L10: Thrombosis and Embolism

Question 1

What is the difference between a thrombus and a clot?

Answer 1

Thrombus–> Solid mass of blood inside the blood vessel (circulatory system)
Clot–> Solid mass outside the vessel wall

Question 2

What is thrombosis?

Answer 2

Process of formation of a blood clot

Question 3

What is Vichrow’s triad?

Answer 3

Explains how a thrombus is formed
Abnormality in two of the following:
1- Vessel wall
2- Blood flow
3- Blood composition

Question 4

How does changes in the vessel wall lead to thrombus formation?

Answer 4

Endothelial damage–> platelets adhere to exposed vWB factor complex
Atheroma, direct trauma, inflammation, haemodynamic stress of hypertension
Normal blood flow usually washes platelets away–> stasis in flow results in formation

Question 5

How do problems in blood flow result in thrombus formation?

Answer 5

Stasis–> slowing of blood
Turbulence–> non lamina flow, not smooth
Platelets have better chance at sticking to the endothelial wall
Veins–> slower flow, valves cause turbulence, pockets of stagnant blood
Slow in cardiac failure, bed rest, immoblised
Turbulent around abnormal heart valves, athersclerotic plaques, aneurysms
Turbulent flow can also cause damage to endothelium

Question 6

How does problems with the blood components lead to thrombus?

Answer 6

Hypercoagulable states--> sticky blood
Increased levels of fibrinogen and factor VIII
Risk increases:
Smokers
Pregnancy and post partum
Post-operative patients
Cancer patient 
Trauma and burns
Oral contraceptive pill etc...
Inherited disorders--> anticoagulation disorders (protein C or S deficiency) antithrombin III deficiency

Question 7

Compare and contrast arterial and venous thrombus?

Answer 7

Arterial 
--> Pale
--> Granular
--> Lines of Zahn
--> Lower cell content
Venous
--> Deep red
--> Gelatinous
--> Soft
--> Higher cell content

Question 8

Formation of a thrombus?

Answer 8

1. Platelets are small–> more concentrated along the endothelium, catch in eddy behind valve, form an aggregate and settle on the wall of vessel (especially if damaged), more platelets aggregate
2. Fibrinogen–> fibrin
3. Binds platelets together and grow out of platelet layer
4. RBC get trapped covering platelets
5. Surface thrombogenic so traps platelets… process continues
6. Produces layers–> Lines of Zahn
7. More obvious in arteries as blood flows over the top

Question 9

How can you tell the difference between post mortum clots and pre-mortum thrombi?

Answer 9

Post mortum–> rubbery, shiny, less layers, not attached to intima

Question 10

What is the difference between a parietal and occlusive thrombus?

Answer 10

Parietal–> attached to the wall of the vessel and restricts lumen
Occlusive–> Fill and obstruct the lumen

Question 11

What do arterial thrombi tend to be?

Answer 11

Parietal

Occlusive tend to form over the atherosclerotic plaque–> cracked open–> can be fatal

Question 12

What is a thrombus in a cardiac valve called?

Answer 12

Vegetation
2-3cm in long and easily embolise
Usually left side of heart–> exposed to greater pressures
Microtrauma exposes thrombogenic subendothelial tissue–> can become infected particularly common in intravenous drug abusers

Question 13

What are the outcomes of thrombi?

Answer 13

Lysis
Propagation 
Organise
Recanalise
Embolise

Question 14

What is lysis?

Answer 14

Most likely when thrombi are small
Complete dissolution of thrombus
Fibrinolytic system active
Blood flow re-established

Question 15

What is propagation?

Answer 15

Progressive spread of thrombosis
Distally in arteries
Proximally in veins

Question 16

What organisation?

Answer 16

Reparative process
Ingrowth of fibroblasts and capilliaries (similar to granulation tissue)
Lumen remains obstructed

Question 17

What is recanalisation?

Answer 17

New channel lined with endothelium runs through occlusion

Restores blood flow

Question 18

What is embolisation?

Answer 18

Part of thrombus breaks off and embolises

Thromboembolism

Question 19

What are the clinical effects of thrombosis?

Answer 19

Artery

• Occlusion–> ischemia, infarction
  
  • -> depends on site and collateral circulation

Vein
- Congestion
- Oedema 
- Ischaemia
- Infarction 
repeated miscarriage- thromboembloism in uteroplacental vasculature

Question 20

What is an embolism?

Answer 20

Blockage of BV by solid, liquid or gas at site distant from origin
>90% are thromboemboli

Question 21

What is a thromboemboli? What are emboli composed of?

Answer 21

Piece of thrombus breaks off from main thrombus
Emboli–> Composed of body fat, bone marrow, material from atheromatous plaques, tumour fragments, parasite, bubbles of air or other gases, debris from injections, amniotic fluid, medial equipment, bits of brain or liver after trauma etc…

Question 22

What is a pulmonary emboli?

Answer 22

Passes from systemic vein–> lungs
Most from deep veins of the thigh and popliteal veins
Most are small and clinically silent
Multiple small= pulmonary hypertension
Large pulmonary emboli= sudden death (60%)

Question 23

What thromboemboli arise in the systemic circulation?

Answer 23

Arise from left heart, aneurysms and thrombi on ulcerated arthersclerosis
Embolise to lower extremities, brain, intestines, kidney, spleen and arms
Thrombi often seen in heart often:
- Infarct in LV–> thrombi on necrotic tissue–> heart beating–> emboli
- Atrial fibrillation–> decreased atrial contraction, dilation of left atrium, stagnation of blood, and thrombus formation
- Vegetations (heart valve thrombus)

Question 24

What are paradoxial emboli? How does it occur?

Answer 24

Pass from systemic veins–> systemic arteries
Bypass the lungs
- Small emboli pass through aterio-venous anastomoses in pulmonary circulation
- Defect in IVS or patent foramen ovalae (coughing or stretching increase RA/RV pressure pass R to L)

Question 25

What is an emboli from an atheroma?

Answer 25

Released into blood when plaque cracks open
Often affects intestine = abdominal pain
TIAs (transient ischameic attacks)–> emboli in brain
Atheroembolus in carotid arteries
Very small so usually break up before lasting damage is done

Question 26

What are fat and bone marrow emboli?

Answer 26

Complications usually from bone fracture can be from liposuction
Fat droplet coalesce–> sucked into venules
Respiratory distress and neurological symptoms (if pass through the lungs into the brain)

Question 27

What are the two types of gas emboli?

Answer 27

Air embolism

• -> Negative pressure in veins in chest and head during inspiration in upright position –> draw in air after trauma of neck and chest
• -> Labour–> air enters uterus, forced into open veins during contraction
• -> Air –> right heart–> frothy mass stops circulation

The bends

• -> Diver–> surrounding air high than land–> increased gases (nitrogen) dissolved in blood–> surface too quickly–> depressurisation gas released into body as bubble–> emboli in blood
• -> nitrogen –> lipid-rich tissue targeted–> CNS

Treatment–> prompt recompression in compression chamber to force gas back into solution

Question 28

What is an amniotic fluid embolism?

Answer 28

Complication of labour and caesarean section
Amniotic fluid–> maternal circulation through tear
Sudden respiratory distress, hypotension, seizures, loss of consciousness and disseminated intravascular coagulation (DIC) (prothrombotic substances in amniotic fluid)
Microscopic emboli are found in the lungs

Question 29

What do we mean by a talcum emboli?

Answer 29

Microscopic foreign body
Lungs of drug abusers
Drugs cut with talcum powder
Pulmonary symptoms

Question 30

What are the complications that arise with a pulmonary embolism?

Answer 30

Massive PE >60% reduction in blood flow= rapidly fatal
Saddle emboli- bifurcation of lungs
Major PE- medium BV blocked, patient SoB +/- blood stained sputum
Minor PE- small peripheral pulmonary arteries block, assymptomatic or minor SoB
Reccurrent minor PR–> pulmonary hypertension

Question 31

How are thromboembolism prevented?

Answer 31

Prophylaxis–> treatment given or action taken to prevent disease
Prevent venous stasis or hypercoagulability
- Mobilise early post-op or illness
- Elevate legs
- Increase venous return–> compression stockings, calf muscle stimulation, passive calf muscle exercises (done by someone else)
- Anticoagulants

Question 32

How are thromboemboli treated?

Answer 32

Clot buster- streptokinase, alteplase (thrombolytic)
Intravenous heparin type drugs
Noval oral anticoagulants (Dabigatran, Rivaroxaban, Apixaban, Edoxaban)–> Riv, Api and Edo anti factor Xa, Dab reversible binds to active site in thrombin
Filters into IVC
Embolectomy–> removal of embolism
Oral warfarin

Question 33

How does warfarin work?

Answer 33

Interferes with Vit K metabolism
Dosage titrated to patients PT results–> INR results (international normalised ratio)- ratio of patient’s PT to normalised control

Question 34

How does Heparin work?

Answer 34

Forms an irreversible complex with antithrombin III resulting in activation

Question 35

How does Aspirin work?

Answer 35

Antithrombogenic
Irreversably acetylates an enzyme of prostagladin synthesis (cyclooxygenase)
Platelets can’t produce thromboxane A2 –> powerful platelet aggregator
Formation of haemostatic plug inhibited

Question 36

What are the predisposing factors for a deep vein thrombosis?

Answer 36

Immobility/ bed rest--> reduced flow rate
Post operative
Pregnancy/ post partum
Oral contraceptives
Severe burns 
Cardiac failure
Disseminated cancer
All cause stickier blood--> hypercoaguable state