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The Cardiovascular System > Atheroma, Thrombosis, Embolism and Infarction > Flashcards

Atheroma, Thrombosis, Embolism and Infarction Flashcards

1
Q

What are atheromas

A

Fibro-fatty plaques.

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2
Q

What are the main locations of atherosclerosis

A

Elastic and medium to large muscular arteries. Common in the aorta and its branches. Not common in the pulmonary circulation.

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3
Q

What are some genetic conditions that increase the risk of atherosclerosis

A

Hypercholesterolaemia or genetic hyperlipodaemia.

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4
Q

Name the risk factors for atheroma

A

Age, male sex, genetics, hyperlipidaemia, hypertension, smoking, diabetes.

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5
Q

What is the first step in the parthenogenesis of atherosclerosis

A

Endothelial injury or dysfunction

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6
Q

What substances accumulate in the tunica intima during atheroma formation

A

Low density lipoproteins and foam cells.

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7
Q

Describe the process of the parthenogenesis of atheroma formation.

A
  1. Endothelial injury or dysfunction
  2. accumulation of LDL and foam cells in the intimal layer of the blood vessel wall
  3. smooth muscle proliferation from the medial layer
  4. fibrosis which forms a fibro-lipid plaque.
  5. Plaque injury to make the atheroma complicated such as thrombosis or haemorrhage.
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8
Q

At what stage does the fatty plaque become irreversible

A

When it gets to the point of forming an early atheroma in which the medial layer of the blood vessel becomes involved.

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9
Q

What are the components of an uncomplicated athermatous plaque

A

Foam cells (fat containing macrophages), smooth muscle cells from the medial layer, lymphocytes, fibrosis and a fibrous cap.

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10
Q

What is the difference between an early and late atheromatous plaque

A

In the early stages there is no involvement of the tunica media. In the late stages smooth muscle cells from the medial layer become involved, however it is still uncomplicated.

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11
Q

What can make a plaque “complicated”

A

Ulceration, haemorrhage, thrombosis.

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12
Q

Why is atherosclerosis more likely to be an issue in coronary arteries compared to the aorta

A

Because coronary arteries are narrower so less obstruction is required.

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13
Q

What are the local complications of atheroma

A
  • calcification
  • ulceration
  • plaque rupture
  • haemorrhage
  • thrombosis
  • aneurysmal dilatation (which can rupture)
  • blood vessel obstruction and downstream ischaemia
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14
Q

What are the systemic complications of atheroma

A

Infarction, stroke, ischaemia, gangrene.

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15
Q

What is a thrombus

A

A solidification of blood constituents that forms within the vascular system during life.

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16
Q

What is thrombosis

A

A pathological process. It is the formation of a thrombus in an uninterrupted vascular system.

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17
Q

When is it normal for thrombus formation to occur

A

In an interrupted vascular system when it is associated with injury.

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18
Q

When is a blood clot not termed a thrombus

A

If it forms outside the vascular system or after dear

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19
Q

What are the risk factors for thrombosis

A

Endothelial injury, abnormal blood flow and hypercoagulability

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20
Q

What is the name given to the three risk factors for thrombosis - endothelial injury, abnormal blood flow and hypercoagulability

A

Virchow’s triad

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21
Q

What is the most common cause of endothelial injury

A

Atheroma

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22
Q

What is a cause of hypercoagulability

A

Increased clotting factors and platelets present after surgery.

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23
Q

Give examples of things which cause endothelial injury leading to thrombosis and when this may occur.

A

1) Ulcerated atheromatous plaques - occurs in the aorta, carotid arteries, iliac and femoral arteries, coronary arteries.
2) Left ventricular endocardium injury - occurs after MI
3) Abnormal cardiac valves - occurs in rheumatic fever, infective endocarditis, prosthetic valves.

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24
Q

How does abnormal blood flow result in thrombus formation

A

It prevents the dilution of clotting factors, prevents the inflow of inhibitors of clotting factors and promotes endothelial cell activation.

25
Q

What can be the result of turbulent blood flow

A

The development of arterial and cardiac thrombi.

26
Q

What can be the result of stasis

A

The formation of venous thrombi.

27
Q

What are come genetic predispositions to hypercoagulability

A

Protein S or protein C deficiency

28
Q

What is a mural thrombus

A

A mural thrombus is present on the wall of the structure.

29
Q

Where do mural thrombi often form

A

The cardiac chambers

30
Q

What is an occlusive thrombus

A

Occlusive thrombi obstruct the vessel completely.

31
Q

What is the name given to thrombosis in a vein

A

Phlebothrombosis

32
Q

What is thrombophlebitis

A

Inflammation in a vein with subsequent thrombosis.

33
Q

What is shown in histology of thrombi

A

Alternating pale and dark “lines of Zahn”.

34
Q

What is shown by the pale lines of Zahn

A

Fibrin and platelets.

35
Q

What is shown by the dark lines of Zahn

A

Red blood cells.

36
Q

What are the complications of thrombosis

A

Occlusion of an artery or vein, embolism - arterial (in the legs or brain) or venous (to the heart and lungs).

37
Q

What is the end result of arterial occlusion

A

Loss of pulse distal to the thrombus, the area will become cold, pale and painful and eventually the tissue will die and gangrene will result.

38
Q

What is the end result of thrombosis in the superficial veins of the leg

A

Congestion, swelling, pain and tenderness

39
Q

What is the result of thrombosis in the deep veins of the leg

A

There can be foot and ankle oedema however it may also be asymptomatic and only recognised when it embolises.

40
Q

What is an embolus

A

A detached intravascular liquid or gaseous mass that is carried by the blood to a site distant from its origin.

41
Q

What is a thromboembolus

A

An embolus arising from a thrombus (99% of cases)

42
Q

What are some rare forms of emboli

A

Bone or bone marrow fragments, atheromatous debris, fat droplets, tumour cells, foreign bodies, bubbles of air or nitrogen.

43
Q

What is the origin of most pulmonary emboli

A

Thrombi in the deep veins of the lower leg, and second most commonly from the pelvis.

44
Q

How can you tell after death that what is present in the blood vessel is an embolus

A

The calibre of an embolus is different from that of the vessel it becomes lodged in.

45
Q

What is the name given to an embolus that lodges at the bifurcation of an artery

A

A saddle embolus

46
Q

What is the outcome associated with saddle emboli

A

Collapse and sudden death

47
Q

What is a paradoxical embolism

A

A pulmonary embolism that gains access to the systemic circulation as a result of an interatrial or interventricular defect.

48
Q

What is often a feature of pulmonary infarction

A

They are often haemorrhagic.

49
Q

What is an infarct

A

An area of ischaemic necrosis

50
Q

What causes an infarct

A

Occlusion of arterial supply or venous drainage in a particular tissue.

51
Q

What are the factors which influence the development of an infarct

A
  • The nature of the vascular supply (single or dual)
  • The rate of development of the occlusion
  • The vulnerability of the affected tissue to hypoxia
  • The oxygen content of the blood
52
Q

How does the nature of the vascular supply affect the development of an infarct

A

A lot of organs have a single blood supply however some such as the lung and the small bowel have a dual blood supply. In these organs when one blood vessel is obstructed, the other will still be supplying blood so infarct will not happen as quickly.

53
Q

Which type of tissues are more vulnerable to hypoxia as a result of infarct

A

Those which are more metabolically active such as the heart.

54
Q

What are the three types of infarct

A

Red (haemorrhagic), white (anaemic) and septic.

55
Q

In what situations does a red (haemorrhagic) infarct form

A

When there is venous occlusion (so blood cannot be returned through the venous system and pressure builds), in loose tissues and in tissue with a dual blood supply.

56
Q

In what situations does a white (anaemic) infarct form

A

When there is arterial occlusion and in solid organs such as the heart and the spleen.

57
Q

In what situations does a septic infarct form

A

In infected infarcts.

58
Q

What can be seen in histology of an infarct

A

Ischaemic coagulative necrosis (minutes to days), an inflammatory response (hours - 7 days), reparative response (1-2 weeks) and scarring (2 weeks-2 months)

59
Q

What is the repair process in infarction

A

Inflammation and scarring as infarct is irreparable.

The Cardiovascular System (15 decks)

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