patho quiz 4 heart disease.txt

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patho quiz 4 heart disease.txt
2011-03-25 10:24:28
patho quiz heart disease

patho quiz 4 heart disease
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  1. congestive heart failure.
    inability of the heart to eject the blood delivered to it by the venous system. Congestive heart failure may involve any of the four chambers.
  2. What is Backward failure
    :results from increased congestion of venous circulation
  3. What is forward failure?
    results from inadequate cardiac output
  4. What are the four common causes of left side congestive failure? How do these causes contribute to left side failure?
    • Left side failure is characterized by the inability to pump oxygenated blood to the systemic circulation. Common causes include:
    • o Systemic hypertension
    • o Mitral or aortic valve disease
    • o Ischemic heart disease
    • o Primary disease of the myocardium
  5. What are the two common causes of right side congestive heart failure? How do these causes contribute to right side failure?
    • Right side failure is characterized by the inability to effectively accept blood from the venous circulation or to deliver blood to the pulmonary circulation. Common causes include:
    • o Left ventricle failure  results in failure of heart to accept blood from pulmonary circulation
    • o Pulmonary thromboembolism  blockage of the pulmonary artery or its branches
  6. What is Concentric hypertrophy-
    muscle wall increases in thickness without increase in chamber size  adaptation to increase in pressure load (hypertension, valvular stenosis [stuck valves])
  7. What is Eccentric hypertrophy-
    muscle wall increases in thickness and chamber size- adaptation to increase in volume load (valvular regurgitation [leaky valve] or abnormal shunts)
  8. What are common clinical features of congestive heart failure?
    • Dyspnea (breathlessness)  left side pulmonary edema and congestion
    • Soft tissue edema  right side
    • Muscle fatigue (not enough oxygen)
    • Enlarged heart (hypertrophy from trying to pump too much)
    • Irregular heart beat and rhythm (arrythmia)
    • Lung rales (characteristic sounds from lung edema)
  9. What is the definition of ischemic heart disease?
    Ischemic heart disease refers to a group of related syndromes resulting from myocardial ischemia- an imbalance between cardiac blood supply (perfusion) and myocardial oxygen demand. In most cases, IHD is caused by a narrowing of the coronary arteries by atherosclerosis. This disease is also commonly termed coronary heart disease or coronary artery disease.
  10. What four clinical syndromes are associated with ischemic heart disease?
    • Angina pectoris (chest pain)
    • Acute myocardial infarction
    • Chronic IHD with congestive heart failure
    • Sudden cardiac death
  11. 7. What are the two common causes for acute changes in vascular lumen diameter?
    • Acute plaque changes can result in IHD
    • Coronary artery vasoplasm/vasoconstriction can result in IHD
  12. What is the mechanism of typical angina pectoris?
    blood flow to cardiac muscle cannot keep pace with increased demand for cardiac function
  13. What causes typical angina?
    increased exertion and sress
  14. What is the cause of variant angina?
    coronary artery spasm
  15. What are the symptoms of varient angina?
    occurs at rest
  16. What is the mechanism of crescendo angina?
    progressive narrowing of coronary arteries that may precede MI
  17. What are the symptoms of crescendo angina?
    Increased frequency of chest pain and more intense attacks
  18. What is Myocardial infarction-
    development of an area of myocardial necrosis caused by local ischemia
  19. WHat is the Pathogenesis of MI
    • Most common cause is coronary artery thrombosis
    • Necrosis begins within 20-30 minutes of occlusion
    • Area of necrosis (infarction) reaches full size within 3-6 hours
    • Location and size of infarct is dependent on the site of the occlusion (chich coronary artery and how distal)
  20. What are the Morphological Changes of MI
    • First 30 minutes: no gross and microscopic change, reversible
    • 30 min-4 hour: no gross and microscopic change, irreversible process begins
    • 4hr: a sequential process of cell death, hemorrhage, edema, coagulation, fibrosis
    • It takes > 2 months to complete the scarring
  21. What are the Clinical features of MI
    • Severe crushing substernal chest pain. In 10-15% of patients the MI is preceded by unstable angina not relieved by nitroglycerin
    • Rapid, weak pulse and shortness of breath. This is associated with decreased blood pumping capacity
  22. How do CK levels vary
    elevated within 2-4 hrs after an MI and peak at 24-48 hours after. It returns to normal 72 hrs after
  23. How do Troponin levels vary
    elevated within 2-4 hrs after an MI and peak at 48 hours. They remain elevated for 4-7 days after.
  24. What are Complications of MI
    • Cardiogenic shock and pulmonary congestion and edema due to impaired left ventricle function
    • Arrythmias
    • Myocardial rupture can occur 3-7 days after infarction due to heart wall weakening
    • Progression to chronic ischemic heart disease associated with congestive heart failure
  25. Understand the causes of hypertensive heart disease.
    Hypertensive heart disease is characterized by left ventricular hypertrophy (thickening of the muscle wall with no increase in chamber volume. It is an adaptive change to permit the increased pumping pressure the heart is required to generate in response to systemic vascular hypertension
  26. What are the Characteristics of hypertensive heart disease
    • Hypertrophoc myocardium is poorly perfused by capillaries and is in a state of chronic ischemia. This stimulated mild inflammation and deposition of fibrous material that impairs contraction and relaxation and can ultimately lead to heart failure.
    • Chronic ischemic state also sensitizes tissue to ischemic damage by cardiac infarction
    • Hypertension increases the risk of atherosclerosis
    • Combination leads to increased incidence of MI and increased severeity of ischemic damage by MI
  27. What is Stenosis-
    • the failure of a valve to open completely, thereby obstructing forward flow
    • It is typically the consequence of valve calcification or scarring
    • It demands additional pumping pressure by the heart. This leads to concentric hypertrophy of the heart
  28. What is Regurgitation-
    • the failure of a valve to close completely, thereby permitting reverse blood flow
    • It is typically the consequence of valve destruction or distortion of the supporting structures
    • It demands additional pumping volume by the heart. This leads to eccentric hypertrophy of the heart
  29. What is Rheumatic fever
    (a type of valvular heart disease)
  30. What is the Pathogenesis of rheumatic fever
    • Hypersensitive immune reaction to group A strep
    • Antibodies against group A strep cross-react with normal cellular proteins causing ADCC and inflammatory damage
  31. What is Chronic rheumatic heart disease 
    • irreversibly deformity of one or more cardiac valves
    • Leads to stenosis (more common) or incompetence
    • Pulmonary congestion
    • Hypertrophy of right ventricle and atrium
    • Concentric hypertrophy of left atrium
    • Chronic aortic valve stenosis
    • Increased pressure load on left ventricle
    • Concentric hypertrophy
    • Left ventricle failure
  32. What are clinical features of rhumatic fever
    • Acute rheumatic carditis  inflammatory changes in all 3 layers of the heart
    • " Aschoff bodies (heart muscle)
    • " Fribrinous pericarditis (pericardium)
    • " Endocardium inflammation
    • " Mitral and aortic valves
    • " Minor; does not contribute to valvular dysfunction
  33. Understand the characteristics of mitral valve prolapse. Connective tissue structural protein defects
    Valve is characteriscally Floppy, Incompetent
  34. What are the characteristics of DCM?
    progressive hypertrophy, dilation, contractile dysfunction
  35. What are the characteristics of HCM?
    myocardial hypertrophy, abnormal diastolic filling, powerful contractions
  36. What are the charicteristics of restrictive?
    decrease in ventricular compliance--> impaired ventricular filling
  37. What causes DCM?
    viral infection, alcohol abuse, toxic insult, inheretid mutations
  38. What causes HCM?
    genetic mutations
  39. What is the outcome of DCM?
    heart is enlarged and flabby, thrombi and emboli develop, ineffective contraction, leads to CHF, need transplant
  40. What is the outcome of HCM?
    Increased pulmonary venous pressure, exertional dyspnea, ventricular arrythmia
  41. What is the outcome of restrictive CM?
    CHF, pulmonary congestion, right side failure