Patho 2 Unit 1

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  1. How does coronary artery disease (CAD; atherosclerosis of the coronary a.) present itself clinically?
    - Angina pectoris (chest pain)

    - Chronic ischemic heart disease w/ CHF

    - Acute myocardial infarction (MI)

    - Sudden cardiac death
  2. What is the underlying mechanism of coronary a. disease?
    Myocardial ischemia
  3. How do atherosclerotic lesions cause acute coronary syndromes?
    1) Fissuring of plague w/ clotting

    2) Plague ruptures w/ emobolization

    3) Results in thromboemboli
  4. What results from an imbalance between myocardial oxygen demand and myocardial bloody supply?
    Ischemic heart disease
  5. How does coronary occlusion affect myocardial cells?
    • @ 10 sec: become hypoxic from inadequate oxygen
    • @ 10 mins: lose ability to contract
    • @ 20 min: necrosis begins
  6. What are 4 conditions that increase oxygen demand to the heart?
    - High systolic BP

    - Increased ventricular volume

    - Increased thickness of the myocardium

    - Increased HR
  7. Healthy coronary a. are able to _____ to (increase/decrease) the flow of oxygenated blood to the _____.
    Healthy coronary a. are able to dilate to increase the flow of oxygenated blood to the myocardium.
  8. Narrowing the coronary a. by ___% impairs the flow enough to affect the cell during exertion.
    Narrowing the coronary a. by 50% impairs the flow enough to affect the cell during exertion.
  9. What is angina pectoris?
    Chest pain caused by myocardial ischemia
  10. What causes the actual pain during angina pectoris?
    Buildup of lactic acid

    Abnormal stretching of the ischemic m.
  11. What disorders are associate with angina pectoris?

    Profuse sweating

  12. What are the two types of angina?
    - Stable

    - Unstable
  13. What causes stable angina? Is it predictable?
    Luminal narrowing and hardening of the arterial walls (atherosclerosis)

  14. What causes unstable angina? Is it predictable?
    Combination of vasospasm and atherosclerotic lesions

    Unpredictable; often occur at rest
  15. What are some factors that affect the clinical presentation of ischemic disease?


    Type (Fibrolipid plague more likely to rupture)

    Speed @ which it develops

    Extent of disease in other branches

    Other diseases that increase oxygen demand
  16. What factors can drugs target to help with myocardial ischemia?



    L. ventricular volume

    The goal is to reduce oxygen consumption of the myocardium.
  17. What is MI?
    Myocardial infarction is prolonged ischemia (>20 min) which leads to irreversible hypoxic injury, cellular death, and tissue necrosis.
  18. Where does necrosis begin with MI?
    Necrosis begins in the subendocardial region and extends in the next 3-6 hrs.
  19. Can ischemic tissue around necrosis be healed?
    Ischemic tissue around the area of necrosis may or may not be irreversibly damaged at the outset.
  20. MI leads to glycolysis (use of glycogen stores for energy) which then causes what?
    Accumulation of hydrogen ions and lactic acid, causing acidosis and eventual heart failure
  21. Oxygen deprivation that occurs with MI also causes what?
    Electrolyte imbalance which excites the myocardium leading to dysrhythmias (90% of individuals w/ MI).
  22. What functional changes occur as a result of MI?
    Decreased contractility, SV, and ejection fraction

    Increased end-systolic volume

    SA node malfunction
  23. List the 4 main coronary a.
    - RCA

    - LCA

    - LCX

    - LAD
  24. Where does occlusion of the RCA cause infarction?
    Poterior infarction

    30% of all cases
  25. Where does occlusion of the LCX cause infarction?
    Lateral infarction

    20% of all cases
  26. Where does the occlusion of the LAD cause infarction?
    Anterior infarction (widowmaker)

    50% of all cases
  27. Where does occlusion of the l. coronary a. cause infarction?
    Anterolateral infarction

    Massive MI
  28. What affects the ability to repair an infarct? Is there inflammation?
    The site and size of the lesion

    MI causes a sever inflammatory reaction
  29. What are the problems with collagen repair of infarcts?
    Collagen matrix that is initially deposited is weak and may be stressed within 10-14 days post-infarct

    After 6 weeks, necrotic area is replaced by scar tissue, which cannot contract and relax (non compliant) like healthy heart tissue
  30. When do infarcts typically rupture?
    May occur anytime within the first 2 weeks (usually between days 4-7)
  31. What percentage of MI cases lead to rupture? What does rupture often cause?
    13% of MI cases lead to rupture

    Rupture of an infarct often leads to fatal cardiac tamponade (hemopericardium)
  32. What are some clinical manifestations of MI?
    Sudden chest pain



    Cardiovascular changes

    Increased creatine kinase and lactic dehydrogenase
  33. When are patients at the highest risk for sudden death?
    Within the first 24 hours after onset.
  34. What are some treatments of MI?
    Aspirin (inhibits platelets)

    Thrombolytic agents

    Supplemental oxygen

    Pain relief

    Bed rest w/ gradual return to activities

    Dietary measures
  35. What is the most common complication associate with MI?
    Cardiac arrythmia
  36. What percentage of MI cases result in sudden coronary death?
  37. Describe the normal conduction system of the heart
    SA Node - atria - AV node - AV bundle - R & L bundle branches - purkinje fibers
  38. What does it mean that cardiac myocytes are autorhythmic?
    They depolarize at regular time intervals without external stimulation

    Cardiac m. is an excitable tissue
  39. What is a sinus rhythm?
    A normal cardiac rhythm, originates at SA node
  40. _____ can be caused by abnormal rate or the abnormal conduction of impulses.
    Arrythmias can be caused by abnormal rate or conduction.
  41. What does the seriousness of an arrythmia depend on?
    Its hemodynamic consequences (how much it affects blood flow)
  42. Valvular damage can be either congenital or ____.
    Valvular damage can be either congenital or acquired.
  43. What can cause acquired valvular dysfunction?




  44. Abnormal valves are more susceptible to ____.
    Abnormal valves are more susceptible to infection,
  45. What are 3 hemodynamic burdens that occur with abnormal valves?


  46. What is valvular stenosis?
    Valve orifice is constricted and narrowed, impeding the forward flow of blood
  47. What do pressure increases in a chamber (like with valvular stenosis) cause?
    Myocardial hypertophy - cardiomegaly
  48. What are the consequences of valvular dysfunction?
    Changes in pre/afterload

    Enlarged chamber

    Decreased contractility and ejection fraction

    Increased diastolic pressure

    Ventricular failure from overworking
  49. How does one get rheumatic heart disease?
    It is immunologically mediated.

    3% of strep (sequella of group A) leads to acute rheumatic fever; 10% of ARF cases lead to rheumatic heart disease
  50. Rheumatic heart disease happens in ____ episodes.
    Rheumatic heart disease happens in recurrent episodes.
  51. What is rheumatic heart disease?
    Acute carditis +

    Chronic valvular deformities
  52. What are some examples of ventricular escape beats?
    Atrial standstill

    AV block
  53. Does calcific aortic stenosis occur gradually or acutely?
    Gradually, often age-related
  54. What is MV prolapse?
    Cusps of the MV "billow upward" or prolapse into the atrium during systole

    Cusps become thickened

    Often asymptomatic

    Patients may request antibiotics before dental work
  55. Elongated chordae tedinae are often seen with what?
    MV prolapse
  56. MV prolapse has a high incidence in whom?
    Young women
  57. What is infective (bacterial) endocarditis?
    Masses of thrombotic debris and organisms infect the aortic and mitral valves
  58. Why is infective endocarditis hard to treat?
    Because of the avascular nature of valves, antibiotics can't reach
  59. What are the 2 forms of bacterial endocarditis?
    - Acute: organisms with high virulence

    - Subacute: organisms of lower virulence
  60. What is virulence?
    The strength, potency, or danger of a pathogen
  61. What are some conditions that increase the risk of infective endocarditis?
    Preexisting conditions

    Prosthetic valves

    IV drug abuse and indwelling catheters

    Hemodynamic trauma

    Chronic valve diseases
  62. Describe the etiology of infective endocarditis
    Infection occurs when organisms are implanted on the endocardial surface during episodes of bacteremia
  63. Describe the steps of the pathogenesis of endocarditis
    Bacteria erode endothelium

    Site of injury covered with fibrin/platelet clot

    Inflammatory cells and bacteria invade the thrombus

    Bacteria invade valves and destroy connective tissue

    Inflammation heals by fibrosis causing deformity and vegetations
  64. What are some clinical features of bacterial endocarditis?

    Cardiac murmurs (most characteristic)

    Systemic emboli

    Renal lesions

    Negative blood cultures

    May result in CHF and valvular regurgiation/stenosis


    (was almost always fatal before antibiotics)
  65. What is myocarditis and what are the different etiologies?
    Heart wall inflammation

    Viruses (most common)



    Cardiac allograft rejection

    Drug hypersensitivity
  66. What are the 2 types of pericarditis?
    - Primary: uncommon, usually infectious

    - Secondary: due to MI, cardiac surgery, radiation
  67. What are the possible outcomes of pericarditis?

    Resolution without complication

    progress to chronic fibrosis
  68. What are cardiomyopathies and what is the etiology?
    Heart diseases resulting from a primary abnormality in the myocardium

    Idiopathic etiology
  69. What are the 3 major froups of cardiomyopathies?


  70. What is dilated cardiomyopathy?
    Congestive cardiomyopathy

    Progressive dilation of the chambers leading to weak contractions

    Associated with alcohol abuse, toxic insult, or viral
  71. What is hypertrophic cardiomyopathy?
    Thickened walls leading to abnormal ventricular diastolic filling

    Ineffective ejection because EDV is so small
  72. What is restrictive cardiomyopathy?
    Decrease in ventricular compliance

    Inelastic ventricle leading to EDV and SV
  73. What can all 3 cardiomyopathies lead to?
Card Set:
Patho 2 Unit 1
2012-04-10 05:58:22

Unit 1 (Quiz 1): Alts. of Cardiovascular Function pt. 2 I didn't make cards on ECGs and congenital heart defects
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