Pharm: H

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Pharm: H
2014-04-13 20:12:52

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  1. plaque buildup on the inner lining of the affected artery, with resulting arterial narrowing and decreasing blood supply to the heart is called:
    coronary artery disease
  2. when heart cells have an insufficient blood supply (a state myocardial ishcemia), what is the result:
    heart cells arent able to contract as well
  3. typically with increased demands of exercise and stress, a pt. with CAD may feel increased pain from lactic acid, why is lactic acid produced:
    the heart cells are so deficient in oxygen they cant meet basic metabolic needs
  4. with increased activity the hardened coronary arteries are not able to:
    dilate to increase the blood flow to the heart
  5. how is anginal pain usually described:
    crushing or constricting
  6. SOB
    diaphoresis (sweating profusely)
    increased BP and HR

    are the s/sx of:

    what are the s/sx caused by:
    anginal pain

    the s/sx are caused by the lactic acid of anaerobic metabolism and from the SNS stimulation brought on by hypoxia
  7. which (2) situations usually precipitate angina as they increase the demands on the heart.

    exercise or emotioinally charged stiutations

    why: increased the demand for O2 to produce more energy
  8. if the pain after exercise or emotionally charged situations does not subside after 5-10 minutes of rest, what could be happening: (2)
    • unstable angina
    • MI
  9. angina at rest (with no activity) is more serious because:
    the heart cant even get the minimum O2 supply

    must be tx'ed emergently.
  10. situations of increased frequency, intesnity or duration of angina is also considered:
    unstable angina
  11. angina caused by coronary artery spasm, not often assoicated with CAD and occurs unpredictably is called:
    vasospastic (prinzmetal's) angina
  12. medications that relieve angina do so by decreasing the hearts O2 demand. list the classes that preform the following:

    decreasing O2 need by decreasing afterload:
    anti-hypertensive medications
  13. medications that relieve angina do so by decreasing the hearts O2 demand. list the classes that preform the following:

    decreasing force of contractions:
    negative inotropics
  14. medications that relieve angina do so by decreasing the hearts O2 demand. list the classes that preform the following:

    decreasing the HR:
    beta blockers
  15. medications that relieve angina do so by decreasing the hearts O2 demand. list the classes that preform the following:

    decreasing the preload via venous dilation (more blood stays in the veins):

    nitrates also dilate the cornonary arteries to increase the oxygen demand
  16. the termination of an acute angial attack is usually accomplished with:
    rapid acting organic nitrates
  17. preventing or decreasing the frequency of angina attacks is usually accomplished with:
    beta blockers, CCBs, or long acting nitrates
  18. what is the MOA for organic nitrates:
    they are metabolized to nitric acid, a very powerful vasodilator that is produced naturally by healthy arteries
  19. which stage of cardiac output do organic nitrates work on:

    decrease preload and afterload

    nitrates relax arterial and venous smooth muscles, decreasing the hearts workload and O2 demand
  20. considering that coronary arteries with arteriosclerosis are less able to dilate, how do nitrates primarily give relief:
    by decreasing preload
  21. what is the preganancy category for organic nitrates:
    pregnancy category C
  22. how do organic nitrates work to decrease prinzmetals' angina (vasospastic): (2)

    what is the result of the (2) mechanisms:
    • decrease arterial spasms
    • causing coronary artery relasxation and dilation

    result: increasing the blood flow to the heart
  23. short acting nitrates are used for:
    acute angina episodes
  24. how is short acting nitrates ususally administered:

    how long do short acting nitrates usually take to start working:
    • administered: sublingual
    • take to start working: only a few minutes
  25. what are long acting nitrates used for:
    to decrease the frequency and severity of angina.
  26. name one long acting nitrate:
    isosorbide (isordil)
  27. tolerance develops rapidly with L/T nitrates, especially with higher and/or frequent doses.

    how can this be resolved: (2)
    • giving it only 1x or 2x/day
    • taking off the patch for half of the day
  28. why is transdermal nitroglycerin only left on for 1/2 of the day?
    because tolerance can develop rapidly
  29. when a nitrate patch is prescribed, list (3) things to keep in mind of applying and removing the patch:
    • wash the area thoroughly after patch removal
    • rotate patch sites
    • wear gloves when applying (its usually an ointment placed on a patch with a scale on it)
  30. why is headache a common side effect of nitrates:
    due to cerebral blood vessel dilation
  31. a side effect of nitrates may be reflex tachycardia, although it does decrease over time. 

    what is often prescribed to combat the reflex tachycardia:
    beta blockers
  32. before starting on a nitrate tx, what should be determined about their chest pain:
    the frequency and severity
  33. pt. care of nitrate tx should include checking the BP before starting and frequenly during the tx.

    what should you do if hypotension develops: (2)
    • hold the PO dose
    • remove the patch
  34. Topical and PO nitrates should be held when:
    the pt. is receiving IV nitrates
  35. decreased cardiac output
    intracrainal pressure
    head injury
    acute MI

    .... are contraindications of:
  36. what drugs absolutely cannot be taken when a pt. uses nitrates: (2)
    • alcohol
    • sidlenafil (viagra)
  37. nitrates and anti hypertensive in concurrent use should be watched cautiously because:
    the hypotensive effects can be compounded
  38. the pt. on nitrates should avoid alochol to avoid:
    sever hypotension
  39. when the pt. has taken a sublingual nitrate, remind them that they should sit or lay down to prevent fainting.

    the pt. should call 911 if there is no chest pain relife after how many SL NTGs:
    after 3 NTGs
  40. what are the s/sx of nitrate overdose:
    • blurred vision
    • dry mouth
    • severe headache
  41. what instructions should be given to a pt. about the storage for SL NTGs:
    • protect the nitrates from light and heat
    • keep the tablets in their original container and away from moisture, light and heat
  42. how often should SL NTG rx be replaced:
    every 6 months
  43. what is the MOA for beta blockers for the relife of chest pain:
    decrease the cardiac workload by decreasing the heart rate
  44. how do beta blockers compare to nitrates for the relief of chest pain:
    • beta blockers decrease the frequency and severity of chest pain from activity as well as nitrates
    • beta blockers do not develop tolerance, as nitrates do
  45. beta blockers should be used with caution for pts with which (4) conditions:
    • asthma (bronchospams)
    • COPD (bronchospams)
    • heart failure
    • diabetes melletsis (masks hypoglycemia)
  46. what are the (3) side effets of beta blockers:
    • weakness
    • fatigue
    • poor exercise tolerance
  47. list the (5) contraindications of beta blockers
    • bradycardia
    • 2nd or 3rd degree heart block
    • decompensated heart failure
    • cardiogenic shock
    • hypotension
  48. what is the MOA for CCBs for the tx of CAD:

    which stage of cardiac output do CCBs work on:
    blocks Ca++ movement into the heart and/or blood vessel smooth muscle

    they decrease the afterload of the heart, and thus the hearts O2 demand
  49. CCBs' also increase O2 supply to the heart because CCB's:
    dilate the coronary arteries
  50. list the (4) adverse effects of CCB's
    • headache
    • dizziness
    • constipation
    • peripheral edema
  51. pt. care for the use of CCBs should include checking the pts. VS, and do not give the med if the pt. is:
  52. some CCBs can worsen heart failure becuase they:
    decrease heart contractility
  53. list the (3) contraindications of CCBs:
    • sick sinus syndrome
    • 3rd degree AB block w/o a pacer
    • severe hypotension
  54. XR CCB doses shoud NOT be:
    split or crushed!
  55. describe why CCBs should never be stopped abruptly:
    it could result in myocardial ischemia or MI
  56. when are thrombolytics used:
    emergently with MI
  57. what is the MOA of thrombolytics:
    they work by activiating plasmin which breaks down the clot fibrin matrix
  58. how long does it take for thrombolytics to start working:
    about 20 minutes
  59. when can a 2nd dose of thrombolytics be administered:
    30 minutes after the 1st dose
  60. thrombolytics are often followed by which class of drugs:
    anti- coagulants
  61. what is therapeutic range for thrombolytics:

    what is the half life of thrombolytics:
    narrow therapeutic range

    very short half life
  62. active bleeding
    recent surgery
    recent LP (lumbar puncture) or bx (biopsy)
    CVA hx
    GI bleeding
    recent delivery
    decreased platelet count
    bleeding disorders
    septic thrombophlebitis
    renal or liver failure

    .... is the contraindication of:
  63. what is a common after a thrombolytic reperfusion:
  64. how long can increased bleeding las for once a thrombolytic drug has been given:
    2-4 days
  65. which drugs are given at the first signs of an MI:

    describe why these are given:
    anti-platelet drugs

    they decrease clot formation but dont dissolve  clots
  66. list the (3) anti-platelet drugs:
    • ASA
    • clopidogrel (plavix)
    • ticlopidine (ticlid)
  67. which drug is usually started right after an acute MI event to prevent new clot formation:
    IV heparin

    then.. they are switched to coumadin or enoxorparin
  68. what would be given during an MI:

    because the heart damaged by an MI is very prone to arrhythmias and doesnt tolerate nitrates well

    beta blockers help with that, as they slow impulse conduction and suppress some dysrhymeias.

    they also block catecholamines on the heart
  69. what drug class is ususally started soon after an MI but not until the pt. is stable and thrombolytics are D/C'ed:
    ACE inhibitors