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IMED2002 UWA > Thrombosis, Embolism, and Tissue Infarction > Flashcards

Thrombosis, Embolism, and Tissue Infarction Flashcards

1
Q

What are the types of ways in which blood clotting occurs?

A

Clotting can be physiological (response to injury) or pathological (cause of tissue damage/death)

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2
Q

What is the cause of most vascular disease?

A

Narrowing or blockage of the lumen of blood vessels resulting in tissues being deprived of oxygen and nutrients and causing a buildup of toxic metabolites that cause damage and cell death.

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3
Q

What is ischaemia the result of?

A

Reduced blood flow (May have normal oxygen content)

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4
Q

What causes ischaemia?

A

Usually due to obstruction of blood vessel (thrombosis, embolus, microvascular disease, etc)

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5
Q

What causes tissue damage as a result of ischaemia?

A

Drop in ATP generation anf then failure of Na pump causes a cascade of events such as cell swelling, calcium influx, repture of lysosomes and membrane rupture, production of toxic metabolites and free radicals

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6
Q

What are the external symptoms of ischaemia?

A

Pale

Painful

Perishing

Cold

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7
Q

What is hypoxia?

A

Deficiency of oxygen in the blood available to tissues.

Reduced oxidative respiration in cells

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8
Q

What causes hypoxia?

A

Reduced oxygenation due to cardiorespiratory failure / asphyxia.

Decreased carrying capacity due to anaemia or CO poisoning

Drop in blood volume

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9
Q

What is the end result of ischaemia?

A

Necrosis

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10
Q

What happens to a cell during necrosis?

A

Cell swells -> Cell blebs -> Contents begin leaking out

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11
Q

What is an infarct?

A

An area of ischaemic necrosis caused by occlusion of vascular supply to the affected tissue.

Infarction is the process that leads to an infarct.

Arterial occlusion cause infarctions

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12
Q

What causes arterial occlusions?

A

Thrombus

Embolus

Vasospasm

Expansion of atherosclerotic plaque

Torsion or compression of vessels

Trauma

Vasculitis

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13
Q

At what point is ischaemia of the heart irreversible?

A

At the point of infarction

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14
Q

What are the most common and important causes of ischaemia and infarction?

A

Thrombosis and embolus

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15
Q

What is virchow’s triad?

A

Endothelial injury

Abnormal blood flow

Hypercoagulability

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16
Q

What causes clot formation?

A

Virchow’s triad

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17
Q

What causes endothelial injury?

A

Direct physical injury

Chemical/metabolic abnormality (drugs or hypercholesterolaemia)

Atherosclerosis

Infection

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18
Q

What does endothelial injury lead to?

A

Activation of endothelial cells, they change gene expression to a pro-coagulant state.

Downregulation in thrombomodulin and subsequent overactivity of thrombin.

Inflammation of endothelium downregulated protein C and other anticoagulant proteins

Antifibrinolytic effects - plasminogen inhibitors decreased production of t-PA

Activation of platelets

Major contributor to thrombosis in high flow / high pressure environment

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19
Q

What type of flow is normal?

A

Laminar blood flow (straight line flow)

20
Q

What is abnormal blood flow?

A

Turbulent flow in which there are counter currents which puts lots of shearing force on blood vessel walls and creates pockets of stasis.

21
Q

What is stasis?

A

Pockets of areas where blood is relatively not moving.

22
Q

How does stasis contribute to clotting?

A

Allows activation of clotting cascade, platelet aggregation and activation, fibrin aggregation.

Keeps platelets and clotting factors in contact with the vessel wall.

Prevents washout and dilution of activated clotting factors by fresh flowing blood and the inflow of clotting factor inhibitors

23
Q

What causes hypercoagulability?

A

Any disorder of the blood that predisposes to thrombosis. Can be primary (genetic) or secondary (acquired)

24
Q

What are the causes of primary thrombophilia?

A

Primary:
Factor V abnormalities [2% to 15% of caucasians carry a single-nucleotide variation in factor V called factor V leiden causing a loss of antithrombotic counterregulatory pathway, heterozygotes have a 5x increased risk of venous thrombosis and homozygotes have a 50x increase.

Prothrombin abnormalities:
1 - 2% of the population carry a single nucleotide variation in the prothrombin gene causing elevated prothrombin levels and 3x increased risk of venous thrombosis

25
Q

What are the causes of secondary thrombophilia?

A

Immobilisation

Major trauma

Malignancy

DIC: breakdown of cell membrane in some bacteria such as neisseria meningitidis in septicaemia leads to consumption of clotting factors

Consumptive coagulopathy

Many others

26
Q

What are the characteristics of thrombi?

A

They are attached to vessel surface and tend to propagate towards the heart and may detatch

Thrombi can have laminations called the lines of Zahn.

Large thrombi attached to wall of heart or aorta are called mural thrombi

27
Q

What do the lines of Zahn look like?

A

platelet and fibrin layers alternating with darker red cell-rich layers.

Only seen in flowing blood making them distinguishable from clots formed in postmortem state.

Higher flow = more prominent laminations

28
Q

What are large thrombi attached to the wall of the heart or aorta called?

A

Mural thrombi

29
Q

Where do arterial or cardiac thrombi more likely to arise?

A

At sites of endothelial injury or turbulence.

30
Q

What do arterial and cardiac clots look like?

A

They tend to be platelet rich and often occlusive and more likely to have lines of Zahn.

31
Q

Where do venous thrombi occur?

A

Typically at sites of stasis.

They can form a long cast within the lumen.

32
Q

How do venous thrombi differ from arterial thrombi?

A

Can form long cast within lumen

tend to have more enmeshed RBCs, fewer platelets, and less often have lines of zahn (due to more time for aggregation)

Deep vens of lower extremities most often affected.

Can occur in upper extremities, periprostatic plexus, or ovarian and periuterine veins.

Arterial thrombus = turbulent flow and stasis causing thrombus

Vein thrombus = Stationary for long time causing thrombus

33
Q

What are possible sequelae of Clots?

A

Propagation (extension of clot longitudinally or build up of additional layers

Dissolution (activation of fibrinolysis; after several hours fibrin polymerisation makes thrombus resistant to plasmin-induced proteolysis.

Occlusion (Thrombus blocks lumen)

Organization and recanalisation (Organisation: ingrowth of endothelial cells, smooth muscle cells, and fibroblasts. Recanalisation: Capillary channels form within the fibrotic clot partially reestablishing lumen)

34
Q

What are emboli?

A

Embolus is a detatched intravascular solid, liquid, or gaseous mass that is carried by the blood from point of origin to a distant site where it causes tissue dysfunction or infarction.

35
Q

What are the types of embolic material?

A

Thromboemboli (pulmonary vs systemic)

Air/Gas emboli

Fat emboli

Amniotic fluid emboli

Septic emboli

Foreign body emboli

36
Q

What are the types of thromboemboli?

A

Pulmonary

Systemic (infarcts of heart, lung, bowel, spleen)

37
Q

What are the effects of PE?

A

Blood stops reaching involved lung

Leads to VQ mismatch

Increased right ventricular pressure

38
Q

What does large embolus in the lung do?

A

Can lead to acute right heart failure (cor pulmonale) and sudden death.

(this is sometimes caused by saddle embolus at bifurcation of pulmonary arteries)

39
Q

What do smaller emboli in the lung do?

A

Pulmonary haemorrhage +/- infarct and hypoxia depending on size and other factors.

40
Q

What happens if there are multiple small emboli in the lung?

A

Can lead to chronic pulmonary hypertension and chronic right heart failure

41
Q

What are possible sequelae of pulmonary emboli?

A

Lysis of the embolus

Superimposed thrombus (another thrombus forms behind the embolus due to static blood)

Organisation and recanalisation

42
Q

Where do systemic thromboemboli typically occur?

A

Often arterial/cardiac origin

Lodge in vessels at bifircations or narrowing sites.

Lead to localised infarcts in area of vascular supply (bowel, brain, kidney, spleen, lung)

43
Q

What cause air or gas emboli?

A

Air -surgical or trauma

Gas - often nitrogen (at high pressure more nitrogen dissolves into blood and when divers return to low pressure this results in bubbles forming within the microvasculature. (Can damage brain, lungs, joints, and heart)

44
Q

What causes fat emboli?

A

Trauma caused by fracture of long bone.

Causes mechanical obstruction and biochemical irritant.

Can trigger intravascular coagulation

45
Q

What are amniotic fluid emboli?

A

Rare but critical complication of labour

Tear in placental membrane or uterine veins allow amniotic fluid (including hair, foetal skin, and fat) into maternal circulation.

Can trigger disseminated intravascular coagulation (DIC)

46
Q

What causes septic and foreign body emboli?

A

Colonies of bacteria/fungi can detach and lodge elsewhere.

47
Q

Summary:

A

Meaning of ischaemia/infarction

Meaning of thrombosis, pathophysiology of thrombosis and possible consequences

Meaning of embolism

Thromboemboli and other forms of emboli

IMED2002 UWA (29 decks)

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