NR439 Pharmacodimes

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  1. What is pharmacodynamics?
    Study of biochemical and physiologic effects of drugs and the molecular mechanisms by which those effects are produced. STUDY OF WHAT DRUGS DO TO THE BODY AND HOW THEY DO IT
  2. How id drug action determined?
    Determined by where and how a drug interacts with the body.
  3. How are THREE sites of drug action determined?
    • 1. May enter where intended to act (antacids)
    • 2. Lipids solubility: allows drugs to interact with the lipids and proteins in cell membranes
    • 3. May be directed to specific types of cells via receptors
  4. What are receptors?
    Any functional macromolecule in a cell to which a drug binds to produce its effects
  5. Why bind to drug receptor?
    To either block or mimic normal receptor activity. DRUGS CAN'T DO ANYTHING IN BODY THAT BODY DOESN'T ALREADY KNOW HOW TO DO.
  6. What impact does the number of different receptors have?
    Number of different receptors determines variety of responses. Increased receptor response increases potential for side effects.
  7. What is the simple occupancy theory?
    Assumes ability to bind and influence receptor.
  8. Describe the relationship between the response and number of receptors in the simple occupancy theory.
    Intensity of response proportional to # of receptors occupied. (lots of receptors occupied=intense response)
  9. What happens when all available receptors have been occupied?
    Maximum response occurs.
  10. What is the modified occupancy theory?
    Assumes indepence of affinity and intrinsic activity.
  11. What is affinity?
    Strength of attraction between drug and receptor. Higha ffinity drugs are very potent.
  12. What is intrinsic activity?
    Ability of drug to activate recptor after binding.
  13. What kind of effect does high intrinsic-activity have?
    Maximum efficacy.
  14. What is the Dose Response Curve?
    As dosage is increased, the response becomes progressively larger (GRADED). Must indiviually adjust for each patient.
  15. What are the THREE phases of Dose Response?
    • Phase I-occurs at low dose, too low to measure
    • Phase II-increased dose produces increased response. Response is graded.
    • Phase III. Increase in dose no longer elicits response. Curve flattens.
  16. Which phase iin the dose response is graded?
    Phase II.
  17. What is Maximum Efficacy?
    Largest effect a drug can produce.
  18. How is maximum efficacy graphed?
    Height of dose-response curve.
  19. What is relative potency?
    Amoutn of drug needed to elicit effect.
  20. What are AGONISTS?
    Mimic the body's own regulatory molecules and activate receptors.
  21. What are ANTAGONISTS?
    Produce their effects by preventing receptor activation.
  22. What is a competitive antagonist?
    Binds reversibly.
  23. What is a noncompetitive antagonist?
    Binds irreversibly. Reduces the maximal response that an agonist can elicit.
  24. What are PARTIAL AGONISTS?
    Mimic action like agonists but with reduced intensity. Can also act as antagonist.
  25. How does an alpha-adrenergic antagonist work?
    • 1. Blocks alpha receptors on blood vessels.
    • 2. Stimulation of alpha receptors promot vasocontriction.
    • 3. This blocks response and causes vasodilation.
    • *Given to lower blood pressure.
  26. What is my dog's name?
  27. How do Beta Blockers work?
    • Antagonistic action.
    • Block beta receptors in the heart which:
    • -reduce heart rate
    • -reduce force of contraction
    • -reduce velocity of impulse condition
  28. What are TWO ways in which we classify receptors?
    Classify according to affinity for agonist or antagonist. According to location within the cell or cell membrane.
  29. What is an idiosyncratic reaction?
    Genetic difference
  30. How might an allergic reaction be triggered?
    Might be triggered by drug or metabolite of drug
  31. What is the therpeutic index?
    Measure of drug's safety. Ration of LD50 (Lethal Dose) to its ED50.
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NR439 Pharmacodimes
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