WEEK 2 PPT CAD STABLE ANGINA

  1. What is the most common type of cardiovascular disease?
    coronary artery disease (CAD)
  2. TRUE OF FALSE: CAD is not asymptomatic & cannot develop chronic stable angina (chest pain). *
    FALSE: CAD may be asymptomatic or develop chronic stable angina (chest pain)
  3. What are the more serious manifestations of CAD? 2
    unstable angina & MI
  4. What is the term used for unstable angina & MI?
    acute coronary syndrome (ACS)
  5. What does "athere" mean?
    fatty mush
  6. What does "skleros" mean?
    hard
  7. Atherosclerosis is referred to as the?
    hardening of the arteries
  8. What is "atheromas"?
    fatty deposits
  9. Atheromas or fatty deposits prefer which arteries?
    coronary arteries
  10. Atherosclerosis begins as?
    soft deposits of fat that harden with age
  11. What is the major cause of CAD?
    atherosclerosis
  12. CAD is characterized by?
    lipid deposits within the intima of an artery
  13. What plays a major role in the development of atherosclerosis? 2
    endothelial injury & inflammation
  14. What is the nonspecific marker of inflammation?
    C-reactive protein (CRP)
  15. Which organ produces C-reactive protein (CRP)?
    liver
  16. What are the stages of atherosclerosis? 3
    • 1. fatty streaks
    • 2. fibrous plaque
    • 3. complicated lesion
  17. At which stage does the earliest lesions of atherosclerosis occur?
    fatty streaks
  18. Fatty streaks is characterized by?
    lipid-filled smooth muscle cells
  19. What happens during the second stage of atherosclerosis (fibrous plaque stage)? *
    progressive changes in the endothelium of the arterial wall begins
  20. Which is the most dangerous & final stage in the development of the atherosclerotic lesion?
    complicated lesion
  21. What is collateral circulation? *
    arterial anastomoses or connections within the coronary circulation
  22. What happens when plaque blocks the normal flow of blood through a coronary artery & the resulting ischemia is chronic?
    increased collateral circulation develops
  23. Why is it that collateral circulation is inadequate with rapid-onset CAD?
    because time is inadequate for collateral development
  24. Give an example of rapid-onset CAD.
    familial hypercholesterolemia
  25. Besides rapid-onset CAD, what else can cause inadequate time for collateral development?
    coronary spasm
  26. What are the non modifiable risk factors for CAD? 5
    • 1. age
    • 2. gender
    • 3. ethnicity
    • 4. family history
    • 5. genetic predisposition
  27. What are the modifiable risk factors for CAD? 10
    • 1. elevated serum lipids
    • 2. hypertension/increased blood pressure
    • 3. tobacco use
    • 4. physical inactivity
    • 5. obesity
    • 6. diabetes
    • 7. metabolic syndrome
    • 8. psychological state
    • 9. homocysteine level
    • 10. substance abuse
  28. What is the desired level of cholesterol?
    less than 200 mg/dL
  29. What is the desired level of triglycerides?
    less than 150 mg/dL
  30. What is the desired level of high-density lipoproteins (HDLs)?
    above 60 mg/dL
  31. What is the desired level of low-density lipoproteins (LDLs)?
    less than 70 mg/dL
  32. Treatment for CAD is based on which guidelines?
    10-year risk score
  33. What is the blood pressure range for hypertension?
    >140/90 or >130/80 mm Hg
  34. What is the patient teaching for patients with prehypertension?
    begin lifestyle changes
  35. Those with stage 1 or 2 hypertension often require?
    more than one drug to reach therapeutic goals
  36. Give examples of catecholamine. 2
    • 1. epinephrine
    • 2. norepinephrine
  37. What causes catecholamine release in tobacco smoke?
    nicotine
  38. What does tobacco smoke do to LDL and HDL levels?
    • 1. increases LDL levels ("bad cholesterol")
    • 2. decreases HDL levels ("good cholesterol")
  39. Tobacco smoke releases?
    toxic oxygen radicals
  40. What does tobacco smoke do to carbon monoxide levels?
    increases it
  41. How do you manage or prevent CAD?
    with prevention and early treatment
  42. Why is it extremely important to identify people at risk for CAD? *
    because clinical manifestations of CAD will not be apparent in the early stages of the disease
  43. Which subjective data would you assess when screening for CAD?
    • 1. health history including family history
    • 2. environmental patterns (ex: diet, activity, social habits)
    • 3. psychosocial history
    • 4. values and beliefs about health and illness
  44. Which objective data would you assess when screening for CAD?
    presence of cardiovascular symptoms
  45. How would people that are considered high-risk manage CAD?
    by controlling modifiable risk factors
  46. How could you encourage lifestyle changes for persons that are high-risk for CAD? 3
    • 1. through patient teaching (education)
    • 2. clarification of personal values (so the patient can identify their vulnerability to various risks)
    • 3. setting realistic goals (so the patient can choose which risk factor(s) to change first)
  47. What is the FITT formula?
    • Frequency (how often)
    • Intensity (how hard)
    • Type (isotonic)
    • Time (how long)
  48. What is the recommended frequency and time for physical fitness? *
    30 minutes most days + weight training 2 days a week
  49. Regular physical activity contributes to? 3
    • 1. weight reduction
    • 2. reduction of >10% in systolic blood pressure
    • 3. helps increase HDL levels ("good cholesterol")
  50. What is the nutritional therapy for CAD management? 4
    • 1. decrease saturated fats and cholesterol
    • 2. increase complex carbohydrates and fiber
    • 3. decrease red meat, egg yolks, and whole milk
    • 4. increase omega-3 fatty acids
  51. What are the 2 types of omega-3 fatty acids?
    • 1. eicosapentaenoic acid (EPA)
    • 2. docosahexaenoic acid (DHA)
  52. What is the recommended daily intake for total fats (includes saturate fat calories)?
    25-35% of total daily calories
  53. What is the recommended daily intake for saturate fats?
    <7% of total daily calories
  54. What is the recommended daily intake for cholesterol?
    <200 mg
  55. What is the recommended daily intake for plant stanols or sterols?
    2 g
  56. What is the recommended daily intake for dietary fiber?
    10-25 g of soluble fiber
  57. What is the recommended daily intake for total calories?
    only enough calories to reach or maintain a healthy weight
  58. Give an example of moderate-intensity physical activity.
    brisk walking
  59. What are some examples of saturated fats that should be consumed sparingly? 5
    • 1. animal fat (bacon, lard, egg yolk, dairy fat)
    • 2. oils (coconut, palm oil)
    • 3. butter
    • 4. cream cheese
    • 5. sour cream
  60. What are some examples of monounsaturated fats? 5
    • 1. fish oil
    • 2. oils (canola, peanut, olive)
    • 3. avocado
    • 4. nuts (almonds, peanuts, pecans)
    • 5. olives (green, black)
  61. What are some examples of polyunsaturated fats that should be consumed primarily? 5
    • 1. vegetable oils (safflower, corn, soybean, flaxseed, cottonseed)
    • 2. some fish oil, shellfish
    • 3. nuts (walnuts)
    • 4. seeds (pumpkin, sunflower)
    • 5. margarine
  62. If diet and exercise is ineffective in managing CAD, which drug is most widely used to lower lipid levels?
    HMCCoA reductase inhibitors (statins)
  63. What are some examples of statins? 3
    • 1. atorvastatin (Lipitor)
    • 2. simvastatin (Zocor)
    • 3. rosuvastatin (Crestor)
  64. What is the mechanism of action of statins? *
    inhibit cholesterol synthesis, decrease LDL, increase HDL
  65. What are the side effects of statins? 3
    • 1. myopathy (disease of muscle tissues)
    • 2. hepatotoxicity
    • 3. GI side effects
  66. When simvastatin (Zocor) is also used with gemfibrozil (Lopid) or niacin (Niaspan), it increases the risk for?
    rhabdomyolysis
  67. What are the signs and symptoms of rhabdomyolysis? 2
    • 1. increased creatinine levels
    • 2. muscle pain
  68. Besides statins, what is another drug that restricts lipoprotein production?
    niacin (Niaspan)
  69. What is the mechanism of action of niacin (Niaspan)? *
    lowers LDL ("bad cholesterol") and triglyceride by inhibiting synthesis + increases HDL levels ("good cholesterol")
  70. What are the side effects of niacin (Niaspan)? 4
    • 1. flushing
    • 2. pruritus
    • 3. GI side effects
    • 4. orthostatic hypotension
  71. What should you tell the patient in regards to flushing when taking niacin (Niaspan)? *
    flushing especially of the face and neck may occur within 20 minutes after taking the drug and may last for 30-60 minutes
  72. Besides statins and niacin, what is another drug that restricts lipoprotein production?
    fabric acid derivative (Lopid)
  73. What is the mechanism of action of fabric acid derivatives? *
    decreases triglycerides and increases HDL levels ("good cholesterol")
  74. What is the side effect of fabric acid derivatives (Lopid)?
    GI side effects
  75. Which drug increase lipoprotein removal?
    bile acid sequestrants
  76. What are some examples of bile acid sequestrants? 2
    • 1. cholestyramine (Questran)
    • 2. colesnvelam (WelChol)
  77. What is the mechanism of action of bile acid sequestrants?
    increases conversion of cholesterol to bile acids
  78. What are the side effects of bile acid sequestrants? 2
    • 1. GI side effects
    • 2. it binds with other drugs
  79. Which drug decreases cholesterol absorption?
    ezetimibe (Zetia)
  80. What is the mechanism of action of ezetimibe (Zetia)?
    decreases absorption of dietary and biliary cholesterol
  81. What are the side effects of ezetimibe (Zetia)? 3
    • 1. GI side effects
    • 2. upper respiratory symptoms
    • 3. arthralgia
  82. Which antiplatelet drug is given for CAD?
    low-dose aspirin (81 mg)
  83. Which alternative antiplatelet drug is given if aspirin is not tolerated?
    clopidogrel (Plavix)
  84. Aspirin is recommended for? *
    men >45 and high-risk women + a 10-year CAD risk of >20%
  85. CAD in older adults causes? *
    increased incidence and mortality
  86. For older adults, what are the necessary guidelines that need to be modified for physical activity? 5
    • 1. longer warm-up
    • 2. longer periods of low-level activity
    • 3. longer rest period between sessions
    • 4. avoid extremes of temperature
    • 5. engage in physical activity for 30 minutes on most days
  87. What is angina?
    chest pain
  88. Angina is a manifestation of?
    reversible myocardial ischemia
  89. What causes angina or chest pain?
    increased demand for oxygen or a decreased supply of oxygen
  90. What happens in angina or chest pain? *
    lactic acid irritates the nerve fibers and causes pain the cardiac nerves
  91. Angina or chest pain can radiate to? 4
    • 1. shoulders
    • 2. neck
    • 3. lower jaw
    • 4. arms
  92. What are the symptoms of angina or chest pain? 5
    • 1. pressure/ache
    • 2. squeezing, heavy, choking, or suffocating sensation
    • 3. rarely sharp or stabbing
    • 4. indigestion or burning
    • 5. can radiate to various locations
  93. Chronic stable angina refers to?
    chest pain
  94. Describe the onset of chronic stable angina. 3
    • 1. intermittent
    • 2. has the same pattern of onset, duration, and intensity of symptoms
    • 3. has a 5-15 minute duration
  95. What does a 12-lead electrocardiogram (ECG) often show in chronic stable angina? 2
    • 1. ST segment depression
    • 2. and or T-wave inversion
  96. What does an ST segment depression and or T-wave inversion indicate?
    ischemia
  97. How is chronic stable angina controlled? *
    with drugs on an outpatient basis
  98. What are the different types of chronic stable angina? 5
    • 1. silent ischemia
    • 2. nocturnal angina
    • 3. angina decubitus
    • 4. prinzmetal's (variant) angina
    • 5. microvascular angina
  99. What is silent ischemia? *
    ischemia that occurs in the absence of any subjective symptoms
  100. Silent ischemia is associated with?
    diabetic neuropathy
  101. How do you confirm silent ischemia? *
    ECG changes with a Holter monitor
  102. What is nocturnal angina? *
    chest pain that occurs only at night but not necessarily during sleep
  103. What is angina decubitus?
    chest pain that occur only while lying down
  104. How is angina decubitus relieved? *
    by standing or sitting
  105. What is prinzmetal's (variant) angina? *
    rare form of angina that often occurs at rest usually in response to a spasm or a major coronary artery
  106. Prinzmetal's (variant) angina is seen in patients with a history of? 3
    • 1. migraine headaches
    • 2. raynaud's phenomenon
    • 3. heavy smoking
  107. TRUE OR FALSE: In prinzmetal's (variant) angina, spasm may occur in the absence of CAD.
    TRUE
  108. What is microvascular angina? *
    chest pain that occurs in the absence of significant atherosclerosis or coronary spasm
  109. In microvascular angina, chest pain is related to? *
    myocardial ischemia that is associated with atherosclerosis or spasm of the small distal branch vessels of the coronary microcirculation
  110. Chest pain that is due to myocardial ischemia from atherosclerosis or spasm of the small distal branch vessels of the coronary microcirculation is known as?
    coronary microvascular disease (MVD)
  111. Coronary microvascular disease (MVD) affects?
    small, distal coronary arteries
  112. What is the goal of collaborative care for CAD? *
    decrease oxygen demand and or increase oxygen supply
  113. What is the first line drug therapy for the treatment of angina?
    short-acting nitrates
  114. What is the mechanism of action of short-acting nitrates? *
    dilates peripheral and coronary blood vessels
  115. What are some examples of short-acting nitrates? 2
    • 1. nitroglycerin (NTG) SL
    • 2. nitrolingual spray
  116. How would you instruct the patient on how to take nitroglycerin? 2
    • 1. if no relief in 5 minutes, call EMS
    • 2. if some relief, repeat every 5 minutes for a maximum of 3 doses
  117. How long does NTG SL or NTG translingual sprays lasts for?
    30-40 minutes
  118. What is the recommended dose of an NTG translingual spray? *
    1 metered spray on the tongue (do not inhale)
  119. What happens when the bottle for NTG tabs are opened? *
    the tabs lose potency and should be replaced every 6 months
  120. SL NTG should cause which sensation when taken? *
    tingling (otherwise it might be outdated)
  121. Can patients use NTG prophylactically before starting an activity that is known to cause angina?
    yes
  122. Why are long-acting nitrates given?
    to reduce angina incidence
  123. What are the main side effects of long-acting nitrates? 2
    • 1. headache
    • 2. orthostatic hypotension
  124. What are the methods of administration for long-acting nitrates? 3
    • 1. oral
    • 2. topical (ointment)
    • 3. transdermal controlled-release (silicone gel, polymer matrix)
  125. What are some examples of oral long-acting nitrates? 2
    • 1. isosorbide denigrate (Isordil)
    • 2. isosorbide mononitrate (Imdur)
  126. What other drugs are given for chronic stable angina? 4
    • 1. angiotensin-converting enzyme (ACE) inhibitors.
    • 2. B-adrenergic blockers
    • 3. calcium channel blockers
    • 4. sodium current inhibitors
  127. Angiotensin-converting enzyme (ACE) inhibitors is recommended for? *
    patients with chronic stable angina that are at a higher risk for a cardiac event
  128. What places patients at a higher risk for a cardiac event? 2
    • 1. EF<40%
    • 2. DM
  129. What is an example of angiotensin-converting enzyme (ACE) inhibitors?
    lisinopril (Zestril)
  130. Angiotensin-converting enzyme (ACE) inhibitors result in? *
    vasodilation and reduced blood volume
  131. What can angiotensin-converting enzyme (ACE) inhibitors prevent or reverse for patient who have had an MI?
    ventricular remodeling
  132. Angiotensin-converting enzyme (ACE) inhibitors are contraindicated with? 2
    • 1. cough
    • 2. angioedema
  133. B-adrenergic blockers are recommended for which patients? 2
    • 1. those with left ventricular dysnfunction
    • 2. have a history of MIs
  134. What is the mechanism of action of B-adrenergic blockers? *
    decreases myocardial contractility, HR, SVR, and BP, which reduces the myocardial oxygen demand
  135. What are some examples of B-adrenergic blockers? 3
    • 1. carvedilol (Coreg)
    • 2. metoprolol (Lopressor, Toprol XL)
    • 3. bisoprolol (Zebeta)
  136. What are some of the side effects of B-adrenergic blockers? 8
    • 1. bradycardia
    • 2. hypotension
    • 3. wheezing from bronchospasm
    • 4. GI side effects
    • 5. weight gain
    • 6. depression
    • 7. fatigue
    • 8. sexual dysfunction
  137. B-adrenergic blockers are contraindicated in patients with? 3
    • 1. severe bradycardia
    • 2. acute heart failure
    • 3. asthma
  138. Why are B-adrenergic blockers used cautiously in diabetic patients?
    because they mask signs of hypoglycemia
  139. What happens when B-adrenergic blockers are stopped abruptly? *
    it may result in an increase in the number and intensity of angina attacks
  140. When are calcium channel blockers used? *
    when B-adrenergic blockers are ineffective or is contraindicated
  141. What are the primary effects of calcium channel blockers? 4
    • 1. systemic vasodilation with decreased SVR
    • 2. decreased myocardial contractility
    • 3. coronary vasodilation
    • 4. decreased HR
  142. What are the 2 groups of calcium channel blockers?
    • 1. dihydropyridines
    • 2. nondihydropyridines
  143. What is the difference between dihydropyridines and nondihydropyridines? *
    dihydropyridines have more vasodilatory effects while nondihydropyridines have more rate and contractility effects
  144. What is an example of dihydropyridines (calcium channel blocker)?
    amlodipine (Norvasc)
  145. What is an example of nondihydropyridines (calcium channel blocker)? 2
    • 1. verapamil (Calan)
    • 2. diltiazem (Cardizem)
  146. What do calcium channel blockers do to serum digoxin levels? *
    it enhances it, therefore, monitor patient for signs and symptoms of digoxin toxicity
  147. Which nondihydropyridines (calcium channel blocker) can cause constipation especially in older adults?
    verapamil (Calan)
  148. When are sodium current inhibitors used?
    when the patient has not had an adequate response to other antianginals
  149. What is an example of a sodium current inhibitor?
    ranolazine (Ranexa)
  150. Ranolazine (Ranexa) is contraindicated with? *
    patients who have a long QT interval or are taking QT-prolonging drugs
  151. Why is ranolazine (Ranexa) contraindicated in patients who have a long QT interval or are taking QT-prolonging drugs?
    because ranolazine (Ranexa) already prolongs QT interval
  152. What is an example of a QT-prolonging interval drug?
    fluoxetine (Prozac)
  153. What are the common side effects of ranolazine (Ranexa)? 4
    • 1. dizziness
    • 2. nausea
    • 3. constipation
    • 4. headache
  154. What are the diagnostic studies for CAD? 7
    • 1. chest x-ray
    • 2. lab studies
    • 3. 12-lead ECG
    • 4. calcium-score screening heart scan
    • 5. echocardiogram
    • 6. exercise stress test
    • 7. pharmacologic nuclear imaging
  155. How does the calcium-score screening heart scan help in diagnosing CAD?
    it locates calcium deposits in plaques
  156. Why is cardiac catheterization/coronary angiography done diagnostically in CAD?
    to visualize blockages
  157. Why is cardiac catheterization/coronary angiography done interventional in CAD?
    to open blockages
  158. What is a percutaneous coronary intervention (PCI)? *
    its when a catheter with a deflated balloon tip is inserted into the appropriate coronary artery
  159. What is a balloon angioplasty? *
    its when the deflated balloon tip is positioned in the blockage and is inflated
  160. What is the end result of a balloon angioplasty?
    vessel dilation and a larger vessel diameter
Author
kmartinez7
ID
332632
Card Set
WEEK 2 PPT CAD STABLE ANGINA
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WEEK 2 MS2 PPT REVIEW
Updated