Pharm Test 1

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Pharm Test 1
2012-09-06 21:45:19
Pharmacology Autonomic Pharamacology LSU

Principles of Pharmacology and Autonomic Pharmacology
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  1. Butyrlcholinesterase
    Found in the blood plasma an enzyme that breaksdown succinylcholine
  2. Neostigmine
    Antidote for non-deploarizing NMJ blocking agents
  3. Succinycholine
    Depolarizing blocker (non-competitive)
  4. Pancuronium
    Non-Depolarizing Blocker (competitive)
  5. D-Tubocuraine
    Non-Depolarizinf Blocker (Competitive) 
  6. NMJ Blocking Agents
    Used in surgery to promote skeletal muscle relaxtion. intubation, main controlled ventilation, paralysis of skeletal muscle in area of surgery.
  7. 5 key steps in neurotransmission
    Synthesis, Storage, Release, Recognition, Metablosim 
  8. Irreversible inhibitors of AChE
    Insectidices (malathion, parathion, diazinon) Nerve Gases (sarin, soman, tabun)
  9. Edrophonium
    Very short acting used for diagnosis of myasthnia gravis 
  10. Neostigmine
    Dose not penetrate CNS used to treat myasthnia gravis
  11. Physostimine
    Tx poisioning with muscarinic agent. Penetrates CNS
  12. Atropine Overdose
    • Dry as a bone
    • Hot as a Pistol
    • Red as a beet
    • Blind as a bat
    • Mad as a hatter
  13. Atropine and Scopolamine
    • Anitmusacarnic
    • Belladona Alkaloids
    • Pre-op to reduce salivation/bronchial secretions, reduce intestinal motiltiy, treat overactive bladder, used for opthalmolgical examinations mydriasis, prevent motion sickness, tx asthama, treat AChE inhibitor poisioning
  14. Cevimeline
    No nicotinic effect, Orally treat sjogren's syndrome (difficulty with salivation and sweating)
  15. Bethanecol
    No nicotinic effect, somewhat selective for urinary bladder, orally for treatment of post-op urniary retention
  16. Pilocarpine
    No nicotinic effects selective to salivary glands, tx of xerostomia, topically to tx glaucoma. Adverse effect over stimulation of muscarinc receptors
  17. The 3 steps in pharmokinectics:
    • Absorption
    • Distrubution 
    • Elimination (clearance)
  18. Absorption
    Transfer of drug from site of action to systemic circulation
  19. Distrubution
    Transfer of drug from systemic circulation to tissue
  20. Elimination
    • Removal of the drug from the body
    • Metabolism mainly by the liver and excretion through renal or hepatobiliary
  21. Primary means by which drugs cross membranes
    Passive Diffusion: Low molecular weight drugs that are both water a lipid soluble dissolve in membrane and cross to the other side
  22. What is PKa
    Pka: is the pH at which half of the drug is in its ionized form. 50% charged and 50% uncharged
  23. Means of transfer across membrane
    • Filtration
    • Transport Mechanisms: Facilitated Diffusion and Active Transport
  24. Passage of molecules through pores or pourous structures as in the renal glomerulus
  25. Requires no energy for transport but requires a carrier. Drugs bind to carrier by noncovalent mechanisms chemically similar drugs compete for carrier.
    Facilitated Diffusion
  26. Requires Energy and has a carrier. Creates a rxn to be transported
    Active Transport
  27. Fraction of an oral dose that appears in systemic circulation
  28. Bioavailabilty/Influences on Absorption
    • Reduced by 1st pass effect 
    • Altered by chenges in GI motility 
    • Can be reduced by other substances present in the GI tract (antacids inhibit absorption of tetracyclines)
  29. Plasma Protein Binding
    • Protein bound drug cannot distribute to tissues or be elminated.
    • Bound drug is pharmacologically inactive
    • Only free unbound drug is available for Distribution to sites of action and for Elimination. 
    • One drug can displace another from binding site (causing a drug drug interaction)
  30. Things affecting drug Distrubtion: is
    • Blood Flow (ie. stroke pts has decrease blood flow)
    • pH differences b/w plasma and intracellular barrier
    • Specialized barriers: Blood-Brain Barrier
    • Tissue factors affecting accumulation or binding of drug (ie. edema)
  31. What is responsible for the metabolism of many drugs and where is it located?
    The Cytochrome P450 system (CYP) and it is found in the Liver
  32. Conversion of drug to a different chemical structure
  33. Where does Biotransformation occur and by what enzymes
    In the liver and by the CYP P450
  34. What is a Phase 1 Reaction?
    (nonsynthetic) Oxidation Reduction Reaction by Oxygenases and Reductases
  35. What is a Phase 2 Reaction?
    (Synthetic) Formation of conjugates by Tranferases; drugs are conjugated with a sugar an amino acid or sulfate. Phase 2 drugs are easier to metabolize
  36. Biotransformation: Relative to Parent Compound
    • Metabolite is more water soluble
    • Metabolite may be less active
    • Metabolite may be more active: -Prodrug: INACTIVE DRUG UNTIL CONVERTED TO ACTIVE FORM BY THE BODY
    • Metabolite may be inactive
    • Metabolite may be less toxic
    • Metabolite may be more toxic 
  37. Increase elimination of weak acid in the urine
    by alkalinizing the urine
  38. Akalinize the Urine using
    Bicarbonate or Diuretic Acetazolamide which increase bicarb in the urine
  39. To increase elimantion of weak bases 
    Acidify the Urine
  40. Acidify the urine with
    Ammonium Chloride
  41. Enterohepatic Recycling
    drug conjugate secreted into the bile and reconverted to parent compound by intestinal bacteria can be reabsorbed from small intestines-Recycling (Can extend the duration of the drug in the body)
  42. First Order Elimination
    Contant Percentage of drug eliminated per unit time
  43. Plasma Half Life (t1/2)
    Time necessary to reduce plasma drug levels by one half. 
  44. Capacity Limited (Zero Order) Elimination
    Constant amount of drug eliminated per unit time (ie. 50mg/4hr)
  45. Receptors are
    Regulatory proteins that interact with a drug or hormone and initiate a cellular response
  46. Affinity
    How well the drug binds (STRENGTH/LOVE). Drugs that interact with receptor to prduce a response
  47. Efficacy is
    The capacity of a drug to produce a response after it binds
  48. Agonist
    Has Affinity and Efficacy
  49. Antagonsist
    Has ONLY Affinity
  50. Full Agonist
    Can produce full response; Efficacy=1
  51. Partial Agonsit
    Produce a response less that that of a full agonist; Efficacy >0 but <1
  52. Inverse Agonist
    Produce a response less than that of a full agonsist; Efficacy<0
  53. Competitive Antagonsit
    • Have Affinity
    • Have NO Efficacy
    • Block the binding by an agonsit to its receptor
    • Blockade can be OVERCOME (SURMOUNTABLE)
    • Reduce the Potency of agonist
  54. Noncompetitve Antagonist
    • Have Affinity
    • Have NO Efficacy
    • Block the binding by an agonsit to its receptor
    • Reduce the Efficacy of Agonist
  55. Allosteric Modulators
    Can only prevent so much of the agonist from binding can't shut off site completely but can only modulate it. Causes the protein to change shape so the agonsit can't bind
  56. SLUDE Effect what Receptors and What does it stand for
    • Muscarinic Recptors
    • Salivation
    • Lacrimation
    • Urination
    • Defecation
    • Emesis
  57. Beta 1
    • INCREASE contractile force
    • Increase HR (TACHYCARDIA)
    • Increase Renin Release
  58. B2
    DECREASE vasodilation and TPR (bronchorelaxation, mydriasis, decreased urination and GI motility, utureus relax)
  59. A1 and A2
    INCREASE Vasoconstriction and TPR
  60. Dopamine
    DA, B1, A1. Increase UO 
  61. NE (Norepinephrine)
    A1 A2 and B1
  62. Epi
    • A1 A2 B1 B2
    • Tx Asthma 
    • Anaphylatic Shock
    • Cardiogenic Shock
    • Prolong action of local anesthetics
    • Topical hemostatic agent
  63. Dopamine
    • Tx CHF
    • DA B1 A1
  64. Alpha Agonists
    • 1. Pheneylephrine (a1)
    • 2. Methoxamine (a1)
    • 3. Oxymetazoline (a1 and a2 in periphary)
    • 4. Tetrahydrozoline (a1)
    • 5. Nephazoline (a1)
    • 6. Ephdrine/Pseudoephedrine (a1)
    • 7. Clonidine (a2, Tx site of action is the CNS)
  65. Beta Agonist Nonselective B1/2
    Isoproterenol Tx CHF increase pulse no change in MAP
  66. Beta Agonist Selective B2
    • 1. Albuterol
    • 2. Terbutaline
    • 3. Metaproterenol
    • Bronchodilators inhaled agents. can decrease BP and increase HR cause syncope. *B2 is important on arterioles
  67. Beta Agonist  Selective B1
    Dobutamine tx CHF increase CO
  68. CNS Adrenergic Agent
    • Clonidine (a2 agonist) Antihypertensive.
    • Initially it increase BP but cross BBB it decrease BP can cause sleepiness and no ejaculation. it contracts vessels barroreflux do not work because it decreases HR and BP
  69. Nonselective A1 and A2 receptor antagonsit used for OD of alpha agonsits used in pt with pheochromocytoma
  70. Selective a1 receptor antagonsits
    • Prazosin (drug of choice for A1) Terazosin (water soluble don't block A2 in the brain)
    • Used tx as antihypertensive agents
  71. Beta Antagonists
    • OLOL
    • NonSelective B1 and B2 Propanolol Pindolol Timolol Nadolol
    • Selective B1AMA= Atenolol Metropolo Acebutolol (B1 went to the AMA)
    • Nonselective B1 B2 A1 Carvedilol Labetalol
  72. Indirect Acting Adrenergic Agonsits
    • Tyramine (dieatry substance)
    • Ephedrine
    • Pseudoephedrine
    • Amphetamine
    • influenece nerve terminal release of NE binds to alpha and beta
  73. Uptake Blockers
    • Cocaine
    • Tricyclic Antidepressants
  74. Neuronal Blockers Inhibits NE release also cause NE depletion and can damage NE neurons
  75. Neuronal Blockers Deplets NE stores by inhibiting uptake of NE, NE then metabolized by intraneuronal MAO
  76. MAO Monoamine Oxidase Inhibitors
    • Pargyline
    • Tranylcypromine

    Tyramine (or other drugs that promote NE release) may cause markedly increased BP in patients taking MAO inhibitors