Patho- Ch 18

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hjones18
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151038
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Patho- Ch 18
Updated:
2012-04-30 00:27:40
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Cardiovascular disorders
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patho ch 18
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  1. Define Coronary Heart Disease
    Any disease in which there is narrowing of the coronary arteries
  2. Define Arteriosclerosis
    General term for arterial changes

    Degenerative changes in small arteries and arterioles
  3. What is the pathology for Arteriosclersis
    Thickening, loss of elasticity and calcification of the arterial walls
  4. Eventually the lumen narrows and results in ischemia and necrosis to tissues
  5. What is Atherosclerosis
    Form of arteriosclerosis that has Atheromas


    The thickening and hardening of the arteries are caused by deposits of lipds, cells, fibrin, cellular debris and often attached to thrombus (hardens over time)
  6. Effects of Atherosclerosis
    Decrease perfusion to organs

    Increase platelet adhesion

    Promote the dev. of an aneurysm
  7. Endothelial injury begins formation of Atheromas which results in elevated levels of what
    C-reactive proteins
  8. What adheres to tunica intima and causes an atheroma
    Leukocytes (lymphocyte, monocyte-macs) and platelets
  9. Define Fatty streaks
    Earliest atheroscerotic lesions

    • Common in children during 1st year
    • Thin flat yello discolorations in tunica intima of arteries
    • Consist of lipid filled smooth muscle cells or macs
  10. Describe plaque
    Characteristic lesion of advancing atherosclerosis
  11. Plaque is thought to develop from what
    Fatty streaks- cellular proliferation, lipid accumulation and ct formation occur
  12. Plaque protudes into _________ of an artery
    Lumen


    Lipids continue to lay down pushing the endothelial cells of the tunica intima to the center
  13. The mass of plaque also invades the _________
    tunica media
  14. what is hyperlipidemia
    blood levels that are in LDL (low density lipoproteins)

    High cholesterol content


    BAD GUYS
  15. elevated blood cholesterol levels cause monocytes to attach to the endothelium and they migrate into the subendothelial spaces and become ______
    macs
  16. Macs release _____ that alter the LDL
    free radicals (compounds with unpaired electrons)
  17. Altered LDL is ________ to the endothelium
    • Toxic
    • This destroys the enothelium and exposes subendothelial tissues
    • Macs phagocytize altered LDL
    • Macs die and release lipds into plaque
  18. After macs release lipds into plaque a ____ _____ forms
    fibrous scar

    • causes loss of elasticity
    • weakens vessel
  19. Atheromas calcify which may lead to dev. of an ____
    aneurysm
  20. How is a thrombus formed
    Platelets athere to rough damaged surface of arterial wall
  21. Platelets release ______
    Prostaglandin
  22. Prostaglandin causes _____ and ______
    inflammation and vasospasm


    This promotes platelet adhesion forming a thrombus.
  23. Describe total occlusion
    A lesion that progresses and occludes areterial opening= results in thrombus!
  24. Where do total occlusions typically form
    Large arteries- aorta, coronary, carotid and iliac
  25. What is a bifurcation
    curves where arteries taper
  26. Turbulant blood flow in bifurcation may lead to dev. of _____
    atheroma
  27. 2 consequeces of atheromas
    • transient ischemic attacks
    • cerebrovascular accident- CVA/stroke
  28. what is myocardial ischemia
    Narrowing of blood vessel that causes the myocardium to become ischemic
  29. Myocardial ischemia has _____ periods of insufficient oxygen
    intermittent
  30. Myocardial ischemia causes
    • cardiac muscles cells do not recieve sufficient O2
    • Cells remain alive but can not function normally
  31. Myocardial Infarction/MI =
    Heart attack
  32. MI causes ____ of cardiac muscles cells
    Death
  33. MI has ____ ischemia
    • Persistent
    • more than 20 mins=irreversible cell death!
  34. Compete occlusion of coronary artery will cause ____
    MI
  35. What are the Risk factors of CAD
    • Hyperlipidemia
    • Hypertension
    • Smoking
    • Diabetes
    • Genetic predisposition
    • Gender
    • Obesity
    • Sedentary lifesyle
  36. Hyperlipidemia
    • Strong link between CAD and elevated plasma lipoproteins
    • modifiable risk factor
    • causes atherosclerosis
  37. LDL is
    Low Density Lipoprotein/High cholesterol content

    Less than 180 mg/dl
  38. HDL is
    Low cholesterol content

    Greater than 40 mg/dl
  39. Total cholesterol
    150-250
  40. Triglycerides
    75-160 mg/dl
  41. Hypertention is a _____ risk factor
    Modifiable
  42. Hypertension is _____ blood pressure
    elevated
  43. Smoking causes
    Increase HR

    Increase BP

    Promotes platelet adhesion

    Modifiable risk factor
  44. Myocardial Ischemia is an _____ in O2 demand and _____in O2 supply
    Increase, decrease
  45. Myocardial Ischemia may result from
    Myocardial hypertrophy in which the heard has outgrown its blood supply
  46. Signs of myocardial ischemia
    • angina pectoris (transient)
    • substernal chest discomfort
  47. Pain may radiate to
    neck, left arm and left shoulder (Derived from common nerve pathways)
  48. Precipitating factors in angina attacks
    • running upstairs
    • getting angry
    • resp inf with fever
    • cold weather
    • eating a large meal
  49. what are 3 types of angina
    • stable
    • variant
    • unstable
  50. Describe stable angina
    • Predictable- increase physical activity
    • rest usually helps
  51. Describe Variant Angina
    • Caused by vasospasms of coronary arteries
    • usually occurs at rest or during sleep
  52. Describe unstable angina
    • Most serious form
    • occur at rest
    • prolonged pain
    • longer than 20 mins
    • could result in break in an atheroma
  53. Diagnostic Tests
    • ECG/EKG
    • Exercise stress test
    • Thallium scan
    • Coronary angiography
  54. Treatment
    • Decrease oxygen demand
    • eliminate predisposing factors
    • stop activity
    • avoid stress
    • rest
    • nitroglycerin
  55. Nitroglycerin is _____
    • vasodialator
    • decreases peripheral resistance
    • decrease BP
  56. Angina is a ______
    WARNING of a possible MI
  57. Etiology of MI
    • Atherosclerosis
    • Coronary Thrombosis
  58. Most infactions are _____
    Transmural
  59. An embolus is
    part of a thrombus that breaks off-results in occlusion
  60. most infarcations involve _____ ventricle
    LEFT (systemic circulation)
  61. Pathology of MI
    • Cell injury
    • Cells can withstand ischemia for 20 mins before cell death
    • Cell death
    • causes release of intracellular enzymes through damaged cell membranes
    • Lymphatics pick up enzymes and transports to blood stream
  62. Enzymes can be detected with _____ tests
    serologic
  63. Functional changes in an MI
    • Decrease cardiac contractility
    • Decrease stroke volume
    • Decrease in Cardiac output
  64. Signs of classic MI
    • Severe chest pain
    • substernal pain
    • silent myocardial infarction
    • nausea
    • diaphoresis (sweating)
  65. Classic signs of MI VItal Signs
    • Blood Pressure- Hypotension
    • Pulse- Rapid and Weak
    • Low grade fever
  66. 3 cardiac enzymes
    • CK-MB
    • LDH
    • AST
  67. Blood tests will be _____ for enzyme levels
    elevated
  68. Which is the most specific enzyme for MI
    CK-MB
  69. _____ is the best marker for myocardial injury
    Troponin
  70. Blood tests for MI
    • CBC- leukocytosis
    • C-reactive protein-elevated
    • ESR-elevated
  71. Other diagnostic tests
    • Arterial blood gases (if shock is pronounced)
    • Serum electrolytes (pot and sod levels are elevated)
  72. Complications
    • Cardia Arrhythmias (most common)
    • palpitations
    • tachycardia
    • bradycardia
    • skipped heartbeats

    Cardogenic shock (if left vent is great imparied)

    Congestive heart gailure (SV declines)

    Ruptured ventricular wall

    Thromboembolism

    Sudden cardiac death
  73. Factors that precipitate conduction irregularities
    • Hypoxia
    • Increased pot (released from necrotic cells)
    • Acidosis
    • Drug toxicities
  74. Treatment
    • Decrease O2 need of heart
    • bedrest
    • oxygen therapy
    • anticoagulants (heparin or warfarin)
  75. 3 Thrombolytic agents
    • tPA
    • Streptokinase
    • Urokinase
    • Dissolve blood clots-promote vasodialation
  76. Analgesics are administered for ____ relief
    Pain
  77. Stool softeners prevent _____
    straining
  78. Treatment of arrhythmias
    • Cardioversion
    • Defibrillation
    • Pacemaker
    • Angioplasty and coronary stent implant
    • Coronary artery bypass
    • Cardiac transplant
  79. Define CHF
    • The pumping ability of the heart is progressively imparired and can no longer meet the needs of the body
    • May present as acute but is usually chronic
  80. CHF usually occurs as a ____
    complication
  81. Etiology of CHF
    • Coronary artery disease
    • Myocardial infarction
    • Hypertension
    • Cardiac valvular disease
    • Arrhythmias
    • Congenital heard defects
  82. Left sided CHF is
    Aortic valve stenosis
  83. Right sided CHF is
    Pulmonary valve stenosis
  84. Essential hypertension effects ____ ventricle first
    Left
  85. Pulmonary disease
    Increase work load for right vent
  86. When heart fails blood flow is reduced into systemic circulation and to the ____
    kidneys
  87. The kidneys stimulate ____ and _____
    • renin-angiotensin secretion
    • vasoconstriction
    • These increase resistance which the left vent myst eject blood
  88. Pulmonary disease is referred to as
    Cor Pulmonale
  89. Kindeys also cause secretion of _____
    aldosterone
  90. Aldosterone results in
    • Increase blood volume
    • Reabsorption of sodium
    • Water retention
  91. Increased afterload and preload lead to ___
    cardiomegaly (increase hr)
  92. 2 effects when heart cant keep up
    • SV and CO decrease- less blood reaching organs and tissues-decreased cell function (forward effect)
    • Return of blood is impeaded (back up effect)
  93. Signs of Left sided heart failure
    • Left ventricle weakens and cant empty
    • back up of blood in pulmonary veins
    • high presssure in capillaries leads to pulmonary edema
    • Dyspnea
    • Orthopenea
    • Hemoptysis
    • Rales
  94. Signs of Right sided heart failure
    • Back up of blood in vena cavae
    • Congestion of peripheral organs and extremeties
    • swollen legs
    • Distention of neck veins
    • Hepatomegaly and splenomegaly
    • Ascites
    • abdominal distension
  95. Diagnostic procedures
    • History and physical
    • Chest xray
    • arterial blood gases
    • EKG
  96. Complications
    • Pulmonary edema
    • Multiple organ failure
    • Hypopfusion
    • Slowed brain function
    • Renail failure-retention of sod and chloride
  97. Treatment
    • Replace defective valves
    • pacemaker
  98. Medications
    • Digoxin (enhances myocardial contractions)
    • Antihypertensives
    • Flu vaccine
  99. Describe Rheumatic heart disease
    • Systemic inflammatory disease- joints hear cns skin
    • causes serious irreprarable damage
    • seen in children 5-15
  100. Etiology of rheumatic fever
    • infection of throat-upper resp
    • group A beta-hemolytic streptococci pyogenes
    • After untreated strep throat
  101. Pathophysiology of rheumatic fever
    • causes inflammation
    • autoimmune response results in cardiac damage
    • scar tissue forms in hear-causes rheumatic heart disease
  102. Signs of rheumatic fever
    • Mitral stenosis-Vegetations
    • Cyanosis
    • Dyspnea and fatigue
    • Murmurs
  103. Diagnostic tests
    • Echocardiogram
    • CBC-leukocytosis
    • Antitrertolysin O titer is elevated
    • ESR and C reactive are elevated
  104. Complications
    • Bacterial endocardidtis (infected vegetations)
    • valvular vegetations give rise to emboli (can cause infarctions)
    • Rheumatic heard disease(does not develop until a decade after initial infection)
    • CHF
  105. Treatment
    • NO cure
    • bed rest
    • surgery
    • antibiotics
    • prohylactic
    • asprin
  106. prognosis
    surgery prolongs life

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