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

Atheroscelerosis and Peripheral Vascular disease Tutorial Flashcards

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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?

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A
  1. Thrombus generation (late)

2. Cytokine and growth factor release

24
Q

What is the function of T lymphocytes?

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A

Macrophage activation

25
What is the function of vascular smooth muscle cells?
1. Migration and proliferation 2. Collagen synthesis 3. Remodelling & fibrous cap formation
26
What basis does atherosclerosis have?
inflammatory
27
What did the CANOS trial involve?
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
What type of mechanisms connect lipids and inflammation in atherosclerosis?
Multiple mechanisms including cholesterol crystal formation
29
What happens if WBC are activated excessively or inappropriately?
injure host tissue
30
What are the main inflammatory cells in atherosclerosis?
macrophages, which are derived from blood monocytes
31
How are macrophage subtypes regulated?
d by combinations of transcription factors binding to regulatory sequences on DNA
32
What are the two main classes of macrophages?
- Inflammatory macrophages | - Resident macrophages
33
What do inflammatory macrophages do?
adapted to kill micro-organisms (germs)
34
What do resident macrophages do?
1. Normally homeostatic - suppress inflammatory activity 2. Alveolar resident macrophages - surfactant lipid homeostasis 3. Osteoclasts - calcium and phosphate homeostasis 4. Spleen - iron homeostasis
35
What are LDL?
1. Synthesised in liver | 2. Carries cholesterol from liver to rest of the body including arteries
36
What is the structure of LDLs?
1. docking molecule 'molecular addresses for fat delivery' 2. lipid monolater (like cell membrane) but one molecule thick 3. Cargo fat for fuel
37
What is HDL?
Carries cholesterol from ‘peripheral tissues’ including arteries back to liver (=“reverse cholesterol transport”)
38
What are oxidised LDLs?
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
How are LDLs trapped?
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
How are LDLs modified?
oxidation - represents partial burning
41
How do LDLs become oxidatively modified?
by free radicals
42
What happens to the oxidised LDLs?
phagocytosed by macrophages and stimulates chronic inflammation
43
What is the process of chronic inflammation from LDLs?
1. LDLs 2. LDL oxidation 3. Phagocytosis by macrophages 4. Macrophages now known as 'foam cells' 5. Chronic inflammation
44
What is familial hyperlipidemia (FH)?
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
How is the LDL receptor expression regulated?
negatively regulated by intracellular cholesterol
46
How is cholesterol synthesis regulated?
negatively regulated by cellular cholesterol
47
How do you lower plasma cholesterol?
HMG-CoA reductase inhibitors (= “statins”)
48
What happens to cholesterol in LDLR-negative patients?
macrophages accumulate cholesterol
49
Where is there a second LDL receptor?
- not under feedback control | - in atherosclerotic lesions. -‘scavenger receptor’ since they hoover up chemically modified LDL
50
What are scavenger receptors?
family of pathogen receptors that ‘accidentally’ bind OxLDL
51
What are macrophage scavenger receptor A known as?
Known as CD204
52
What do CD204 bind to?
1. oxidised LDL 2. Gram-positive bacteria like Staphylococci & Streptococci 3. dead cells
53
What is macrophage scavenger receptor B known as?
CD36
54
What does CD36 bind to?
1. oxidised LDL 2. malaria parasites 3. dead cells
55
How are macrophages used in inflammation?
- Activation of 'bug detector' pathways - Aterial Ox-LDL deposits - Balance with homeostasis
56
How are macrophages used in homeostasis?
- Safe clearance - Reverse cholesterol transport - Aterial Ox-LDL deposits - Balance with inflammation

Z YEAR 2 BRS CARDIO (18 decks)

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