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1st Year Medicine > Atheroma, Thombus And Embolism. > Flashcards

Atheroma, Thombus And Embolism. Flashcards

0
Q

What is a thrombosis?

A

Pathological corruption of haemostasis. Formation of solid or semi solid mass of blood constituents of blood within the vessels.

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1
Q

What are the two main functions of haemostasis?

A

Maintain blood in a fluid, clot free state.

Induce haemostatic plug at site of vascular injury.

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2
Q

What is virchows triad?

A

Changes in the blood vessel wall.
Changes in the blood constituents.
Changes in the blood flow.

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3
Q

What are the functions of an endothelial cell?

A

Maintains a permeability factor.
Elaborates anticoagulant and prothrombin molecules e.g. Fibrinogen.
Produce ECM.
Modulate blood flow and vascular permeability.
Regulates inflammation and immunity.
Regulates cell growth.
Play a role in LDL oxidation.

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4
Q

What is hyaline arteriosclerosis?

A

Plasma proteins forced into the vessel walls?

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5
Q

What is hypercoagulability?

A

Any alteration in the coagulation pathway which predisposes to thrombus. Usually genetic or acquired.

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6
Q

What are three possible mechanisms of genetic hyper-coagulability conditions?

A

Factor V mutations. Cane be defects in anti-coagulation pathways e.g. Anti thrombin III deficiency. Could also be defects in fibrinolysis.

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7
Q

What are some high risk acquired hypercoagulable states?

A

MI, immobilisation, tissue damage, cancer, prosthetic heart valves, DIC, hepatic induced thrombocytopaenia and antiphospholipid syndrome.

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8
Q

What are some low risk acquired hypercoagulability states?

A

AF, cardiomyopathy, nephrotic syndrome, oral contraceptives, late pregnancy, sickle cell anaemia and smoking.

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9
Q

What are two types of blood flow disruptions?

A

Turbulence and stasis?

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10
Q

What are the results of disruption of laminar blood flow?

A

Platelets come into contact with epithelium. Clotting factors not diluted by normal blood flow. Inform of anticoagulant factors is slowed allowing thrombi to persist. Endothelial activation is promoted.

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11
Q

What situations can lead to turbulence and stasis?

A 
Impaired venous drainage beading to DVT.
Non contractile areas of myocardium following MI.
Aneurysms.
A fib.
Mitral valve stenosis.
Left atrial dilatation.
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12
Q

What are the different morphologies of thrombus?

A

Arterial, mural and venous.

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13
Q

What is an arterial thrombus?

A

Often occlude the lumen. They are associated with atheroma and have firm attachment to the wall, they show lines of Zahn.

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14
Q

Where are common sites for arterial thrombi?

A

Coronary, femoral and cerebral.

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15
Q

Where do we get mural thrombi?

A

Ventricles (heart) and aortic aneurysms.

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16
Q

What can a mural embolism of the heart cause?

A

MI’s and arrhythmias.

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17
Q

What is the appearance of mural thrombi and why?

A

Look laminated due to alternating light and dark bands.
Light - platelet and fibrin.
Dark - RbC and wbc bands.
These are called lines of Zahn.

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18
Q

What are venous thrombosis otherwise called?

A

Plebothomboses.

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19
Q

What blood flow are venous thrombosis often related to?

A

Stasis.

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20
Q

What is the appearance of venous thrombi?

A

Reddish blue and form casts which are adherent to the walls.

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21
Q

What are the most common venous thrombi?

A

Popliteal, femoral, iliac and pelvic.

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22
Q

What is probably the most important venous thrombi?

A

DVT of the calf.

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23
Q

What are four fates of thrombi?

A

Proximal propagation - small to large vessel.
Embolisation resolution - fibrinolysis.
Organisation - granulation tissue
DIC.

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24
Q

What is an embolism?

A

Detached intra vascular solid, liquid or gaseous mass, carried by the bloodstream to a site distant from the point of origin.
99% are thromboemboli.

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25
Q

What different types of emboli are there?

A

Thrombo, fat, marrow, air, septic, amniotic and tumour.

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26
Q

Where do 95% of pulmonary thromboembolisms come from?

A

95% from large leg veins e.g. Popliteal , iliac and femoral.

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27
Q

How do DVT in the leg travel to the lungs?

A

Via the IVC.

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28
Q

What do pulmonary infarcts look like?

A

They are wedge shaped and firm.

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29
Q

What symptoms do we get with pulmonary infarcts?

A

Chest pain, haemostasis and dyspnoea.

30
Q

What is a paradoxical embolus?

A

Usually thrombus emboli cannot infarction in the peripheral arterial circulation. They can only do this if patient has rare AV septal defect. If this happens its a paradoxical embolus.

31
Q

What causes fat emboli and what happens?

A

Follow major soft tissue trauma e.g. Pelvis and femur. Fatty marrow enters venules and most globules arrest in the lungs causing dyspnoea. Can be fatal.

32
Q

What can happen to the patient if a fatty embolus reaches the peripheral circulation?

A

Skin rashes and CNS confusion.

33
Q

What can cause gas/air embolisms?

A

Barotrauma e.g. The bends. Can also occur during delivery/abortion.

34
Q

What arteries can gas/air emboli occlude?

A

Commonly pulmonary arteries and rarely coronary arteries.

35
Q

How much gas is required to form an air/gas embolism that can cause harm and why?

A

100mls. Need to overcome the filtering of the lungs.

36
Q

What is an amniotic embolism?

A

Occurs postpartum when fluid enters torn veins and embolisms to the lungs.

37
Q

What does an amniotic embolism cause?

A

Marked oedema, often DIC and 80% result in death.

38
Q

What is a systemic embolism? Where do they originate and what do they cause?

A

One that travels through the arterial circulation.
80% originate from thrombi within heart chambers or valves e.g. AF, mural thrombus or post MI/aneurysm.
Almost always cause infarct mostly to the legs causing gangrene. But some arms, brain or visceral infarct.

39
Q

What is arteriosclerosis?

A

Affects the small arteries and arterioles.
Have hyaline and hyperplastic types.
Associated with DM and hypertension.

40
Q

What is monckeberg medial calcification sclerosis?

A

Calcification of medium sized arteries in those over 50 years old.

41
Q

What is atherosclerosis a disease of?

A

Small to medium arteries.

42
Q

What is an atherosclerotic plaque made of and what happens as it increases in size?

A

Plaque made of a raised focal lesion of intima, a lipid core of cholesterol and esters. Lipoproteins and a fibrous cap.
As plaque size increases, luminal diameter decreases, blood flow reduces and ischaemia occurs.

43
Q

Where in artery walls are atherosclerotic plaques situated?

A

Essentially intimal but the medial structure is progressively degraded, causing weakening of the wall and aneurysm development.

44
Q

What is the most common underlying cause for thrombotic events?

A

Atherosclerosis.

45
Q

What age and race is atherosclerosis most commonly found in?

A

All races and ages.

46
Q

Where is atherosclerosis most commonly found?

A

Aorta, coronary arteries and cerebral arteries.

47
Q

What can atherosclerosis of the cerebral arteries cause?

A

Ischaemia encephalopathy dementia.

48
Q

What are the risk factors for atherosclerosis?

A

Age, sex, genetics, hypertension, smoking, diabetes, hyperlipidaemia. Lack of exercise, obesity, high carb diet, saturated/trans fats.
Oestrogen if status e.g. Post menopause and the pill. Infection and inflammation.

49
Q

What have protective roles in atherosclerosis?

A

Alcohol and HDL.

50
Q

How many stages are there in the formation of atherosclerotic plaques?

A

6.

51
Q

What is stage 1 in the pathogenisis of atherosclerotic plaques?

A

Chronic endothelial injury.

52
Q

What are steps 2-4 in the pathogenisis of atherosclerotic plaques?

A

Endothelial dysfunction causes: increased permeability, monocyte adhesion, monocyte emigration and platelet adhesion.

53
Q

What is stage 5 in the pathogenisis of atherosclerotic plaques?

A

Macrophage activation has multiple roles:
Generation of reactive O2 species leading to oxidation of lipoproteins.
Cytokines production promotes chemotaxis and leukocyte adhesion.
Production of growth factors contributing to smooth muscle proliferation.

54
Q

What is stage 6 in the pathogenisis of atherosclerotic plaques?

A

Lipoprotein oxidation. This is more easily ingested by macrophages and acts as chemotactic factors for monocytes. Increases monocyte adhesion and inhibits macrophage motility, trapping macrophages within the plaque.
This stimulates cytokines and growth factor release which directly damages endothelial and smooth muscle cells and induces antibody responses.

55
Q

How are foam cells produced? What does this form and is it reversible?

A

Macrophages and smooth muscle cells engulf the lipids to become foam cells. Visible as a fatty streak on the wall of an artery. Is reversible at this stage if cholesterol is reduced.

56
Q

What happens if hypercholesterolaemia persists after fatty streak formation?

A

Smooth muscle proliferation and collagen deposition convert the fatty streak into a mature fibrofatty atheroma.

57
Q

What four places are fibrofatty atheroma commonly distributed?

A

Thoracic aorta - mainly arch branch points.
Carotid artery bifurcations - especially internal carotid.
Circle of Willis.
Coronary arteries - Ostia and the lad.

58
Q

What vessels normally avoid fibrofatty plaques?

A

Arms and associated vessels.

59
Q

What three sequelae categories come from fibrofatty plaque formations?

A

Resolution, repair and complications.

60
Q

What happens during resolution of fibrofatty plaques?

A

Fatty streak lipids are re absorbed (high dose statins).

61
Q

What happens during repair of fibrofatty plaques?

A

Stabilisation by fibrosis (scarring). Thick cap/total fibrosis or calcification.

62
Q

What complications can come from fibrofatty plaques?

A

Ulceration of atheromatous plaque and thrombosis.
Haemorrhage into plaque with rupture and embolism of plaque contents.
Ongoing narrowing giving critical stenosis.
Aneurysm formation.

63
Q

What are the steps in atherothrombis formation?

A

Normal ==> fatty streak ==> fibrous plaque ==> atherosclerotic plaque plaque rupture/fissure and thrombosis.

64
Q

What are some complications of atherothrombosis?

A

Stenosis, thrombosis, aneurysm, dissection, embolism and ischaemia.

65
Q

What is arterial stenosis?

A

Narrowing of the arterial lumen, causing reduced elasticity, reduced blood flow in systole and tissue ischaemia.

66
Q

Where are common sites of arterial stenosis and what does this cause?

A

Coronary arteries.
Carotid arteries - TIA, stroke and vascular dementia.
Renal arteries - hypertension and renal failure.
Peripheral arteries - claudication and lower limb ischaemia.

67
Q

What happens to cardiac tissue during cardiac fibrosis?

A

Loss of myocytes which are replaced by fibrous tissue. Causes loss of contractility and reduced elasticity, which in turn reduces filling.

68
Q

What is arterial dissection?

A

Splitting within the media by flowing blood. The false lumen is filled with blood within the media.

69
Q

What are some causes of arterial dissection?

A

Usually middle age +- atheroma.

Marfans, pregnancy, atheroma, hypertension, trauma and coarction.

70
Q

What can arterial dissection result in?

A

Sudden collapse and has a high mortality rate.

71
Q

What is atherosclerosis?

A

Progressive disease characterised by a build up of plaque within the arteries.

72
Q

What are atherosclerotic plaques made from?

A

Fatty substances, cholesterol, cellular waste, calcium and fibrin.

73
Q

What two things can happen to an atherosclerotic plaque?

A

Bleeding into the plaque or formation of a clot on its surface.

1st Year Medicine (64 decks)

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