Atheroma, Thrombosis and Ebolism Flashcards

1
Q

What is atherosclerosis?

A

Degeneration of arterial wall characterised by fibrosis, lipid deposition and inflammation.
-limits blood circulation and predisposes thrombosis.

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2
Q

What are the commonly affected vessels of atherosclerosis?

A
  • Bifurcations
  • Abdominal aorta
  • Coronary arteries
  • Popliteal arteries
  • Carotid vessels
  • Circle of Willis
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3
Q

What are the non-modifiable risk factors of atherosclerosis? (4)

A
  • Age
  • Male
  • FH
  • Genetic
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4
Q

What are the modifiable risk factors of atherosclerosis? (5)

A
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes
  • CRP
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5
Q

Why does atherosclerosis arise?

A

Due to chronic injury and repair of the endothelium.

-1st step = endothelial injury

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6
Q

What are the main causes of atherosclerosis? (4)

A
  • Haemodynamic injury
  • Chemicals
  • Immune complex deposition
  • Irradiation
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7
Q

Describe the process of atheroma formation.

A
  • Hyperlipidaemia and endothelial injury&raquo_space; lipid accumulation in intima
  • Monocytes ingest the lipid&raquo_space; foams cells (fatty streak)
  • Foam cells secrete chemokines&raquo_space; attract more monocytes/lymphocytes/smooth muscles cells
  • Forms ATHEROSCLEROTIC PLAQUE
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8
Q

What is the structure of an atheromatous plaque?

A
  • Fibrous cap (superficially)
  • Necrotic centre
  • Media (deep)
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9
Q

What is the fibrous cap of an atheromatous plaque composed of? (4)

A
  • Smooth muscle cells
  • Macrophages
  • Foam cells
  • Collagen
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10
Q

What is the necrotic centre of an atheromatous plaque composed of? (4)

A
  • Cell debris
  • Cholesterol
  • Foam cells
  • Calcium
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11
Q

What is thrombosis?

A

Solidification of blood contents in the vessel during life.

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12
Q

How is thrombosis different to a clot? (3)

A
  • Thrombosis is during life, clot is stagnant blood
  • Thrombosis is dependent on platelets, clots are enzymatic processes
  • Thrombosis is firm, clots are elastic/adopt shape of the vessel
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13
Q

What are platelets?

A

Fragments of megakaryocytes in the bone marrow.

-circulate in the blood and help form clots

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14
Q

How are platelets activated?

A

They bind to collagen exposed by endothelial damage&raquo_space; activation.

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15
Q

What do activated platelets secrete? (2)

A
  • Alpha granules; fibrinogen, fibronectin, PDGF

- Dense granules; chemotactic chemicals

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16
Q

What is Virchow’s triad?

A

The 3 factors required for thrombosis;

  • intimal surface of vessel
  • blood flow (stasis/turbulence)
  • blood constituents (mediators)
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17
Q

How does an arterial thrombus form?

A
-Turbulence
>> loss of endothelial cells
>> exposure of collagen
>> platelet adherence and activation
>> THROMBUS FORMATION
18
Q

What are the lines of Zahn?

A

Rib-like markings characteristic of thrombi near the heart or aorta.

19
Q

What factors contribute to venous thrombosis? (3)

A
  • Intimal changes; valves
  • Change in blood flow; immobile
  • Change in blood constituents; mediators/FV leiden/oestrogen
20
Q

What are cardiac thrombi known as?

A

Mural thrombi.

-occur over areas of endomyocardial injury

21
Q

What are the main causes of cardiac thrombi? (4)

A
  • MI
  • Myocarditis
  • Arrhythmias
  • Cardiomyopathy
22
Q

What is the general sequence of embolism formation?

A
Occlusion of vessel (thrombus)
>> resolution
>> incorporation into vessel wall
>> recanalisation
>> embolisation
23
Q

What is an embolus?

A

A mass of material in the vascular system able to lodge in a vessel and block it.

24
Q

What are the different types of emboli?

A
  • Exogenous/endogenous

- Solid/liquid/gas

25
Q

What is the most common emboli?

A

Pulmonary embolism.

26
Q

What are the main risk factors for venous thromboembolism (VTE)?

A

ACQUIRED - immobility, malignancy, heart failure. oestrogens, obesity, pregnancy
GENETIC - thrombotic disorders

27
Q

Name 2 genetic disorders that are risk factors for venous thromboembolism.

A
  • Factor V leiden

- Protein S deficiency

28
Q

What are the clinical effects of venous emboli?

A

SMALL - usually asymptomatic
MEDIUM - acute respiratory and cardiac failure
LARGE - death (‘saddle emboli’)

29
Q

Where do systemic emboli arise? (2)

A
  • Heart (MI/AF)

- Arterial circulation (atheroma)

30
Q

Where do systemic emboli always travel to?

A

The lungs.

-pulmonary emboli

31
Q

What do infective emboli usually form from?

A

Vegetations on infected heart valves.

32
Q

What can infective emboli lead to?

A

Mycotic aneurysm formation.

33
Q

How do tumour emboli form?

A

Bits may break off a tumour as they penetrate vessels.

34
Q

Do tumour emboil usually cause immediate physical problems?

A

No.

35
Q

What are the main forms of gas emboli?

A
  • Air

- Nitrogen

36
Q

How does air get into vessels to form gas emboli?

A

Obstetric procedures/chest wall injury.

->100ml to cause clinical effects

37
Q

How does nitrogen get into vessels to form gas emboli?

A

Decompression sickness.

  • divers/tunnel workers
  • enter bones/joints/lungs
38
Q

How do amniotic fluid emboli form?

A

Increased uterine pressure during labour&raquo_space; AF may enter maternal uterine veins
-can lodge in lung&raquo_space; respiratory distress

39
Q

How many patients with significant trauma are found to have fat emboli at post-mortem?

A

~80%.

40
Q

What do far emboli cause?

A

Sudden onset of respiratory distress.

41
Q

How do foreign body emboli often form?

A

Particles injected intravenously.

-e.g. talc in IVDUs&raquo_space; granulomatous reaction