pharm detailed antiangina

  1. metabolic change in the heart caused by imbalance of O2 supply and demand
    accumulation of lactic acid, which causes pain
  2. 3 electrophysiologic change caused by decreased O2 in heart
    • ST segment changes
    • T changes
    • arrythmia
  3. contractile changes caused by decreased O2 in the heart
    wall motion abnormalities
  4. the bottom-line role of drugs used to treat angina pectoris
    restore balance between myocardial O2 supply and demand
  5. organic nitrates -- treat what? how?
    • angina
    • decrease O2 demand
  6. beta blockers treat angina how?
    decrease O2 demand

    best for treating stable angina than the other types
  7. Ca++ channel blockers
    treat what? how?
    • angina
    • increase O2 supply -- do it by reducing contractability of muscles --> dilation ---> increased blood supply
  8. 3 primary drug categories to treat angina, and their basic roles
    • organic nitrates: decrease O2 demand
    • beta blockers: decrease O2 demand
    • Ca++ channel blockers: increase O2 supply
  9. stable angina 
    brought on by what?
    primary characteristic of it?
    • activity
    • O2 demand greatly exceeds supply
  10. treatment of stable angina -- which types of meds?
    • mainly organic nitrates and beta blockers
    • but Ca++ channel blockers can be used (due to their effect on myocardium and peripheral vasculature rather than their ability to dilate coronary arteries)
    • usually treated with a combo of antianginal drugs
  11. variant angina - primary problem? his description of this type?
    • O2 supply to myocardium decreases bc of coronary artery vasospasm
    • happens when you find out your wife is cheating
  12. first choice drug for variant angina
    • Ca++ channel blockers
    • long lasting nitrates can be added for management of severe forms
  13. what can trigger variant angina
    • endogenous vasoconstrictive agents
    • emotional and environmental stim (cheating wife) can also cause the coronary arteries to constrict
    • * can occur when pt is at rest
  14. unstable angina
    several serious and potentially life-threatening forms of myocardial ischemia associated with thrombosis in the coronary arteries MI

    it's a combo of stable and variant - increased myocardial O2 demands at the same time as coronary vasoconstriction

    can begin with activity or happen when at rest
  15. Prinzmetal's ischemia
    • aka variant angina
    • it's called spontaneous, but really it's just that something other than exercise, such as stress, is triggering the angina
  16. organic nitrates - basic role?
    dilate vascular smooth muscle to produce vasodilation throughout body (not just coronary vessels)
  17. how do organic nitrates impact the heart? 2 ways
    • dilation in systemic venous system --> decreased amount of blood returning to heart (cardiac preload)
    • dilation of systemic peripheral arterioles --> decreased pressure against which the heart must pump (cardiac afterload)
  18. 2 organic nitrate drugs
    • nitroglycerin
    • isosorbide dinitrate
  19. nitrates are drug precursors. They become active when converted to __ within __
    • nitrous oxide
    • vascular smooth muscle
  20. nitrous oxide (nitrates turn into this) do what?
    cause vasodilation
  21. how do nitrous oxides cause vasodilation? (remember, organic nitrates become nitrous oxides)
    increase the production of cyclic guanosine monophosphate (c-GMP) in muscle cells, --> cGMP acts as a second messenger that initiates phosphorylation of specific contractile proteins --> inhibition of smooth muscle contraction
  22. nitroglycerin -- type of drug? role? ways to take it, in order from fastest to slowest acting?
    • organic nitrate
    • antianginal - treatment and prevention

    sublingual (1-3), buccal (2-3), oral (20-45), transdermal (30 min)
  23. isosorbide dinitrate
    type of drug?
    how it differs from the other drug of this class?
    • organic nitrate -- treatment and prevention of angina
    • antianginal and hemodynamic effects last longer than nitorgylcerine
  24. isosorbide dinitrate - given how for acute vs prevention
    • acute - sublingually, buccally, or chewable tablets
    • prevention - oral tablets
  25. beta-adrenergic blockers -- basic role? how?
    • decrease HR and force of myocardial contractions
    • by antagonizing beta-1 receptors on myocardium --> decrease in work the heart must perform & decrease in myocardial O2 demand
  26. can beta-adrenergic blockers be given prophylactically?
    yes - can prevent onset of angina by balancing myocardial O2 supply and demand
  27. atenolol and metoprolol are what kind of drug?
    cardioselective beta-1 antagonists
  28. blockers that bind to both beta-1 and 2 receptors may induce what side effect in who? so they should be given what?
    • bronchoconstriction in pts w asthma
    • cardioselective beta-1 antagonists (atenolol or metoprolol)
  29. how do Ca++ channel blockers work?
    block entry of calcium into vascular smooth muscle --> less actin-myosin interactions --> relaxation & dilation of blood vessels
  30. the impact of Ca++ blockers?
    coronary dilation --> more O2 in myocardium
  31. can Ca++ blockers do systemic vasodilation?
    yes, although their primary role is to dilate coronary arteries, they do some systemic vasodilation, so some of their antianginal effects may be due to how they decrease myocardial work load by reducin cardiac pre and afterload
  32. how do Ca++ blockers impact cardiac striated cells?
    • by reducing the amount of calcium in them, they decrease their contractility and O2 demand
    • by altering conduction of electrical activity can treat cardiac arrhythmia
  33. 2 Ca++ channel blockers
    • diltiazem
    • nifedipine
  34. diltiazem
    type of drug?
    • Ca++ channel blocker
    • vasodilate coronary arteries and peripheral vasculature
    • some depression of electrical conduction in SA and AV nodes
    • may --> slight bradycardia
  35. nifedipine
    type of drug
    • it's a Ca++ channel blocker, 
    • it's of dihydropyridine class of drugs
  36. nifedipine -- Ca++ channel blocker and of diydropyridine class -- does what?
    • selectively blocks Ca++ channels in vascular smooth muscle rather than cardiac striated muscles
    • dilate coronary arteries and periph vasc w/o affecting heart excitability and contractility
  37. side effects of nitrates and Ca++ channel blockers that may be an issue during a PT session
    peripheral vasodilation that can lead to HoTN, orthostatic hotn, dizziness, syncope
  38. nitrous oxide increases production of what?
    c-GMP (cyclic guanosine monophosphate)
Card Set
pharm detailed antiangina