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2011-09-08 22:55:03

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  1. Most of the blood flow in the left coronary artery occurs during ___________.
    Diastole -- because compression of the left ventricle during systole produces a force greater than the arterial pressure in the branches of the left coronary artery
  2. Most of the blood flow in the right coronary artery occurs during ____________.
    Systole -- because aortic pressure is greater than right ventricular pressure
  3. What four factors determine myocardial oxygen demand?
    • Heart Rate
    • Contractility
    • Preload -- or Diastolic Wall Tension
    • Afterload -- or Systolic Wall Tension
  4. ____________ binds to the beta-1 receptor.
    This activates ____________, which converts ATP to cAMP.
    cAMP activates _______________, which phosphorylates __________ calcium channels. As a result, with the next action potential, more calcium will enter the cell.
    It also phosphorylates __________ receptors. As a result, more calcium will be released from the SR with the next action potential.
    The enhanced levels of calcium lead to more binding of __________________ which allows enhanced interactions of cross-bridges, resulting in a more forceful contraction.
    • Norepinephrine
    • Adenylyl Cyclase
    • Phosphokinase A (PKA)
    • L-type
    • Ryanodine
    • Troponin C
  5. What is defined as discomfort or pain associated with an imbalance between myocardial oxygen supply and demand?
  6. What type of angina is described as typical angina that occurs with exertion? The cause is usually an atheromatous lesion on a coronary artery that reduces its diameter. With additional effort, myocardial oxygen demand increases, but the artery is too narrow for adequate blood flow.
    Stable Angina
  7. What type of angina is associated with a vasospasm of a coronary artery that temporarily reduces the diameter of a coronary artery? This can happen at any time; it is not dependent on effort.
    Variant (Prinzmetal) Angina
  8. What type of angina is usually caused by the rupture of an atherosclerotic clot? This is a medical emergency because it often predicts that myocardial infarction and possibly sudden death are about to occur. This angina occurs at rest.
    Unstable Angina
  9. What is it called when the aortic valve has only 2 leaflets? What are the implications of this?
    • Congenital Bicuspid Aortic Valve
    • Usually no complications early, but may result in stenosis of the aortic valve in later years
  10. What type of valvular abnormality results in pressure overload of the chamber? This leads to muscle hypertrophy, and may eventually lead to failure.
    Valve Stenosis
  11. What type of valvular abnormality results in volume overload of the chamber? This leads to chamber dilation, and may eventually lead to failure.
    Valvular Insufficiency (Regurgitation)
  12. What is a primary cause of functional mitral regurgitation? What is this common in?
    • Dilation of left ventricle: valve itself is normal, but regurgitation occurs because the leaflets are pulled apart
    • Ischemic Heart Disease
  13. Acute rheumatic fever occurs because the body develops an immune reaction to what?
    Group A Streptococcus (almost always streptococcal pharyngitis)
  14. What is the main long-lasting complication of acute rheumatic fever? What is most commonly involved with this?
    • Cardiac Valvular Disease
    • Most commonly involves mitral valve, often with involvement of the aortic valve as well
  15. What are the two most common manifestations of acute rheumatic fever?
    • Pancarditis -- inflammation of myocardium, pericardium, and endocardium
    • Migratory polyarthritis of large joints
  16. What are the Jones critera used in the diagnosis of? What are its basic requirements?
    • Acute Rheumatic Fever
    • Must be: 1, serologic evidence of previous streptococcal infection, and 2, presence of sufficient number of clinical manifestations of disease (carditis, arthritis, etc)
  17. What are considered pathognomonic for acute rheumatic heart disease?
    Anitschkow Cells -- "caterpillar cells," nuclear chromatin forms a slender, wavy ribbon resembling a caterpillar in the center of the pale nucleus
  18. What are collections of T-cells, plasma cells, and distinctive macrophages called Anitschkow cells called? What are these found in?
    • Aschoff Bodies
    • Acute Rheumatic Heart Disease
  19. Identify the pathology below:
    What disease is this found in?
    • Entire structure is an Aschoff Body
    • Can see Anitschkow Cells within it
    • Pathognomonic for Acute Rheumatic Heart Disease
  20. Identify the pathology below:
    • Acute Rheumatic Valvulitis
    • Arrows point to the verrucae on the cusps of the valve
  21. What is a pericardial friction rub (due to inflammation of the pericardium) seen in, along with weak heart sounds, tachycardias, and arrhythmias?
    Acute Rheumatic Heart Disease
  22. What does the valve damage that occurs during acute rheumatic fever result in?
    Hemodynamic abnormalities, turbulence, ongoing fibrosis, and scarring
  23. What valve is nearly always involved in Chronic Rheumatic Heart Disease (65-70%)?
    Mitral Valve
  24. In chronic rheumatic heart disease, there is leaflet thickening, commissural fusion and shortening of the mitral valve. This leads to thickening and fusion of the chordae tendinae. What does this result in?
    Mitral Stenosis ("fish mouth valve")
  25. What is the most common aquired valve abnormality?
    Aortic Stenosis
  26. What is this the most common cause of: nodular calcium deposits in valve cusps which protrude into sinuses of Valsalva and block valve opening?
    Aortic Stenosis
  27. What is the most common cause of mitral stenosis?
    Rheumatic Heart Disease
  28. A mitral valve prolapse is a weakening of mitral valve leaflets resulting in prolapse of leaflets back into the left atrium during systole. This is usually of no clinical significance. However, how is it detected? Confirmed diagnosis?
    • Detected by mid-systolic "click" on auscultation -- squatting maneuver
    • Confirm diagnosis by echocardiogram
  29. Identify the pathology below:
    Mitral Valve Prolapse: arrows point to the "ballooned-out" mitral valve cusps which are bulging into the left atrium
  30. Identify the pathology below (first is normal):

    • Normal valve on top has well-organized collagen (blue stain) within the valve leaflet
    • The abnormal valve (bottom) has loose, disorganized tissue
  31. What is it called when there are degerative calcium deposits in the fibrous ring (annulus) of the mitral valve? This is usually not associated with significant consequences.
    See pathology below:
    Mitral Annular Calcification
  32. What is infective endocarditis usually caused by? What is the treatment for this?
    • Bacterial Infections -- Bacteremia, with seeding of valve
    • Weeks of antibiotic treatment; some cases require surgical intervention
  33. Infective endocarditis is traditionally divided into acute versus subacute forms. The acute form is less common, and is typically an infection of a previously normal valve by virulent organisms. What type of organisms most often cause this form?
    Staphylococcus aureus
  34. Infective endocarditis is traditionally divided into acute versus subacute forms. The subacute form is more common, and involves an infection of a previously diseased valve by a less virulent organism. What type of organism most often causes this?
    Streptococcus viridans
  35. What is the most consistent feature of infective endocarditis?
  36. Which patient seems more sick, one with acute infective endocarditis or one with the subacute form?
    Acute -- rapidly developing fever, chills, and weakness
  37. What is Duke's Criteria used to diagnose? What are these criteria?
    • Infective Endocarditis
    • Fever, Systolic Murmur, Multiple Blood Cultures, TEE
  38. What two valves are most commonly involved in infective endocarditis?
    Aortic and Mitral
  39. What side of the heart is commonly involved in infective endocarditis in IV drug users?
    Right Side
  40. Identify the pathology below:
    Infective Endocarditis
  41. What is a rare disease that is caused by the deposition of small, sterile thrombi on leaflets (cusps) of cardiac valves? This is often associated with underlying cancer, especially mucinous adenocarcinomas. It may be associated with hypercoagulable states, or with indwelling catheters. This is composed of bland thrombi; there is no inflammatory reaction; it may be a source of emboli.
    See pathology picture below:
    Nonbacterial Thrombotic Endocarditis (NBTE)
  42. What is a rare disease caused by vegetations on mitral or tricuspid valves or endocardium occassionally seen in SLE? This may be located on valve surfaces, on the undersurface of valves, on chordae tendinae, or on endocardium. It is composed of finely granular, fibrinous material. Active valvulitis may be present.
    Endocarditis of SLE -- Libman-Sacks Disease)
  43. Carcinoid Heart Disease is characterized by tumors of various organs (most often GI tract) that may be associated with production of bioactive products: serotonin, histamine, etc. Patients with extensive hepatic metastasis may develop this type of heart disease. It usually manifests as what? Where is this limited to?
    • Tricuspid Insuffiency, plus or minus Pulmonary Valve Insufficiency
    • Right Side of Heart
  44. What is the major complication associated with a mechanical heart valve? With a bioprosthetic one?
    • Thrombosis: must be maintained on prophylactic anticoagulation for life
    • Degeneration of Valve
    • Both may be complicated by Infection
  45. What cell type lines the pericardium?
    Mesothelial Cells
  46. The majority of cases of idiopathic pericarditis are probably due to what?
    Viral Infections
  47. What two viruses account for most cases of pericarditis?
    • Coxsackie
    • ECHO
  48. What are three common Immune-Mediated causes of pericarditis?
    • Rheumatoid Arthritis
    • SLE
    • Scleroderma
  49. What is a common miscellaneous cause of acute pericarditis?
  50. Identify the pathology below:
    Acute Pericarditis
  51. Most patients with acute pericarditis are asymptomatic. In symptomatic patients, what is the most common presenting symptom?
    Pleuritic Chest Pain that is decreased by leaning forward, and worsened by lying down
  52. What is a common physical exam finding in a patient with acute pericarditis?
    Pericardial "Friction Rub"
  53. What is commonly seen on diagnostic evaluation for acute pericarditis?
    • May have elevation of troponin I & CK-MB
    • Diffuse ST segment elevation
  54. What is the typical treatment for acute pericarditis?
    • NSAIDs
    • Colchicine sometimes used
  55. What is caused by chronic inflammation and scarring of the pericardium? This can be due to any cause of pericarditis. It results in the pericardium constricting the heart, leading to decreased venous return and right heart filling, and thus decreased cardiac output. Physiologically, this is equivalent to a cardiac tamponade due to effusion.
    Constrictive Pericarditis
  56. What two things are relatively commonly associated with constrictive pericarditis?
    • Radiation
    • Rheumatoid Arthritis
  57. What is it called when fluid is collected in the pericardial sac? What is the most serious complication of this?
    • Pericardial Effusion
    • Cardiac Tamponade
  58. What is described as compression of the right side of the heart by pericardial effusion, preventing venous return to the heart? What does this result in?
    • Cardiac Tamponade
    • A marked decrease in cardiac output
  59. What are two common, specific causes of Pericardial Effusion?
    • Uremia
    • Hemopericardium
  60. What four causes of Pericardial Effusion have the highest risk of progressing to Cardiac Tamponade?
    • Bacterial Infection
    • HIV Infection
    • Hemopericardium
    • Malignant Pericardial Effusions
  61. How does Cardiac Tamponade present?
    • Right Heart Failure
    • Hypotension
  62. What is the Beck Triad for Cardiac Tamponade? What other symptoms is pathognomic?
    • Beck Triad: Hypotension, Muffled Heart Sounds, Elevated Jugular Venous Pulse
    • Paradoxical Pulse: abnormally large drop in systemic arterial pressure during inspiration -- >10 mmHg drop in systolic pressure
  63. What is the key diagnostic test for cardiac tamponade? What can be seen on chest radiograph?
    • Echocardiography: should show perfusion
    • Chest Radiograph: water bottle heart
  64. What is the typical presentation of Cardiac Tamponade?
    • Tachycardia
    • Diaphoresis
    • Cool Extremities
    • Peripheral Cyanosis
    • Hypotension with reduced pulse pressure
    • Marked Jugular Venous Distention
    • Paradoxical Pulse
  65. How is an effusion without tamponade treated? With?
    • Treat underlying cause; NSAIDs; Colchicine
    • Immediate infusion of saline; Pericardiocentesis; Pericardial Window
  66. What are the most common primary cardiac tumors?
    Atrial Myxomas
  67. What are the most common malignant primary cardiac tumors?
  68. What are the most common sites of origin of metastasis to the heart?
    Lung and Breast
  69. What gender is most commonly affected in Atrial Myxomas? Are the majority of cases familial or sporadic?
    • Women
    • Sporadic
  70. Familial myxomas are associated with what syndrome? How are these typically inherited? What are the other manifestations of this syndrome?
    • Carney Syndrome
    • Autosomal Dominant
    • Myxomas in cardiac & extracardiac sites; hyperpigmented skin lesions; endocrine hyperactivity; variety of noncardiac tumors
  71. Where do cardiac myxomas typically grow from? Are they sessile or pedunculated? What stem cell type are they believed to arise from?
    • Interatrial Septum
    • Pedunculated
    • Multipotent Mesenchymal Stem Cells
  72. What are the common complications of Cardiac Myxomas?
    • Systemic Symptoms -- fever, chills, malaise
    • Embolic Phenomena
    • Intracardiac Obstruction
  73. Identify the pathology below:
    Left Atrial Myxoma -- tumor is the reddish, polypoid mass surrounded by clot within the left atrial cavity
  74. Identify the pathology below:
    Atrial Myxoma -- scattered stellate or spindled cells and capillaries within a loose, pale stroma
  75. What is the main cardiac manifestation of a myxoma? What can this cause?
    • Mechanical obstruction to mitral valve
    • Dizziness, dyspnea, cough, pulmonary edema, heart failure
    • Diastolic murmur and tumor "plop"
  76. What is a tumor "plop" heard in?
  77. How are myxomas diagnosed?
    • Echocardiography is initial test of choice
    • Chest CT or Cardiac MRI may be helpful
  78. What is the treatment method and prognosis for myxomas?
    • Surgical Excision
    • Prognosis is good, with rare recurrence
  79. What is the second most common primary cardiac tumors?
    • Lipomas -- benign tumors composed of fat cells; these are well circumscribed
    • Of no clinical significance
  80. What is a non-circumscribed collection of fat cells in the atrial septum called?
    • Lipomatous Hypertrophy of the Atrial Septum
    • Of no clinical significance
  81. What are the third most common primary cardiac tumors? Where are these usually located?
    • Papillary Fibroelastoma -- resemble sea anemones
    • Located on heart valves
    • Of no clinical significance, but can be source of emboli
  82. What are the most common cardiac tumors in infants and young children? What are these often associated with? What are these composed of, and what is the prognosis?
    • Cardiac Rhabdomyomas
    • Tuberous Sclerosis
    • Composed of bizarre, markedly enlarged myocytes
    • Often regress spontaneously, but may cause obstruction of valve orifice or cardiac chamber
  83. What are the second most common malignant cardiac tumors?
  84. What are the primary symptoms associated with heart failure?
    • SOB
    • Fatigue
    • Edema
    • Congestion
  85. In which type of heart failure does the heart not develop adequate force to eject enough blood? The result of this is that the contractility of the heart is reduced, leading to reduced ejection fraction and dilated ventricle. What is the most common example of this?
    • Systolic Heart Failure
    • Myocardial Infarction
  86. In which type of heart failure does the heart have problems filling? The primary problem is that the heart loses compliances, and becomes stiffer. As a result, the heart cannot relax adequately, limiting filling. What is a common cause of this?
    • Diastolic Heart Failure
    • Systemic Hypertension
  87. What is the New York Heart Associated Classification based on? What are the classes?
    • Exercise Capacity
    • Class I: There is cardiac disease, but the patient is asymptomatic
    • Class II: Dyspnea with heavy exertion
    • Class III: Dyspnea with light exertion
    • Class IV: Dyspnea at rest
  88. What is the American College of Cardiology and American Heart Association classifications for heart failure?
    • Stage A: patient has risk factors for heart failure
    • Stage B: patient is asymptomatic for heart failure
    • Stage C: patient has symptoms of heart failure
    • Stage D: patient is refractory to treatment or at the end stage of heart disease
  89. What receptor protein does cholesterol interact with for absorption?
    Niemann-Pick C1-like 1 Protein (NPC1L1)
  90. What are the largest plasma lipoproteins, as well as the least dense?
  91. As chylomicrons travel through the circulation, tissues that synthesize __________ (skeletal and cardiac muscle, adipose tissue, and breast tissue of lactating women) partially metabolize them.
    Lipoprotein Lipase
  92. The liver removes chylomicron remnants from the blood when the _______ component binds to receptors on hepatocytes. What are the two receptor types that bind this? Hepatocytes then absorb the remants via receptor-mediated endocytosis
    • ApoE
    • Low Density Lipoprotein Receptors (LDLR) & LDL Receptor-related Protein (LRP)
  93. The liver is the primary regulator of cholesterol levels in the body. Hepatocytes regulate cholesterol by controlling its synthesis, which is based on the levels of cholesterol in the hepatocytes. Cholesterol is synthesized in a multi-step process. What is the rate-limiting step?
    Conversion of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) to mevalonate using the enzyme HMG-CoA reductase
  94. Cholesterol and cholesteryl esters, along with apoB-100, triglycerides, and phospholipids, are combined by the liver into _________, and then secreted by exocytosis into the blood stream.
    Very Low Density Lipoproteins (VLDLs)
  95. Very Low Density Lipoproteins (VLDLs) are partially digested by lipoprotein lipase in striated muscle and adipose tissue to release monoglycerides and free fatty acids which are then taken up by these tissues. This produces VLDL remnants, which are also term what?
    Intermediate-Density Lipoproteins (IDLs)
  96. Intermediate-Density Lipoproteins (IDLs) can interact with hepatic lipase, which partially digests them, releasing monoglycerides and free fatty acids that are then taken up by the liver. In this process apoE is removed. What are the resulting lipoproteins termed?
    Low-Density Lipoproteins (LDLs)
  97. What structures regulate the blood levels of cholesterol?
  98. What is the major apoprotein in HDLs?
  99. Cholesterol is a major culprit in the development of what?
    Atheromatous Plaques
  100. What is the recommendation for total cholesterol? LDL-C? HDL-C? Ratio of total cholesterol to HDL-C? Ratio of LDL-C to HDL-C?
    • Total Cholesterol: < 200 mg/dl
    • LDL-C: < 130 mg/dl
    • HDL-C: > 40 mg/dl male; > 50 mg/dl female
    • Ratio TC to HDL: 5:1
    • Ratio LDL to HDL: 3:1
  101. What is considered Borderline to High in total cholesterol? High?
    • 200-239 mg/dl
    • > 240 mg/dl
  102. What is considered Borderline to High in LDL-C? High?
    • 130-159 mg/dl
    • > 160 mg/dl
  103. Triglyceride levels greater than _________ mg/dl can lead to pancreatitis, which is the major problem with high triglycerides.
  104. What is the major problem with high triglycerides (> 1000 mg/dl)?
  105. What are tumorous masses of lipids contained in foam cells, and associated with plasma cholesterol levels greater than 300 mg/dl?
  106. What hypertriglyceridemia is a recessive genetic disease where there is too little lipoprotein lipase so that chylomicrons cannot be metabolized? This can lead to severe lipemia (2000-3000 mg/dl of triglycerides). This disorder might not be discovered until the patient has an acute attach of pancreatitis. Xanthomas, hepatosplenomegaly, and hypersplenism may occur, and foam cells can be found in bone marrow, liver, and spleen.
    Primary Chylomicronemia
  107. What hypertriglyceridemia results from a failure to adequately remove triglyceride-rich lipoproteins? This leads to increases in VLDL and chylomicrons. Factors that increase VLDL secretion from the liver (such as obesity, alcohol, diabetes, and estrogens) aggravate the condition. Xanthomas, epigastric pain, and pancreatitis may be present depending on the severity of the disease.
    Familial Hypertriglyceridemia
  108. What hypertriglyceridemia is characterized by increased levels of VLDL, LDL or both? The increases in triglycerides and cholesterol are generally moderate. Xanthomas are usually absent.
    Familial Combined Hyperlipoproteinemia
  109. What hypertriglyceridemia involves a defect in apoE synthesis? This can lead to a huge increase in plasma triglycerides (> 1000 mg/dl).
    Familial Dysbetalipoproteinemia
  110. What hypercholesterolemia is associated with mutations in the LDL receptor which prevent cholesterol uptake in the liver? This is an autosomal dominant disorder. This is very rare. People with this can have atherosclerosis when they are children, and MIs before they are 20. Tendon xanthomas can be present.
    Familial Hypercholesterolemia
  111. In what hypercholesterolemia is apoB-100 damaged, which impairs binding of LDLs to hepatocytes and other cells? Plasma LDLs decrease. Tendon xanthomas can be present.
    Familial Ligand-Defective Apolipoprotein B
  112. What hypercholesterolemia is associated with lipoprotein(a)? This is found in atherosclerotic plaques and is associated with a higher risk of coronary artery disease. Levels of Lp(a) can range from 0 to over 500 mg/dl. This is associated with enhanced atherogenesis.
    Lp(a) Hyperlipoproteinemia
  113. Rare genetic disorders, such as ________ disease and ________ deficiency, as well as familial ____________, have reduced HDL which can lead to atherosclerosis.
    • Tangier Disease
    • LCAT Deficiency
    • Familial Hypoalphalipoproteinemia