Atheroma, Thrombosis & Embolism (13) Flashcards Preview

EMS - Mechanisms of Disease > Atheroma, Thrombosis & Embolism (13) > Flashcards

Flashcards in Atheroma, Thrombosis & Embolism (13) Deck (35):
1

Atherosclerosis

Degeneration of arterial walls characterised by fibrosis, lipid disposition and inflammation which limits blood circulation and predisposes to thrombosis

2

Commonly affected vessels

Bifurcations (turbulent flow), abdominal aorta, coronary arteries, popliteal arteries, carotid vessels, circle of willis

3

What are non modifiable risk factors?

Age, male, FH, genetic

4

What are modifiable risk factors?

Hyperlipidaemia (LDL:HDL), hypertension, smoking, diabetes, CRP, increased homocysteine, stress

5

Pathophysiology

Due to chronic injury and repair of endothelium, in presence of hyperlipidaemia - lipid accumulates in intimate, monocytes migrate (VCAM1) and ingest lipid > foam cells (fatty streak) - secrete chemokines attracting more monocytes/macrophahes, lymphocytes, smooth muscle cells > proliferate and secrete connective tissue (atherosclerotic plaque)

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Causes of endothelial injury

Haemodynamic injury, chemicals, immune complex deposition, irradiation

7

Plaque - fibrous cap

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

8

Plaque - necrotic centre

Cell debris, cholesterol crystals, foam cells, calcium

9

After athersclerosis

Occlusion, wearing of vessel walls (aneurysm), erosion (thrombosis)

10

Thrombosis

Solidification of blood contents formed in vessel during life

11

Blood clot

Stagnant blood, enzymatic process, elastic, adopts shape of vessel

12

Thrombus

Within the body during life, dependent on platelet, firm

13

What are platelets?

Fragments of megakaryocytes in bone marrow, circulate in blood stream

14

How do platelets become activated?

Bind to collagen exposed by endothelial damage

15

What do platelets secrete?

Alpha granules - fibrinogen, fibronectin, PDGF (platelet derived growth factor)

Dense granules - chemotactic chemicals

16

Virchow's triad

Thrombus formations requires changes in
- Intimal surface of vessel
- The pattern of blood flow
- Blood constituents

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Plaque rupture causes

Turbulent flow and intimal change

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Hyperlipidaemia causes

Change in blood constituents

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Arterial thrombus formation

- Lipid-filled cells
- Loss of endothelial cells and exposure to collagen
- Platelet adherence and activation
- Thrombus formed of alternating layers of platelets, fibrin and RBCs

20

Venous thrombosis

Intimal change - valves
Change in blood flow - immobile
Change in blood constituents - inflammatory mediators (infection, malignancy), factor V leiden, Oestrogen

21

Cardiac thrombosis

Mural thrombi, occur in MI, myocarditis, arrhythmias, cardiomyopathy (areas of injury)

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Sequelae of thrombosis

Occlusion, resolution, incorporation into vessel wall, recanalisation and EMBOLISATION

23

Embolus

A mass of material in vascular system able to lodge in a vessel and block it (endo/exogenous, sold, liquid/gas)

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Pulmonary emboli

Most common, common cause of hospital mortality

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Acquired risk factors for VTE

Immobility, malignancy, previous VTE, heart failure, oestrogen, obesity, pregnancy, renal disease, smokers

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Genetic/hereditary risk factors for VTE

Thrombotic disorders - FV Leiden, Protein S deficiency

27

Clinical effects of PE

Small - starts asymptomatic > pulmonary hypertension (if multiple)

Medium - acute respiratory and cardiac failure (V/Q mismatch, RV strain)

Large - death (saddle emboli)

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Systemic emboli arts with

Heart (MI/AF), arterial circulation (atheroma)

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Infective embolism

Vegetations on infected heart valves > mycotic aneurysm formation

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Tumour embolism

May break off as tumours penetrate vessels, major route of dissemination

31

Air embolism

Obstetric/chest wall injury, >100ml to cause clinical effects

32

Nitrogen embolism

Decompression sickness, increase pressure absorb more N2, N2 bubbles enter bones, joints and lungs (Divers, tunnel workers)

33

Amniotic fluid embolism

Increased uterine pressure during labour may force AF into maternal uterine veins, lodge in lungs > respiratory distress

34

Fat embolism

80% patients with significant trauma (fractures and bones), sudden onset respiratory distress (fatal 15%)

35

Foreign body embolism

Particles injected IV e.g. talc in IVDUs > granulomatous reaction