Vascular pathology Flashcards

(42 cards)

1
Q

Define thrombosis

A

The formation of a blood clot in a blood vessel (artery or vein)

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2
Q

What is Virchow’s triad?

A

The three factors which predispose to thrombi (blood clots in vessels)

1) Endothelial injury/dysfunction
2) Hypercoagulability
3) Haemodynamic changes (stasis/turbulence)

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3
Q

What is endothelial injury/dysfunction?

A

Physical endothelial damage or endothelial cell dysfunction

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4
Q

What are the causes of endothelial injury/dysfunction?

A
  • Hypertension
  • Toxins from tobacco smoke
  • Hyperlipidaemia, chronic hyperglycaemia
  • Bacterial endotoxins
  • Medical devices
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5
Q

What does endothelial injury/dysfunction result in?

A
  • loss of protective layer that discourages attachement of cells and clotting proteins
  • change in the gene expression pattern to a phenotype that is proinflammatory and prothrombotic
  • Main cause of arterial or intracardiac (within the heart) thrombi
  • These thrombi are rich in platelets and so are treated with antiplatelet drugs, e.g. aspirin
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6
Q

Describe some characteristics of relative stasis

A
  • Slow flowing blood in veins, e.g. prolonged immobility, long operations
  • Loss of laminar flow
  • Contributes to endothelial dysfunction
  • Decreased washout of coag factors, increased cell contact with epithelium
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7
Q

Describe some characteristics of turbulent blood flow

A
  • Chaotic flow with focal stasis and loss of laminar flow
  • Contributes to endothelial injury (shear stress) and/or dysfunction
  • Occurs in arterial vessels (e.g. narrowed arteries (stenosed), branch points)
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8
Q

Name some causes of hypercoagulability

A

Inherited disorders of coagulation factors e.g.:
Factor V Leiden mutation – this mutation makes factor V resistant to inhibition, goes into overdrive
Antithrombin III deficiency
Protein C or S deficiency

Acquired disorders, e.g.:
Dehydration
Tobacco smoke, obesity
Pregnancy, hormonal contraceptive use
Disseminated cancer
Postoperative 
Heparin-induced thrombocytopenia. Develop antibodies to the heparin
Antiphospholipid syndrome. Autoimmune disease.
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9
Q

What is Budd-Chiari syndrome?

A

hepatic vein thrombosis; abdo pain / ascites / hepatomegaly

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10
Q

Give some examples of superficial venous thrombosis

A

e.g. anterior chest wall (Mondor’s disease) or varicose vein thrombosis, with painful thrombophlebitis; usually of little clinical significance

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11
Q

What is Paget-Schroetter disease?

A

thrombosis of axillary or subclavian vein (arm vein)

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12
Q

What is deep vein thrombosis and what are the signs and symptoms?

A

venous thrombus forming in the deep veins of the leg or pelvis (iliac veins)

swelling, pain, tenderness, erythema, increased temperature

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13
Q

What things can increase the risk of deep vein thrombosis?

A

1) Bed rest and immobilisation – reduced muscle action and slow venous return -> stasis
2) Pregnancy – stasis due to enlarging uterus and hypercoagulability
3) Post-surgical – stasis due to immobilisation, vascular injury and release of procoagulant factors

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14
Q

What is the clinical consequence of thrombi?

A

Cause obstruction to blood flow or embolisation (later)

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15
Q

What can happen if there’s a thrombus in an artery?

A

ischaemia and infarction of tissues
Ischaemia → restriction in blood supply resulting in oxygen insufficiency for cellular metabolism
Infarction → tissue death (necrosis) due to inadequate blood supply (ischaemia)

Limb artery thrombosis → limb ischaemia
Coronary artery thrombosis → myocardial infarction
Cerebrovascular artery thrombosis → stroke

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16
Q

What is propagation of a thrombus?

A
  • Enlargement and growth along the vessel due to further platelet and fibrin deposition
  • Can lead to vascular occlusion and/or embolism
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17
Q

What is embolisation?

A
  • Embolus → A detached intravascular solid, liquid or gas that is carried by the blood to a site distant from its point of origin
  • Detachment of part or all of thrombus from site of origin to lodge at a distant site (thromboembolism)
  • Can cause occlusion and infarction
18
Q

What is resolution/dissolution of a thrombus?

A
  • Fibrinolysis and autolytic degeneration of cellular components of thrombus
  • Restoration of blood flow
19
Q

What is organisation of a thrombus?

A

Ingrowth of granulation tissue and fibrous repair

20
Q

What is recanalisation of a thrombus?

A

new channel forms in organising thrombus

21
Q

What are the different types of embolism?

A
  • Thromboembolism – dislodged thrombus; most common
  • Fat embolism – droplets of fat from e.g. fractures, orthopaedic procedures, massive soft tissue injury, liposuction
  • Air (gas) embolism – e.g. decompression sickness, medical procedures
  • Amniotic fluid embolism – triggers serious allergic reaction if it goes into mother’s circulation

Unless otherwise specified it is thrombus embolising

22
Q

What are some common sites of arterial thromboembolism?

A

Heart – most commonly left ventricle or left atrium

  • Ventricular thrombus secondary to myocardial infarction
  • Atrial fibrillation
  • Infected heart valve – endocarditis (→ septic embolism, with distal infection)

Arterial vessels

  • Atheromatous plaque
  • Aortic aneurysms – abnormal dilatation of a blood vessel
23
Q

Describe the cause and effects of pulmonary thromboembolism

A

Due to embolism from DVT
Route of embolism:
DVT → IVC → right side of heart → pulmonary circulation

Effect depends on size:
Tiny vessel occlusion → asymptomatic
Multiple tiny emboli over a prolonged period → pulmonary hypertension
Small / medium vessels occlusion → symptomatic +/- infarction

Signs and symptoms: shortness of breath, pleuritic chest pain (pain on inspiration), cough and haemoptysis, tachycardia, tachypnoea, hypoxia

Major pulmonary arteries (e.g. saddle embolus) → sudden death

24
Q

Name the 3 types of arteries

A

1) Elastic arteries
2) Muscular arteries
3) Small arteries and arterioles

25
Describe elastic arteries
(large arteries, generally >10mm) - Pulmonary arteries, aorta and main it’s main branches… - Brachiocephalic trunk, common carotid, subclavian, common iliacs - Need to be elastic as relatively thin compared to diameter, so can stretch/recoil with systole/diastole - Media is thick; mainly layers of elastin/collagen, very little smooth muscle - Adventitia has vasa vasorum – small blood vessels
26
Describe muscular arteries
(medium arteries, 0.1mm to 10mm) - Generally, the other “named” arteries - Media is between thin internal/external elastic layers, and primarily made of smooth muscle (but gradual transition from elastic arteries) - Less elastic but capacity for vasoconstriction
27
Describe small arteries and arterioles
(<0.1mm) - Have an internal elastic layer only - Small arteries have up to 8 smooth muscle layers in media - Arterioles have one or two layers (<30 mm) - Deliver blood to capillaries; can control flow by dilating/contracting - Origin of most peripheral vascular resistance, so useful in regulating BP
28
Describe the structure of veins
- Same three layers as arteries (intima/media/adventitia) - Intima and media are thinner than arteries - Adventitia tends to be the most developed layer - Overall, thinner wall compared to lumen Large veins have vasa vasorum – blood supply Small veins known as venules (10-50mm diameter)
29
Define arteriosclerosis
- “hardening of the arteries” - Generic terms for arterial wall thickening and loss of elasticity - Three specific types
30
What are the three types of arteriosclerosis?
1) Arteriolosclerosis 2) Mönckeberg medial sclerosis 3) Atherosclerosis (most common)
31
What is arteriolosclerosis?
- Affects small arteries/arterioles, may result in distal ischaemia - Usually seen with hypertension or diabetes
32
What is Mönckeberg medial sclerosis?
- Calcific deposits in muscular arteries, usually in over-50s - Lesions do not restrict lumen – not clinically significant
33
What is atherosclerosis?
- Progressive arteriosclerosis of medium/large arteries due to atheromatous plaque
34
What are the 4 stages of atherogenesis?
1) Chronic endothelial injury 2) Endothelial dysfunction 3) Fatty streak development 4) Atheroma development
35
What happens in stage 1 (Chronic endothelial injury) of atherogenesis?
- Lesions develop in tunica intima of large/medium arteries following endothelial injury - Predisposing factors include: LDL hyperlipidaemia, diabetes, hypertension, smoking, some viral/bacterial infections (e.g. HIV, HCV, CMV, H. pylori)
36
What happens in stage 2 (endothelial dysfunction) of atherogenesis?
- Increased permeability to LDL cholesterol - Increased adherence of WBCs to endothelium - Reactive oxygen species from endothelial injury oxidise LDL in intima - Monocytes enter tunica intima → macrophages
37
What happens in stage 3 (fatty streak development) of atherogenesis?
- Macrophages phagocytose oxidised LDL → foam cells (spongy cytoplasm appearance due to being loaded with lipid-containing vesicles) - Foam cells + infiltrated T-lymphocytes form fatty streak (initial atherosclerotic lesion)
38
What happens in stage 4 (atheroma development) of atherogenesis?
- Smooth muscle cells migrate from media and proliferate to surround deposits - Fibroblasts form a protective layer around the lesion (fibrous cap) - The final atheromatous plaque contains a combination of: - Smooth muscle cells, macrophages, T-cells, foam cells, cholesterol deposits and cellular debris - Progression: accumulation of lipids and loss of integrity of endothelium - Advanced lesions: thin tunica media, calcification of lipid deposits, necrosis
39
What do fatty streaks look like macroscopically and microscopically?
Macroscopic: Begin as minute yellow, flat areas that coalesce into elongated lesions, 1 cm or more in length.  Microscopic: Composed of lipid-filled foamy macrophages but are only minimally raised and do not cause any significant flow disturbance 
40
What does an atherosclerotic plaque look like macroscopically and microscopically?
Macroscopic: intimal thickening and lipid accumulation; whitish-yellow raised lesions up to 1.5cm diameter (can coalesce) Thrombus overlying ruptured plaques look red-brown Microscopic: three key components - Cells: smooth muscle cells, macrophages, T cells - Extracellular matrix: collagen, elastic fibres, proteoglycans - Intra/extracellular lipids Lumen, fibrous cap, central core (mainly lipid)
41
What are the clinical consequences of atheroma formation?
1) Thrombosis due to ulceration and rupture of atheroma plaque Occludes blood supply → ischaemic necrosis (infarction) 2) Distal embolisation of atheromatous debris post-rupture (e.g. trash foot) 3) Intermittent ischaemia from stenosis (narrowing) E.g. angina, intermittent claudication, mesenteric ischaemia 4) Destruction of underlying vessel → aneurysm formation Secondary rupture/thrombosis
42
What are some other causes of infarction other than thrombus/atheroma?
1) Vasospasm eg. cerebral vasospasm after subarachnoid haemorrhage 2) Dissecting aortic aneurysm - rip in the intima 3) Extrinsic compression eg. by tumour, or oedema (compartment syndrome) 4) Twisting eg. testicular torsion