to keep the temp normal by warming fluids,heated ventilation and warm environment.
Slide 74-

ACQUIRED DISORDERS MASSIVE TRANSFUSION
Slide 75-

MASSIVE TRANSFUSION Defined as more than 10 units of transfused blood or replacement of the pts total blood volume within 24 hrs. Pts have thrombocytopenia,low fibrinogen and prolonged PT. These changes result from low temperature of blood,increased citrate level,increased k level,low pH,decreased ca level. Tt is by infusion of FFP,PLATELETS.
Slide 76-

ABNORMAL HAEMOSTASIS
Slide 77-

Misappropriately applied haemostasis
Slide 78-

ABNORMAL THROMBOSIS CLINICAL FEATURE SCORE 1.Active cancer 1 2.Paralysis, paresis, plaster 1 immobilisation 3.Bed ridden, major surgery 1 4.Tenderness on deep veins 1 5.Entire leg swollen 1 6.Calf swelling > 3 cms 1 7.Collateral superficial veins 1 ( non-varicose) 8.Pitting edema 1 9.Alternative diagnosis likely - 2
Slide 79-

POST-OP THROMBOSIS WHY? 1. NO MUSCLE CONTRACTION 2. FIBRINOGEN , PLATELET,vWF, FACTOR VIII 3. DECREASED ANTITHROMBIN III 4. SEPSIS 5. DAMAGE TO VEINS
Slide 80-

POST-OP THROMBOSIS PREVENTION: Intermittent compression or electrical stimulation Aspirin, dextran, di-pyridamole Low dose heparin, low molecular weight heparin Early mobilization Hydration T E D stockings
Slide 81-

ABNORMAL THROMBOSIS Prophylaxis RISK PATIENTS RECOMMENDED LOW Age < 40 Early ambulation Surgery < 30 mts Leg exercises No added risk factors MODERATE Age > 40 Heparin 5000 u S/C 12 hrly Abdominal / Thoracic beginning 2 hr pre – op. surgery > 30 mts External pneumatic Neurosurgery compression RISK OF DVT 20 – 30 %
Slide 82-

ABNORMAL THROMBOSIS Prophylaxis RISK PATIENTS RECOMMENDED HIGH Hip # LMWH Hip replacement Knee replacement + Open prostatectomy Ext. pneumatic Gyanecologic malignancy compression RISK 40 – 70 %
Slide 83-

ABNORMAL THROMBOSIS Investigations: Phlebography Plethysmography Radionucleotide scanning I 125 fibrinogen uptake Ultrasound & Duplex scanning
Slide 84-

ABNORMAL THROMBOSISTreatment PRINCIPLES 1.Prevent embolism 2.Prevent progression 3.Restore patency 4.Preserve valve function 5.Prevent chronic venous insufficiency
Slide 85-

ABNORMAL THROMBOSIS Treatment Heparin L M W H Oral anticoagulants Thrombolytic therapy Thrombectomy Vein grafting I V C filter Angioplasty & Stenting
Slide 86-

Surgery in patients on anticoagulants DRUG BLEEDING ELECTIVE EMERGENCY RISK SURGERY SURGERY 1 .HEPARIN Low / Moderate Discontinue high dose Same as elective Give low dose heparin High risk Discontinue 6 – 12 hrs Discontinue before surgery Give Protamine sulphate 2. L M W H -- Discontinue 12 – 24 hrs before surgery especially in high risk group
Slide 87-

Surgery in patients on anticoagulants DRUG BLEEDING ELECTIVE EMERGENCY RISK SURGERY SURGERY 3. Warfarin LOW Adjust dose to I N R < 2.5 Discontinue warfarin MODERATE ‘’ Discontinue warfarin FFP to decrease INR to < 2.5. HIGH Discontinue & allow P T to Discontinue warfarin normalize. Substitute with FFP , Vit K to heparin . normalize PT.
Slide 88-

Surgery in patients on anticoagulants Aspirin: Discontinue 1 week before surgery. Platelet transfusion DDAVP In emergency surgery Fibrinolytics: Wait for half life 6 min for TPA 23 min for Streptokinase 16 min for Urokinase EACA: Only in emergency. Weigh benefit Vs risk
Slide 89-

ABNORMAL HAEMOSTASIS BLEEDING
Slide 90-

ABNORMAL HAEMOSTASISBleeding Liver disease: Causes 1.Varices, gastritis, haemorrhoids 2.P T prolonged 3.Reduced platelets 4.Increased fibrinolysis 5.D I C Treatment Vit K, F F P, plasma exchange, platelet transfusion, DDAVP
Slide 91-

ABNORMAL HAEMOSTASIS Bleeding: Haemophilia Christmas disease Von-Willebrand disease
Slide 92-

Haemophilia Haematologist & laboratory Comfortable surgeon Blood bank Rehabilitation team No inhibitor Schedule surgery on Monday or Tuesday
Slide 93-

Haemophilia Pre-op orders : No IM medications No ASA containing compounds MINOR SURGERY: Factor VIII to 100 % Post-op EACA for 7-10 days MAJOR SURGERY: Factor VIII to 100 % ( 40 – 50 u/kg ) Keep at 30-50 % for 10 – 14 days Mild haemophilia: DDAVP , Cryoprecipitate
Slide 94-

ABNORMAL HAEMOSTASIS Bleeding: Haemophilia Christmas disease Von-Willebrand disease
Slide 95-

Christmas disease Minor surgery - EACA or Tranexamic acid 20 – 50 % activity for 2-5days Major surgery – Factor IX to 100 % activity for 7 – 10 days DDAVP no use
Slide 96-

ABNORMAL HAEMOSTASIS Bleeding: Haemophilia Christmas disease Von-Willebrand disease
Slide 97-

Von-Willebrand disease Type I : DDAVP for 2-3 days ( 0.3 microgram / kg ) Type II : more need for blood products DDAVP: vWF in 30 mts from storage site
Slide 98-

ABNORMAL HAEMOSTASIS Thrombocytopenia safe surgery- 50,000 - 100,000 / micro litre maintain values for 1 week treat cause
Slide 99-

ABNORMAL HAEMOSTASIS Aids: Cautery Laser Topical absorbable haemostat Gelatin sponge Oxidized regenerated cellulose Collagen Thrombin Fibrin seal
Slide 100-

ABNORMAL HAEMOSTASIS Aids: Packing Pharmacologic agents Trasylol Epsilon aminocaproic acid Tranexemic acid Desmopressin acetate
Slide 101-

ABNORMAL HAEMOSTASIS BLOOD PRODUCTS: FFP Cryoprecipitate Platelets
Slide 102-

CONCLUSION The more exotic these approaches become, the more one is compelled to emphasize that gentle handling, precise dissection and accurately applied haemostasis constitute much the art of surgery. Injecting, burning, stuffing, and scorching wounds is not likely to lead to a higher plateau of accomplishment. John A Collins , M.D
Slide 103-

THANK YOU