Ischaemic heart disease Flashcards

1
Q

What are the non-modifiable risk factors for IHD?

A
  • age
  • sex (males>females)
  • family history of CVD
  • ethnicity
  • genetics e.g. hypercholesterolaemia
  • previous history
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2
Q

What are the modifiable risk factors for IHD?

A
  • high blood pressure
  • total cholesterol
  • smoking
  • diabetes
  • BMI
  • smoking
  • diet
  • exercise
  • stress
  • low socioeconomic state
  • alcohol
  • medications
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3
Q

What is ischaemic heart disease/coronary heart disease?

A
  • heart problem caused by narrowed coronary arteries that supply blood to the heart muscle (demand>supply)
  • manifests as myocardial infarction and ischemic cardiomyopathy
  • some deaths are sudden due to acute coronary occlusion
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4
Q

What is angina?

A
  • chest pain
  • sometimes mistaken for indigestion or heart burn
  • aching, burning, fullness, heaviness, numbness, pressure, squeezing
  • radiation to arms, back, jaw, neck, shoulder
  • occur w/ high or low bp
  • sometimes syncope
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5
Q

What can cause obstruction to coronary blood flow?

A
  • atheroma
  • thrombosis
  • spasm
  • embolus
  • coronary ostial stenosis
  • coronary arteritis
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6
Q

What can cause a general decrease of oxygenated blood flow to myocardium?

A
  • anaemia
  • carboxyhaemoglobulinaemia
  • hypotension causing decreased coronary perfusion pressure
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7
Q

What is a stable atherosclerotic plaque?

A
  • fibrous cap surrounding lipid-rich necrotic core
  • fibrous cap provides effective barrier preventing plaque rupture
  • T-reg cells and macrophages produce TGF-beta, which maintains fibrous cap quality by stimulating collagen production in SMCs
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8
Q

How does a plaque become vulnerable?

A
  • due to unresolved inflammation, which causes thinning of the fibrous cap
  • thin areas of fibrous cap are prone to rupture, exposing prothrombotic components to platelets and coagulation factors–> thrombus formation
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9
Q

How do patients present with CHD/IHD?

A
  • asymptomatic plaque
  • chronic stable angina= stable fixed atherosclerotic plaque (narrowing)
  • acute coronary syndromes: unstable angina (plaque disruption and platelet aggregation), non-ST elevation MI (thrombus) , STEMI (thrombus blocking vessel)
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10
Q

What is a coronary embolus?

A

when a blood clot breaks away and blocks a more distal artery

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11
Q

How does acute coronary occlusion occur?

A
  • in people w/ underlying atherosclerotic disease
  • local blood clot/thrombus formation–> grows until occludes vessel (can also become embolus)
  • N.B. local muscular spasm of a coronary artery can also add to occlusion
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12
Q

What is the role of collateral vessels in acute hypoxia?

A
  • dilate within seconds of an acute episode

- double by the 2nd or 3rd day and reach normal or almost normal coronary flow within about 1 month

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13
Q

What is the role of collateral vessels in chronic atherosclerotic plaque patients?

A

slow occlusion occurs, so collaterals can develop at same time while atherosclerosis becomes more and more severe

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14
Q

What causes death after a MI?

A
  • decreased cardiac output
  • systolic stretch (dead tissue)
  • ventricular fibrillation
  • rupture of infarcted area
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15
Q

What risk assessment tools are used for IHD?

A
  • JBS3

- q-risk

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16
Q

What serum markers are used in patients with suspected acute cardiac events?

A
  • troponin (I or T)
  • creatine kinase w/ MB isozymes
  • lactate dehydrogenase and isozymes
  • serum aspartate aminotransferase
17
Q

What biomarkers can predict death following a MI?

A
  • B-type natriuretic peptide
  • CRP
  • homocysteine
  • renin
  • urinary ACR
18
Q

What are the ECG findings in IHD?

A
  • stable angina: normal ECG but during stress test, might see ST depressions (indicates IHD)
  • unstable angina/NSTEMI: ST depressions and T wave inversion
  • acute MI/STMI: ST elevation w/ T wave inversion
19
Q

When is echocardiography used?

A

to see which area of the heart is damaged following an MI

20
Q

What is the gold standard investigation for detecting stenosis?

A

coronary CT angiography

21
Q

What are HMG-CoA reductase inhibitors?

A
  • they lower LDL levels, raise HDL levels and lower triglyceride levels
  • e.g. atorvastatin
22
Q

What are bile acid sequestrants?

A
  • block enterohepatic circulation of bile acids and inc. decal loss of cholesterol
  • e.g. cholestyramine
23
Q

What are calcium channel blockers?

A
  • relax coronary smooth muscle and produce coronary vasodilation, improving myocardial oxygen delivery
  • e.g. amlodipine
24
Q

What are beta-blockers?

A
  • block symapathetic stimulation of heart
  • reducing HR and contractility
  • decreasing myocardial oxygen demand–> relieving angina
25
Q

What are antianginal agents?

A
  • ronalazine
  • new
  • relieve ischaemia by reducing myocardial cellular sodium and calcium overload
  • works on ion channels
  • relaxes heart
26
Q

What is percutaneous coronary intervention?

A
  • angiography and stent placement
  • common to treat stable CAD
  • improves blood flow by placing stent and compressing plaque
27
Q

What is coronary artery bypass grafting?

A
  • vessel from another part of body create a graft that allows blood to flow around blocked/narrowed coronary artery
  • open heart surgery for people w/ severely narrowed coronary arteries