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Yr 2 - EMS > Atheroma, thrombosis and embolism > Flashcards

Atheroma, thrombosis and embolism Flashcards

1
Q

What is an atheroma?

A

Intimal lesion that protrudes into a vessel wall.

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2
Q

What are the 5 main steps of atheroma formation?

A
  1. Endothelial dysfunction
  2. Formation of lipid layer or fatty streak within the intima
  3. Migration of leukocytes and smooth muscle cells into the vessel wall
  4. Foam cell formation
  5. Degradation of extracellular matrix
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3
Q

What allows circulating LDLs into the intima?

A

Disruption of endothelial barrier due to endothelial dysfunction

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4
Q

When do macrophages become foam cells?

A

When monocytes enter the intima, they differentiate into phagocytic macrophages. These phagocytic macrophages may become foam cells when they absorb lipoproteins

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5
Q

What does an atheroma lesion consist of?

A

A raised lesion with a soft core of lipid (mainly cholesterol and cholesterol esters) and is covered by a fibrous cap.

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6
Q

What does the fibrous cap of an atheroma consist of?

A

Smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin

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7
Q

What does the central necrotic core of an atheroma consist of?

A

Cell debris, cholesterol crystals, foam cells, calcium

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8
Q

Diagram of atherosclerosis

A
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9
Q

Why are sites of birfucation common for atheromas?

A

Blood flow is often turbulent here

  • E.g. abdominal aorta; particularly around branches
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10
Q

What vessels are commonly affected by atheromas?

A
  • Abdominal aorta
  • Coronary arteries
  • Popliteal arteries
  • Carotid vessels
  • Circle of Willis
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11
Q

What are the non-modifiable risk factors for atheroma?

A
  • Increasing age
  • Male gender
  • Family history
  • Genetic abnormalities
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12
Q

What are the modifiable risk factors for atheroma?

A
  • Hyperlipidemia (LDL:HDL)
  • Hypertension
  • Cigarette smoking
  • Diabetes
  • CRP (inflammation)

These factors can damage endothelium and cause an influx of lipids

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13
Q

How does atherosclerosis begin?

A

Starts with damage or injury to the inner layer of an artery

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14
Q

What may cause damage to inner layer of an artery?

A
  • High blood pressure
  • High cholesterol
  • An irritant, such as nicotine
  • Certain diseases, such as diabetes
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15
Q

How does atherosclerosis then develop in response to the endothelial injury?

A

Response to injury hypothesis:

  • Atherosclerosis develops as a chronic inflammatory response
  • Lesion progression occurs through interactions of modified lipoproteins, monocyte-derived macrophages, T-lymphocytes, and the normal cellular constituent of the arterial wall.
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16
Q

Describe mechanism of how atheroma forms

A
  • Damage allows influx of lipids into intima
  • Marcophages recruited and activated to try and engulf lipid –> forming foam cells
    • ​Sometime die which causes an excess of extracellular lipid
  • Smooth muscle cells infiltrate and proliferate and try to lay down collagen –> conenctive tissue forms a thin fibrous cap on the surface
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17
Q

What are foam cells?

A

A type of macrophage that localise to fatty deposits on blood vessel walls, where they ingest low-density lipoproteins and become laden with lipids, giving them a foamy appearance.

I.e. foam cells are fat-laden macrophages containing LDLs

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18
Q

How does the fibrous cap on the atheroma form?

A

Smooth muscle cells laying down collagen –> connective tissue forms fibrous cap

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19
Q

Basic response to injury hypothesis for atheroma?

A
  1. Chronic endothelial injury
  2. Endothelial dysfunction (increased permeability, monocyte adhesion and emigration)
  3. Smooth muscle emigration from media to intima, macrophage activation
  4. Macrophages and smooth muscle cells engulf lipid
  5. Smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid
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20
Q

What is the earliest lesion in atherosclerosis?

A

Fatty streak

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21
Q

What is a fatty streak composed of?

A

Lipid filled foamy macrophages (i.e. macrophages that have ingested fat)

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22
Q

Describe appearance of fatty streaks

A

These lesions are not significantly raised and do not cause flow disturbance

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23
Q

Do all fatty streaks progress to atheromatous plaques?

A

No - but coronary fatty streaks begin to form in adolescence at the same anatomical sites that later tend to develop plaques

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24
Q

What does a fatty streak then progress to?

A
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25
Q

What does an atherosclerotic plaque consist of?

A

Intimal thickening and lipid accumulation

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26
Q

Describe appearance of an atheroslerotic plaque

A

Appears white and yellow raised plaques which often have superimposed thrombus on the plaque that appear red

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27
Q

Does an atherosclerotic plaque impinge on the vessel lumen? What is effect of this?

A

Yes - causes turbulent blood flow:

  • There may be damage to overlying endothelium and thrombus can start to appear on surface
  • Causes stenosis (narrowing) of vessel lumen
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28
Q

Diagram of atherosclerosis development

A
  1. Initial lesion
  2. Fatty streak
  3. Intermediate lesion
  4. Atheroma
  5. Fibroatheroma
  6. Complicated lesion
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29
Q

How does an initial lesion mainly progress to an atheroma?

A

Growth mainly by lipid addition

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30
Q

How does an atheroma progress to a fibroatheroma?

A

Increased smooth muscle and collagen (cap forms and core of extracellular lipid)

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31
Q

How does a fibroatheroma progress to a complicated lesion?

A

Thrombosis and/or hermatoma

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32
Q

What are the 4 seque of atherosclerotic plaques?

A
  1. Rupture, ulceration or erosion of the plaque
  2. Haemorrhage into plaque
  3. Atheroembolism
  4. Aneurysm formation
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33
Q

The plaque is at danger of rupturing, ulcerating or eroding. What would this cause?

A

This will expose the blood to highly thrombogenic substances (cholesterol and tissue that was under the fibrous cap) and induce thombosis –> blood clots which can block flow in the artery

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34
Q

What can cause a haemorrhage into a plaque?

A

If there is damage to one of the blood vessels feeding the plaque or the overlying endothelium

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35
Q

What happens during haemorrhaging into a plaque?

A

Blood rapidly enters plaque and expands it –> can lead to occlusion

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36
Q

What is atheroembolism?

A

Damage to overlying surface, bits of atheroma can break off and travel in the bloodstream as emboli

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37
Q

How can atherosclerotic plaques lead to aneurysm formation?

A

Over time, plaques may cause the artery wall to weaken due to atrophy –> can lead to an aneurysm

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38
Q

What does sequelae mean?

A

a condition which is the consequence of a previous disease or injury.

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39
Q

What is a thrombus?

A

A blood clot that occurs inside the vascular system

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40
Q

What are the 2 types of thrombosis?

A
  1. Arterial
  2. Venous
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41
Q

How does arterial thrombosis typically occur?

A

Usually occurs after the erosion or rupture of an atherosclerotic plaque

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42
Q

What is venous thrombosis most commonly due to?

A

Stasis

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43
Q

What is Virchow’s Triad?

A

Describes 3 factors that are ciritical important in the development of venous thrombosis:

  1. Stasis of blood flow
  2. Hypercoagulability
  3. Endothelial injury
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44
Q

How can endothelial injury lead to thrombosis?

A

Expose blood to factors within the underlying tissue which promote clotting cascade to cause a thrombus to form

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45
Q

How can abnormal blood flow lead to thrombosis?

A

Prothrombotic factors are able to build up and antithrombotic factors may not be abel to be brought into the area

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46
Q

How can hypercoagulabiliy lead to thrombosis?

A

A hypercoagulable state is the medical term for a condition in which there is an abnormally increased tendency toward blood clotting (e.g. Factor V Leiden)

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47
Q

Difference in cause of arterial and venous thrombosis?

A

Arterial: typically from rupture of atheromatous plaque

Venous: typically from combination of factors from Virchow triad

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48
Q

Difference in location between arterial and venous thrombosis?

A

Arterial: left heart chambers, arteries

Venous: venous sinusoids (a small irregularly shaped blood vessel) of muscle and valves of veins

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49
Q

Why does venous thrombosis typically appear near valves and sinusoids?

A

Sinusoids –> allow pooling of blood

Valves –> areas of turbulence

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50
Q

What diseases can arterial thrombosis lead to?

What diseases can venous thrombosis lead to?

A

Arterial:

  • Acute coronary syndrome
  • Ischaemic stroke claudication

Venous:

  • Deep vein thrombosis
    • Pulmonary embolism
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51
Q

What is claudication?

A

a condition in which cramping pain in the leg is induced by exercise, typically caused by obstruction of the arteries.

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52
Q

Difference in composition of arterial and venous thrombus?

A

Arterial: mainly platelets

Venous: mainly fibrin

53
Q

How is arterial thrombosis treated?

A

Anti-platelet agents (e.g. clopidogrel)

54
Q

How is venous thormbosis treated?

A

Anticoagulants e.g. warfarin, rivaroxaban

55
Q

Components of Virchow’s Triad

A
56
Q

What are the risk factors for endothelial damage?

A

Endothelial dysfunction (endothelium usually helps regulate clotting and vascular relaxation so dysfunction can lead to problems)

  • Smoking
  • Hypertension

Endothelial damage

  • Surgery
  • Catheter (PICC line)
  • Trauma
57
Q

What are the 2 categories of hypercoagulability?

A
  1. Hereditary
  2. Acquired
58
Q

What are the hereditary factors of hypercoagulability\?

A
  • Factor V Leiden
  • Prothrombin
  • Protein C and S deficiency
59
Q

What is Factor V Leiden?

A

An inherited disorder of blood clotting –> a specific gene mutation that results in thrombophilia

This mutation means that Factor V (a cofactor of the clotting cascade) is resistant to inhibition by protein C

60
Q

What is normal effect of Factor V?

A

Is a procoagulant molecule that interacts with other clotting proteins including activated factor X and PT to increase the production of thrombin

I.e. helps convert prothrombin into thrombin

61
Q

What is Factor V normally degraded by?

A

Protein C

62
Q

What can a deficiency in Factor V lead to?

A

Predisposition for haemorrhage (lack of clotting)

63
Q

What is Prothrombin G20210A?

A

Mutation in the prothrombin gene causes people to produce more prothrombin than is normal which increases conversion of fibrinogen to fibrin

A genetic condition that increases the risk of blood clot

64
Q

How can a Protein C and S deficiency lead to clotting?

A

Protein S and Protein C are both natural anticoagulants:

  • Protein C: regulates activities of Factor VIIIa and Factor Va (cofactors in the activation of factor X and prothrombin respectively)
  • Protein S: functions as cofactor to protein C in th inactivation of Factor VIIIa and Factor Va
65
Q

What are protein C and S dependent on?

A

Vitamin K

66
Q

What are the acquired causes of hypercoagulability?

A
  • Cancer
  • Chemotherapy
  • HRT
  • High oestrogen states (e.g. the pill)
  • Pregnancy
  • Obesity
  • HIT
67
Q

How can high oestrogen lead to increased risk of clots?

A

Oestrogen, like many lipophilic hormones, affects the gene transcription of various proteins. Thus, oestrogen increases plasma concentrations of these clotting factors by increasing gene transcription

68
Q

What is HIT?

A

Heparin induced thrombocytopenia - the development of thrombocytopenia (a low platelet count), due to the administration of various forms of heparin, an anticoagulant.

Heparin is a blood thinner used to prevent blood clots. With HIT, your body reacts to heparin in a way that may cause clots instead of preventing them.

Thrombocytopenia means you have a low level of platelets, which are blood cells that help your blood clot. Usually, low platelets would cause you to bleed. But the reaction to heparin may cause clots instead.

69
Q

How can HIT lead to thrombosis?

A

Patient may develop antibodies to heparin which in turn leads to thrombosis

These antibodies bind to heparin and activate platelets –> prothrombotic

70
Q

What are the causes of stasis?

A
  • Immobility
  • Polycythaemia
71
Q

How can immobility lead to thrombosis?

A

Using muscles less, less squeezing of venous blood back to heart

72
Q

What is polycythaemia? How can it lead to thrombosis?

A

An increase in the number of red blood cells. The extra cells cause the blood to be thicker, and this, in turn, increases the risk of other health issues, such as blood clots

73
Q

Are platelets involved in a clot?

A

No

74
Q

Where can clots occur?

A

Outside a vessel (test tube or hematoma) or inside but only postmortem

75
Q

What colour is a clot?

A

Red

76
Q

Is a clot attached to a vessel wall?

A

No

77
Q

describe appearance of clot

A

Red, gelatinous

78
Q

Are platelets involved in a thrombus?

A

Yes

79
Q

Where does a thrombus occur?

A

Only inside a vessel

80
Q

Describe colour of a thrombus in an artery and vein

A

Red –> venous

Pale –> arterial

81
Q

Is thrombus attached to vessel wall?

A

Yes

82
Q

What are the sequelae of thrombosis?

A
  • Occlusion of vessel (can cause downstream ischaemia or infarction)
  • Dissolution (may be broken down and resolves itself)
  • Incorporation into vessel wall (may lead to narrowing of vessel lumen)
  • Recanalisation (new blood vessels grow into thrombus)
  • Embolisation (part of thrombus can break up and travel to another organ where it can cause blockage of a vessel)
83
Q

What is an embolus?

A

A mass of material in the vascular system able to become lodged in the vessel and block its lumen

84
Q

Where are most emboli derived from?

A

Thrombi - most common are pulmonary embolus derived from DVT which breaks off, travels through venous system into pulmonary arteries

85
Q

Types of emboli:

A
  • Thrombus derived
  • Atheromatous plaque material (bits can break off if overlying fibrous cap is damaged OR if there is haemorrhage into plaque)
  • Vegetation on heart valves
  • Fragments of tumour (causing metastasis)
  • Amniotic fluid
  • Gas
  • Fat
86
Q

How can vegetation on heart valves lead to emboli?

A

If heart valves are damaged then this can predispose to thrombi forming on surface as endothelium is damaged and due to turbulent blood flow.

These thrombi can sometimes become infected –> causes infective carditis, become fragile and can break off

87
Q

What does the effect of a pulmonary embolus depend on?

A

The size of the embolus

88
Q

How can a small emboli lodge?

A

Can lodge in pulmonary vasculature –> causes increased pressure and therefore pulmonary hypertension

This means right hand side of heart has to work harder –> can get heart failure secondary to lung disease, this is called ‘cor pulmonale’

89
Q

What is ‘cor pulmonale’?

A

An alteration in the structure and function of the right ventricle (RV) of the heart caused by a primary disorder of the respiratory system. Pulmonary hypertension is often the common link between lung dysfunction and the heart in cor pulmonale

90
Q

What are dangers of large pulmonary emboli?

A

Can lodge in bifurcation of pulmonary artery and blocks it entirely –> sudden death

91
Q

Where do pulmonary emboli tend to arise/go?

A

Arise from thrombi that form in the venous system that travel through the veins, into the right side of the heart, through the pulmonary artery and lodge in a smaller vessel

92
Q

Where do systemic emboli tend to arise from?

A

Not from veins but from arterial system - generally originate from the heart (left side) or atheromatous plaque

93
Q

How can systemic emboli be a sequelae of myocardial infarction?

A

Death of myocardium and overlying endocardium –> predisposes to thrombosis due to damage

Also, part of the heart is no longer functioning correctly which can cause turbulence –> thrombus can form over area of myocardial infarction

94
Q

How can atrial fibrillation lead to systemic emboli?

A

Turbulence and pockets of stasis due to mal coordination of atria –> thrombus formation

95
Q

What is infective endocarditis? How can it lead to systemic emboli?

A

Infective endocarditis is an infection in the heart valves or endocardium –> can cause thrombi

96
Q

What 4 major issues can systemic emboli cause?

A
  • CVA (Cerebrovascular accident - a stroke, emboli become lodged in circulation of brain)
  • TIA (Transient Ischemic Attack - a temporary blockage of blood to the brain similar to a stroke (“mini-strokes)” but leave no lasting brain damage or residual symptoms
  • Gangrene - eath of body tissue due to either a lack of blood flow, commonly affects extremeties
  • Bowel necrosis - reduced flow to the GI tract (secondary to vascular occlusion)
97
Q

What is paradoxical embolism?

A

A paradoxical embolism refers to an embolus which is carried from the venous side of circulation to the arterial side, or vice versa.

98
Q

What is the response-to-injury hypothesis behind atherosclerosis?

A

Chronic inflammatory response to endothelial injury to the arterial wall

99
Q

What causes endothelial injury?

A
  • hyperlipidaemia
  • high blood pressure
  • immune reactions
  • an irritant (e.g. nicotine)
  • diabetes
100
Q

What follows endothelial injury?

A
  1. Monocytes adhere and emigrate into lesion
  2. Smooth muscle emigrates from the media to the intima, leading to monocytes differentiating into macrophages
  3. Macrophages and smooth muscle cells engulf the lipid, macrophages become foam cells and a fatty streak appears on the lining
  4. Smooth muscle proliferation, collagen and other ECM deposition
  5. Extracellular lipid continues to develop, leading to a fibro-fatty atheroma
101
Q

What causes macrophages to become foam cells?

A

They engulf the lipid

102
Q

What is the earliest lesion in atherosclerosis?

A

Fatty streak - beginning as multiple minute yellow spots that coalesce into streaks

103
Q

What is a fatty streak composed of?

A

Lipid filled foamy macrophages

104
Q

How do fatty streaks affect flow?

A

Not significantly raised and do not cause flow disturbance.

105
Q

What follows a fatty streak?

A

Atherosclerotic plaque

106
Q

Appearance of an atherosclerotic plaque?

A

Appears white-yellow and superimposed thrombus on the plaque appears red

107
Q

What does an atherosclerotic plaque consist of?

A

Intimal thickening and lipid accumulation

108
Q

How do atherosclerotic plaques affect flow?

A

Impinges on the vessel lumen

109
Q

What follows an atherosclerotic plaque?

A

Complicated lesion –> can lead to thrombosis

110
Q

What are the possible sequelae of atherosclerosis?

A
  1. Rupture, ulceration or erosion of the intimal surface
  2. Haemorrhage into plaque
  3. Athero-embolism
  4. Aneurysm formation
111
Q

What is result of rupture, ulceration or erosion of the intimal surface?

A

Exposes the blood to highly thrombogenic substances and induces thrombosis, lumen occlusion and maybe ischaemia

112
Q

What is a thrombus?

A

A solid mass of blood constituents formed within the vascular system in vivo.

113
Q

Where can a thrombus occur?

A

Can occur in the arterial system (most commonly superimposed on atheroma) or the venous system (most commonly due to stasis)

114
Q

Arterial vs venous thrombosis

A
115
Q

What are the 3 factors of Virchow’s Triad?

A
  1. Endothelial injury
  2. Hypercoagulability
  3. Stasis
116
Q

What can cause endothelial damage?

A

smoking, hypertension, surgery, catheter, trauma

117
Q

What can cause hypercoagulability?

A

can be hereditary (Factor V Leiden, Prothrombin G20210A, Protein C/S deficiency) or acquired (cancer, chemotherapy, pregnancy, obesity)

118
Q

What can cause stasis?

A

immobility or polycythemia

119
Q

What is polycythaemia?

A

an increase in the number of red blood cells in the body which causes the blood to be thicker

120
Q

Once a thrombus develops, what can happen?

A
  • Will occlude the vessel
  • May dissolve
  • May be incorporated into vessel wall –> causing recanalisation
  • May embolise –> problem
121
Q

What is an embolus?

A
  • Mass of material in the vascular system able to become lodged in the vessel and block its lumen
  • 99% are thomrbi derived
122
Q

What else can form an embolus?

A
  • Atheromatous plaque material
  • Vegetation on heart valves (infective carditis)
  • Fragments of tumour (causing metastasis)
  • Amniotic fluid
  • Gas
  • Fat
123
Q

What are the 2 types of emboli?

A

Systemic or pulmonary

124
Q

What can a systemic embolus cause?

A

Generally originating from the heart (myocardial infarction/atrial fibrillation) or an atheromatous plaque. Can cause cerebral infarction, gangrene, bowel necrosis.

125
Q

Why are areas of turbulent blood flow more vulnerable to atherosclerotic plaques?

A

Frictional force exerted on blood-vessel walls –> endothelial injury

126
Q

What is thrombophilia?

A

A condition in which there’s an imbalance in naturally occurring blood-clotting proteins, or clotting factors

127
Q

What is cor pulmonale?

A

The enlargement and failure of the right ventricle of the heart as a response to pulmonary hypertension

128
Q

What can cause cor pulmonale?

A

Acute:

  • Massive PE
  • Injury due to mechanical ventilation

Chronic:

  • COPD (most common)
  • Chronic PE
129
Q

What is the medical term for a stroke?

A

Cerebrovascular accident (CVA)

Yr 2 - EMS (60 decks)

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