Session 5: Thrombosis and Embolism Flashcards

1
Q

Definition of thrombus.

A

A solid mass formed from the constituents of the blood within the heart or vessels during life.

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2
Q

Definition of thrombosis.

A

Process of formation of a thrombus.

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3
Q

What three things are thrombosis dependent on?

A

Virchow’s triad:
Changes in vascular wall (endothelial damage)
Changes in blood flow (turbulent or slow flow)
Changes in the blood itself (hypercoagulability)

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4
Q

Referring to Virchow’s triad, when is arterial and cardiac thrombi likely to form?

A

When there is a site of endothelial damage or turbulent flow.

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5
Q

Referring to Virchow’s triad, when is venous thrombi likely to form?

A

Often seen where there is stasis.

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6
Q

How many components of Virchow’s triad are needed to produce thrombus?

A

Seems like only two out of three like stasis and hypercoagulability.

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7
Q

Give common causes of endothelial damage in vessels.

A

Myocardial infarction
Secondary to the haemodynamic stress of hypertension
Scarred heart valves
Trauma
Surgery
Inflammation
Surface of atherosclerotic plaque when they break open.

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8
Q

Explain how endothelial damage can lead to thrombus formation.

A

When there is a breach in the endothelium as in clotting platelets will adhere to exposed von Willebrand factor/factor VIII complex.

This is usually no problem when the blood flow is swift like in an artery because the platelet thrombi won’t be able to grow. This is because the swift blood flow will continuously wash away platelets, chemical mediators and clotting factors.

However if there is also stasis in the vessel this can allow the thrombus to grow bigger.

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9
Q

Referring to the stasis and endothelial damage, where are you most likely to see thrombus formation?

A

In veins because the blood flow is slower in veins.

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10
Q

What else in veins increases risk of thrombus formation?

A

The valves causing pockets of stagnant flow and also turbulent flow.

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11
Q

Give examples of conditions where blood flow might be particularly slow/turbulent in the veins.

A
Pregnancy where the woman is not moving
PAtiens on bed rest or immobilised
Lack of muscular contraction in the calves result in blood stasis.
Cardiac failure
Ulcerated atherosclerotic plaques
Within aneurysm
Around abnormal heart valves
After MI
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12
Q

What else can blood stasis/turbulent flow cause?

A

It can cause endothelial damage itself.

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13
Q

Causes of hypercoagulability

A
Pregnancy
After surgery
Fractures
Burns
Smoking
Cancer
Oral contraceptive pill
Factor V Leiden
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
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14
Q

How can pregnancy, post-surgery, trauma and burns result in hypercoagulability?

A

Increased circulating levels of fibrinogen and factor VIII leading to the increased coagulability

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15
Q

Where are you likely to see thrombus?

A

Platelets flow in the blood by the sides at the surface of the endothelium. This means that platelets are more likely to aggregate behind a valve. This is particularly common in endothelial injury or haemostasis. In surgery palettes aggregate more easily as well and platelet collection will grow more quickly.

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16
Q

Explain formation of a thrombus.

A

E.g. in haemostasis fibrinogen binds the platelets together and fibrin will grow out of the platelet layer. The fibrin will then trap red blood cells. This means a white layer (platelets) will be covered by a red layer (fibrin and red blood cells).
The surface of the red layer is thrombogenic and this means that platelets will adhere to the exposed fibrin. In this way a second white layer of platelets is formed. This happens over and over again, rinse and repeat.

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17
Q

Upon examination you can see the laminations by the naked eye. Thrombus is therefore a laminated structure.
What are the laminations called?

A

Lines of Zahn.

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18
Q

How do arterial thrombi and venous thrombi differ in appearance?

A

Arterial thrombi have more obvious lines of Zahn than venous thrombi.

Arterial:
Pale
Lines of Zahn
Granular
Low cell content
Venous:
Soft
Gelatinous
Deep red
Higher cell content
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19
Q

Post-mortem blood will clot and form thrombi.

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

A

Post-mortem thrombi have no laminations at all.

They are also more rubbery and shiny than pre-mortem thrombi and they are not attached to the intima.

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20
Q

Pain is not always present in thrombus formation. However it can be, why would it be?

A

It is usually painful in the superficial veins.

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21
Q

What is thrombophlebitis?

A

Painful superficial thrombi with associated inflammation in the wall of the vein.

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22
Q

What is a parietal thombus?

A

When the thrombus is attached to the wall of the vessel and restricts the lumen.

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23
Q

What is an occlusive thrombus?

A

When the thrombus fill and obstruct the lumen.

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24
Q

What do arterial thrombi tend to be? Parietal or occlusive?

A

Arterial thrombi tend to remain parietal. This is because of the flow of the blood in the arteries.

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25
Q

When can occlusive thrombi form in the arteries?

A

They usually form over an atherosclerotic plaque that has cracked open.

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26
Q

What is a vegetation? What’s the danger of vegetations`

A

A thrombus on a cardiac valve. They easily embolise.

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27
Q

Where do vegetations most commonly form? Why?

A

On the valves of the left heart.
Because they are exposed to greater pressures and therefore also to microtrauma which exposes thrombogenic subendothelial tissue.

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28
Q

What are the outcome of thrombi?

A
Resolution
Propagation
Organisation
Recanalisation
Embolisation
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29
Q

Explain resolution.

A

The thrombus dissolves

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30
Q

Explain propagation.

A

Progressive spread of the thrombosis and the thrombi will grow bigger and bigger.

This happens distally in arteries and proximally in veins.

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31
Q

Explain organisation.

A

Thrombus undergoes fibrous repair and forms a fibrous scar on the wall of the vessel.

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32
Q

Explain recanalisation.

A

In an occluding thrombus new channels lined with endothelium can run through the occlusion itself and restore blood flow. However the blood flow will have significantly smaller capacity than original vessel.

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33
Q

Explain embolisation. (Briefly)

A

Part of the thrombus breaks of and embolisms. This is called a thromboembolism when the embolus comes from a thrombus.

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34
Q

Thrombi that form where are more likely to embolise?

A

In the lower limbs such as the femoral, iliac and popliteal veins.

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35
Q

Most common clinical effects of thrombosis.

A

Occlusion of an artery at the site of the thrombus leading to ischaemia and infarction like in a myocardial infarction.

Pulmonary embolism, cerebrovascular accident from embolism

Congestion and oedema can lead to pain and skin ulcerations.

Repeated miscarriage.

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36
Q

What is an embolus?

A

A solid, liquid or gas that is carried by the blood and large enough to become impacted in a vascular lumen.

37
Q

Define embolism.

A

Sudden blocking of an artery by a thrombus or foreign material which has been brought to its site of lodgement by the blood current.

38
Q

What is a thromboembolus?

A

Embolus the arise from thrombus.

They are the most common emboli and when they occur they often occur in multiples.

39
Q

Drawing from that an embolus can be a solid, liquid or gas. More specifically, give examples of what an embolus can be.

A
Body fat
Bone marrow material from atherosclerotic plaque
Tumour fragments
Parasites
Bubbles of air or other gases
Debris injected intravenously
Amniotic fluid
Medical equipment
Bits of brain or liver after trauma.
40
Q

Can embolisation occur in veins? Why?

A

No. Because blood flow from smaller to larger vessels.

41
Q

When would objects carried by blood in veins embolise?

A

They go through right heart and embolise in the pulmonary arteries.

42
Q

Can embolisation occur in arteries? Why?

A

Yes. Because arteries go from larger to smaller.

43
Q

Where do pulmonary emboli most commonly arise?

A

From thrombi in the deep veins of the thigh and the popliteal vein.

44
Q

Symptoms of small pulmonary emboli.

A

Most pulmonary emboli are small and clinically silent.

Multiple small emboli can cause pulmonary hypertension.

45
Q

Complications of large pulmonary emboli.

A

When they result n more than 60% occlusion it can cause sudden death, cor pulmonale (right-sided heart failure) or cardiovascular collapse.

46
Q

What is a saddle emboli?

A

Large emboli that become lodged astride the bifurcation of an artery so it blocks both branches.

47
Q

Where do saddle emboli most commonly occur? What are the complications?

A

Usually in the bifurcations of the pulmonary arteries resulting in sudden death.

48
Q

Where do thromboembolism in the systemic arteries most commonly arise?

A

From the left heart, aneurysms and thrombi on ulcerated atherosclerosis.

49
Q

Where do thromboemboli in systemic arteries embolise?

A

To the lower extremities, brain, intestines, kidneys, spleen and arms.

50
Q

Where in the left heart can thrombi be seen?

A

Necrotic endothelium in the ventricular cavity
Left atrium
Valves

51
Q

Why would you see thrombi form on necrotic endothelium in the ventricular cavity?

A

Infarcts commonly affect the left ventricle. The necrotic endothelium is thrombogenic.
When the heart beats these often embolise.

52
Q

Why do you see thrombi form in the left atrium?

A

This is most commonly in atrial fibrillation causing decreased atrial contraction, dilatation of the left atrium and stagnation of blood. This can lead to thrombus formation.

53
Q

What are 80% of systemic thromboembolism from?

A

Cardiac mural thrombi in association with MI or atrial fibrillation.
Cardiac mural just means parietal in the heart.

54
Q

What are paradoxical emboli?

A

Thromboemboli that form in the systemic veins and embolism to the systemic arteries by bypassing the lungs somehow.

55
Q

How can paradoxical emboli occur?

A

Small emboli can pass through the arteriovenous anastomoses in the pulmonary circulation. This is how fat droplets pass through the lungs in fat embolism as well.

Larger emboli can only enter the systemic circulation by passing through a defect like an interventricular septum defect (VSD) or by a patent foramen ovale (PFO). In addition to the septal defect there must also be a production of increased pressure in the right side of the heart which is greater than in the left to push the thrombus thought the defect. This can be due to coughing, lifting or straining.

56
Q

What is an atheroma?

A

A gruel-like necrotic material that is present in atherosclerotic plaques.

57
Q

When might atheroemboli occur?

A

Can happen spontaneously and also during surgery or catheterisation for coronary artery disease.

58
Q

Where do atheroemboli commonly embolise?

A

To the intestine and present with abdominal pain.

Another common embolisation from atheroemboli is to the brain causing TIA.

59
Q

What is a TIA?

A

A transischaemic attack which are episodes of neurological dysfunction that appear suddenly, last minutes to hours and then disappear. They should have been resolved within 24 hours.

They are the result of microscopic emboli. Commonly atheroemboli from carotid arteries but can also be thromboemboli from the left heart.

60
Q

What most commonly cause fat emboli?

A

Complication of bone fractures or after liposuction.

61
Q

How come a bone fracture can result in fat emboli?

A

When a bone is fractured the bone marrow fat cells that are injured break up and release oil droplets which are sucked into gaping venules which have been damaged in the fracture.

62
Q

When do symptoms of fat embolism present?

A

Usually one to three days after the fracture.

63
Q

Why is there a delay between bone fracture and the fat embolism?

A

Because the oil droplets will coalesce over a period of a few days before being sucked into the venules.

64
Q

What are common symptoms of fat emboli? (Main category)

A

Respiratory symptoms and neurological symptoms.

65
Q

Why would you get resp. symptoms?

A

If the fat emboli lodge in the lungs.

66
Q

Why would you get neurological symptoms?

A

If droplets manage to squeeze through the lung in the same way as thromboemboli (arteriovenous anastomoses)

67
Q

Other symptoms of fat embolism.

A
Renal failure (emboli to kidneys)
Petechial rash (emboli to skin)
68
Q

Causes of air embolism.

A

Since there is negative pressure in the veins of the chest and head during inspiration in the upright position the veins can draw in air after trauma of the neck and chest.

An air embolism can also occur during labour as air can enter the uterus and be forced into open veins during uterine contraction.

69
Q

Where will air emboli end up from trauma to neck and chest?

A

Since they enter via veins they will end up in the right heart. Here they will start to bubble and gather as a frothy mass that stop circulation.

70
Q

What are the bends?

A

Gas embolism from nitrogen. Particularly nitrogen embolism that forms bubbles in skeletal muscle and joints which are very painful.

71
Q

What are the chokes?

A

Nitrogen embolism in lung tissue.

72
Q

How do nitrogen emboli occur?

A

Most commonly when a diver is breathing air underwater the pressure is higher down below which means increased amounts of gases become dissolved in the blood and body tissues. If a diver now resurfaces too quickly the sudden decrease in pressure can result in dissolved gases coming out of solution and being released into the body as bubbles.

These bubbles distort the tissues and act as emboli in blood.

73
Q

Why is nitrogen a particular problem?

A

Because nitrogen is fat soluble and when it comes out of the solution it produces persistent bubbles and focal ischaemia in lipid-rich tissues like the CNS.

74
Q

How do you treat the bends?

A

By prompt recompression in a special compression chamber to force the gas back into solution.
After this slow decompression will ensue.

75
Q

Causes of amniotic fluid embolism.

Mechanism behind the embolism.

A

Complication of labour and caesarean section when amniotic fluid enters the maternal circulation through a tear in the amniotic membranes.

76
Q

Symptoms and signs of amniotic fluid embolism.

A

Sudden respiratory distress, hypotension, seizures, loss of consciousness and DIC.

77
Q

What are microscopic emboli of foetal origin?

A

Emboli from foetus like epithelial squares, lanugo hair and meconium.
Usually embolise to lungs.

78
Q

What is a talcum embolus?

A

Microscopic foreign bodies with high drugs have been cut.

Found in the lungs of IV drug users.

79
Q

Prevention and treatment of thromboembolic disease.

A
General prophylaxis
Aspirin
Heparin
Warfarin
Filters
80
Q

Explain general prophylaxis.

A

Preventing venous stasis or preventing hypercoagulability.
E.g. in stasis patients after surgery or illness you encourage them to mobilise early. During and after and operation a leg can be elevated to increase venous return.

Also compression stocking, calf muscle stimulation, passive calf muscle exercises.

81
Q

Explain action of aspirin.

A

Antithrombogenic by irreversibly acetylating an enzyme of prostaglandin synthesis called cyclooxygenase. This means that platelets can’t produce thromboxane A2 which is a platelet aggregator.

82
Q

When is aspirin used?

A

To reduce risk of MI and stroke.

Prophylaxis against DVT in patients who are taking long haul flights.

83
Q

Action of heparin.

A

Forms irreversible complexes with antithrombin III.

84
Q

When is heparin used?

A

Prophylaxis against thrombosis but also to treat thrombosis. Given subcutaneously or intravenously.

85
Q

Action of warfarin.

A

Interferes with vitamin K metabolism (reactivation of vitamin K to the active form used in blood clotting).
It can take a few days for this drug to start working because all the vitamin K needs to be used up.

86
Q

When is warfarin used?

A

Prophylaxis against thrombosis and also to treat thrombosis.

87
Q

What is special about the dosage of warfarin?

A

It is titrated to the patients PT test specifically to the INR results.

88
Q

Explain INR briefly.

A

International normalised ratio forming a ratio of the patient’s PT to a normal control.

89
Q

What are filters?

A

Umbrella shaped filter in the inferior vena cava to prevent pulmonary emboli.