Atheroma, Thrombosis & Embolism (13) Flashcards

1
Q

Atherosclerosis

A

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

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2
Q

Commonly affected vessels

A

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

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3
Q

What are non modifiable risk factors?

A

Age, male, FH, genetic

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4
Q

What are modifiable risk factors?

A

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

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5
Q

Pathophysiology

A

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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6
Q

Causes of endothelial injury

A

Haemodynamic injury, chemicals, immune complex deposition, irradiation

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7
Q

Plaque - fibrous cap

A

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

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8
Q

Plaque - necrotic centre

A

Cell debris, cholesterol crystals, foam cells, calcium

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9
Q

After athersclerosis

A

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

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10
Q

Thrombosis

A

Solidification of blood contents formed in vessel during life

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11
Q

Blood clot

A

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

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12
Q

Thrombus

A

Within the body during life, dependent on platelet, firm

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13
Q

What are platelets?

A

Fragments of megakaryocytes in bone marrow, circulate in blood stream

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14
Q

How do platelets become activated?

A

Bind to collagen exposed by endothelial damage

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15
Q

What do platelets secrete?

A

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

Dense granules - chemotactic chemicals

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16
Q

Virchow’s triad

A

Thrombus formations requires changes in

  • Intimal surface of vessel
  • The pattern of blood flow
  • Blood constituents
17
Q

Plaque rupture causes

A

Turbulent flow and intimal change

18
Q

Hyperlipidaemia causes

A

Change in blood constituents

19
Q

Arterial thrombus formation

A
  • 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
Q

Venous thrombosis

A

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

21
Q

Cardiac thrombosis

A

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

22
Q

Sequelae of thrombosis

A

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

23
Q

Embolus

A

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

24
Q

Pulmonary emboli

A

Most common, common cause of hospital mortality

25
Acquired risk factors for VTE
Immobility, malignancy, previous VTE, heart failure, oestrogen, obesity, pregnancy, renal disease, smokers
26
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)
28
Systemic emboli arts with
Heart (MI/AF), arterial circulation (atheroma)
29
Infective embolism
Vegetations on infected heart valves > mycotic aneurysm formation
30
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