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Cardiorespiratory 2 > Atherosclerosis and Coronary Artery Disease > Flashcards

Atherosclerosis and Coronary Artery Disease Flashcards

1
Q

what is atherosclerosis

A

• Thickening of arterial wall which then loses elasticity, the wall becomes hardened

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2
Q

what is atherosclerosis primary due to

A

formation of fatty plaques in the arterial wall which cause it to narrow

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3
Q

what diseases does atherosclerosis cause

A
  • Coronary artery disease
    - Cerebrovascular disease
    • Peripheral artery disease
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4
Q

what is the basic formation of atheroma

A
  1. Endothelial damage
  2. Uptake of modified LDL particles adhesion and infiltration of macrophages
  3. Small muscle proliferation and formation of a fibrous cap
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5
Q

what is function of the endothelium

A
  • contains vasodilators
  • responds to vasoconstrictors
  • involved in thrombosis as it has anticoagulant and procoagulant
  • inflammatory factors - interacts with leucocytes
  • has receptors
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6
Q

what does endothelium dysfunction mean

A

this is an imbalance between vasodilating and vasoconstricting substances

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7
Q

what causes endothelial damage

A
  • Shear stress
  • Toxic damage
  • High levels of lipids (Hyperlipidemia)
  • Viral or bacterial infection (Chlamydia pneumoniae)
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8
Q

How do fatty streaks form

A
  • Endothelial damage/oxidised LDLs - attract monocytes
  • Monocytes bind to/cross endothelium
  • Transformed into macrophages which accumulate oxidised LDLs
  • Fat-laden cells foam cells appear as fatty streaks
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9
Q

name the 5 types of lipoprotein

A
  • Chylomicrons
  • VLDL (very low-density lipoprotein)
  • IDL (intermediate-density lipoprotein)
  • LDL (low-density lipoprotein)
  • HDL (high-density lipoprotein)
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10
Q

the lower the density of the lipoprotein…

A

The lower the density of a lipoprotein the more lipid it contains relative to the amount of protein

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11
Q

name the ways in which LDLs are modified

A
  • oxidation

- glycation

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12
Q

how does oxidation modify LDL

A
  • facilitated by reactive oxygen species (free radicals)

* Oxidised LDL stimulates expression of inflammatory mediators including adhesion molecules for monocytes

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13
Q

how does glycation modified LDL

A
  • facilitated by high glucose levels (diabetes mellitus)
  • higher [glycated LDL] present in diabetes
  • glycated LDL more likely to be oxidised
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14
Q

how are LDL normally uptakes

A

• LDL-receptor recognises apolipoprotein B100
• Negative feedback
- internal accumulation of LDL by macrophages
- decreasing LDL surface receptors
- decreasing LDL uptake

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15
Q

how is LDL taken up by scavenge receptors

A
  • But modified LDL uptake via scavenger receptor
  • No negative feedback - uptake unlimited
  • LDL accumulates in large droplets - foam cells
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16
Q

how does the fatty streak convert to a mature plaque

A
  • Endothelial cells and macrophages release growth factors (esp. platelet derived growth factor)
  • Cause proliferation of Smooth Muscle Cells in intima & collagen production
  • Breakdown of internal elastic lamina - atrophy
  • Smooth muscle Cells also become foam cells - uptake of modified LDL
  • Formation of a plaque
  • Collagen forms fibrous cap (fragile)
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17
Q

name some complications of atherosclerosis

A
  • Stroke
  • Coronary artery disease – angina and MI
  • Aneurysm
  • Renal artery stenosis
  • Peripheral vascular disease (peripheral arterial occlusive disease) – ulcers, peripheral neuropathy, gangrene
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18
Q

what is the purpose of coronary circulation

A
  • Ensure adequate oxygenation of myocardium at all levels of cardiac activity
  • Oxygenation requirements increase with increased cardiac output (exercise)
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19
Q

if the coronary arteries narrow what are the two main outcomes

A
    • angina

* - myocardial infarction

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20
Q

what are the types of coronary artery lesion

A

stenotic

non stenotic

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21
Q

what does a stenotic coronary artery lesion lead to

A
  • thick fibrotic cap
  • Leads to ischemia
  • Angina
  • Positive exercise test
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22
Q

what does a non stenotic coronary artery lesion lead to

A
  • Thin cap
  • Susceptible to rupture
  • Formation of thrombus
  • Myocardial infarction
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23
Q

what are the ECG changes of MI

A
  • STEMI
  • pathological Q waves
  • T waves become elevated
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24
Q

what cardiomyocytes is troponin found in

A

Troponin only found in cardiomyocytes (cardiac I and T): evidence of cell death

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25
Q

what is troponin used as

A

evidence of cell death

Very specific biomarker for cardiomyocyte death

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26
Q

describe what stable plaques lead to

A
  • Slow growing
  • Fibrin cap matures (not prone to rupture)
  • Reduced blood flow
  • Stable angina (exertional)
  • when a stable plaque increases in volume it causes stenosis of the lumen and limits flow causing stable angian
27
Q

what happens in unstable plaques

A
  • Grow quickly as result of rapid lipid deposition
  • Thin fibrin cap
  • Fragile cap ruptures
  • haemorrhage from plaque
  • release of platelet tissue factor (clotting cascade)
  • collagen exposed causing platelet aggregation
  • Thrombus formation
  • Reduces lumen diameter
  • May occlude lumen completely (MI)
28
Q

what is the difference between stable and unstable plaques

A

Stable

  • Slow growing
  • Fibrin cap matures (not prone to rupture)
  • Reduced blood flow
  • Stable angina (exertional)
  • when a stable plaque increases in volume it causes stenosis of the lumen and limits flow causing stable angian

Unstable
• Grow quickly as result of rapid lipid deposition
• Thin fibrin cap
• Fragile cap ruptures
• haemorrhage from plaque
• release of platelet tissue factor (clotting cascade)
• collagen exposed causing platelet aggregation
• Thrombus formation
• Reduces lumen diameter
• May occlude lumen completely (MI)

29
Q

what is a difference between NSTEMI and a STEMI

A

NSTEMI

  • ECG is non diagnostic
  • rupture coronary plaque with subocculsive thrombus

STEMI

  • ECG diagnostic
  • ruptured coronary plaque with occlusvie thormbus
30
Q

what are the modifiable risk factors for CVD

A
  • Smoking - Regular smokers are twice as likely to have a heart attack.
  • Weight - Overweight or obese people are more likely to have high cholesterol, a major factor in heart disease.
  • High Blood Pressure - Can often show no symptoms but puts strain on the cardiovascular system.
  • Physical activity - Lack of exercise can double the risk of heart attacks.
  • Diabetes - Over time this can damage the heart and blood vessels.
  • Dyslipidaemia
31
Q

what is the normal range for blood cholesterol for adults

A
  • Normally the triglycerides are in the range of 10-190mg/dl
  • TC (total cholesterol) under 200 mg/dl
  • LDL under 130 mg/dl
  • HDL over 40 mg/d
32
Q

how can you reduce blood cholesterol

A
  • exercise
  • diet
  • drugs
33
Q

what are emerging risk factors for atherosclerosis

A
  • Increased Homocysteine (B6, B12 & folic acid deficiencies)
  • Increase oxidant stress
  • Lipoprotein (a) - (LDL + extra apolipoprotein)- more firmly retained in arterial wall
  • Infection (Chlamydia pneumoniae)- inflammation of endothelium
34
Q

How are B-vitamins used for reducing risk factors for atherosclerosis

A
  • Methionine transformed to homocysteine in bloodstream
  • Homocysteine converted to cysteine (B6) - cell folding/antioxidant
  • Homocysteine converted back to methionine (B12 enzymes)
35
Q

what is primary prevention

A
  • This aims to prevent disease or injury before it ever occurs – for people with no history of angina
36
Q

name some lifestyle modifications you can make to prevent atherosclerosis

A
  • Smoking
  • Weight loss
  • Salt intake
  • Hypertension
  • Exercise
37
Q

what drug treatments can you use to prevent atherosclerosis

A
  • Statins – uncertainty in the data for low risk individuals

- Aspirin – heterogeneity in the data

38
Q

what is secondary prevention

A

• Secondary prevention tries to intervene and hopefully put an end to the disease before it fully develops.

39
Q

what is the secondary prevention for angina

A
  • Lifestyle modification
  • beta blocker ± CCB, Sublingual GTN, Aspirin, statin, ACE inhibitor
  • Possible revascularisation (PCI, CABG)
40
Q

what is the secondary prevention for acute myocardial infraction

A
  • Acute: defibrillator and reperfusion (aspirin, ticagrelor, Heparin, PPCI)
  • PCI immediately for STEMI, within 24 – 96 hours NSTEMI
  • Chronic: aspirin, statin, beta blocker, GTN, ticagrelor/prasugrel/clopidogrel, ACE inhibitor
41
Q

what is the immediate treatment for acute myocardial infarction in order to get rid of the clot

A
  • Tissue plasminogen activator (tPA)
  • Endogenous fibrinolytic agent found in endothelial cells
  • facilitates the conversion of plasminogen to plasmin and dissolves the clot
  • Given acutely after myocardial infarction
42
Q

what does streptokinase do

A
  • Thrombolytic medication
  • Directly lysis fibrin in the thrombus
  • Effective early trials to reduce death
43
Q

what is streptokinase usually combined with

A

• Even better when combined with aspirin

44
Q

what is the difference between a low dose and a high dose of aspirin

A
  • Low dose inhibits COX-1

- high dose inhibits COX-2

45
Q

what is the role of COX-1

A

COX-1 converts arachidonic acid into PGH2

46
Q

how does COX-1 cause clots to form

A

COX-1 converts arachidonic acid into PGH2
• PGH2 is precursor for other prostaglandins
Importantly PGH2 converted to thromboxane A2
• Potent stimulator of platelet aggregation

47
Q

how does aspirin prevent clot formation

A
  • Irreversible inhibitor of COX in platelets
  • Covalently binds to the enzyme
  • Platelets can’t make new protein (no nucleus)
48
Q

why do we use aspirin specifically when other NSAIDS bind to COX

A
  • Aspirin binds to platelets in portal system following absorption
  • Irreversible inhibition – for the lifetype of the platlet
  • First pass metabolism reduces bioavailable aspirin
  • Deacetylation
  • Avoids systemic effects
  • other NSAIDS increase cardiovascular mortality - this causes a rise in blood pressure
  • thought to be due to inhibitor of COX-2 in the macular dense of the kidneys
49
Q

what are the three things that beta blockers do

A
  • Decrease heart rate
  • Decrease contractility
  • Decrease systemic vascular resistance
  • These decrease myocardial oxygen demand
50
Q

describe how beta blockers work

A
  • Propanolol: non-selective β adrenoceptor antagonist
  • Use β1 preferring antagonist (atenolol)
  • It increases the end diastolic volume and increases the ejection time
51
Q

who should not have beta blockers

A
  • Propanolol: non-selective β adrenoceptor antagonist

- Contraindicated in asthmatics/COPD – causes bronchoconstriction

52
Q

What is afterload

A

is the amount of resistance the heart must overcome to open the aortic valve and push the blood volume out into the systemic circulation

53
Q

where are beta 1 adrenoreceptors expressed

A
  • on the SAN- increase HR
  • on cardiomyocytes- increase contractility
  • in peripheral arteries- vasoconstriction
  • Activated by noradrenaline in the SNS
54
Q

What do ACE inhibitors do

A
  • preventing conversion of (inactive) angiotensin I to (active) angiotensin II
  • Decrease in BP due to prevention of AngII vasoconstriction
55
Q

what do calcium channel blockers do

A
  • Decrease heart rate
  • Decrease contractility
  • Increase coronary artery vasodilation
  • Decrease total peripheral resistance
  • These decrease myocardial oxygen demand
56
Q

where are calcium channels expressed

A
  • the SAN and cardiomyocytes (L and T type)- mediate the cardiac action potential
  • Cardiac arteries and peripheral arteries
  • Involved in smooth muscle contraction
57
Q

name some L type calcium channel blockers

A

• Amplodipine, nifedipine are L type calcium channel blockers

58
Q

what is the mechanism of action of statins

A
  • HMG-CoA reductase is the rate limiting step in cholesterol synthesis
  • Statins are competitive inhibitors of HMG-CoA
  • Decreased hepatic cholesterol synthesis upregulates LDL receptor synthesis
59
Q

what do statins do

A

• Increases clearance from blood

- Decrease plasma triglycerides and increase HDL

60
Q

how does nitric oxide work in the cardiovascular system

A
  • NO activates guanylate cyclase to form cGMP
  • cGMP stimulates dephosphorylation of myosin light chain
  • Causes vascular smooth muscle relaxation and consequent vasodilation
  • Increase O2 supply, decrease preload (venous blood pressure) so decrease O2 demand
61
Q

What happens when you inhibit P2Y12

A
  • ADP found in platelets and stimulates platelet aggregation
  • Positive feedback mechanism for platelet aggregation
  • P2Y12 receptors found on platelets
  • Inhibition of P2Y12 has anti-platelet aggregation properties
  • Prevents thrombus formation
62
Q

What is PCI

A

Percutaneous Coronary Intervention

63
Q

What is CABG

A

Coronary Artery Bypass Graft

Cardiorespiratory 2 (43 decks)

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