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

    Eventually the lumen narrows and results in ischemia and necrosis to tissues
  4. 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)
  5. Effects of Atherosclerosis
    Decrease perfusion to organs

    Increase platelet adhesion

    Promote the dev. of an aneurysm
  6. Endothelial injury begins formation of Atheromas which results in elevated levels of what
    C-reactive proteins
  7. What adheres to tunica intima and causes an atheroma
    Leukocytes (lymphocyte, monocyte-macs) and platelets
  8. 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
  9. Describe plaque
    Characteristic lesion of advancing atherosclerosis
  10. Plaque is thought to develop from what
    Fatty streaks- cellular proliferation, lipid accumulation and ct formation occur
  11. Plaque protudes into _________ of an artery
    Lumen


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

    High cholesterol content


    BAD GUYS
  14. elevated blood cholesterol levels cause monocytes to attach to the endothelium and they migrate into the subendothelial spaces and become ______
    macs
  15. Macs release _____ that alter the LDL
    free radicals (compounds with unpaired electrons)
  16. 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
  17. After macs release lipds into plaque a ____ _____ forms
    fibrous scar

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


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

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

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

    Increase BP

    Promotes platelet adhesion

    Modifiable risk factor
  43. Myocardial Ischemia is an _____ in O2 demand and _____in O2 supply
    Increase, decrease
  44. Myocardial Ischemia may result from
    Myocardial hypertrophy in which the heard has outgrown its blood supply
  45. Signs of myocardial ischemia
    • angina pectoris (transient)
    • substernal chest discomfort
  46. Pain may radiate to
    neck, left arm and left shoulder (Derived from common nerve pathways)
  47. Precipitating factors in angina attacks
    • running upstairs
    • getting angry
    • resp inf with fever
    • cold weather
    • eating a large meal
  48. what are 3 types of angina
    • stable
    • variant
    • unstable
  49. Describe stable angina
    • Predictable- increase physical activity
    • rest usually helps
  50. Describe Variant Angina
    • Caused by vasospasms of coronary arteries
    • usually occurs at rest or during sleep
  51. Describe unstable angina
    • Most serious form
    • occur at rest
    • prolonged pain
    • longer than 20 mins
    • could result in break in an atheroma
  52. Diagnostic Tests
    • ECG/EKG
    • Exercise stress test
    • Thallium scan
    • Coronary angiography
  53. Treatment
    • Decrease oxygen demand
    • eliminate predisposing factors
    • stop activity
    • avoid stress
    • rest
    • nitroglycerin
  54. Nitroglycerin is _____
    • vasodialator
    • decreases peripheral resistance
    • decrease BP
  55. Angina is a ______
    WARNING of a possible MI
  56. Etiology of MI
    • Atherosclerosis
    • Coronary Thrombosis
  57. Most infactions are _____
    Transmural
  58. An embolus is
    part of a thrombus that breaks off-results in occlusion
  59. most infarcations involve _____ ventricle
    LEFT (systemic circulation)
  60. 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
  61. Enzymes can be detected with _____ tests
    serologic
  62. Functional changes in an MI
    • Decrease cardiac contractility
    • Decrease stroke volume
    • Decrease in Cardiac output
  63. Signs of classic MI
    • Severe chest pain
    • substernal pain
    • silent myocardial infarction
    • nausea
    • diaphoresis (sweating)
  64. Classic signs of MI VItal Signs
    • Blood Pressure- Hypotension
    • Pulse- Rapid and Weak
    • Low grade fever
  65. 3 cardiac enzymes
    • CK-MB
    • LDH
    • AST
  66. Blood tests will be _____ for enzyme levels
    elevated
  67. Which is the most specific enzyme for MI
    CK-MB
  68. _____ is the best marker for myocardial injury
    Troponin
  69. Blood tests for MI
    • CBC- leukocytosis
    • C-reactive protein-elevated
    • ESR-elevated
  70. Other diagnostic tests
    • Arterial blood gases (if shock is pronounced)
    • Serum electrolytes (pot and sod levels are elevated)
  71. 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
  72. Factors that precipitate conduction irregularities
    • Hypoxia
    • Increased pot (released from necrotic cells)
    • Acidosis
    • Drug toxicities
  73. Treatment
    • Decrease O2 need of heart
    • bedrest
    • oxygen therapy
    • anticoagulants (heparin or warfarin)
  74. 3 Thrombolytic agents
    • tPA
    • Streptokinase
    • Urokinase
    • Dissolve blood clots-promote vasodialation
  75. Analgesics are administered for ____ relief
    Pain
  76. Stool softeners prevent _____
    straining
  77. Treatment of arrhythmias
    • Cardioversion
    • Defibrillation
    • Pacemaker
    • Angioplasty and coronary stent implant
    • Coronary artery bypass
    • Cardiac transplant
  78. 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
  79. CHF usually occurs as a ____
    complication
  80. Etiology of CHF
    • Coronary artery disease
    • Myocardial infarction
    • Hypertension
    • Cardiac valvular disease
    • Arrhythmias
    • Congenital heard defects
  81. Left sided CHF is
    Aortic valve stenosis
  82. Right sided CHF is
    Pulmonary valve stenosis
  83. Essential hypertension effects ____ ventricle first
    Left
  84. Pulmonary disease
    Increase work load for right vent
  85. When heart fails blood flow is reduced into systemic circulation and to the ____
    kidneys
  86. The kidneys stimulate ____ and _____
    • renin-angiotensin secretion
    • vasoconstriction
    • These increase resistance which the left vent myst eject blood
  87. Pulmonary disease is referred to as
    Cor Pulmonale
  88. Kindeys also cause secretion of _____
    aldosterone
  89. Aldosterone results in
    • Increase blood volume
    • Reabsorption of sodium
    • Water retention
  90. Increased afterload and preload lead to ___
    cardiomegaly (increase hr)
  91. 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)
  92. 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
  93. 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
  94. Diagnostic procedures
    • History and physical
    • Chest xray
    • arterial blood gases
    • EKG
  95. Complications
    • Pulmonary edema
    • Multiple organ failure
    • Hypopfusion
    • Slowed brain function
    • Renail failure-retention of sod and chloride
  96. Treatment
    • Replace defective valves
    • pacemaker
  97. Medications
    • Digoxin (enhances myocardial contractions)
    • Antihypertensives
    • Flu vaccine
  98. Describe Rheumatic heart disease
    • Systemic inflammatory disease- joints hear cns skin
    • causes serious irreprarable damage
    • seen in children 5-15
  99. Etiology of rheumatic fever
    • infection of throat-upper resp
    • group A beta-hemolytic streptococci pyogenes
    • After untreated strep throat
  100. Pathophysiology of rheumatic fever
    • causes inflammation
    • autoimmune response results in cardiac damage
    • scar tissue forms in hear-causes rheumatic heart disease
  101. Signs of rheumatic fever
    • Mitral stenosis-Vegetations
    • Cyanosis
    • Dyspnea and fatigue
    • Murmurs
  102. Diagnostic tests
    • Echocardiogram
    • CBC-leukocytosis
    • Antitrertolysin O titer is elevated
    • ESR and C reactive are elevated
  103. 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
  104. Treatment
    • NO cure
    • bed rest
    • surgery
    • antibiotics
    • prohylactic
    • asprin
  105. prognosis
    surgery prolongs life
Author:
hjones18
ID:
151038
Card Set:
Patho- Ch 18
Updated:
2012-04-30 04:27:40
Tags:
Cardiovascular disorders
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patho ch 18
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