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Dr. Shubhangi Agale
Associate Professor
Grant Govt Medical
College, Mumbai.
Functions of Normal Hemostasis
Maintain blood in a fluid and clot free
state
Induce a rapid and localised
hemostatic plu...
 Normal flow of liquid blood is
maintained by following properties of
endothelial cells
Antiplatelet properties
Anticoa...
Thrombosis
Definition:
Formation of solid
plug any where in
intact cardiovascular
system from
constituents of
blood duri...
Differential Diagnosis
1. Blood clot: A mass of coagulated blood
formed in vitro e.g. in a test tube.
2. Haematoma: Extra ...
Effects of Thrombosis :
“ Life threatening”
1. Ischaemic injury: Thrombi may
decrease/ stop the blood supply to part of
an...
Pathogenesis
Three primary influences predispose to
thrombus formation (Virchow triad)
Endothelial injury
Stasis or tur...
1. Endothelial Injury
1. Role of vessel wall.
2. Role of Platelets.
3. Role of coagulation system.
Role of vessel wall:-In...
Endothelial Injury
Intact endothelium has following functions-
1. Protects the flowing blood from thrombogenic
influence o...
A leads to –
Exposure of subendothelium ( collagen,
elastin, fibronectin,laminin,
glycosaminoglycans)which are
Thrombogen...
Conditions where vascular injury
predispose to formation of thrombi
Endocardial injury in myocardial
infarction, cardiac ...
Endothelial dysfunction without
endothelial loss
Hemodynamic stresses of Hypertension
Turbulent flow over scarred valves...
2. Alteration in Normal Blood Flow
Turbulence
a) Causes endothelial injury or dysfunction,
b) Forms counter currents and ...
Stasis and Turbulence
Bring platelets into contact with endothelium
Prevent dilution of clotting factors
Retard inflow ...
2. Alteration of blood flow
Formation of arterial and cardiac thrombi is
facilitated by turbulence in the blood flow.
St...
3. Hypercoagulability
Any alteration of the coagulation
pathways that predisposes to
thrombosis.
A) Primary or Genetic.
1....
4. Rare
a) Antithrombin III deficiency
b) Protein C
c) Protein S deficiency
d) Fibrinolysis defects
Hypercoagulability
Hypercoagulability
Secondary (Acquired):
A) High risk:
1. Prolonged bed rest/immobilisation
2. Myocardial infarction,
3. A...
Gross appearance
Arterial thrombi-White, mural,
firm ,pale.
Venous thrombi- red, occlusive, soft,
gelatinous.
Mixed or ...
Types of thrombi
Antemortem Thrombi.
1. Gross-
Dry,granular,firm,friab
le
2. Adherant to vessel
wall.
3. Shape- May or may...
Microscopy
Composition depends upon rate of flow of
blood.
Lines of Zahn are formed by light staining
aggregated platele...
Sites for Thrombi
Any where in cardiovascular system
Variable in size and shape
Arterial: at ulcerated Atherosclerotic ...
Mitral valve stenosis
Atrial fibrillation
Stasis due to hyperviscosity syndrome
(Polycythemia)
Deformed red cells (Sic...
Cardiac Thrombi
Vegetations of infective endocarditis.
Maccallum patch in RHD.
Myocardial infarction-subendocardial.
B...
Arterial Thrombi
Usually occlusive
Sites: Coronary, Cerebral, Femoral
Thrombus on atherosclerotic plaque or
sometimes v...
Arterial thrombi
Aorta:aneurysms,arteritis.
Coronary arteries:atherosclerosis.
Mesentric artery:atherosclerosis,arterit...
Venous thrombi
Veins of lower limbs:deep veins of legs,varicose
veins.
Popliteal,femoral and iliac veins:postoperative
s...
Arterial vs Venous Thrombus
Grossly: Thrombi are friable, a mixture of red and
gray in irregular layers, dull, and attach...
Capillary Thrombi
Vasculitis.
Acute inflammatory lesions.
Disseminated intravascular
coagulation.
Fate of Thrombus
Propagation: May accumulate more
platelet and fibrin leading to fibrosis
and inflammation
Recanalisatio...
Predisposing Factors
Primary(Genetic)factors:
1. Defficiency of antithrombin,Protien C / S.
2. Defects in fibrinolysis.
3....
1. Heart diseases- MI, CHF, RHD,
Cardiomyopathy.
2. Atherosclerosis.
3. Aneurysms of Aorta.
4. Varicose veins.
5. Nephroti...
Clinical Effects of Thrombosis
Cardiac thrombi- sudden death,
thromboembolism
Arterial thrombi- sudden death,
thrombosis...
Clinical Correlation
Arterial Thrombi: Obstruction of coronary
arteries (Myocardial infarction), cerebral,
Renal arteries...
Clinical Correlation
Deep Venous Thrombi: (Popliteal, femoral,
Iliac)
Occurs in cardiac failure due to stasis
Immobalis...
SUMMARY
Definition
Effects of thrombi
Pathogenesis
Virchow’s triad
Antemortem / postmortem thrombi
Gross appearance
...
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
Thrombosis- Dr. Shubhangi V. Agale
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Thrombosis- Dr. Shubhangi V. Agale

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Thrombosis
Definition:
Formation of solid plug any where in intact cardiovascular system from constituents of blood during life.

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Thrombosis- Dr. Shubhangi V. Agale

  1. 1. Dr. Shubhangi Agale Associate Professor Grant Govt Medical College, Mumbai.
  2. 2. Functions of Normal Hemostasis Maintain blood in a fluid and clot free state Induce a rapid and localised hemostatic plug at a site of vascular injury Hemostasis and thrombosis are regulated by: the vascular wall,
  3. 3.  Normal flow of liquid blood is maintained by following properties of endothelial cells Antiplatelet properties Anticoagulant properties Endothelium
  4. 4. Thrombosis Definition: Formation of solid plug any where in intact cardiovascular system from constituents of blood during life.
  5. 5. Differential Diagnosis 1. Blood clot: A mass of coagulated blood formed in vitro e.g. in a test tube. 2. Haematoma: Extra vascular accumulation of blood clot e.g. into the tissues. 3. Haemostatic plug: Blood clots formed in a healthy individual at the site of injury.
  6. 6. Effects of Thrombosis : “ Life threatening” 1. Ischaemic injury: Thrombi may decrease/ stop the blood supply to part of an organ/ tissue and cause ischaemia which may subsequently result in infarction. 2. Thromboembolism: The thrombus or its part may get dislodged and be carried along in the blood stream as embolus to lodge in a distant vessel e.g. Pulmonary embolism.
  7. 7. Pathogenesis Three primary influences predispose to thrombus formation (Virchow triad) Endothelial injury Stasis or turbulence of blood flow Hypercoagulability of blood
  8. 8. 1. Endothelial Injury 1. Role of vessel wall. 2. Role of Platelets. 3. Role of coagulation system. Role of vessel wall:-Integrity of vessel wall is important to maintain normal blood flow.
  9. 9. Endothelial Injury Intact endothelium has following functions- 1. Protects the flowing blood from thrombogenic influence of subendothelium. 2. Elaborates few anti thrombotic factors like heparin like substance,thrombomodulin,inhibitors of platelet aggregation,fibrinolysis-TPA. 3. Release of prothrombotic factors- Thromboplastin,von Willibrand’s factor,platelet activating factor,inhibitor of TPA.
  10. 10. A leads to – Exposure of subendothelium ( collagen, elastin, fibronectin,laminin, glycosaminoglycans)which are Thrombogenic. Brief vasoconstriction of small blood vessels –to reduce the blood flow. Major significance in arterial thrombi/in heart. Vasculr injury::
  11. 11. Conditions where vascular injury predispose to formation of thrombi Endocardial injury in myocardial infarction, cardiac surgery, prosthetic valves. Ulcerated plaques in athrosclerosis. Hypertension, Diabetis Mellitus, cigarette smoking. Arterial diseases.
  12. 12. Endothelial dysfunction without endothelial loss Hemodynamic stresses of Hypertension Turbulent flow over scarred valves Bacterial toxins Homocystinuria Hypercholesterolemia Radiation Products absorbed from cigarette smoke
  13. 13. 2. Alteration in Normal Blood Flow Turbulence a) Causes endothelial injury or dysfunction, b) Forms counter currents and local pockets of stasis Stasis: Disrupts normal blood flow Normal blood flow (Laminar): Platelets flow centrally separated from the endothelium by plasma
  14. 14. Stasis and Turbulence Bring platelets into contact with endothelium Prevent dilution of clotting factors Retard inflow of clotting factor inhibitor and permit the build-up of thrombi Promote endothelial cell activation, predisposing to local thrombosis
  15. 15. 2. Alteration of blood flow Formation of arterial and cardiac thrombi is facilitated by turbulence in the blood flow. Stasis initiates the venous thrombi even without evidence of endothelial injury. In turbulence and stasis, the normal axial flow of blood is disturbed so that the platelets come into contact with the endothelium. Inhibitors of coagulation fail to reach the site of thrombus resulting in enlargement of the thrombus site.
  16. 16. 3. Hypercoagulability Any alteration of the coagulation pathways that predisposes to thrombosis. A) Primary or Genetic. 1. Mutation in factor V gene (Leiden) 2. Mutation in Prothrombin gene. 3. Mutation in Methyltetrahydrofolate gene.
  17. 17. 4. Rare a) Antithrombin III deficiency b) Protein C c) Protein S deficiency d) Fibrinolysis defects Hypercoagulability
  18. 18. Hypercoagulability Secondary (Acquired): A) High risk: 1. Prolonged bed rest/immobilisation 2. Myocardial infarction, 3. Atrial fibrillation 4. Tissue damage (surgery, fracture, burns, cancer) 5. Prosthetic cardiac valves, 6. DIC 7. Heparin induced thrombocytopenia 8. Antiphospholipid antibody syndrome
  19. 19. Gross appearance Arterial thrombi-White, mural, firm ,pale. Venous thrombi- red, occlusive, soft, gelatinous. Mixed or laminated- Alternate red & white layers –Lines of Zahn.
  20. 20. Types of thrombi Antemortem Thrombi. 1. Gross- Dry,granular,firm,friab le 2. Adherant to vessel wall. 3. Shape- May or may not fit their vascular contours. 4. Surface contains apparent lines of Zahn. Postmortem clots. 1. Gross-Gelatinous, soft, rubbery. 2. Weakly attached. 3. Take the shape of vessel or its bifurcation. 4. The surface is chicken fat yellow covering the underlying red currant jelly.
  21. 21. Microscopy Composition depends upon rate of flow of blood. Lines of Zahn are formed by light staining aggregated platelets admixed with fibrin and dark staining layer of red cells. Red thrombi have more abundant red cells leucocytes & platelets entrapped in fibrin meshwork.
  22. 22. Sites for Thrombi Any where in cardiovascular system Variable in size and shape Arterial: at ulcerated Atherosclerotic plaque Cardiac: MIAuricular appendage, Stenotic valve Vessel bifurcation due to turbulence Venous thrombi: At site of stasis Firmly attached at the point of origin Arterial: Thrombi grow retrograde Venous: Thrombi extend towards heart
  23. 23. Mitral valve stenosis Atrial fibrillation Stasis due to hyperviscosity syndrome (Polycythemia) Deformed red cells (Sickle cell anemia) Clinical settings contributing to thrombosis
  24. 24. Cardiac Thrombi Vegetations of infective endocarditis. Maccallum patch in RHD. Myocardial infarction-subendocardial. Ball valve thrombus. Atrial appendages.
  25. 25. Arterial Thrombi Usually occlusive Sites: Coronary, Cerebral, Femoral Thrombus on atherosclerotic plaque or sometimes vasculitis Firmly adherent to injured endothelium Gray-white, friable
  26. 26. Arterial thrombi Aorta:aneurysms,arteritis. Coronary arteries:atherosclerosis. Mesentric artery:atherosclerosis,arteritis. Arteries of limbs:atherosclerosis,diabetes mellitus, Buerger’s disease, Raynaud’s disease. Renal artery: atherosclerosis,arteritis. Cerebral artery:atherosclerosis,vasculitis.
  27. 27. Venous thrombi Veins of lower limbs:deep veins of legs,varicose veins. Popliteal,femoral and iliac veins:postoperative stage,postpartum. Pulmonary veins:CHF,pulmonary hypertension Hepatic and portal vein:portal hypertension Superior vena cava:infections in head and neck Mesentric veins:volvulus,intestinal obstruction
  28. 28. Arterial vs Venous Thrombus Grossly: Thrombi are friable, a mixture of red and gray in irregular layers, dull, and attached to the endothelium Arterial thrombus: Dry, friable gray masses composed of almost regularly arranged layers of platelets and fibrin, irregularly mixed with small amounts of darker red coagulated blood (White or conglutination thrombus) Venous thrombus: Red, gelatinous (Stasis or red coagulation thrombus)
  29. 29. Capillary Thrombi Vasculitis. Acute inflammatory lesions. Disseminated intravascular coagulation.
  30. 30. Fate of Thrombus Propagation: May accumulate more platelet and fibrin leading to fibrosis and inflammation Recanalisation: Reestablish vascular obstruction Embolisation: Thrombi may dislodge Dissolution: Removed by fibrinolytic activity Organisation: Thrombi may induce flow
  31. 31. Predisposing Factors Primary(Genetic)factors: 1. Defficiency of antithrombin,Protien C / S. 2. Defects in fibrinolysis. 3. Mutation in Factor V. Secondary (acquired) factors: 1. Prolonged bed rest / Immobilisation. 2. Use of oral contraceptives. 3. Cigarette smoking. 4. Tissue damage: trauma,fractures,burns.
  32. 32. 1. Heart diseases- MI, CHF, RHD, Cardiomyopathy. 2. Atherosclerosis. 3. Aneurysms of Aorta. 4. Varicose veins. 5. Nephrotic syndrome. 6. Dissseminated cancers. Clinical conditions predisposing to thrombosis
  33. 33. Clinical Effects of Thrombosis Cardiac thrombi- sudden death, thromboembolism Arterial thrombi- sudden death, thrombosis of coronary artery Venous thrombi-thromboembolism, skin, thrombophlebitis, Capillary thrombi- DIC
  34. 34. Clinical Correlation Arterial Thrombi: Obstruction of coronary arteries (Myocardial infarction), cerebral, Renal arteries, and arteries of spleen Venous Thrombi: Congestion and ed ema distal to obstruction, may embolise to lung (Pulmonary embolism) causing death Superficial venous Thrombi: Congestion, swelling, pain, tenderness (rarely embolise)
  35. 35. Clinical Correlation Deep Venous Thrombi: (Popliteal, femoral, Iliac) Occurs in cardiac failure due to stasis Immobalisation Release of procoagulant substances from tissues: Puerperium, Amniotic fluid infusion into circulation in delivery Hypercoagulability: late pregnancy, Postpartum period Release of tumor associated procoagulant
  36. 36. SUMMARY Definition Effects of thrombi Pathogenesis Virchow’s triad Antemortem / postmortem thrombi Gross appearance Microscopy Types of thrombi Fate of thrombus Predisposing Factors Clinical Effects of Thrombosis
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Thrombosis Definition: Formation of solid plug any where in intact cardiovascular system from constituents of blood during life.

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