Card Set Information

2012-05-18 16:21:04

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  1. ACh Receptors: Na+/K+ channels
    Nicotinic ACh receptors
  2. ACh Receptors: G-protein-coupled receptors
    Muscarinic ACh receptors
  3. G protein linked 2nd messengers: a1

    NE and Epi

    increase vascular smooth muscle contraction, pupillary, sphincters
  4. G protein linked 2nd messengers: a2

    NE and Epi

    decrease sympathetic outflow
  5. G protein linked 2nd messengers: B1

    NE and Epi

    increase heart rate, contractility, renin release
  6. G protein linked 2nd messengers: B2

    NE and Epi

    vasodilation, bronchodilation, decreased uterine tone, increased HR and contractility
  7. G protein linked 2nd messengers: M1


  8. G protein linked 2nd messengers: M2


    Decrease heart rate and contractility of atria
  9. G protein linked 2nd messengers: M3


    increased bronchoconstriction, bladder contraction
  10. G protein linked 2nd messengers: D1


    renal vascular relaxation
  11. G protein linked 2nd messengers: D2


    Brain NT release
  12. G protein linked 2nd messengers: H1


    increased nasal mucous production
  13. G protein linked 2nd messengers: H2


    increase gastric acid
  14. G protein linked 2nd messengers: V1

    ADH (vasopressin)

    increase vascular smooth muscle contraction
  15. G protein linked 2nd messengers: V2

    Vasopressin (ADH)

    increase water permeability and reabsorption in kidney collecting tubules
  16. What are the symptoms of excess parasympathetic activity?
    • Diarrhea
    • Urination
    • Miosis
    • Bronchospasm
    • Bradycardia
    • Excitiation of CNS / Skeletal muscle
    • Lacrimation
    • Sweating
    • Salivation
  17. Name the cholinomimetic direct agonists and their primary use.
    Bethanechol - ileus, urinary retention (Bethany call to relieve bowels and bladder)

    Carbachol - glaucoma

    Pilocarpine - stimulates tears, sweat, saliva

    Methacholine - Dx asthma
  18. Name the anticholinesterases (indirect agonists) and their primary use.
    Neostigmine - ileus, urinary retention

    PyRIDostigmine - myasthenia gravis (gets RID of MG)

    Physostigmine - Glaucoma, atropine OD

    Edrophonium - Dx MG

    Echothiophate - glaucoma

    Donepezil - alzheimers

    Galantamine - alzheimers

    Rivastigmine - alzheimers
  19. How do you treat organophosphate poisoning?
    Atropine + Praloxidime
  20. Most common NMJ disorder. Autoantibodies to postsynaptic AChR.

    Ptosis, Diplopia, Weakness worsen with muscle use
    Myasthenia Gravis
  21. Name the muscarinic antagonists (besides atropine) and their primary use
    Benztropine - Parkinsons (Park my Benz)

    Scopolamine - Motion Sickness

    Ipratropium - Asthma / COPD

    Oxybutynin, Glycopyrrolate, Tolterodine, Darifenacin, Solefenacin, Trospium - urinary retention

    Methscopolamine - Peptic Ulcer
  22. Describe the effects of Atropine
    Blocks DUMBBELLS

    increase dilation and cycloplegia, body temp

    decrease secretions, motility and urgency in cystitis
  23. What is the mnemonic for Atropine?
    • Hot as a Hare
    • Dry as a Bone
    • Mad as a Hatter
    • Red as a Beet
    • Blind as a Bat
    • Bloated as a Toad
  24. When is atropine contraindicated?
    • BPH
    • Hyperthermia
    • Glaucoma
    • Delirium
    • Ileus/Obstruction
  25. What group of genes are responsible for skeletal development?
    HOX genes
    • 1 - Vesamicol
    • 2 - Hemicholinium
    • 3 - Acetyl Co A
    • 4 - Ca2+
    • 5 - Botulinim Toxin (flaccid paralysis)
    • 6 - Black widow spider Toxin
    • 7 - Choline Acetyltransferase
    • 1 - tyrosine hydroxylase
    • 2 - Metyrosine
    • 3 - Reserpine
    • 4 - Guanethidine (stops vesicle release)
    • 5 - Amphetamines, Ephedrine, Tyramine (increases NE release)
    • 6 - Cocaine, amphetamines, TCA's (prevent reuptake)
  26. Describe Gq pathways
    Phopholipase C -> PIP2 ->

    a) IP3 -> increase Ca2+ intracellular -> Ca2+ binds calmodulin -> activate CaM kinase

    b) DAG -> activate protein kinase C
  27. Tyrosine kinase receptors are associated with what?
    Growth factors
  28. What enzymes are used in the catabolism of NE?
    COMT - methylates

    MAO - oxidizes

    then excrete in urine
    • 1 - dorsal root ganglion
    • 2 - dorsal horn (sensory)
    • 3 - lateral horn
    • 4 - ventral horn (motor)
    • 5 - ventral root
    • 6 - white communicating rami (toward dot)
    • 7 - grey communicating rami
    • 8 - sympathetic ganglion
  29. Name the sympathomimetic drugs, their primary receptor and their primary function.
    Epinephrine - A1, A2, B1, B2 - anaphylaxis, glaucoma

    Norepinephrine - A1, A2, B1 - Septic Shock - but reflex brady!

    Isoproterenol - B1, B2 - AV block (reflex tachy)

    Dopamine - A1, A2, B1, B2, D1 - Cardiogenic Shock

    Dobutamine - B1 - Cardiogenic Shock

    Phenylephrine - A1, A2 - nasal decongestion

    Metaproterenol and Albuterol - B1 and B2 - asthma

    Salmeterol - B1 and B2 - long term asthma

    Terbutaline - B1 and B2 - reduce premature contractions

    Ritodrine - B2 only - reduce premature contractions
  30. Name the indirect sympathomimetics and their primary function.
    Amphetamine - Narcolepsy, ADD, Obesity

    Ephedrine and Tyramine- nasal decongestion, urinary incontinence

    Cocaine - vasoconstriction
  31. Name the sympathoplegics and their primary function.
    Clonidine and a-methyldopa - a2 agonists - HTN with renal disease.
  32. What drug do you give hypertensive pregnant women?
  33. Name the nonselective alpha blockers and their primary receptor and use.
    Phenoxybenzamine - A1 and A2 - pheochromocytoma

    Phentolamine - A1 and A2 - HTN crisis (MAO inhibitors eating tyramine foods)
  34. Name the a1 blockers and their primary use.
    Prazosin, Terazosin, Doxazosin - HTN, Urinary retention in BPH
  35. This drug class has 1st dose hypotension
    A1 blockers
  36. Name the a2 blockers and their primary use.
    Mirtazapine - depression for elderly (increases sleep and appetitie)

  37. Describe what happens after alpha blockade with phentolamine (non selective alpha blocker):
    • B2 vasodilation is unopposed - reversal of blood pressure change

  38. Describe what happens after alpha blockade with phentolamine (non selective alpha blocker):
    • No B effects means suppression, but not reversal
  39. Name the B1 selective Beta Blockers
    A BEAM

    • Acebutolol
    • Betaxolol
    • Esmolol
    • Atenolol
    • Metoprolol
  40. Name the effects of Beta Blockers and applications for use:
    HTN - decrease cardiac output and renin secretion

    Angina - decrease heart rate and contractility

    MI - decrease mortality

    SVT - decrease AV conduction (propranolol and esmolol)


    Glaucoma - decrease secretion of aqueous humor
  41. What B blocker would you give for thyroid storm?
  42. What are the common side effects of B Blockers?
    • sedation
    • impotence
    • exacerbation of asthma
    • bradycardia
    • AV block
    • increased blood glucose
  43. What patients should be given B blockers with CAUTION?
    • diabetics
    • asthmatics
    • CHF
    • Cocaine users

  44. What is Km? What is Vmax?
    Km - the amount of substrate needed to get 1/2 Vmax.

    A low Km means the enyzme loves the substrate. Just eating that shit up.

    Vmax = maximum velocity (how fast is substrate bindind enzyme)

  45. What is a noncompetitive inhibitor?
    Doesn't bind active site - therefore, doesn't compete.

    Noncompetitive inhibitors are in no hurry because they have no competition, so they bring Vmax and efficiency DOWN.
  46. Competitive or Noncompetitive?

    Resembles substrate
    Binds active site
    Increases Km
    Decreases potency
    Competitive Inhibitor
  47. Name the 4 equations you need to know for pharmacokinetics.
    1) Vd = amount of drug in body/ plasma drug concentration

    2) Cl = 0.7 x Vd / T1/2

    3) Ld = Cp x Vd

    4) Md = Cp x Cl

  48. What order elimination?
    Zero order

  49. What order elimination?
    First order
  50. Vmax or Km?


    amount of drug needed for a given effect
  51. Vmax or Km?

    Vmax - maximal effect a drug can produce

  52. Describe what happens to Km
    Right shift = less potent

    Km increases

  53. Describe what happens to Vmax
    Down shift - Vmax decreases

    less efficient

  54. Describe what happens to Vmax and Km
    Left shift and down shift - Km increases, Vmax decreases

    Less efficient, more potent
  55. Therapeutic Index: give formula and explain

    lethal dose/ effective dose = therapeutic index

    high index = safer
  56. Name 4 drugs with low therapeutic index
    • Warfarin
    • Phenobarbital
    • Lithium
    • Digoxin
    • Anti-seizure drugs too
  57. What drug do you use to treat benzo overdose?
  58. What are 3 drugs that have zero order elimination?
    PEA -

    • Phenytoin
    • Ethanol
    • Aspirin
  59. Ionized species are trapped and eliminated easily. What do you treat a weak acid drug overdose with?
    a base

  60. Ionized species are trapped and eliminated easily. What do you treat a weak base drug overdose with?
    an acid

    Ammonium Chloride
  61. Phase I metabolism describes what 3 processes?
    • Hydrolysis
    • Oxidation
    • Reduction

    "HOR" - Cytochrome P450 is Phase I
  62. Phase II metabolism describes what three processes?
    • Glucuronidation
    • Acetylation
    • Sulfation

    "GAS" - Geratric patients lose Phase I and rely on this, they are Gassy.
  63. Name the P450 Inducers:

    • Macrolides (Erythromycin)
    • Amiodarone
    • Grapefruit
    • Isoniazid
    • Cimetidine

    • Ritonavir
    • Acute Alcohol
    • Cipro
    • Ketoconazole
    • Sulfonamides
  64. Name the P450 Inhibitors
    Queen Barb Steals Phen Phen and Refuses Greasy Carbs

    • Quinidine
    • Barbiturates
    • St John's Wart
    • Phenytoin
    • Rifampin
    • Griseofulvin
    • Carbamazepine

    Chronic Alcohol Use
  65. What is the general biproduct of a phase I metabolism? Phase II?
    Phase I - polar water soluble metabolites

    Phase II - very polar inactive metabolites
  66. What overdose can be treated with bicarb? With ammonium chloride?
    Bicarb - Aspirin OD

    Ammonium Chloride - Amphetamine OD
  67. Describe the steps in ethanol metabolism
    ethanol -> alcohol dehydrogenase -> acetaldehyde -> acetaldehyde dehydrogenase -> acetate
  68. What drug inhibits alcohol dehydrogenase? When would you use it?

    Antidote for methanol or ethylene glycol poisoning
  69. What drug inhibits acetaldehyde dehydrogenase?

    discourage alcohol abuse
  70. Drug suffix: ane
    inhaled anesthetics
  71. Drug suffix: azine
  72. Drug suffix: ipramine
  73. Drug suffix: oxin
    cardiac glycoside
  74. Drug suffix: tidine
    H2 blockers
  75. Drug suffix: dronate
  76. Drug suffix: mustine
  77. Drug suffix: caine
    local anesthetics
  78. Drug suffix: cycline
    protein synthesis inhibitors (tetracyclines)
  79. Drug suffix: phylline
  80. Drug suffix: terol
    B2 agonists
  81. Drug suffix: triptyline
  82. Drug suffix: sartan
  83. Drug suffix: stigmine
    indirect muscarinic agonist
  84. Drug suffix: curonium
    paralytic, non depolarizing NMJ blocker
  85. Drug suffix: glitazone
    TZD's (diabetes)
  86. Drug suffix: dipine
    CCB's (dihydropyridines)
  87. Name the Sulfa Drugs

    • Probenecid
    • Sulfasalazines
    • Sulfonylureas
    • Thiazides

    • Furosemide
    • Acetazolamide
    • Celecoxib
    • TMP-SMX
    • Sumatriptan