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

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
Q

Acquired risk factors for VTE

A

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

26
Q

Genetic/hereditary risk factors for VTE

A

Thrombotic disorders - FV Leiden, Protein S deficiency

27
Q

Clinical effects of PE

A

Small - starts asymptomatic > pulmonary hypertension (if multiple)

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

Large - death (saddle emboli)

28
Q

Systemic emboli arts with

A

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

29
Q

Infective embolism

A

Vegetations on infected heart valves > mycotic aneurysm formation

30
Q

Tumour embolism

A

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

31
Q

Air embolism

A

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

32
Q

Nitrogen embolism

A

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

33
Q

Amniotic fluid embolism

A

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

34
Q

Fat embolism

A

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

35
Q

Foreign body embolism

A

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

EMS - Mechanisms of Disease (21 decks)

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