thrombosis
DESCRIPTION
Lecture for 3rd year medical students on ThrombosisTRANSCRIPT
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Thrombosis
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Normal haemostasis
Well regulated process Maintain blood in a fluid, clot free
state in normal vessels Induce rapid and localized
haemostatic plug at the site of vascular injury
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Thrombosis Formation of a solid mass from the constituents of blood within the vasculature (blood
vessels / chambers of heart) During life
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The pathologic opposite of haemostasis is thrombosis
An inappropriate activation of normal haemostatic process in uninjured vasculature or thrombotic occlusion of a blood vessel after relatively minor injury
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Mechanism of thrombosis Platelets adhere to
endothelium forming a projecting mass
Liberation of thromboplastins from platelet aggregate leads to initiate coagulation cascade
Blood clot formation occurs
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Pathogenesis
Three primary influences predispose to thrombus formation.
These are described as Virchow’s triad
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Virchow’s triad
There are three main factors leading tothrombosis Damage to the endothelial cell layer
of blood vessel Changes to the flow of blood Alteration to the constituents of blood
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Endothelial factors
Normal vascular tree is lined by endothelial cells
Endothelium prevents elements of blood coming into contact with the subendothelial connective tissue which is highly thrombogenic.
Endothelial cell surface is resistant to thrombus formation normally
Endothelial cells can initiate both thrombogenic and antithrombogenic stimuli
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Thrombotic and antithrombotic mechanisms
Thrombotic ThromboplastinFactor VPAFvWF
Anti-thromboticThrombomodulinAnti thrombin IIIAlpha 2 macroglobulintPA
Normally these two groups are finely balanced to prevent thrombus formation. Damage to endothelium however will favour thrombosis.
Most significant in arterial thrombosis
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Damage to the endothelium
This is of most importance in arterial thrombosis.
The endothelial cell damage could be in the form of
Endothelial cells loss Hydrodynamic stresses causing metabolic
damage eg. Prolonged Hypertension, Turbulance
Toxins and immune mediated mechanisms and radiation
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Endothelial cells loss Atheromatous plaques: ulceration Damage by surgery Arteritis Indwelling vascular catheters Infusion of sclerosing chemicals
Hydrodynamic forces Prolong hypertension Turbulance
Toxins and immune mediated damage
Bacterial toxins Cigarette smoke Immune mediatd: transplant rejection,
immune complex disease Radiation
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Regardless of the cause of endothelial damage, the end results include
Exposure of subendothelial collagen
Adherence of platelets Exposure to tissue factor Local depletion of prostacyclin and
plasminogen activator
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Arterial thrombosis
Seen in coronary arteries, circle of Willis, small arteries of limbs and digits.
Common in aorta due to atherom a or arteriosclerosis
Due to high pressure and rapid flow , these are often platelet variety, exception is laminated thrombus in aneurisms
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Coronary thrombosis
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Occlusive coronary atherosclerosis
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Cardiac thrombosis Thrombi of pale variety
occur on the heart valves in rheumatic endocarditis
Thrombi can be seen on the surface of the infarctions
In SABE, ABE the thrombi are larger, mixed, friable and contain bacteria
In atrial fibrillation thrombi can be seen in the auricular appendage
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Rheumatic vegetations
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Venous thrombosis
Common due to slower flow, lower pressure with easy compressibility and eddy formation around valves
Usually start in the deep veins of the calf, frequently a propagating thrombus extending in to femoral and iliac veins
Common in patients who are immobilized
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Sites of venous thrombosis
Leg veins:immobiliity, post surgery, hypercoagulability
Pelvic veins: pueperal sepsis,post partum, pelvic surgery,
IVC: Tumour, extension from leg
Renal vein: Tumour compression
Portal/hepatic vein: Local sepsis, tumour
Cavernous sinus: Facial sepsis
SVC:Mediastinal tumour Axillary vein: Rucksac,
surgery
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Deep Vein thrombosis
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Deep vein thrombosis
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Preventing deep vein thrombosis
Patients are encouraged to move their legs regularly when confined to bed
Leg muscles are stimulated to contract during long operations using electrodes
Anticoagulants like heparin is used in patients with a risk.
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Venous thrombosis
Abdominal operations,child birth, cardiac disease, varicose veins, inflammation may potentiate the condition.
These are attached to vein wall only in few places
Hence chances of detachment and embolism are common
Can lead to pulmonary embolism
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Capillary thrombosis
Form when capillaries are damaged usually in acute inflammatory processes
Capillaries can be occluded by fibrin thrombi in cases of disseminated intravascular coagulation
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Varieties of thrombosis
White: mainly platelets, mainly seen in arteries where circulation is rapid. Often non occlusive
Red: Start as small platelet aggregate, and then produces fibrin strands entrangling the blood cells
Mixed and laminated: alternate layers of red and white thrombi. Common in aneurisms.
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Effects of thrombosis
Arterial: Infarction Ischaemia No effects if there are adequate
anastomoses
Venous: Anastomoses developed frequently to by
pass the obstruction
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Collateral circulation in venous thrombosis
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Arterial venous
Risk factors Atheroma Immobility
Pathogenesis
Turbulant flowDamaged endothelium
StasisHypercoagulability
Symptoms Sudden onset Slow onset
Complications
InfarctionArterial embolism
Pulmonary embolism
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Arterial & Venous thrombi
In propagation the tail builds up retrograde to the flow
Embolization is manly due to detachment of entire or almost the entire thrombus
The tail extends in the direction of flow (towards heart)
The loosely attached tail can fragment creating an embolus
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Sequels of thrombosis
Propagation
Resolution
Organisation
Recanalisation
Incorporation
Embolism
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Propagation of thrombus If the rate of flow is slow as
in a vein red cells are entrangled in the coagulum
In front and behind the platelet mass blood stagnates. Further formation of fibrin occurs and thrombus extends to the nearest junction
At the junction more platelets get deposited on the end of the mass. This gives the head of the thrombus a pale colour
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Resolution The thrombus is completely removed
leading to complete recanalisation. Occurs commonly in the small veins of
the lower limb as the venous intima contains more plasminogen activator than arterial intima.
By giving streptokinase we can enhance the process of thrombolysis.
But it should be given early after thombosis as the effect is going to be less on polymerised fibrin
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Organization
When the thrombus has formed PMNL and macrophages begin to degrade and digest fibrin
Later granulation tissue grows into the base of the thrombus and is converted into a mass of small blood vessels separated by connective tissue.
This can lead to complete block or partial block
In partial block, ultimately the thrombus shrinks and is covered by endothelial cells
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Recanalisation
Involves production of new endothelium lined channels that convey blood through the occlusive thrombus.
Clefts are produced by shrinkage and digestion of thrombus and are lined by endothelium
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Differences of antemortum thrombi and postmortum clots
Antemortum thrombi
Firm Dry granular
appearance Has lines of Zahn Has a point of
attachment to wall
Post mortum clots Cast of the vein Rubbery gelatinous Red current
jelly/chicken fat Not attached to
vein wall
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Antemortum / Post mortum clots
Antemortum Post mortum
clot clot
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Clinical problems 1 A 65 year old female patient was
admitted to accident and emergency ward with fracture of neck of R femur. Internal fixation was planned in three days time. Two days after the fracture patient complained of pain & swelling in the L calf & ankle.
What is the likely condition? How do you proceed with the
diagnosis?
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Clinical problem 2
A 55 year old female patient who underwent debulking surgery for carcinoma of cervix. On 5 th day of operation she developed sudden chest pain with difficulty in breathing.
ECG showed classical pulmonary embolism changes
What is the likely condition? What measures would have taken to
prevent this incident.
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Clinical problem 3 A 58 year old female patient
complained of swelling & redness in the left foot. On questioning she gives history of travelling from USA 4 days back. On examination she was afebrile.
What is the likely condition? What investigations are needed for
diagnosis? How do you prevent this? What is the management of this
patient?
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A 23 yr old man met with a road traffic accident and was admitted to accident service. He was found to have fractures of R femur, tibia, left femur and left radius. 24 hrs after admission he developed dyspnoea, tachycardia and restlessness. In few hours time patient progresses to a coma. He was found to have a petechial rash.
What is the likely condition? How would you confirm the diagnosis? Explain the pathogenesis of the signs and
symptoms.