Atheroma, Thrombosis and Ebolism Flashcards Preview

Year 2 EMS MoD > Atheroma, Thrombosis and Ebolism > Flashcards

Flashcards in Atheroma, Thrombosis and Ebolism Deck (41):
1

What is atherosclerosis?

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

2

What are the commonly affected vessels of atherosclerosis?

-Bifurcations
-Abdominal aorta
-Coronary arteries
-Popliteal arteries
-Carotid vessels
-Circle of Willis

3

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

-Age
-Male
-FH
-Genetic

4

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

-Hyperlipidaemia
-Hypertension
-Smoking
-Diabetes
-CRP

5

Why does atherosclerosis arise?

Due to chronic injury and repair of the endothelium.
-1st step = endothelial injury

6

What are the main causes of atherosclerosis? (4)

-Haemodynamic injury
-Chemicals
-Immune complex deposition
-Irradiation

7

Describe the process of atheroma formation.

-Hyperlipidaemia and endothelial injury >> lipid accumulation in intima
-Monocytes ingest the lipid >> foams cells (fatty streak)
-Foam cells secrete chemokines >> attract more monocytes/lymphocytes/smooth muscles cells
-Forms ATHEROSCLEROTIC PLAQUE

8

What is the structure of an atheromatous plaque?

-Fibrous cap (superficially)
-Necrotic centre
-Media (deep)

9

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

-Smooth muscle cells
-Macrophages
-Foam cells
-Collagen

10

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

-Cell debris
-Cholesterol
-Foam cells
-Calcium

11

What is thrombosis?

Solidification of blood contents in the vessel during life.

12

How is thrombosis different to a clot? (3)

-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

13

What are platelets?

Fragments of megakaryocytes in the bone marrow.
-circulate in the blood and help form clots

14

How are platelets activated?

They bind to collagen exposed by endothelial damage >> activation.

15

What do activated platelets secrete? (2)

-Alpha granules; fibrinogen, fibronectin, PDGF
-Dense granules; chemotactic chemicals

16

What is Virchow's triad?

The 3 factors required for thrombosis;
-intimal surface of vessel
-blood flow (stasis/turbulence)
-blood constituents (mediators)

17

How does an arterial thrombus form?

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

18

What are the lines of Zahn?

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

19

What factors contribute to venous thrombosis? (3)

-Intimal changes; valves
-Change in blood flow; immobile
-Change in blood constituents; mediators/FV leiden/oestrogen

20

What are cardiac thrombi known as?

Mural thrombi.
-occur over areas of endomyocardial injury

21

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

-MI
-Myocarditis
-Arrhythmias
-Cardiomyopathy

22

What is the general sequence of embolism formation?

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

23

What is an embolus?

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

24

What are the different types of emboli?

-Exogenous/endogenous
-Solid/liquid/gas

25

What is the most common emboli?

Pulmonary embolism.

26

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

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

27

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

-Factor V leiden
-Protein S deficiency

28

What are the clinical effects of venous emboli?

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

29

Where do systemic emboli arise? (2)

-Heart (MI/AF)
-Arterial circulation (atheroma)

30

Where do systemic emboli always travel to?

The lungs.
-pulmonary emboli

31

What do infective emboli usually form from?

Vegetations on infected heart valves.

32

What can infective emboli lead to?

Mycotic aneurysm formation.

33

How do tumour emboli form?

Bits may break off a tumour as they penetrate vessels.

34

Do tumour emboil usually cause immediate physical problems?

No.

35

What are the main forms of gas emboli?

-Air
-Nitrogen

36

How does air get into vessels to form gas emboli?

Obstetric procedures/chest wall injury.
->100ml to cause clinical effects

37

How does nitrogen get into vessels to form gas emboli?

Decompression sickness.
-divers/tunnel workers
-enter bones/joints/lungs

38

How do amniotic fluid emboli form?

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

39

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

~80%.

40

What do far emboli cause?

Sudden onset of respiratory distress.

41

How do foreign body emboli often form?

Particles injected intravenously.
-e.g. talc in IVDUs >> granulomatous reaction