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atherosclerosis and coronary artery disease Flashcards

1
Q

what is arteriosclerosis?

A

thickening of the arterial wall which then loses elasticity

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2
Q

what does sclerosis mean

A

hardening

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3
Q

what is the most common form of arteriosclerosis?

A

atherosclerosis

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4
Q

how does arteriosclerosis manifest clinically?

A

coronary artery disease
cerebrovascular disease
peripheral artery disease

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5
Q

what is atherosclerosis?

A

plaque builds up inside the arteries over many years –> narrows artery

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6
Q

what are the main functions of the endothelium?

A
  • Vasomotor tone – vasodilators (NO/PGI2) and vasoconstrictors (angiotensin II/endothelin)
  • Thrombosis – anticoagulant and procoagulant, platelet inhibitors/activators
  • Inflammatory factors – leucocyte interactions
  • Cellular adhesion molecules – receptors
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7
Q

explain the classic mechanism of atheroma formation?

A

o Endothelial damage
o Uptake of modified LDL particles
o Adhesion and infiltration of macrophages
o Smooth muscle proliferation and formation of a fibrous cap

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8
Q

why can endothelial damage occur?

A

bc of shear stress, toxic damage, hyperlipidemia, viral or bacterial infection (e.g. Chlamydia penumoiae)

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9
Q

why is damaged endothelium dysfunctional?

A

inappropriate vasoconstriction and reduced antithrombotic properties

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10
Q

how do macrophages infiltrate the endothelium?

A
  • Endothelial damage and the oxidised LDLs attract monocytes
  • Monocytes bind to/cross endothelium
  • Monocytes  macrophages which accumulate oxidised LDLs
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11
Q

name types of lipoprotein?

A

chylomicrons, VLDL (very low density), IDL (intermediate density), LDL (low density), HDL (high density)

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12
Q

how does the density of a lipoprotein relate to how much lipid it contains relative to protein?

A

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

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13
Q

how can LDLs be modified?

A

oxidation

glycation

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14
Q

what facilitates oxidation of LDL?

A

Oxidation – facilitated by reactive oxygen species (free radicals)

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15
Q

what facilitates glycation of LDL?

A

Glycation – facilitated by high glucose levels (diabetes mellitus)

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16
Q

in what conditions is higher glycated LDL present?

A

diabetes

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17
Q

what type of LDL is more likely to be oxidised?

A

glycated LDL

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18
Q

what does oxidised LDL stimulate?

A

expression of inflammatory mediators inc adhesion molecules for monocytes

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19
Q

what do LDL receptors recognise?

A

apolipoprotein B100

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20
Q

describe the negative feedback mechanism of the normal uptake of LDL?

A

internal accumulation of LDL by macrophages so decreased LDL surface receptors –> decreased LDL uptake

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21
Q

why is the uptake of modified LDL unlimited?

A

modified LDL not recognised by LDL-receptor
uptake is done via the scavenger receptor
no negative feedback –> uptake unlimited

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22
Q

what are foam cells?

A

when LDL accumulates in large droplets

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23
Q

what are fatty streaks?

A

fat laden foam cells

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24
Q

how do fatty streaks become mature plaques?

A
  • endothelial cells and macrophages release growth factors to cause SMC proliferation in the intima + collagen production
  • breakdown of IEL –> atrophy
  • SMC become foam cells - uptake modified LDL
  • formation of a plaque
  • collagen forms a fibrous plaque
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25
Q

name complications of atherosclerosis

A
  • Stroke
  • Coronary artery disease – Angina, MI
  • Aneurysm
  • Renal artery stenosis
  • Peripheral vascular disease (peripheral arterial occlusive disease) –> leads to ulcers, peripheral neuropathy and gangrene
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26
Q

what is the purpose of the coronary circulation?

A
  • supplies oxygen rich and nutrient rich blood to the heart
  • ensures adequate oxygenation of the myocardium
  • oxygen requirements increase with increased cardiac output
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27
Q

what are the short term consequences of narrowing the coronary arteries?

A

reduces blood flow –> reduced oxygenation (ischaemia) –> pain

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28
Q

what are the long term consequences of narrowing the coronary arteries?

A

angina and myocardial infarction

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29
Q

what are the types of coronary artery lesions?

A

stenotic

non-stenotic

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30
Q

describe stenotic coronary artery lesions?

A

thick fibrotic cap
leads to ischaemia
angina
+ve exercise test

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31
Q

describe a non-stenotic coronary artery lesion

A

thin cap; susceptible to rupture; formation of thrombus; myocardial infarction

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32
Q

what are the two main clinical manifestations of CAD?

A

angina and myocardial infarction

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33
Q

what is the diagnostic challenge of CAD?

A

to determine whether or not the patient with chest pain has flow limiting coronary obstructions

34
Q

what are methods of functional testin of evidence of ischaemia?

A

ETT, SPEC, stress echo, stress cMR

35
Q

what are the methods of anatomical testing for evidence of obstructive disease?

A

CTCA

36
Q

what are the clinical manifestations of myocardial infarction?

A
  • rise and/or fall of troponin
    one of the following;
    o Symptoms of ischaemia
    o New ST segment or T wave changes or new left bundle branch block on ECG
    o Pathological Q wave on ECG
    o Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
    o Identification of an intracoronary thrombus by angiography
37
Q

why is troponin evidence of myocardial infarction?

A

only found in cardiomyocytes - evidence of cell death

38
Q

summarise stable plaques

A

Increasing plaque volume causes stenosis of the lumen and limits flow

39
Q

why do unstable plaques grow quickly?

A

bc of rapid lipid deposition

40
Q

summarise how unstable plaques work?

A
  • grow quickly
  • thin fibrin cap
  • cap ruptures and releases platelet tissue factor - collagen exposed causing platelet aggregation
  • thrombus formation
  • reduces lumen diameter
  • may occlude lumen completely (MI)
41
Q

what method of imaging can be used to observe plaques?

A

ultrasound

42
Q

what are risk factors for cvd?

A

smoking, weight, high BP, physical activity, diabetes, dyslipidemia

43
Q

what are non-modifiable risk factors for CVD?

A

age, sex, ethnicity, family history

44
Q

what are the normal desirable levels of blood cholesterol?

A
  • Total cholesterol should be <200mg/dL
  • LDL cholesterol should be <130mg/dL
  • HDL cholesterol should be >60mg/dL
45
Q

what is the aim of primary prevention?

A

aims to prevent the disease or injury before it ever occurs for people with no history of angina

46
Q

what are methods of primary prevention?

A

•Lifestyle modification; smoking, weight loss, salt intake, hypertension, exercise

Drug treatments
o Statins – uncertainty in the data for low risk individuals
o Aspirin

47
Q

what is the aim of secondary prevention?

A
  • Tries to intervene and hopefully put an end to the disease before it fully develops
  • Trying to reduce the number of new/severe cases
48
Q

name methods of secondary prevention for angina

A

o Lifestyle modification
o Beta blocker + CCB, sublingual GTN, aspirin, statin, ACE inhibitor
o Possible revascularisation (PCI, CABG)

49
Q

name methods of secondary prevention for acute myocardial infarction

A

defibrillator and reperfusion (aspirin, ticagrelor, heparin, PPCI)
oPCI immediately for STEMI, within 24-96 NSTEMI

50
Q

name methods of secondary prevention for chronic myocardial infarction

A

aspirin, statin, beta blocker, GTN, ticagrelor/prasugrel/clopidogrel, ACE inhibitor

51
Q

what drug is given acutely after a myocardial infarction?

A

tissue plasminogen activator

52
Q

what is tissue plasminogen activator?

A
  • Endogenous fibrinolytic agent found in endothelial cells

* Facilitates conversion of plasminogen to plasmin and dissolves the clot

53
Q

what is streptokinase used to treat?

A

thrombolytic medication

54
Q

how does streptokinase work?

A

directly lyses fibrin in the thrombus

55
Q

what does a low does of aspirin inhibit?

A

COX-1

56
Q

what does a high dose of aspirin inhibit?

A

COX2

57
Q

what does COX-1 do?

A

converts arachidonic acid into PGH2 (precursor for other prostaglandins)
• PGH2 converted to thromboxane A2 – strong stimulator of platelet aggregation

58
Q

what type of COX inhibitor is aspirin?

A

irreversible

59
Q

where does aspirin bind to platelets?

A

in portal system following absorption

60
Q

what effects do beta blockers have?

A
  • Decrease heart rate, contractility and systemic vascular resistance
  • Decrease myocardial O2 demand
61
Q

what is propanolol?

A

beta blocker

non-selective B adrenoceptor antagonist

62
Q

what is propanolol contraindicated in?

A

asthmatics and COPD

63
Q

what should you use instead of propanolol in asthmatics and COPD?

A

B1 preferring antagonist (atenolol)

64
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
65
Q

what are ACE inhibitors?

A

RAAS system preventing conversion of inactive angiotensin I to active angiotensin II

66
Q

how do ace inhibitors decrease blood pressure?

A

due to prevention of AngII vasoconstriction

67
Q

what type of drug is ramipril?

A

ace inhibitor

68
Q

what effect do calcium channel blockers have?

A
  • Decrease heart rate + contractility
  • Increase coronary artery vasodilation
  • Decrease total peripheral resistance
  • Decrease myocardial O2 demand
69
Q

where are calcium channels expressed?

A

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

70
Q

name L type calcium channel blockers

A

amplodopine

nifedipine

71
Q

what is the rate limiting step in cholesterol synthesis?

A

HMG-CoA reductase

72
Q

what drugs are competitive inhibitors of HMG-CoA?

A

statins

73
Q

what effects do statins have?

A
  • Decreased hepatic cholesterol synthesis upregulates LDL receptor synthesis –> increases clearance from blood
  • Decreases plasma triglycerides and increase HDL
74
Q

why are statins considered more effective than stents?

A

o Statins affect all of the cholesterol deposition in coronary arteries
o Stents/CABG only affect treated artery

75
Q

how does nitric oxide have a vasodilation effect?

A
  • NO activates guanylate cyclase to form cGMP
  • cGMP stimulates dephosphorylation of myosin light chain
  • Causes vascular smooth muscle relaxation and consequent vasodilation
76
Q

what effect does nitroglycerin have?

A

• Increase O2 supply, decrease preload (venous blood pressure) so decrease O2 demand

77
Q

name p2y12 antagonists

A

Clopidogrel/Ticagrelor

78
Q

how do p2y12 antagonists work?

A

• P2Y12 receptors found on platelets
o Inhibition of P2Y12 has anti-platelet aggregation properties
o Prevents thrombus formation

79
Q

what is PCI?

A

Percutaneous Coronary Intervention

80
Q

what is CABG?

A

Coronary Artery Bypass Graft

c2 (37 decks)

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