Risk Factors of Atherosclerosis
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Questions and Answers

What is the primary consequence of chronic excessive dilation of the myocardium?

  • Reduced contractility and stroke volume (correct)
  • Increased stroke volume and cardiac output
  • Hypertrophy of myocytes
  • Increased thickness of the myocardial wall

    • What is the primary goal of treatment for LV systolic heart failure?

  • Reduce aldosterone levels
  • Prolong diastole and increase venous return
  • Reduce symptoms and hospitalization (correct)
  • Improve cardiac output and stroke volume

    • Which of the following is a characteristic of LV diastolic heart failure?

  • Impaired contractility
  • Increased cardiac output
  • Preserved ejection fraction (correct)
  • Reduced ejection fraction

    • What is the effect of beta blockers on the heart?

    <p>Prolong diastole and increase venous return</p> Signup and view all the answers

    Which of the following is a treatment for LV diastolic heart failure?

    <p>Diuretics</p> Signup and view all the answers

    What type of ischemia is seen in unstable angina?

    <p>Supply ischemia</p> Signup and view all the answers

    What is the main difference between stable and unstable angina?

    <p>Type of plaque</p> Signup and view all the answers

    What is the diagnostic test for stable ischemic heart disease?

    <p>Stress test</p> Signup and view all the answers

    What is the treatment for acute coronary syndrome?

    <p>Revascularization</p> Signup and view all the answers

    What is the pathological change in acute myocardial infarction?

    <p>All of the above</p> Signup and view all the answers

    What is the most common early complication of acute myocardial infarction?

    <p>Arrhythmias</p> Signup and view all the answers

    What is the formula for cardiac output?

    <p>Stroke volume x heart rate</p> Signup and view all the answers

    What is the determinant of stroke volume that depends on venous return to the heart?

    <p>Preload</p> Signup and view all the answers

    What is the result of increased preload on stroke volume?

    <p>Increased stroke volume</p> Signup and view all the answers

    What is the type of infarction seen in main artery occlusion?

    <p>Transmural infarction</p> Signup and view all the answers

    According to the Frank-Starling law, what is the effect of increased venous return on the heart?

    <p>Increased end-diastolic volume and stroke volume</p> Signup and view all the answers

    What is the primary factor that determines afterload?

    <p>Peripheral vascular resistance and blood pressure</p> Signup and view all the answers

    What is the characteristic feature of left ventricular systolic heart failure?

    <p>Reduced stroke volume with unchanged or increased end-diastolic volume</p> Signup and view all the answers

    What is the effect of myocardial ischemia and infarction on the heart?

    <p>Decreased myocardial contractility and stroke volume</p> Signup and view all the answers

    What is the primary cause of left ventricular diastolic heart failure?

    <p>Hypertension</p> Signup and view all the answers

    What is the clinical significance of reduced blood ejected forward in systolic heart failure?

    <p>Target organ damage and pulmonary vascular congestion</p> Signup and view all the answers

    What is the primary mechanism of the sympathetic nervous system in response to heart failure?

    <p>Increased myocardial contractility and heart rate</p> Signup and view all the answers

    What is the effect of chronic activation of the renin-angiotensin-aldosterone system (RAAS) in heart failure?

    <p>Maladaptive responses, including venous overstretching and decreased contractility</p> Signup and view all the answers

    What is the primary mechanism of cardiac remodeling in heart failure?

    <p>Mechanical stress on the myocardium, leading to ventricular dilation</p> Signup and view all the answers

    What is the characteristic feature of left ventricular diastolic heart failure?

    <p>Equally decreased end-diastolic volume and stroke volume, with preserved ejection fraction</p> Signup and view all the answers

    What is the primary mechanism by which smoking contributes to the development of atherosclerosis?

    <p>Production of reactive oxygen species leading to oxidative stress</p> Signup and view all the answers

    What is the result of glucose binding to blood lipids and proteins in diabetes?

    <p>Formation of advanced glycation end products</p> Signup and view all the answers

    What is the mechanism by which hypertension contributes to the development of atherosclerosis?

    <p>Shear mechanical stress on endothelial cells</p> Signup and view all the answers

    What is the primary consequence of excessive LDL deposition in the endothelium?

    <p>Oxidation of LDL and formation of a soft lipid-loaded core</p> Signup and view all the answers

    What characterizes a complicated atherosclerotic plaque?

    <p>May rupture causing acute thrombosis</p> Signup and view all the answers

    What is the consequence of oxidative LDL attracting macrophages in atherosclerosis?

    <p>Degrades collagen of the cap leading to rupture</p> Signup and view all the answers

    What is the result of the rupture of an atherosclerotic plaque?

    <p>Activation of platelets and clotting cascade</p> Signup and view all the answers

    What type of atherosclerotic plaque is characterized by a thin capsule and inflammatory core?

    <p>Unstable plaque</p> Signup and view all the answers

    Study Notes

    Risk Factors of Atherosclerosis and Mechanism

    • Smoking: produces reactive oxygen species, leading to oxidative stress, damage to endothelial cells, and increased permeability, resulting in accumulation of lipoprotein in the subendothelial space
    • Diabetes: glucose binds to blood lipids and proteins, forming Advanced Glycation End products (AGEs), which interact with and damage endothelial cells, leading to accumulation of lipoproteins in the subendothelial space
    • Hypertension (HTN): shear mechanical stress on endothelial cells, decreasing nitric oxide production, leading to vasoconstriction and increased endothelial permeability
    • Dyslipidemia (elevated LDL): increased LDL in the blood, leading to accumulation of lipoprotein in the subendothelial space

    Formation of Atherosclerotic Plaque

    • Excessive LDL deposition in the endothelium, leading to oxidation and formation of a soft, lipid-loaded core
    • Platelet activation, growth factor release, and formation of a hard, fibrotic cap
    • Types of atherosclerotic plaques: uncomplicated (slowly growing, asymptomatic), complicated (rupture, symptomatic), and unstable (rupture before occlusion)

    Ischemic Heart Disease Syndromes

    • Stable Ischemic Heart Disease (uncomplicated, stable plaque): chest pain, pressure, or tightness with activity, relieved with rest
    • Acute Coronary Syndrome (complicated, unstable plaque): acute onset of chest pain or pressure at rest, due to rupture of atherosclerotic plaque with thrombosis
    • Unstable Angina (reversible ischemia): acute onset of chest pain or pressure at rest, due to rupture of atherosclerotic plaque with thrombosis
    • Acute Myocardial Infarction (irreversible infarction): acute onset of chest pain or pressure at rest, due to rupture of atherosclerotic plaque with 100% thrombosis

    Diagnosis and Treatment

    • Diagnosis of Stable Ischemic Heart Disease: normal ECG during rest, ST depression during stress test, and negative cardiac enzymes
    • Diagnosis of Acute Coronary Syndrome: resting ECG (ST depression), negative cardiac enzymes, and anticoagulant and revascularization treatment
    • Diagnosis of Acute Myocardial Infarction: resting ECG (ST depression or elevation), elevated cardiac enzymes, and treatment with anticoagulant and revascularization
    • Treatment for Coronary Artery Syndrome: anticoagulant, revascularization, and aspirin to reduce platelet aggregation

    Pathological Changes in Acute Myocardial Infarction

    • Myocardial oxygen deprivation, leading to anaerobic metabolism, accumulation of lactate, and calcium influx into cells, causing cellular death (necrosis)
    • Necrosis starts within 30 minutes, completes within 6-12 hours, and is recognized by macrophages within 3-7 days, leading to fibrosis and diminished heart function

    Complications of Acute Myocardial Infarction

    • Early complications: arrhythmias, cardiogenic shock, and acute rupture of cardiac structures
    • Late complications: pericarditis, heart failure, and ventricular remodeling

    Cardiac Output and Failure

    • Cardiac Output: stroke volume x heart rate
    • Stroke volume: end diastolic volume - end systolic volume
    • Ejection fraction: stroke volume divided by end diastolic volume
    • Stroke volume determinants: contractility, preload, and afterload
    • Left Ventricular Systolic Heart Failure (HF with reduced EF): weak ventricular contraction, decreased stroke volume, and decreased cardiac output
    • Left Ventricular Diastolic Heart Failure (HF with preserved EF): impaired ability to relax and accommodate volume, reduced end diastolic volume, and reduced stroke volume
    • Causes of LV systolic HF: MI/ischemia, HTN, valvular disease, and rare diseases (myocarditis)
    • Causes of LV diastolic HF: long-standing HTN, myocardial ischemia and infarction, and valvular disease

    Compensatory Mechanisms

    • Sympathetic nervous system activation: increases myocardial contractility, heart rate, and cardiac output
    • Renin-angiotensin-aldosterone system (RAAS) activation: increases sodium and water retention, leading to increased preload and cardiac output
    • Cardiac remodeling: mechanical stress on myocardium, leading to increased LV size, accommodation of increased end diastolic volume, and increased cardiac output

    Diagnosis and Treatment of Heart Failure

    • Diagnosis of LV systolic HF: echo (reduced LV contractility, reduced EF), chest x-ray (cardiomegaly, pulmonary congestion/edema), and treatment with beta blockers and ACE/ARBs
    • Diagnosis of LV diastolic HF: echo (preserved EF, hypertrophy of wall), chest x-ray (pulmonary congestion/edema), and treatment with diuretics and SGLT2 inhibitors

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    Description

    This quiz covers the risk factors of atherosclerosis, including smoking, diabetes, and hypertension, and their mechanisms of action on the endothelial cells and blood lipids.

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