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Year 1 Semester 2 > Atherosclerosis, thrombosis, embolism and infarction > Flashcards

Atherosclerosis, thrombosis, embolism and infarction Flashcards

1
Q

Define atherosclerosis

A
  • Athere = gruel; Sclerosis = hardness

- Literal meaning is hardening of the arteries

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2
Q

What arteries does atherosclerosis mainly affect?

A
  • Elastic arteries

- Medium to large muscular arteries

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3
Q

Describe atheromas

A
  • Fibro-fatty plaques
  • Intimal fibrous cap
  • Central core rich in lipids
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4
Q

What are the risk factors for atherosclerosis?

A
  • Age - older –> higher risk
  • Sex - male more common
  • Genetics
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes mellitus
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4
Q

What are the risk factors for atherosclerosis?

A
  • Age - older –> higher risk
  • Sex - male more common
  • Genetics
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes mellitus
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5
Q

What is involved in the pathogenesis of atherosclerosis?

A
  • Chronic endothelial injury/dysfunction
  • Role of lipids
  • Role of macrophages
  • Smooth muscle proliferation
  • Formation of a fibro-lipid plaque
  • Injury to the plaque - thrombus formation
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6
Q

Causes of chronic endothelial injury/dysfunction

A
  • Haemodynamic disturbances
  • Hypercholesterolemia
  • Hypertension
  • Smoking
  • Toxins
  • Viruses
  • Immune reactions
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7
Q

What happens in chronic endothelial injury/dysfunction?

A
  • Leukocyte adhesion
  • Increases production of vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), P-selectin, E-selectin
  • These molecules cause more monocyte adhesion and increased endothelial permeability therefore increased monocyte migration ending up in tunica intima
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8
Q

What role do lipids play in atherosclerosis?

A

Hyperlipidaemia (LDL cholesterol):

  • Impairs endothelial function
  • Accumulates within intima
  • Causes oxidative modification of LDL:
  • ingested by macrophages via SCAVANGER receptors = foam cells
  • chemotactic for monocytes
  • inhibit the motility of macrophages
  • stimulates release of cytokines
  • cytotoxic to endothelial and smooth muscle cells
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9
Q

What is the role of macrophages in atherosclerosis?

A

-Engulf oxidised LDL = foam cells
-Secrete:
IL1 (interleukin 1)
TNF (tumour necrosis factor)
MCP1 (monocyte chemotactic protein 1)
Growth factors (PDGF, FGF, TNF)
Interferon alpha, TGF-beta
-These secretions cause further attraction of monocytes into intima and phagocyte more LDL cholesterol

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9
Q

What is the role of macrophages in atherosclerosis?

A

-Engulf oxidised LDL = foam cells
-Secrete:
IL1 (interleukin 1)
TNF (tumour necrosis factor)
MCP1 (monocyte chemotactic protein 1)
Growth factors (PDGF, FGF, TNF)
Interferon alpha, TGF-beta
-These secretions cause further attraction of monocytes into intima and phagocyte more LDL cholesterol
-Fatty streaks appear

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10
Q

What does LDL cholesterol stand for?

A

Low-density lipoprotein cholesterol

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10
Q

What does LDL cholesterol stand for?

A

Low-density lipoprotein cholesterol

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11
Q

Role of smooth muscle proliferation

A
  • Fatty streaks mature into mature fibro-fatty atheroma
  • Smooth muscle proliferates which helps in the formation of fibrous tissue causing the fibrous cap
  • In the centre, the immobile foamy cells will eventually die
  • Once these cells are dead, LDL cholesterol crystallises and groups together in the centre forming lipid necrotic debris
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12
Q

Why is it good to include antioxidants in one’s diet?

A

Prevents LDL from being oxidised so cannot be engulfed by macrophages

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12
Q

Why is it good to include antioxidants in one’s diet?

A

Prevents LDL from being oxidised so cannot be engulfed by macrophages

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13
Q

What causes smooth muscle to migrate to tunica intima?

A

Cytokines and growth factors released by the foam cells

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14
Q

Morphology of atheroma

A
  • Atheromatous (fibro-fatty, fibro-lipid) plaque
  • Patchy and raised white to yellow 0.3-1.5cm
  • Core of lipid
  • Fibrous cap
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15
Q

Which vessels are most commonly affected?

A
  • Abdominal aorta
  • Coronary arteries
  • Popliteal arteries
  • Descending thoracic aorta
  • Internal carotid arteries
  • Vessels of the circle of Willis
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16
Q

What complications can take place with atheromas?

A
  • Calcification
  • Rupture or ulceration
  • Haemorrhage
  • Thrombosis
  • Aneurysmal dilatation
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17
Q

Clinical issues if complications happen

A
  • Thrombosis
  • Calcification
  • Aneurysmal dilatation
  • Ischaemic events: heart, brain, lower extremities, other organs
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18
Q

What are primary preventions of atherosclerosis?

A
  • Stop smoking
  • Control hypertension
  • Weight reduction
  • Lowering total LDL
  • Reduce calories intake
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18
Q

What are primary preventions of atherosclerosis?

A
  • Stop smoking
  • Control hypertension
  • Weight reduction
  • Lowering total LDL
  • Reduce calories intake
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19
Q

What are secondary preventions of atherosclerosis?

A
  • Prevent complication
  • Antiplatelet drugs in thrombosis
  • Lower blood lipid levels
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20
Q

What are lipoproteins?

A

Central core of hydrophobic lipid
-triglycerides or cholesterol esters

Hydrophilic coat of polar substances

  • phospholipids
  • free cholesterol
  • associated proteins - apoproteins or apolipoproteins
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21
Q

How do the 5 main lipoprotein classes vary?

A
  • core lipids
  • apoproteins
  • size
  • density
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22
Q

What are the 5 main classes of lipoproteins?

A
  • High density lipoprotein (HDL)
  • Intermediate density lipoproteins (IDL)
  • Low density lipoproteins (LDL)
  • Very low density lipoproteins (VLDL)
  • Chylomicrons
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23
Q

How do the lipoproteins interact with cholesterol?

A

Chylomicrons transport triglycerides and cholesterol esters from the GI to tissues

  • Split by lipoprotein lipase to release free fatty acids (FFAs)
  • FFAs taken up by muscle and adipose tissue

Chylomicron remnants taken up in the liver
-cholesterol stored, oxidised to bile acids or released to VLDL

VLDL transport cholesterol and newly synthesised triglycerides to tissues
-TGs removed from VLDL leaving LDL with a high cholesterol (taken up by cells or liver)

HDL absorbs cholesterol from cell breakdown and transfers it to VLDL and LDL

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24
Q

What is hyperlipidaemia?

A

An increase in the plasma concentration of lipids

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25
Q

What are the dangers of plasma cholesterol and LDL?

A

Increased plasma cholesterol associated with increased LDL is a risk factor for atheromatous disease
-may lead to atherosclerosis, ischaemic heart disease, myocardial infarction & cerebral vascular accidents

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25
Q

What are the dangers of plasma cholesterol and LDL?

A

Increased plasma cholesterol associated with increased LDL is a risk factor for atheromatous disease
-may lead to atherosclerosis, ischaemic heart disease, myocardial infarction & cerebral vascular accidents

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26
Q

What is the average total cholesterol level in the UK?

A

5.7mmol/L

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27
Q

What is the ideal cholesterol level?

A

<5mmol/L

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28
Q

What is a mildly high cholesterol level?

A

5 to 6.4mmol/L

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29
Q

What is a moderately high cholesterol level?

A

6.5 to 7.8mmol/L

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30
Q

What is a very high cholesterol level?

A

> 7.8mmol/L

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31
Q

What else other than the cholesterol level must be taken into account when determining how high cholesterol is?

A
  • the ratio between good (HDL) and bad (LDL) cholesterol

- other risk factors for cardiovascular disease e.g. smoking, diabetes, high blood pressure

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32
Q

How do lipid lowering drugs work?

A
  • Reducing production of lipoproteins or

- Increasing their removal from the blood

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33
Q

What is the aim when using lipid lowering drugs?

A

Reduce plasma cholesterol

  • Lifestyle modification (diet and exercise) is first step
  • Drug therapy should be secondary
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34
Q

What 3 source is cholesterol derived from?

A
  • De novo synthesis in liver
  • Uptake from circulating LDLs
  • Uptake of chylomicron remnants
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35
Q

What are the actions of different drug types?

A
  • Sequester bile acids in the intestine/Decrease hepatic stores of cholesterol e.g colestyramine
  • Inhibit transport protein for cholesterol in the brush border of enterocytes in the duodenum e.g ezetimibe
  • Alter the levels of plasma lipoproteins e.g fenofibrate, bezafibrate, gemfibrozil & nicotinic acid
  • Inhibit the synthesis of cholesterol in the liver e.g simvastatin, pravastatin, atorvastatin, rosuvastatin
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36
Q

How does cholestyramine affect cholesterol levels?

A
  • Binds to bile in intestine
  • More bile excreted out, less goes into liver
  • Cholesterol then used to increase bile levels in liver causing a decrease in cholesterol levels
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37
Q

How does ezetimibe affect cholesterol levels?

A

Binds to sterol carrier proteins in the brush border of the enterocytes, inhibiting them and preventing uptake of cholesterol and so it then cannot bind to chylomicrons and be taken to the liver

38
Q

What do fibrates do?

A
  • Increase the action of lipoprotein lipase

- Decrease secretion of VLDL resulting in larger uptake of LDL in the liver

39
Q

What is a secondary action of the cholesterol lowering drugs?

A

Increased expression of LDL receptors in the liver resulting in more LDL uptake

40
Q

How successful are bile-sequestering drugs such as colestryramine?

A

Bile-sequestering drugs plus inhibitors of cholesterol byosynthesis can lower blood cholesterol by 50%

41
Q

What are some clinical uses of fibrates?

A
  • Mixed dyslipidaemia (i.e. raised serum triglyceride as well as cholesterol)
  • In patients with low HDL and high risk of atheromatous disease (e.g. type 2 diabetes)
  • Combined with other lipid-lowering drugs in patients with severe treatment resistant dyslipidaemia
42
Q

What does nicotinic acid (niacin) do?

A

Vitamin with lipid lowering properties

  • decreases VLDL production which leads to a decrease in LDL
  • ALso activates lipoprotein lipase
43
Q

What are statins?

A

-Hydroxymethlglutamyl-coenzyme A reductase (HMG-CoA reductase) inhibitors

44
Q

What is HMG-CoA reductase?

A
  • Major rate-limiting step in cholesterol synthesis

- Converts HMG-CoA to mevalonic acid (MVA)

45
Q

What are some long-lasting HMG-CoA reductase inhibitors?

A
  • Simvastatin
  • Pravastatin
  • Atorvastatin
  • Rosuvastatin
45
Q

What are some long-lasting HMG-CoA reductase inhibitors?

A
  • Simvastatin
  • Pravastatin
  • Atorvastatin
  • Rosuvastatin
46
Q

What are the two outcomes of the mevalonate pathway?

A
  • Cholesterol synthesis

- Protein prenylation

47
Q

What is protein prenylation?

A
  • Addition of lipid tails to small GTPase signalling molecules
  • Ensures they are localised correctly
47
Q

What is protein prenylation?

A
  • Addition of lipid tails to small GTPase signalling molecules
  • Ensures they are localised correctly
48
Q

What are some clinical uses of statins?

A
  • Secondary prevention of myocardial infarction and stroke in those who have atherosclerotic diseases
  • Primary prevention of arterial disease in patients with high serum cholesterol
  • Atorvastatin lowers serum cholesterol in familial hypercholesterolaemia
49
Q

What are some side effects of lipid lowering drugs?

A
  • Statins: myositis, angio-oedema, GI disturbances, insomnia, rash
  • Fibrates: myositis (especially in patients with renal impairment), GI disturbances
  • Colestyramine and ezetimibe: GI symptoms (nausea, abdominal bloating, constipation, diarrhoea)
  • Nicotinic acid: flushing, palpations, GI disturbances
50
Q

What are the two PCSK9 inhibitors?

A

Alirocumab and evolcumab

51
Q

What do PCSK9 inhibitors do?

A
  • PCSK9 is an enzyme that mediates the degradation of LDL receptors on surface of liver cells
  • Inhibiting this enzyme increases the amount of LDL bound and removed by the liver
52
Q

Define thrombus

A

A thrombus is a solidification of blood contents that forms within the vascular system during life

53
Q

What is thrombosis?

A

Thrombosis is a pathological process. It denotes the formation of a thrombus within the noninterupted vascular system

54
Q

What role does endothelial injury play in thrombosis?

A

-Important in the formation of thrombi is the heart and arteries

Examples of thrombi development:

  • Left ventricle at sites of myocardial infarction
  • On ulcerated plaques in advanced atherosclerosis
  • Injured endocardium (cardiac surgery, myocarditis)
  • Valves with inflammatory valve disease, and prosthetic valves
55
Q

What are some causes of endothelial injury?

A
  • Radiation injury
  • Chemical agents: exogenous and endogenous
  • Bacterial toxins or endotoxins
  • Immunologic injuries
  • Neoplastic involvement
55
Q

What are some causes of endothelial injury?

A
  • Radiation injury
  • Chemical agents: exogenous and endogenous
  • Bacterial toxins or endotoxins
  • Immunologic injuries
  • Neoplastic involvement
56
Q

What is platelets’ role in thrombosis?

A

After injury to a vessel, platelets undergo three important reactions:

  • Adhesion
  • Secretion
  • Aggregation
56
Q

What is platelets’ role in thrombosis?

A

After injury to a vessel, platelets undergo three important reactions:

  • Adhesion
  • Secretion
  • Aggregation
57
Q

What do turbulence and stasis do and which cardiovascular structures does each have more of an impact on?

A
  • Disrupt laminar flow
  • Prevent the dilution of coagulation factors
  • Retard the inflow of inhibitors of clotting factors
  • Promote endothelial cell activation
  • Turbulence contributes to the development of arterial and cardiac thrombi
  • Stasis contributes to venous thrombosis
58
Q

What is hypercoagulability?

A

An alteration of the blood coagulation mechanism that in some way predisposes thrombosis

59
Q

What are the two ways of causing hypercoagulability?

A
  • Primary (genetic)

- Secondary (acquired)

60
Q

What are some examples of primary primary risks that cause hypercoagulability?

A
  • Mutation in the factor V gene - Leiden mutation
  • Antithrombin III deficiency
  • Protein C ans S deficiency
61
Q

What re some high and low secondary risk examples that cause hypercoagulability?

A
  • High risk: bed rest (immobilisation), MI, tissue damage, CA, prosthetic valves, DIC
  • Low risk: AF, cardiomyopathy, nephrotic syndrome, oral contraceptive, sickle cell anaemia, smoking
62
Q

What are the three types of thrombi?

A
  • Mural thrombi
  • Arterial thrombi
  • Venous thrombosis (plebothrombosis)
63
Q

Explain mural thrombi

A
  • Applied to one wall of underlying structure

- Occur in the capacious lumina of the heart chambers and aorta

64
Q

Explain arterial thrombi

A
  • Usually occlusive
  • May be mural
  • Frequent in coronary arteries, cerebral arteries and femoral arteries
  • Grey-white and friable
65
Q

Explain venous thrombosis (phlebothrombosis)

A
  • Invariably occlusive and dark red

- Affect the veins of the lower extremities (90%) - deep calm, femoral, popliteal, iliac veins

65
Q

Explain venous thrombosis (phlebothrombosis)

A
  • Invariably occlusive and dark red

- Affect the veins of the lower extremities (90%) - deep calm, femoral, popliteal, iliac veins

66
Q

What is thrombophlebitis?

A

A vein becomes inflamed and then thrombosed

67
Q

What are some clinical features of thrombi?

A
  • They cause obstruction of arteries and veins

- They provide possible sources of emboli

68
Q

What are some clinical features of arterial thrombosis?

A
  • Loss of pulses distal to the thrombus
  • Area becomes perishing cold, pale, painful and there may be paraesthesia
  • Eventually tissue dies and gangrene results
69
Q

What are some clinical features of venous thrombosis?

A

Superficial (saphenous system):
-Congestion, swelling, pain, tenderness (rarely embolise)

Deep:

  • Foot and ankle oedema, Homans’ sign
  • Could be asymptomatic and recognised only when they have embolised
70
Q

How can we treat thrombosis?

A
  • Stockings (prevention)
  • Anticoagulant drugs. These aim to prevent the clot growing any larger and to prevent or stop an embolism
  • Currently there are two main forms of anticoagulant drugs: heparin (i.v or s.c) and warfarin (orally)
71
Q

What is an embolus?

A

A detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

72
Q

Where do most emboli arise from?

A

Thrombi (99%) - thromboembolism

73
Q

What are some rare forms of emboli?

A
  • Bone or bone marrow fragments
  • Atheromatous debris
  • Droplets of fat
  • Bits of tumour
  • Foreign bodies (such as bullets)
  • Bubbles of air or nitrogen
73
Q

What are some rare forms of emboli?

A
  • Bone or bone marrow fragments
  • Atheromatous debris
  • Droplets of fat
  • Bits of tumour
  • Foreign bodies (such as bullets)
  • Bubbles of air or nitrogen
74
Q

What are the different classifications of embolism?

A
  • Pulmonary embolism
  • Systemic embolism
  • Amniotic fluid embolism
  • Air embolism
  • Fat embolism
75
Q

Where do most pulmonary emboli arise from?

A

Thrombi within the large deep veins of the lower leg (95%)

76
Q

What are the 2 main pathophysiologic consequences that emboli can result in?

A
  • Respiratory compromise

- Haemodynamic compromise

77
Q

What might smaller pulmonary emboli cause?

A

Acute respiratory and cardiac problems:

  • Chest pain, dyspnoea, shock, increased LDH, haemoptysis
  • Chest x-ray may disclose a pulmonary infarct as a wedge-shaped infiltrate
  • Emboli can also be detected by pulmonary lung scanning using radionuclides
  • Occlusion puts some strain on the heart which is evident on an ECG
78
Q

What is systemic embolism?

A

Emboli that travel through the arterial circulation

79
Q

Where do most systemic emboli arise from?

A

Thrombi within the heart (80-85%)

80
Q

Are systemic emboli likely to cause infarction?

A

Yes, they almost always cause infarction

81
Q

What are the major sites of lodgement of all systemic emboli?

A
  • Lower extremities (70-75%)
  • Brain (10%)
  • Viscera (mesenteric, renal, splenic) (10%)
  • Upper limbs (7-8%)
82
Q

What is air embolism?

A

The presence of bubbles of air or gas within the circulation obstruct vascular flow and damage tissues just as thrombotic masses

83
Q

What can air embolism also be referred as?

A

Barotrauma

84
Q

What is Caisson disease?

A

If the individual decompresses too rapidly, helium and nitrogen tend to persist to form gaseous emboli within blood vessels and tissues

85
Q

What is the acute form of Caisson disease commonly known as?

A
  • The bends

- The chokes

86
Q

How is caisson disease treated

A

Recompression chamber

86
Q

How is caisson disease treated

A

Recompression chamber

87
Q

What is fat embolism?

A

Minute globules of fat can often be demonstrated in the circulation following

  • fractures of the shafts of long bones
  • and rarely, with soft tissue trauma and burns
88
Q

Describe the pathogenesis of fat embolism

A

The pathogenesis of this symptom complex involve both:

  • Mechanical obstruction - microagregates of neutral fat cause acclusion
  • Chemical injury - free fatty acids released from fat globules result in toxic injury to the vascular endothelium
89
Q

Clinical features of fat embolism

A

Clinically it is characterised by:

  • Pulmonary insufficiency
  • Neurologic symptoms
  • Anaemia and thrombocytopenia

The symptoms appear after latent 24-72 hour period

  • sudden onset of tachypnoea, dyspnoea and tachycardia
  • neurologic symptoms include irritability and restlessness which progress to delirium and coma
90
Q

What is amniotic fluid embolism?

A
  • A rare complication of labour and one cause of maternal mortality (86%)
  • The cause is the infusion of amniotic fluid into the maternal circulation
91
Q

Define infarct

A

An area of ischaemic necrosis caused by occlusion of arterial supply or venous drainage in a particular disease

92
Q

Define necrosis

A

Refers to a spectrum of morphological changes that follow cell death in living tissue, largely resulting from the progressive action of enzymes on the lethally injured cells

93
Q

What are the three types of infarcts?

A

Red (haemorrhagic):

  • venous occlusions
  • in loose tissues
  • in tissues with dual circulation

White (anaemic):

  • arterial occlusions
  • solid organs

Septic or bland

Year 1 Semester 2 (26 decks)

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