Patho Exam 3 - Cardiovascular

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  1. how does gravity play a role in DVT?
    gravity pulls blood down
  2. what are some risk factors for DVT?
    immobility, age, L heart failure, venous stasis, trauma, IV meds, vein wall damage, pregnancy, oral contraceptives, malignancy, genetic coagulopathies, and hypercoagulation
  3. what are venous stasis ulcers?
    cell death and necrosis - no O2 and cell dies
  4. what can chronic venous insufficiency cause?
    hyperpigmentation of lower extremities
  5. what happens with varicose veins?
    blood pools, valves don't shut
  6. what could be some causes/risk factors for orthostatic hypotension?
    anatomic variation with aging, antihypertensive and antidepressant therapy, fluid volume depletion, and venous pooling
  7. what is orthostatic or postural hypotension?
    decrease in both systolic and diastolic arterial BP on standing from a reclining position
  8. what is malignant hypertension an adverse reaction to?
  9. what is malignant hypertension?
    rapid progression in which diastolic is > 140
  10. what are some cerebrovascular complications of complicated hypertension?
    transient ischemic attack (TIA), CVA, cerebral thrombosis, aneurysm, and hemorrhage
  11. what are some cardiovascular complications of complicated hypertension?
    left ventricular hypertrophy, angina, CHF, CAD, MI, sudden death
  12. what are some renal complications of complicated hypertension?
    parenchymal damage, renal arteriosclerosis, renal insufficiency and failure
  13. what is complicated HTN?
    primary and secondary hypertension, damages walls of blood vessel
  14. what are some neurologic disorders that cause secondary hypertension?
    lesions requiring higher systolic BP to maintain perfusion
  15. what are some vascular diseases that cause secondary hypertension?
  16. what are some endocrine disorders that cause secondary hypertension?
    acromegaly, thyroid disturbances, adrenal disorders - estrogen, testosterone, and aldosterone
  17. what are renal disorders that cause secondary hypertension?
    renovascular disease, renin-producing tumors, renal failure
  18. what causes secondary hypertension?
    systemic disease that increases peripheral resistance in blood vessel or cardiac output
  19. what percentage of hypertensive cases are primary?
  20. what is likely responsible for primary hypertension?
    combination of genetic and environmental factors mediated by host of neurohumoral effects
  21. is there a specific cause identified for primary hypertension?
  22. what is primary hypertension also called?
    essential or idiopathic (unknown)
  23. when is hypertension diagnosed?
    2 or more diastolic BP's on 2 or more consecutive visits of 90 or more back-to-back and average of 2 or more visits is > 140 systolic
  24. what are two risk factors for Raynaud disease?
    women who play piano and type of the computer a lot cause fingers need more O2 to function
  25. what is Raynaud phenomenon and Raynaud disease characterized by?
    attacks of vasospasm in small arteries and arterioles of fingers and (less commonly) the toes
  26. is Raynaud phenomenon and Raynaud disease more common in men or women?
  27. what is a risk factors for Buerger's disease/thromboangiitis obliterans?
    heavy smoking
  28. what is another name for thromboangiitis obliterans?
    Buergers disease
  29. is thromboangiitis obliterans more common is men or women?
  30. what is PAD?
    atherosclerotic disease that decreases perfusion to the limbs, especially lower extremities
  31. name three different types of emboli:
    • fat
    • air
    • foreign matter - IV catheter (don't retract IV needle and then reinsert cause slices off pieces of catheter)
  32. what is an embolus?
    obstruction of vessel by an embolus or a bolus of matter that is circulating in bloodstream
  33. what is a thrombus?
    clot that remains attached to vessel wall
  34. describe the 3 different types of an aneurysm:
    • sacular: looks like a berry grown on one side of arterial wall
    • fusiform: all around arterial wall
    • pseudoaneurysm: one layer of artery wall
  35. what is a true aneurysm?
    weakening of vessel wall that involves three layers
  36. what is an aneurysm?
    localized dilation or outpouching of vessel wall or cardiac chamber
  37. are aneurysms venous or artery disorders?
  38. what symptoms do you see in someone with superior vena cava syndrome?
    round head, upper body edema, JVD
  39. what type of cell is injured during atherosclerosis?
    endothelial cells
  40. what is atherogenesis?
    begins with injury to endothelial cells of arteries that causes inflammation
  41. what type of disease is atherosclerosis?
    inflammatory disease
  42. what is atherosclerosis?
    it is a form of arteriosclerosis and is thickening caused by hardening of soft deposits of intra-arterial fat and fibrin that reduce lumen size
  43. what is the only difference between unstable ischemia and an MI?
    • -Unstable ischemia does not have enzymes
    • -MI does have enzymes
  44. why does someone get an MI?
    coronary arteries cannot compensate for lack of O2
  45. do you have positive or negative enzymes with stable and unstable ischemia/angina?
    negative enzymes for both
  46. what happens to an EKG in stable and unstable ischemia/angina?
    STABLE: normal EKG

    UNSTABLE: normal transient ST depression and T wave inversion
  47. what is the difference with NTG (nitroglycerine) with stable and unstable angina/ischemia?
    STABLE: NTG is effective

    UNSTABLE: NTG is not effective
  48. when does angina occur in stable and unstable ischemia?
    STABLE: on exertion, vessels cant dilate in response to demand

    UNSTABLE: occurs at rest
  49. what is the difference with ischemia between stable and unstable angina?
    STABLE: temporary ischemia

    UNSTABELE: advanced but irreversible ischemia
  50. what are the two different types of ischemia?
    stable and unstable
  51. 1. Can you have angina and not have ischemia?

    2. Can you have ischemia and not have angina?
    1. No - if you have angina you always have ischemia

    2. Yes
  52. what is the most common cause of myocardial ischemia and infarction?
  53. list the main symptoms that go with PAD and CAD that help distinguish the two:
    • PAD: increased BP
    • CAD: increased BP AND chest pain
  54. when adiponectin is decreased, what are people at risk for?
    cardiovascular risk
  55. what is the purpose of adiponectin in CAD?
    antiatherogenic hormone - tries to protect tissue
  56. In CAD, which of these two hormones is the good and bad hormone?
    Adipokines is the bad hormone

    Adiponectin is the good hormone
  57. in obese people who have CAD, which of these two hormones are increased or decreased?
    Adipokines are increased

    Adiponectin is decreased
  58. in CAD, where does adipokines come from?
    adipose tissue
  59. what are the two hormones involved with CAD?
    adiponectin and adipokines
  60. when you have ischemia or a clot in CAD, what eventually happens?
    infarction of death of deprived myocardial cells/tissues
  61. what causes diminished blood flow to the myocardium in CAD?
    persistent ischemia (atherosclerosis), or complete occlusion by a clot
  62. what happens to blood flow in CAD?
    diminishes to the myocardium
  63. if you have PAD, are you guaranteed to have CAD?
  64. whats the difference between CAD and PAD?
    PAD is in the periphery and CAD is in the heart
  65. with atherosclerosis, what develops if systemic vascular resistance elevates?
  66. what type of MI is happening with marked elevation in ST segments on EKG, non-stemi or stemi?
  67. what type of MI does stemi go with?
    transmural MI
  68. what type of MI does non-stemi go with?
    subendocardial MI
  69. what type of MI does someone have if there is no ST segment, there's T depression and no Q wave, non-stemi or stemi?
  70. what indicates severity in an MI?
    CPK-MB, LDH, SGOT, troponins I and T indicate severity
  71. what ultimately results in aortic stenosis?
    left ventricular failure
  72. what symptoms occur with aortic stenosis?
    dyspnea and angina
  73. what can cause aortic stenosis?
    rheumatic heart disease, congenital malformation and calcification
  74. valve leaflets or cusps fail to close completely; blood flow continues when valve should be closed, what is this?
    valvular regurgitation/insufficiency/incompetence
  75. what is it when the valvular orifice is constricted or narrowed?
    valvular stenosis
  76. the myocardium is infiltrated with amyloid, hemosiderin or glycogen deposits and the AV valve is incompetent, what is it?
    restrictive cardiomyopathy
  77. why cant the left ventricle squeeze good in restrictive cardiomyopathy?
    it is hardened and stiff
  78. why is there decreased chamber volume in hypertrophic cardiomyopathy?
    there is not enough room for blood in left ventricle
  79. there is hypertropthy of the left ventricle and interventricular septum, chamber volume is normal or decreased and mitral valve is incompetent, what is it?
    hypertrophic cardiomyopathy
  80. why do you hear a murmur in dilated cardiomyopathy?
    cause excess fluid regurgitates into atrium
  81. what can cause dilated cardiomyopathy?
    alcoholism, pregnancy, and infection
  82. left chamber volume and size increases and theres mitral valve incompetence, what is it?
    dilated cardiomyopathy
  83. what are 3 complications of cardiomyopathies?
    ischemic disorders, HTN, and valvular dysfunction
  84. what are cardiomyopathies?
    diverse group of diseases that affect myocardium
  85. what can happen to the sac in cardiac tamponade?
  86. why is it easier for fluid to accumulate around right atrium and right ventricle in cardiac tamponade?
    decreased pressure
  87. in cardiac tamponade, what are the first structures of the heart to be affected?
    right atrium and right ventricle where diastolic pressure are normally lowest
  88. what is pressure from fluid that causes cardiac compression? (squeezing in on heart)
    cardiac tamponade
  89. what can cause pericarditis, but not all the time?
    inflammation of sac
  90. it is a connective tissue disease and there's pericardial effusion... what is it?
  91. can radiation cause pericarditis?
  92. what is pericarditis commonly seen with?
  93. do we know what causes pericarditis?
    no (idiopathic)
  94. what do you hear in pericarditis?
    friction rub
  95. in pericarditis, what happens in the pericardial cavity?
    fluid accumulates
  96. what are 2 symptoms of mitral stenosis?
    orthopnea and pulmonary HTN
  97. what fails in mitral stenosis?
    right ventricular failure
  98. what hypertrophies in the heart in mitral stenosis?
    left atrium and right ventricle
  99. in tricuspid regurgitation, what causes right sided heart failure?
    pulmonary HTN
  100. what causes mitral regurgitation?
    rheumatic heart disease, mitral valve prolapse, and CAD which causes LHF
  101. what are symptoms in mitral regurgitation?
    pulmonary HTN, dyspnea
  102. what are some symptoms/conditions seen in high-output failure?
    anemia, septicemia causes systemic vasodilation and fever, hyperthyroidism
  103. what is inability of the heart to adequately supply blood with nutrients, despite adequate blood and normal myocardial activity?
    high-output failure
  104. what are some symptoms seen in right sided heart failure?
    GI disorders, JVD, dependent edema, and ascites
  105. what happens in right sided heart failure (the process)?
    L failure, decreased RV emptying, increased volume and pressure in RA, increased volume in distensible organs, causing edema and serous effusion
  106. what are symptoms seen in left sided heart failure?
    orthopnea, decreased cardiac output and urinary output, S3 gallop, and blood-tinged sputum
  107. why do you get pulmonary edema with left sided heart failure?
    fluid is transferred from capillaries to alveoli causing pulmonary edema
  108. what happens in left sided heart failure?
    LV fails, increased pressure and volume in LA
  109. what symptoms do you see with infective endocarditis?
    fever, murmur, petechial lesions of skin and mucosa, bacteremia, Osler's nodes
  110. what happens to valves in infective endocarditis?
    blood-borne microbes colonize damaged valve and vegetate
  111. in infective endocarditis, what leads to thrombotic endocarditis?
    prior damage to valves
  112. what causes infective endocarditis?
    staphylococcus aureus, viruses, and fungi
  113. for rheumatic heart disease, what diagnostic blood test is used?
    ant-streptolysi o titer (ASO)
  114. what question do you ask someone if you suspect rheumatic heart disease?
    have you had a Hx of strep throat
  115. what effects/causes does rheumatic heart disease have on the heart?
    causes carditis of all 3 layers of the heart wall, endocaridal inflammation and vegetative growth on valves
  116. what causes rheumatic heart disease?
    sequel to pharyngeal infection with group A beta-hemolytic streptococci (strep throat)
  117. in right sided heart failure do you have symptoms in the body or lungs?
  118. in left sided heart failure do you have symptoms in the body or lungs?
  119. is tricuspid regurgitation left or right sided heart failure?
  120. is mitral regurgitation left or right sided heart failure?
  121. is mitral stenosis left or right sided heart failure?
  122. what are some symptoms of tricuspid regurgitation?
    peripheral edema and ascites
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Patho Exam 3 - Cardiovascular
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