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Z YEAR 2 BRS CARDIO > Atheroscelerosis and Peripheral Vascular disease Tutorial > Flashcards

Atheroscelerosis and Peripheral Vascular disease Tutorial Flashcards

1
Q

What is atheroscelerosis involved in?

A
  1. Neurology (cerebrovascular disease)
  2. Acute medicine (Heart attack / stroke)
  3. Cardiology ( coronary disease)
  4. Cardiac surgery (revascularisation)
  5. Vascular surgery (revascularisation)
  6. Endocrinology (diabetes)
  7. Metabolic medicine (lipids)
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2
Q

What are modifiable risk factors?

A
  1. Smoking
  2. Lipid intake
  3. Blood pressure
  4. Diabetes
  5. Obesity
  6. Sedentary lifestyle
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3
Q

What are non-modifiable factors?

A
  1. Age
  2. Sex
  3. Genetic background
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4
Q

What happens to the risk factor increase?

A

multiplies risk

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5
Q

What has reduced over the last decade?

A
  1. Reduced hyperlipidaemia (statin treatment)

2. Reduced hypertension (antihypertensive treatment)

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6
Q

What has increased?

A

Increased obesity -> Increased diabetes

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7
Q

What type of treatments have improved?

A

New improvements in diabetes treatment have doubtful effect on macrovascular disease

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8
Q

Why is there changing pathology of coronary thrombosis?

A

related to altered risk factors

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9
Q

If risk factors are general why is atherosclerosis focal?

A

turbulence and aerodyanmic

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10
Q

Where do LDL deposits?

A

-Low density lipoproteins (LDL) deposit in the subintimal space -binds to matrix proteoglycans

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11
Q

What is the progression of atherosclerosis?

A
  1. Coronary artery at lesion-prone location
  2. Type II lesion
  3. Type III (preatheroma)
  4. Type IV (atheroma)
  5. Type V (fibroatheroma)
  6. Type VI (complicated lesion)
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12
Q

What happens at a coronary artery at lesion-prone lesion?

A

Adaptive thickening (smooth muscle) - intima thickens

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13
Q

What happens at a type II lesion?

A

macrophage foam cells

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14
Q

What happens at a type III lesion (preatheroma)?

A

small pools of extracellular lipid

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15
Q

What happens at a type IV lesion (atheroma)?

A

core of extracellular lipid (inflammatory)

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16
Q

What happens at a type V lesion (fibroatheroma)?

A

fibrous thickening

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17
Q

What happens at a type VI (complicated lesion)?

A
  • thrombus
  • fissure and hematoma
  • Lipid core breakdown
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18
Q

What is the natural history of atheroscelerosis?

A
  1. Normal
  2. intermediate lesions
  3. Advanced lesions
  4. Complication (e.g. stenosis, plaque rupture)
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19
Q

When is there a window of opportunity for primary prevention?

A

-intermediate lesions
-Advanced lesions
(Life-style changes
Risk factor management)

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20
Q

What are the clinical interventions for complications?

A
  • Secondary prevention
  • Catheter based interventions
  • Revascularisation surgery
  • Treatment of heart failure
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21
Q

What is the function of vascular endothelial cells?

A
  1. Barrier function (e.g. to lipoproteins)

2. Leukocyte recruitment

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22
Q

What is the function of monocyte-macrophages?

A
  1. Foam cell formation
  2. Cytokine and growth factor release
  3. Major source of free radicals
  4. Metalloproteinases
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23
Q

What is the function of platelets?

A
  1. Thrombus generation (late)

2. Cytokine and growth factor release

24
Q

What is the function of T lymphocytes?

A

Macrophage activation

25
Q

What is the function of vascular smooth muscle cells?

A
  1. Migration and proliferation
  2. Collagen synthesis
  3. Remodelling & fibrous cap formation
26
Q

What basis does atherosclerosis have?

A

inflammatory

27
Q

What did the CANOS trial involve?

A
  1. Patients at high risk of atherosclerosis complications injected with antibodies to Interleukin -1 (IL-1) (so could be sued for treatment)
  2. Fewer major adverse cardiovascular events (MACE) mostly stroke and heart attacks in treated patients
28
Q

What type of mechanisms connect lipids and inflammation in atherosclerosis?

A

Multiple mechanisms including cholesterol crystal formation

29
Q

What happens if WBC are activated excessively or inappropriately?

A

injure host tissue

30
Q

What are the main inflammatory cells in atherosclerosis?

A

macrophages, which are derived from blood monocytes

31
Q

How are macrophage subtypes regulated?

A

d by combinations of transcription factors binding to regulatory sequences on DNA

32
Q

What are the two main classes of macrophages?

A
  • Inflammatory macrophages

- Resident macrophages

33
Q

What do inflammatory macrophages do?

A

adapted to kill micro-organisms (germs)

34
Q

What do resident macrophages do?

A
  1. Normally homeostatic - suppress inflammatory activity
  2. Alveolar resident macrophages - surfactant lipid homeostasis
  3. Osteoclasts - calcium and phosphate homeostasis
  4. Spleen - iron homeostasis
35
Q

What are LDL?

A
  1. Synthesised in liver

2. Carries cholesterol from liver to rest of the body including arteries

36
Q

What is the structure of LDLs?

A
  1. docking molecule ‘molecular addresses for fat delivery’
  2. lipid monolater (like cell membrane) but one molecule thick
  3. Cargo fat for fuel
37
Q

What is HDL?

A

Carries cholesterol from ‘peripheral tissues’ including arteries back to liver (=“reverse cholesterol transport”)

38
Q

What are oxidised LDLs?

A
  1. modified LDLs due to action of free radicals on LDL
  2. Not one single substance
  3. Families of highly inflammatory and toxic forms of LDL found in vessel walls
39
Q

How are LDLs trapped?

A
  1. LDLs leak through the endothelial barrier
  2. Trapped by binding to sticky matrix carbohydrates (proteoglycans) in the sub-endothelial layer and becomes susceptible to modification
40
Q

How are LDLs modified?

A

oxidation - represents partial burning

41
Q

How do LDLs become oxidatively modified?

A

by free radicals

42
Q

What happens to the oxidised LDLs?

A

phagocytosed by macrophages and stimulates chronic inflammation

43
Q

What is the process of chronic inflammation from LDLs?

A
  1. LDLs
  2. LDL oxidation
  3. Phagocytosis by macrophages
  4. Macrophages now known as ‘foam cells’
  5. Chronic inflammation
44
Q

What is familial hyperlipidemia (FH)?

A
  1. Autosomal genetic disease main form dominant with gene dosage)
  2. Massively elevated cholesterol (>20mmol/L)
  3. Failure to clear LDL from blood
  4. Xanthomas and early atherosclerosis; if untreated fatal myocardial infarction before age 20
45
Q

How is the LDL receptor expression regulated?

A

negatively regulated by intracellular cholesterol

46
Q

How is cholesterol synthesis regulated?

A

negatively regulated by cellular cholesterol

47
Q

How do you lower plasma cholesterol?

A

HMG-CoA reductase inhibitors (= “statins”)

48
Q

What happens to cholesterol in LDLR-negative patients?

A

macrophages accumulate cholesterol

49
Q

Where is there a second LDL receptor?

A
  • not under feedback control

- in atherosclerotic lesions. -‘scavenger receptor’ since they hoover up chemically modified LDL

50
Q

What are scavenger receptors?

A

family of pathogen receptors that ‘accidentally’ bind OxLDL

51
Q

What are macrophage scavenger receptor A known as?

A

Known as CD204

52
Q

What do CD204 bind to?

A
  1. oxidised LDL
  2. Gram-positive bacteria like Staphylococci & Streptococci
  3. dead cells
53
Q

What is macrophage scavenger receptor B known as?

A

CD36

54
Q

What does CD36 bind to?

A
  1. oxidised LDL
  2. malaria parasites
  3. dead cells
55
Q

How are macrophages used in inflammation?

A
  • Activation of ‘bug detector’ pathways
  • Aterial Ox-LDL deposits
  • Balance with homeostasis
56
Q

How are macrophages used in homeostasis?

A
  • Safe clearance
  • Reverse cholesterol transport
  • Aterial Ox-LDL deposits
  • Balance with inflammation

Z YEAR 2 BRS CARDIO (18 decks)

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