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172 Cards in this Set
- Front
- Back
1. What 3 questions should be asked in every focused cardiac examination history of the patient’s present illness?
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Chest pain, shortness of breath and syncope
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2. What three pulmonary symptoms could be asked in the history of present illness to help separate pulmonic from cardiac induced shortness of breath?
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Orthopnea, PND and productive sputum
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3. What parameter based questions can you ask the patient to separate episodes of stable angina pectoris from unstable angina?
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Changes in frequency and duration. Pain at rest. If episode of angina last 20 min, the damage process starts
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4. What is the most common cause of death in both men and women in this country?
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Atherosclerosis
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5. How long does myocardial ischemia have to last before myocardial damage (myocardial infarction) begins to occur?
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20 min
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6. List 5 major risk factors for the development of coronary artery disease.
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Age, smoking, age, diabetes, cholesterol, family history, obesity, hypertension
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7. Where in the history, other than family history, would be the place to list the atherosclerotic risk factors in a patient with suspected coronary artery disease
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HOPI
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8. In what part of the history would you list cardiac review of systems in a patient with a cardiac problem?
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HOPI
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9. What is the most common diagnosis for episodic syncope upon standing?
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Orthostatic hypotension/ vasovagal syncope
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10. How would you describe a Stokes Adams attack?
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Sudden block in AV conduction leads to syncope, once ventricles establish their own rhythm, patient regain consciousness
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11. Define congestive heart failure.
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The heart is unable to pump blood at a sufficient rate to meet the metabolic demands or can do so at elevated filling pressure
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12. What relatively rare congenital life threatening conditions should you consider in a 20 year old with suspected cardiac induced syncope?
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Wolf-parkinson disease, hypertrophic cardiomyopathy, Long QT
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13. What is the usual chief complaint when mitral regurgitation is severe?
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No symptoms until end stage heart failure. Shortness of breath at end stage
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14. What are the 3 presenting symptoms of a patient with severe aortic stenosis?
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Chest pain, syncope, shortnesss of breath
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15. Which of these 3 complaints in a patient with aortic stenosis is compatable with the shortest life span?
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Shortness of breath
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16. What is the usual chief complaint of patient with severe mitral stenosis?
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Dyspnea
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17. What is the usual presenting symptom of chronic severe AR?
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Shortness of breath
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18. What is the presentation in the emergency department of acute severe AR or MR?
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Pulmonary edema/shock
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19. What is the range of pressure we call prehypertensive?
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120-140 systolic, 80-90 diastolic
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20. What is the normal pulse pressure?
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40
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21. What is the significance of pulsus alternans in a patient?
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Is the finding of an alternating plse volume. Its indicative of congestive heart failure, LV systolic deficiency
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22. What is the significance of a 12 mm or greater paradoxical pulse?
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Paradoxical pulse means that the amplitude decreases with inspiration greater than 10 mm Hg and indicates cardiac tamponade, COPD and pericarditis
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23. What is the finding on carotid palpation in severe aortic stenosis?
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The carotid pulse will register parvus at tardus (weak and late) relative to heart beat. Delay between first heart sound and corresponding pulse in carotid artery.
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24. A patient presents with a murmur, bounding pulses and a pulse pressure of 80. What is your diagnosis?
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Hyperthyroid, truncus arteriousus, post exercise
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25. What is top normal size for a point of maximal impulse (PMI)?
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1-2 cm (5th intercostal space)
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26. In a patient with normal cardiac anatomy, which chamber are you palpating when feeling the PMI?
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Left ventricle
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27. What would be the underlying pathology behind a paradoxical or rocking component of the apical impulse?
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An uncordinate (dyskinetic) apex beat involving a larger area than normal. Ventricular dysfunction possibly post aneurysm or post MI
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28. Which venous pulse can you use to estimate right atrial filling pressure?
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The jugular venous pressure (internal jugular) can be assessed to estimate RA filling pressure
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29. What is the explanation for the a wave seen in the internal jugular pulses?
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Due to atrial contraction
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30. In what heart rhythm abnormality would the a wave disappear?
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In atrial fibrillation
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31. Which heart sound signifies the onset of systole?
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First heart sound (S1)
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32. Diastole begins with what heart sound?
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S2
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33. Why is the S1 sound usually much softer than S2
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AV valves leaflets are not as taught as the aortic and pulmonary valves (semilunar valves)
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34. Where would P2 be most easily heard?
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2 nd intercostal space on the left
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35. Why is A2 louder than P2?
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More pressure in the systemic circulation (pushing back against the aortic valve) than in the pulmonary circulation, the aortic closes with more force
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36. What cardiac event occurs to cause the S4 sound?
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Atrial kick is caused by contraction of the atria to force extra blood into the ventricles prior to systole
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37. When does an S3 gallop occur and what does it signify in an adult?
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Is caused by the flutter of the ventriclular walls as blood rushes in from the atria. It may signify mitral regurgitation or CHF. Decrease ventricular compliance
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38. What abnormalities could cause reverse splitting of A2P2?
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Aortic stenosis, hypertrophic cardiomyopathy, left bundle branch block, ventricular pacemakers
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39. What valves are responsible for early systolic clicks?
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Semilunar
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40. What valve is responsible for mid systolic clicks?
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Opening of a stiffened mitral valve
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41. What is the pathophysiologic explanation of a diastolic snap?
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Opening of stenotic mitral valve
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42. Where, and with what part of your stethoscope, do you listen for left sided cardiac gallops?
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Listen with bell, S3/S4 apeax with patient in left lateral decubitis
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43. What is the response of gallops when you increase pressure on the bell of your stethoscope?
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They dissapear
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44. At what heart rate does the patient develop a summation gallop?
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120. Less time to fill. Diastole is shortened happening all in the same time
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45. How loud does a murmur have to be to cause a thrill?
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Grade 4-6
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46. In addition to the cardiac examination, what other areas of physical examination would be of most interest to you in a cardiac problem? List 4
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Pulmonary, GI, extremities, thyroid, eyes
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47. What other factors or major organ dysfunction can cause peripheral edema?
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Liver failure, RHF, lymphatic obstruction, DVT, kidney failure
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48. What leg statistically swells first in edema?
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Left leg because of iliac vein
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49. What differentiates lymphedema from edema secondary to fluid retention?
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Pitting (fluid, no protein) vs non pitting (lymphedema)
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50. Describe an aortic stenosis mumur.
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Harsh thrill, non-holosystolic, crescendo-decrescendo
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51. In what auscultation site and what position would aortic stenosis be expected to be loudest?
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Right 2nd IC space
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52. What is the radiation pattern of an aortic stenosis murmur?
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Right carotid, clavicle and sternum
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53. Does loudness of AS usually correlate with severity?
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Yes, congestive heart failure
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54. What has occurred when the murmur of severe aortic stenosis decreases?
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CHF
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55. The etiology of dilated cardiomyopathy is:
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Alcohol, defects in cytoskeletal proteins (dystrophin and alpha-actin), volume overload, myocarditis
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56. Describe the murmur of mitral regurgitation and it’s location?
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Pansystolic, radiates to axilla, hear in at PMI 5th IC midclavicular line
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57. Does loudness of MR correlate with severity?
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No
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58. What skeletal abnormalities are associated with mitral valve prolapse?
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Marfans
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59. What maneuver will move the click of mitral valve prolapse later into systole?
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Valsava maneuver (more volume so it will occur later). Squatting increases venous return. Standing decreases ledt ventriclualr volume froom decreased venous return to heart
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60. The murmur of mitral regurgitation will radiate toward the high sternum with an abnormality of which leaflet of the mitral valve?
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Posterior or anterior
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61. What are the other sounds associated with a murmur in mitral valve prolapse?
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Mid systolic click
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62. What would you expect to find on palpation of the PMI of a patient with severe chronic MR
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Shift to the left (increase in diameter)
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63. What is the usual causative factor in the development of mitral stenosis?
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Rheumatic heart disease and congenital
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64. If someone presents with mitral stenosis in their teens, what can you surmise?
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Rheumatic heart disease
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65. Which sex far predominates in the development of mitral stenosis?
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Female
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66. What is the best position and location to hear the murmur of mitral stenosis?
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Left 5th IC space, left lateral position at apex
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67. Which head of the stethoscope do you use to hear mitral stenosis?
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Bell
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68. Describe the mitral stenosis murmur.
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Low pitched rumble, decrescnedo in diastole
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69. What would happen to mitral stenosis murmur if the patient developed atrial fibrillation?
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Presystolic sound dissapears and all you hear is a midsystolic rumble
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70. What is the response of mitral stenosis to exercise?
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Increased. Murmur increased demand of blood. So more has to be pumped through the stenosed valve
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71. Describe the position of the patient and the locations where the murmur of aortic regurgitation is best heard.
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2nd to 4th left interspaces. Patient siting, leaning forward, with breath held after exhalation
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72. What is implied if the murmur of chronic aortic regurgitation is heard best on the right of the sternum?
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A severe murmur, dilation of the root, ventricular hypertophy
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73. Why is the murmur of AR decreshendo?
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Less pressure difference, less blood flow, less sound
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74. In AR and MR what is the best indication of severity.
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Length of murmur
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75. Hypertrophic cardiomyopathy in 50% of people has a familial transmission, describe:
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Massive myocardial hypertrophy without ventricular dilation. Mutations in any of several genes that encode sarcomeric proteins increases the mass and size of the ventricular walls which reduces diastolic filling capacity of the heart
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76, 77, 78 What areas of physical examination and what maneuver will help you differentiate aortic stenosis from Hypertrophic Obstructive Cardiomyopathy on physical examination?
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Carotid: Delayed carotid upstroke in aortic stenosis. The carotid pulse rise quickly in hypertrophic cardiomyopathy
Cardiac:Lateral displacement from cardiac enlargement in hypertrohic cardiomyopathy. No lateral displacement in aortic stenosis Maneuvers: Aotic stenosis murmur heard best with patient sitting and leaning forward. Hypertrophic cardiomyopathy decreases with squatting |
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79. What physical examination sign is pathognomic of atherosclerotic heart disease?
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There isn't one
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80. Which vessel is the most likely cause of an inferior wall MI?
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Posterior interventricular
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81. Which vessel is the most likely cause of a lateral MI?
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Left circumflex artery
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82. Which vessel is the most likely cause of an anterior wall MI?
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LAD left anterior descending
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83. What is the most common abnormality in congenital heart disease?
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VSD, could be bicuspid aortic valves
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84. What is the most common form of congenital heart disease in adults?
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Bicuspid aortic valve
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85. What is the most common cause of an extracardiac shunt?
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PDA
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86. Which congenital heart disease is more common in women:
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ASD, mitral valve prolapse, patent ductus arteriosis, common atrium (one atrium)
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87. Which congenital heart diseases occur most commonly in males?
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Coarction, aortic valve stenosis, tetralogy of Fallot, transposition
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88. Which congenital heart disease has the largest male predominance?
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Bicuspid valve
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89. Which conditions demonstrate increased incidence of patent ductus arteriosus?
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Girls affected more than boys, genetic defect (down syndrome) predispose to PDA, rubella infection, premature infants
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90. Describe the murmur and location of a PDA murmur.
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Harsh machinery-like murmur over left 2 interspace
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91. What will occur in a child with a patent ductus arteriosus with elevated pulmonary vascular resistance?
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It can cause a reversal of flow and switch from a left to right shunt to a right to left shunt
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92. In older children and adults, what is the relationship between the size of a VSD and the murmur?
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The smaller the size, the smaller the leakage, the louder the sound, the bigger the size,the softer the sound
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93. On examination of a newborn, how does a small VSD present?
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Usually asymptomatic unless large. Not heard until a few days
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94. What is the term used to describe the development over time of pulmonary hypertension in congenital heart disease?
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Eisenmenger syndroem: Pulmonary vascualr resistance and right heart pressures reach systemic levels and a right shunt can become a right to left shunt
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95. In the fetus where is the highest percentage oxygen saturation?
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Umbilical vein
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96. What is the most common congenital cardiac defect as a cause of early post birth presentation of congestive heart failure?
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Tetralogy of fallot
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97. Hypoxemia at birth resulting in pulmonary vascular disease, usually presents first as:
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Cyanosis “blue baby syndrome”. Retracted breathing
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98. If this condition persists it presents later with:
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Clubbing of toes and fingers as well as polyctyhemia
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99. A male child presents to clinic with dysmorphic facies, mental retardation, bleeding and pulmonic stenosis. Your diagnosis is:
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Noonan syndrome
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100. Define Kartagener’s syndrome:
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Autosomal recessive disorder of cilia (ciliary dyskinesia) that cuase a respiratory tract problems and may cause congenital heart defects
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101. You are examining a young female patient who is of short stature , has low set ears, broad chest with wide nipples, and a early systolic ejection click and a systolic ejection murmur. What is your diagnosis?
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Turner's syndrome
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102. What is the chromosomal abnormality associated with this condition?
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XO (only one x chromosome
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103. What heart lesions are often associated with this condition?
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Coarction of the aorta, bicuspid aortic valve (40%)
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104. We are seeing a child in pediatric cardiology with a short, flattened facies, upslanted palpebral fissures and mental retardation. What is your diagnosis?
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Down syndrome (trisomy 21)
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105. What is the most significant risk factor for the development of this condition?
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Maternal age over 40
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106. What are the cardiac conditions most often associated with this condition?
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Endocardial cushion defects (AAD, VSD, AV defect)
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107. A thirty five year old man is in your office with chest pain. He is tall, with long limbs, loose ligaments, arachnodactyly, lens dislocation, and aortic regurgitation. What is your diagnosis?
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Marfans syndrome
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108. What is the term for a clot that arises from the veins, passes usually thru an ASD to lodge arterial circulation?
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Paradoxical emobolism
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109. What congenital syndrome is most commonly associated with endocardial cushion defect (atrioventricular canal defect)?
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Down syndrome
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110. What 2 structures does the patent ductus usually connect and in what location?
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Patent ductus arteriosus connects aorta and pulmonary artery
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111. What condition would you suspect in a child when you hear a systolic murmur best posteriorly between the scapulae?
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Coarctation of the aorta
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113. What would you expect upon blood pressure readings in this child?
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High BP in the upper body, low bp in the lower body
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114. What congenital abnormality has a high incidence of this condition?
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Turner syndrome
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115. What happens to a newborn baby born with severe coarctation of the aorta if the associated PDA closes?
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Asymptomatic
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116. What is the underlying pathology in a 40-70 year old man who presents with symptoms of severe aortic stenosis?
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Aortic stenosis, calcification (due to aging)
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117. Where would you expect to hear the murmur of a VSD?
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Tricuspid are of the left sternal edge
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118. What is the correlation between loudness of a VSD murmur and VSD size?
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Louder=small size
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119. What is the term used for the VSD when a loud murmur is present?
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Rogers murmur
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120. What is the mother’s underlying condition in a baby born with Ebstein’s anomaly?
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Wolf parkinson-white
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121. What agent has been thought to increase the development of
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Ebstein’s?; Development of Ebstein's anomaly is common with women who take lithium
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122. How would you describe the anatomical problem in Ebsteins?
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a) Tricuspid displaced into R ventricles, b) anomalous attachment of leaflets, c) dysplastic valve tissue, d) regurgitation related to wolf parkinson-white
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123. What is the usual early presentation of the severe form of this condition
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a) paroxysmal cyanosis, b) tricuspid regurgitation, c) atrial tachycardia
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124. Why should pregnancy be avoided in a female patient with congenital heart disease with Eisenmenger’s physiology?
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Mothers health is at risk if she has pulmonary vascular disease and pulmonary hypertension. Risk of heart failure and arrhythmia
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125. What is the gender of a child born with Noonan syndrome? What is the associated cardiac abnormality?
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Male, pulmonary valve stenosis
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126. What are the four congenital lesions which can present with cyanosis at birth and are considered cardiac emergencies in a new born?
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Tetralogy of fallot, transposition of great arteries, truncus arteriosus, tricuspid atresia
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127. Which condition listed above is the most common?
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Tetralogy is mort common
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128. Describe the heart shape of truncus arteriosis on X-ray:
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Large heart, increased vascularity, right arch
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129. What is expected on examining an X-ray of a patient with tricuspid atresia?
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Square heart, pulmonary oligenia
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130. Transposition is noted by the rapidity of 5the development of what post birth. They usually have:
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Cyanosis, cardioprotective shunts, loud S2, Right ventricular hypertrophy
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131. Closure of any of PDA, VSD or patent foamen ovale in complete transposition induces
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Cyanosis, death
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132. Transposition x-ray appearance:
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Egg on a side
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133. Where is the connection of the pulmonary veins in total anomalous pulmonary venous return if a baby is presenting 12 hours after birth with cyanosis and tachycardia and no murmur
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Subdiaphragmatic, into portal or hepatic vein. Supracardiac into bronchiocephalic vein or supeiror vena cava. Cariac into cardiac sinus or right atrium. mixed
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134. Describe the heart shape on X-ray of tetrology of Fallot:
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Boot shaped heart
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135. What are the components of Tetrology of Fallot?
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VSD, pulmonary stenosis, RVH, overriding aorta
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136. What is the usual cause behind the development of ventricular fibrillation and death?
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Sudden cardiac death, hypercoagulability
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137. What underlying conditions cause ventricular tachycardia in the absence of structural heart disease?
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Monomorphic VT or idiopathic VT, more common in women, induced by exercise, stress, caffeine, homorne. Long QT, brugada syndrome
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138. The 3 main types of non-structural induced ventricular tachycardia are predominantly what type of traits?
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Polymorphic VT, induced by acute ischemia, myocarditis, changes in QT interval
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139. Three findings that should suggest a possible diagnosis of infective endocarditis:
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Major-postive culture or evidence of endocervical involvment (echo or regurgitation) and minor-predisposition, fever, vascualr phenomenon, immunologic phenomenon, microbia evidence
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140. Which form occurs most commonly is on previously abnormal valves?
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Strep epidermis is most common after insertion of prosthetic valves. Subacute endocarditis
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141. What cardiac abnormality is the most common one to develop endocarditis?
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MVP= mitral valve prolapse
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142. What is the most common presentation of a patient with severe acute endocarditis?
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Fever, chest pain, SOB
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143. Characterize the fever pattern in subacute endocarditis.
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Low grade fever
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144. Endocarditis occurs predominately on left sided valves with one exception:
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Tricuspid valve in drug abusers (S. aureus); Tricuspid valve in drug abusers (S. aureus)
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145. What is the most common organism which causes acute endocarditis?
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S. aureus (acute), S. viridans (subacute)
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146. What is the organism most likely responsible for subacute bacterial endocarditis?
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S. viridans (native or S. epidermidis (prosthetic)
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147. What are 2 major criteria for making a diagnosis of endocarditis?
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Blood culture +, echo ID of valve damage
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148. What is the recommended number of and timing of obtaining blood cultures:
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3 cultures, 1 hour apart
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149. What dermatologic findings can be seen on physical examination in endocaditis?
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Janeway lesions, osler nodes, roth spots, splinter hemorrhage
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150. At what age range does acute rheumatic fever usually present?
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Age 6-15
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151. What are the major criteria for acute rheumatic fever?
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Immune response to group A streptococci. Appear 10 day-6 weeks after an episode of pharyngitis, migratory polyarthrits, pancreatitis, subcutaneous nodules, erythema marginatum and syndenham chorea
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152. Which of the major ARF criteria is the most common?
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Carditis
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153. What are the characteristics of the polyarthritis in acute rheumatic fever?
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In which one large joint after another becomes painful and swollen for a period of days and then subsides spontaneously leaving no residual disability
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154. List at least 2 of the findings on physical exam that indicate acute rheumatic carditis.
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Pericardial friction rubs, weak heart sounds, tachy and arrhythmias
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155. What layers of the heart are involved with rheumatic carditis?
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All 3 layers (pericardium, myocardium and endocardium)
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156. What is the pathologic hallmark of rheumatic carditis?
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Aschoff bodies, also Anitschkow cell
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157. What part of the body is typically spared in erythema marginatum?
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Face is spared
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158. What exam finding develops late, but is characteristic of ARF?
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Sydenhams chorea
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159. What does the onset of Sydenham’s chorea and or mitral stenosis have in common
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occur after latent period
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160. What valve murmurs would you expect in the acute phase of rheumatic fever?
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Mitral regurg/stenosis
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161. What organism is responsible for the development of ARF?
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Group A,beta hemolytic strep pyogenes
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162. What is the current antibiotic regimen in the treatment of ARF?
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Course of penicillin to eradicate S. pyogenes
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163, 164. After an episode of ARF, what valve is the most likely to be significantly damaged long term and what population subset will present with symptoms in the 30-50 age range?
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Mitral valve. People with cardiovascualr disease, arthritis, drug abuse, trauma or skin ulcer, alcoholism or drug abuse, malignancy, use of corticosteroids, diabetes mellitus
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165. Pressure in the LA is higher than LV pressure during
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mitral stenosis
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166. What would be the lifestyle modifications you would suggest to a patient with high risk for the development of atherosclerosis?
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Diet low fat, high fiber, exercise 30 min/day, 3-4 times a week, distress, smoking, alcohol cessation
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167. What drug is administered during an episode of angina?
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Nitroglycerin
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168. side effect of Amiodarone
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pulmonary fibrosis
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169. side effect of Procainamide
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hypotension, pericarditis
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170. side effect of Ace inhibitors
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Dry cough
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171. side effect of Cocaine
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Coronary spasm, MI
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172. side effect of Digitalis
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Heart block
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173. side effect of Nitro
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Hypotension
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174. side effect of B blockers
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Heart block and CHF, AV block
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175. side effect of Daunorubicin
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Cardiomyopathy
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176. side effect of Methyl dopa
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hypotension
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