Heart Part 1, UTHSC Fall 2022 D2 Pathology
Heart Part 1, UTHSC Fall 2022 D2 Pathology Heart weight • Varies with body height and weight, 0.4-0.5% of body • Female: ~250 to 320 g, male: ~300 to 360 g Epicardial surface • Smooth and glistening • Epicardial fat Thickness of the free wall • Right ventricle: 0.3 to 0.5 cm • Left ventricle: 1.3 to 1.5 cm Increase in cardiac weight/size = Cardiomegaly • Hypertrophy • Dilation What is the path of blood through the heart? Right Atrium, Tricuspid, Right Ventricle, Pulmonic valve, Pulmonary artery, Lungs, Pulmonary veins, Left Atrium, Bicuspid (Mitral) Valve, Left Ventricle, Aortic valve, Aorta what do cardiac myocytes use almost exclusively for energy needs? oxidative phosphorylation Myocardium extremely vulnerable to ischemia what are the four major arteries that supply blood to the heart muscles? 1. left main coronary artery 2. right coronary artery 3. left anterior descending artery 4. left circumferential artery what are the three layers of the heart wall? epicardium, myocardium, endocardium Endocardium endothelial cells over connective tissue Myocardium cardiac muscle Epicardium connective tissue with blood vessels and nerve fibers, covered by layer of mesothelial cells T/F the epicardium is part of the pericardium True what powers the heart's pumping? due to coordinated contraction and relaxation of the cardiac myocytes what is the effector unit of cardiac muscle? myofibrils what are the subunits to myofibrils? actin, myosin, and other regulatory proteins Cardiac Structure/Myocardium Histology - Striated appearance - Pale pink intercalated disks as intercellular junction for coordinated beating of cardiac myocytes Cardiac Structure/Valves - As extensions of endocardium, maintain unidirectional blood flow - Function depends on the mobility, pliability, and structural integrity of the leaflets or cusps - Leaflets in tricuspid and mitral; cusps in the semilunar valves (aortic and pulmonary) - Tri-layered architecture what are the three major pathological changes to heart valves? - Damage to collagen that weakens the leaflets → mitral valve prolaps - Nodular calcification beginning in interstitial cells → calcific aortic stenosis - Fibrotic thickening → rheumatic heart disease Cardiac Stem Cells - Increasing evidence of presence stem cells in mammalian myocardium, although it is classically considered as a permanent cell population. - 5-10% of normal atrial cellularity , but 1∕100,000 cells in normal ventricle - Cardiac stem cells with very slow rate of proliferation Congestive Heart Failure - A common, usually progressive condition with a poor prognosis - In CHF heart is unable to pump blood at a rate sufficient to metabolic demands of the tissues. Congestive Heart Failure stats In US, 5 million individuals (2% of the population) affected each year, causes 300,000 death/year what is a common end stage of many forms of chronic heart disease? Congestive Heart Failure what is one way the heart will change to help maintain arterial pressure and organ perfusion? myocardial hypertrophy Cardiac Hypertrophy Pathophysiology and Progression to Heart Failure 1. Pressure (systemic hypertension) or Volume overload (aortic stenosis 2. Increase in mechanical work 3. Myocyte adaptation 4. Increase in size (hypertrophy) of myocyte 5. Increase in size and weight of the heart what is the result of Myocyte hypertrophy not being accompanied by a proportional increase in capillary numbers? - weak blood supply for hypertrophied heart while oxygen consumption is elevated - More vulnerability of hypertrophied heart to ischemia-related decompensation - Cardiac failure what is the result of hypertension on the vascular system? Pressure overload what is the result of Valvular Disease on the vascular system? Pressure and/or volume overload what is the result of Myocardial infarction on the vascular system? Regional dysfunction with volume overload what do Hypertension, Valvular Disease, and Myocardial infarction lead to in the heart? increased cardiac work - increased wall stress - cell stretch - hypertrophy and/or dilation - cardiac dysfunction Hypertrophy and/or dilation of the heart is characterized by •↑ Heart size and mass •↑ Protein synthesis •Induction of immediate-early genes • Induction of fetal gene program • Abnormal proteins • Fibrosis • Inadequate vasculature cardiac dysfunction is characterized by • Heart failure (systolic/diastolic) • Arrhythmias • Neurohumoral stimulation what are the causes of left-sided heart failure? - Ischemic heart disease - Hypertension - Aortic and mitral valvular diseases - Primary myocardial diseases what are the consequences of left-sided heart failure? - Passive congestion (blood back up in the pulmonary circulation) - Stasis of blood in the left-sided chambers - Inadequate perfusion of downstream tissues what is the morphology of Left-sided Heart Failure in the heart? Left ventricular hypertrophy (myocyte hypertrophy and interstitial fibrosis) → impaired function → secondary dilation of the left atrium what is the morphology of Left-sided Heart Failure in the lung? • Perivascular congestion and edema → heavy, wet lungs • Progressive edematous widening of alveolar septa • Accumulation of edema fluid in the alveolar spaces • Heart failure cells (hemociderin-laden macrophages) what are the symptoms of left-sided heart failure? • Paroxysmal nocturnal dyspnea • Elevated pulmonary Capillary pressure • Pulmonary congestion Cough Crackles Wheezes Blood-tinged sputum Tachypnea • Restlessness • Confusion • Orthopnea • Tachycardia • Exertional dyspnea
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