BLEEDING AND CLOTTING
ABNORMALITIES
SUPREET KUMAR
BLEEDING
WHAT IS BLEEDING ???
Bleeding, technically called as
HAEMORRHAGING is the loss or
escape of blood from the
circulatory system…
BLEEDING CAN EITHER BE :-
1) EXTERNAL
2) INTERNAL
TYPES OF BLEEDING
A) CLASS I HAEMORRHAGE : 10-15 % of blood
volume
B) CLASS II HAEMORRHAGE : 15-30 % of blood
volume
C) CLASS III HAEMORRHAGE : 30-40 % of blood
volume
D) CLASS IV HAEMORRHAGE : > 40 % of blood
volume
CAUSES OF BLEEDING
A)TRAUMA
- Lacerations
- Incisions
- Contusions
- Crush injuries
B)UNDERLYING MEDICAL CONDNS
- Anatomical defects
- Cancer & infections
- Disorders of hemostasis
- Drugs & Anticoagulation therapy
A DELICATE BALANCE
HEMOSTASIS
HEMOSTASIS is the co-ordinated sequence of
events that eventually stops the bleeding..
EFFECTIVE HEMOSTASIS :-
A) Response should be rapid
B) Response should be localised to the region of
damage
C) Response should be carefully controlled
MECHANISMS THAT REDUCE
BLOOD LOSS
THERE ARE 3 IMP MECHANISMS :-
1) VASCULAR SPASM
2) PLATELET PLUG FORMATION
> Platelet adhesion
> Platelet release action
> Platelet aggregation
3) BLOOD CLOTTING
CLOTTING
BLOOD CLOTTING
DEFINITION :
The process of formation of jelly like substance over
the ends and within the walls of the blood vessels,
with the resultant stoppage of blood flow ..
> Clotting involves a series or a cascade of
chemical reactions that culminates in formation of
FIBRIN THREADS.
> Clotting involves specific substances known as the
CLOTTING FACTORS.
CLOTTING FACTORS
NUMBER NAME OF FACTOR SOURCE ACIVATION
I FIBRINOGEN LIVER COMMON
II PROTHROMBIN LIVER COMMON
III THROMBOPLASTIN PLATELET EXTRINSIC
IV CALCIUM IONS PLATELET
& BONE
ALL PATHWAYS
V LABILE FACTOR LIVER &
PLATELET
EXTRINSIC
AND
INTRINSIC
VII PROCONVERTIN LIVER EXTRINSIC
VIII ANTIHEMOPHILIAC
FACTOR A
LIVER INTRINSIC
CLOTTING FACTORS
NUMBER NAME OF THE
FACTOR
SOURCE ACTIVATION
IX ANTIHEMOPLHILIAC
FACTOR B
LIVER INTRINSIC
X STUART-PROWER
FACTOR /
THROMBOKINASE
LIVER INTRINSIC AND
EXTRINSIC
XI PLASMA
THROMBOPLASTIN
ANTECEDENT
LIVER
INTRINSIC
XII HAGEMAN FACTOR LIVER INTRINSIC
XIII FIBRIN STABILISING
FACTOR
LIVER AND
PLATELETS
COMMON
PATHWAY
THE CLOTTING CASCADE
CLOTTING is a complex cascade of enzymatic reactions in
which each clotting factor activates many molecules of the
next one in a fixed sequence…
CLOTTING CAN BE DIVIDED INTO 3 STAGES
1) THE 2 pathways : EXTRINSIC & INTRINSIC Leading to
formation of PROTHROMBINASE
2) PROTHROMBINASE converts PROTHROMBIN into
enzyme THROMBIN
3) THROMBIN converts soluble FIBRINOGEN into insoluble
FIBRIN
SOME FAQs
1) WHAT IS THE NEED FOR 2 PATHWAYS ??
2) WHAT ARE THESE EXTRINSIC AND INTRINSIC
PATHWAYS ??
3) WHY ARE THEY CALLED SO ??
4) HOW DOES THE INSOLUABLE FIBRIN FORMED IN
THE LAST STEP OF THE CASCADE LEAD TO CESSATION
OF BLEEDING ??
CLOT RETRACTION
ONCE the clot is formed
IT plugs the ruptured area of blood vessel & thus stops
further bleeding
CLOT RETRACTION is the consolidation of the fibrin
clot
AS the clot retracts , it pulls the edges of the damaged
vessels close to each other and bridges the gap caused
due to the trauma or injury and hence leads to arrest of
bleeding
HEMOSTATIC CONTROL MECHANISMS
REGULATION of hemostasis is of optimum
importance
The body has an in built mechanism to CONTROL
AND REGULATE the process of hemostasis.
1) THE FIBRINOLYTIC SYSTEM
2) PROSTACYCLIN
3) NATURAL ANTI COAGULANTS IN BLOOD
WHY DOESN’T THE BLOOD CLOT
WHILE FLOWING THROUGH THE
VESSELS ??
1) THE ENDOTHELIAL LINING OF THE VESSEL
2) AXIAL FLOW OF THE BLOOD
3) VELOCITY OF THE BLOOD FLOW
4) NATURAL ANTICOAGULANTS
DYSREGULATION OF THE
HEMOSTATIC MECHANISM …
> CLOTTING is a dynamic process that involves
AMPLIFICATION and POSITIVE FEED BACK CYCLE.
> DYSREGULATION in the control mechanism can
lead to uninhibited clotting and hence a large clot called
THROMBUS is formed.
> THROMBUS has the potential to clog the vessels
and impair the blood flow that has hazardous
consequences.
THROMBUS FORMATION
VIRCHOW’S
TRIAD
ENDOTHELIAL INJURY
STASIS OF
BLOOD
HYPER
COAGULABI
LITY
VENOUS THROMBI : INITIAL
PHASE
MASSIVE THROMBUS IMPAIRING
BLOOD FLOW
VESSEL OCCLUDED BY THE THROMBUS
AN APPROACH TO BLEEDING DISORDERS
1) HISTORY
* Site of bleeding
* Duration of bleeding
* Precipitating factors of the bleeding
* History of previous operative procedures
* Family history
* History of drug intake
2) EXAMINATION
* Look for BRUISES,PURPURA,TELANGIECTASIA
* Examination of joints ( HAEMOPHILIA )
* stigmata of liver diseases
* SPLEENOMEGALY ( indicates thrombocytopenia )
MANAGEMENT OF BLEEDING
DISORDERS
INVESTIGATIONS TREATMENT
INVESTIGATIONS IN CASE OF A BLEEDING
DISORDER
* PLATELET COUNT
* BLEEDING TIME
* CLOTTING TIME
* PROTHROMBIN TIME
* ACTIVATED PARTIAL THROMBOPLASTIN TIME
* FIBRINOGEN LEVEL
* CLOT RETRACTION TIME
* ACTIVATED CLOTTING TIME
* PLASMA THROMBIN TIME
TREATMENT MODALITIES
* TREATMENT IS DEPENDENT ON THE TYPE OF
BLEEDING DISORDER
* THE MAIN AIM OF THE TREATMENT IS TO
REPLACE THE COMPONENT OR THE FACTOR
WHOSE DEFICIENCY LEADS TO BLEEDING
AN APPROACH TO CLOTTING DISORDERS
1) HISTORY
* Careful history taking is important for evaluation
* Family history should be enquired about
2) EXAMINATION
Careful evaluation of the signs and symptoms
* Pain
* swelling
* Redness at the site and other relevant symptoms
INVESTIGATIONS FOR ABNORMAL CLOTTING
OR THROMBOTIC DISORDERS
1) BLOOD EXAMINATION
* D- DIMER
* CBC
* COAGULATION STUDIES BT,CT,APTT,FIBRINOGEN
* LIVER ENZYMES
2) IMAGING STUDIES
* DOPPLER
* ULTRASOUND
* DUPLEX AND THERMOGRAPHY
TREATMENT MODALITIES FOR ABNORMAL
COAGULABILITY
ANTI-THROMBOTIC DRUGS ARE THE DRUGS USED FOR
TRAETMENT OF HYPER COAGULABILITY
ANTI THROMBOTIC DRUGS
ANTI PLATELET
DRUGS
ANTI
COAGULANTS
FIBRINOLYTIC
AGENTS
ANTI PLATELET DRUGS
1) ASPIRIN
2) THIENOPYRIDINES
* CLOPIDOGREL
* TICLOPIDINE
3) DIPYRIDAMOLE
4) GP II b / III a RECEPTOR ANTAGONIST
* ABCIXIMAB
* TIROFIBAN
ANTI COAGULANTS
1) HEPARIN
2) LMW HEPARIN
3) FONDAPARINUX
4) DIRECT THROMBIN INHIBITOR
* LEPIRUDIN
* BIVALIRUDIN
* ARGATROBAN
FIBRINOLYTIC DRUGS
1) STREPTOKINASE
2) UROKINASE
3) ALTEPLASE
4) TENECTEPLASE
5) RETEPLASE
6) ANISTREPLASE
Bleeding disorders

Bleeding disorders

  • 1.
  • 2.
  • 3.
    WHAT IS BLEEDING??? Bleeding, technically called as HAEMORRHAGING is the loss or escape of blood from the circulatory system… BLEEDING CAN EITHER BE :-
  • 4.
  • 5.
    TYPES OF BLEEDING A)CLASS I HAEMORRHAGE : 10-15 % of blood volume B) CLASS II HAEMORRHAGE : 15-30 % of blood volume C) CLASS III HAEMORRHAGE : 30-40 % of blood volume D) CLASS IV HAEMORRHAGE : > 40 % of blood volume
  • 6.
    CAUSES OF BLEEDING A)TRAUMA -Lacerations - Incisions - Contusions - Crush injuries B)UNDERLYING MEDICAL CONDNS - Anatomical defects - Cancer & infections - Disorders of hemostasis - Drugs & Anticoagulation therapy
  • 8.
  • 9.
    HEMOSTASIS HEMOSTASIS is theco-ordinated sequence of events that eventually stops the bleeding.. EFFECTIVE HEMOSTASIS :- A) Response should be rapid B) Response should be localised to the region of damage C) Response should be carefully controlled
  • 10.
    MECHANISMS THAT REDUCE BLOODLOSS THERE ARE 3 IMP MECHANISMS :- 1) VASCULAR SPASM 2) PLATELET PLUG FORMATION > Platelet adhesion > Platelet release action > Platelet aggregation 3) BLOOD CLOTTING
  • 14.
  • 15.
    BLOOD CLOTTING DEFINITION : Theprocess of formation of jelly like substance over the ends and within the walls of the blood vessels, with the resultant stoppage of blood flow .. > Clotting involves a series or a cascade of chemical reactions that culminates in formation of FIBRIN THREADS. > Clotting involves specific substances known as the CLOTTING FACTORS.
  • 16.
    CLOTTING FACTORS NUMBER NAMEOF FACTOR SOURCE ACIVATION I FIBRINOGEN LIVER COMMON II PROTHROMBIN LIVER COMMON III THROMBOPLASTIN PLATELET EXTRINSIC IV CALCIUM IONS PLATELET & BONE ALL PATHWAYS V LABILE FACTOR LIVER & PLATELET EXTRINSIC AND INTRINSIC VII PROCONVERTIN LIVER EXTRINSIC VIII ANTIHEMOPHILIAC FACTOR A LIVER INTRINSIC
  • 17.
    CLOTTING FACTORS NUMBER NAMEOF THE FACTOR SOURCE ACTIVATION IX ANTIHEMOPLHILIAC FACTOR B LIVER INTRINSIC X STUART-PROWER FACTOR / THROMBOKINASE LIVER INTRINSIC AND EXTRINSIC XI PLASMA THROMBOPLASTIN ANTECEDENT LIVER INTRINSIC XII HAGEMAN FACTOR LIVER INTRINSIC XIII FIBRIN STABILISING FACTOR LIVER AND PLATELETS COMMON PATHWAY
  • 18.
    THE CLOTTING CASCADE CLOTTINGis a complex cascade of enzymatic reactions in which each clotting factor activates many molecules of the next one in a fixed sequence… CLOTTING CAN BE DIVIDED INTO 3 STAGES 1) THE 2 pathways : EXTRINSIC & INTRINSIC Leading to formation of PROTHROMBINASE 2) PROTHROMBINASE converts PROTHROMBIN into enzyme THROMBIN 3) THROMBIN converts soluble FIBRINOGEN into insoluble FIBRIN
  • 20.
    SOME FAQs 1) WHATIS THE NEED FOR 2 PATHWAYS ?? 2) WHAT ARE THESE EXTRINSIC AND INTRINSIC PATHWAYS ?? 3) WHY ARE THEY CALLED SO ?? 4) HOW DOES THE INSOLUABLE FIBRIN FORMED IN THE LAST STEP OF THE CASCADE LEAD TO CESSATION OF BLEEDING ??
  • 21.
    CLOT RETRACTION ONCE theclot is formed IT plugs the ruptured area of blood vessel & thus stops further bleeding CLOT RETRACTION is the consolidation of the fibrin clot AS the clot retracts , it pulls the edges of the damaged vessels close to each other and bridges the gap caused due to the trauma or injury and hence leads to arrest of bleeding
  • 22.
    HEMOSTATIC CONTROL MECHANISMS REGULATIONof hemostasis is of optimum importance The body has an in built mechanism to CONTROL AND REGULATE the process of hemostasis. 1) THE FIBRINOLYTIC SYSTEM 2) PROSTACYCLIN 3) NATURAL ANTI COAGULANTS IN BLOOD
  • 23.
    WHY DOESN’T THEBLOOD CLOT WHILE FLOWING THROUGH THE VESSELS ?? 1) THE ENDOTHELIAL LINING OF THE VESSEL 2) AXIAL FLOW OF THE BLOOD 3) VELOCITY OF THE BLOOD FLOW 4) NATURAL ANTICOAGULANTS
  • 24.
    DYSREGULATION OF THE HEMOSTATICMECHANISM … > CLOTTING is a dynamic process that involves AMPLIFICATION and POSITIVE FEED BACK CYCLE. > DYSREGULATION in the control mechanism can lead to uninhibited clotting and hence a large clot called THROMBUS is formed. > THROMBUS has the potential to clog the vessels and impair the blood flow that has hazardous consequences.
  • 25.
  • 26.
    VENOUS THROMBI :INITIAL PHASE
  • 27.
  • 28.
    VESSEL OCCLUDED BYTHE THROMBUS
  • 29.
    AN APPROACH TOBLEEDING DISORDERS 1) HISTORY * Site of bleeding * Duration of bleeding * Precipitating factors of the bleeding * History of previous operative procedures * Family history * History of drug intake 2) EXAMINATION * Look for BRUISES,PURPURA,TELANGIECTASIA * Examination of joints ( HAEMOPHILIA ) * stigmata of liver diseases * SPLEENOMEGALY ( indicates thrombocytopenia )
  • 30.
  • 31.
    INVESTIGATIONS IN CASEOF A BLEEDING DISORDER * PLATELET COUNT * BLEEDING TIME * CLOTTING TIME * PROTHROMBIN TIME * ACTIVATED PARTIAL THROMBOPLASTIN TIME * FIBRINOGEN LEVEL * CLOT RETRACTION TIME * ACTIVATED CLOTTING TIME * PLASMA THROMBIN TIME
  • 32.
    TREATMENT MODALITIES * TREATMENTIS DEPENDENT ON THE TYPE OF BLEEDING DISORDER * THE MAIN AIM OF THE TREATMENT IS TO REPLACE THE COMPONENT OR THE FACTOR WHOSE DEFICIENCY LEADS TO BLEEDING
  • 33.
    AN APPROACH TOCLOTTING DISORDERS 1) HISTORY * Careful history taking is important for evaluation * Family history should be enquired about 2) EXAMINATION Careful evaluation of the signs and symptoms * Pain * swelling * Redness at the site and other relevant symptoms
  • 34.
    INVESTIGATIONS FOR ABNORMALCLOTTING OR THROMBOTIC DISORDERS 1) BLOOD EXAMINATION * D- DIMER * CBC * COAGULATION STUDIES BT,CT,APTT,FIBRINOGEN * LIVER ENZYMES 2) IMAGING STUDIES * DOPPLER * ULTRASOUND * DUPLEX AND THERMOGRAPHY
  • 35.
    TREATMENT MODALITIES FORABNORMAL COAGULABILITY ANTI-THROMBOTIC DRUGS ARE THE DRUGS USED FOR TRAETMENT OF HYPER COAGULABILITY ANTI THROMBOTIC DRUGS ANTI PLATELET DRUGS ANTI COAGULANTS FIBRINOLYTIC AGENTS
  • 36.
    ANTI PLATELET DRUGS 1)ASPIRIN 2) THIENOPYRIDINES * CLOPIDOGREL * TICLOPIDINE 3) DIPYRIDAMOLE 4) GP II b / III a RECEPTOR ANTAGONIST * ABCIXIMAB * TIROFIBAN
  • 37.
    ANTI COAGULANTS 1) HEPARIN 2)LMW HEPARIN 3) FONDAPARINUX 4) DIRECT THROMBIN INHIBITOR * LEPIRUDIN * BIVALIRUDIN * ARGATROBAN
  • 38.
    FIBRINOLYTIC DRUGS 1) STREPTOKINASE 2)UROKINASE 3) ALTEPLASE 4) TENECTEPLASE 5) RETEPLASE 6) ANISTREPLASE