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  1. Describe the steps for CHOLINERGIC TRANSMISSION
    • 1. Ach is formed with Acetyle Co A (synthesized in the cell mitochondria) + choline that is brought intracellular.
    • 2. Formed ACh is transported into a vesicle with the aid of vesicle associated transporter (VAT)
    • 3. A “quanta” of ACh is stored in each vesicle (approx 1000-50,000 molecules)
    • 4. Vesicles are concentrated at nerve terminal.
    • 5. Held in place by protein.
    • 6. Release (exocytosis) occurs when AP reaches the nerve terminal causing EC calcium to influx.
    • 7. Ca causes vesicles to fuse with membranes and release ACh into the synapse.
    • 8. ACh binds with N1 receptors (pre synaptic) and is hydrolyzed by AChe’s.
  2. Manipulation of ACh release. Name three ways
    • 1. Botulinum toxin blocks binding of ACh vesicle to membrane.
    • 2. Choline transport can be blocked from entering the cell (reducing ACh formation)
    • 3. Hypocalcaemia reduces ACh release.
  3. Direct Acting Cholinergic Agonist, Acetylcholine – organic NT. activates which receptors?
    • 1. Muscarenic
    • 2. Nicotinic
  4. What is the most common method to increase / activate the PSNS?
    1. Using an In Direct Acting Cholinergic Agent
  5. How does an In Direct Acting Cholinergic (Cholinomimetics) agent work?
    • 1. It indirectly activates the PSNS by DECREASING the mechanism to terminate ACh.
    • 2. Indirect acting agents produce their primary effects by inhibiting acetylcholinesterase.
    • 3. By inhibiting ACHe's the endogenous acetylcholine concentration is INCREASED.
  6. What effect does a direct-acting Cholinoceptor stimulants (e.g. ACh)have on the eye?
    • 1. Contraction (miosis)
    • 2. Contraction for near vision
  7. What effect does a direct-acting Cholinoceptor stimulants (e.g. ACh) have on the heart?
    • 1. Sinoatrial node - DECREASE heart rate (negative chronotropy)
    • 2. Atria - DECREASE in contractile strength (negative inotropy), DECREASE in refractory period
    • 3. Atrioventricular node - DECREASE in conduction velocity (negative dromotropy), increase refractory period
    • 4. Ventricles - Small DECREASE in contractile strength
  8. What effect does a direct-acting Cholinoceptor stimulants (e.g. ACh) have on the blood vessels?
    1. Dilation (via EDRF), Constriction (high- dose direct effect)
  9. What effect does a direct-acting Cholinoceptor stimulants (e.g. ACh) have on the lungs?
    • 1. Bronchial muscles - Contraction (bronchoconstriction)
    • 2. Bronchial glands - Stimulation
  10. What effect does a direct-acting Cholinoceptor stimulants (e.g. ACh) have on the Gastrointestinal tract?
    • 1. Motility is INCREASED
    • 2. Sphincters are RELAXED
    • 3. Secretion are STIMULATED
  11. What effect does a direct-acting Cholinoceptor stimulants (e.g. ACh) have on the urinary bladder?
    • 1. Detrusor - CONTRACTION
    • 2. Trigone and sphincter - RELAXATION
  12. What effect does a direct-acting Cholinoceptor stimulants (e.g. ACh) have on the glands?
    1. Sweat, salivary, lacrimal, nasopharyngeal- SECRETION
  13. What forms a bond (varying strength) and inhibits enzymatic degradation of ACh. Ultimately causes an increase in ACh.
    1. Anticholinesterases
  14. Cholinesterase Inhibitor that is used to (treatment of MG) is quaternary amine (does not cross CNS). Short bond
    1. Edrophonium
  15. Cholinesterase Inhibitors that is used to (treatment of MG, reversal of NDMR) is a quaternary amine (does not cross CNS) – intermediate covalent bond
    1. Neostigmine
  16. Cholinesterase Inhibitors that has a prolonged covalent bond with acetylcholinesterase (AChE)
    1. Organophosphate (insecticides) Sarine Nerve Gas
  17. Cholinergic Activation and Clinical Practice (Para sympathomimetic Agonist) for GLAUCOMA
    1. Mechanism of action: Lower IOP by increasing aqueous outflow related to contraction of the ciliary muscle
  18. Cholinergic Activation and Clinical Practice (Para sympathomimetic Agonist) for GI/GU
    • 1. Increased smooth muscle activity in the gut
    • 2. increased secretions
    • 3. reduction of sphincter tones
  19. Cholinergic Activation and Clinical Practice (Para sympathomimetic Agonist) for NMJ
    1. Increase the concentration gradient of ACh in comparison to NDMR
  20. Cholinergic Activation and Clinical Practice (Para sympathomimetic Agonist) for Heart
    1. Reduction in heart rate
  21. Cholinergic Activation and Clinical Practice (Para sympathomimetic Agonist) for CNS
    • 1. tertiary amines will cross BBB
    • 2. may reduce NV and motion sickness
    • 3. can produce mild sedation.
  22. Name the two sets of receptors of the PSNS
    • 1. Nicotinic
    • 2 Muscarinic
  23. If an anticholinergic is given it will block at the N2 (at the NMJ) and cause what reaction?
    1. Muscle relaxation
  24. Blockade of M receptors produce side effects commonly seen antimuscarinic drugs:
    • 1. Atropine
    • 2. Scopolamine
    • 3. Glycopyrulate
  25. Can the drug atropine, a tertiary amine, cross the blood brain barrier?
    • 1. Yes,
    • 2. quat amines do not cross the BBB.
  26. How does Atropine (cholinergic antagonist) affect the CNS
    • 1. Mild dedative effect
    • 2. May reduce Parkinsons Tremor
    • 3. Dilates pupils - may influence CNS evaluation
  27. How does Atropine (cholinergic antagonist) affect the CV
    • 1. Blocks vagal tone leads to tachycardia
    • 2. may block coronary dilation and coronary flow
  28. How does Atropine (cholinergic antagonist) affect the lungs
    1. Mild to moderate bronchodilation
  29. How does Atropine (cholinergic antagonist) affect the GI
    1. Reduced GI motility
  30. Increased cholinergic activity (insecticide or nerve agents) leads to increased PSNS activity can be a
    1. Cholinergic Crisis
  31. During a cholinergic crisis which receptors are effected
    • 1. Nicotinic
    • 2 Muscarinic
  32. Treatment for a Cholinergic Crisis
    • 1. Antimuscarinics are the best method to treat CNS and “peripheral” symptoms (brady, salivation, ect).
    • ATROPINE THE BEST CHOICE
    • 2. No effective anti Nicotinic available. Must use 2-PAM Chloride or similar agent to help regenerate AChe’s
  33. Atropine (cholinergic antagonist) contraindications for use
    • 1. Glaucoma
    • 2. Elderly men with prostate enlargement
    • 3. Gastric Ulcers
  34. Where does adrenergic transmission occur
    1. ONLY in the POSTganglionic SNS
  35. Describe the steps for ADRENERGIC TRANSMISSION
    • 1. Tyrosine is brought intracellular (like Choline). Binds with Dopa makes Dopamine.
    • 2 Dopamine is transported into vesicle transporter (VMAT) and is converted to NE.
    • 3. Norepi is stored in post synaptic nerve vesicles at the terminals.
    • 4. Ca2+ helps with the release via exocytosis
  36. Termination for adrenergic transmission is carried out in three different ways, name them.
    • 1. Reuptake -into the nerve terminal by NET or into perisynaptic glia or other cells
    • 2. Dilution by diffusion from receptors - simple diffusion away from the receptor site (with eventual metabolism in
    • the plasma or liver)
    • 3. Metabolism by enzymes (MAO and COMT)
    • 4. Norepi action is brief and termination is efficient
  37. Uptake vía active transport is done
    • 1. Vesicle cytoplasm
    • 2. Move norepi back into vesicle
    • 3. 80 percent of Norepi is terminated through re-uptake
    • 4. Uptake is the site of action for may drugs.
  38. What is the rate liming step for adrenergic transmission
    1. THE CONVERSION OF TYROSINE TO DOPAMINE IS THE RATE LIMITING STEP TO CATACHOLAMINE DEVELOPMENT.
  39. Manipulation of Noriepi release, nome three ways.
    • 1. Block the transport of Tyrosine - can be blocked with reserpine
    • 2. Inhibit of VMAT protein that will block the conversion of Dopamine to NE
    • 3. Block/inhibit NE transporter (carries NE back into cell after release). - cocaine, tricyclic antidepressants
  40. Adrenergic Agonists manipulate what
    1. SNS
  41. Effects of the SNS are due to what
    1. NE
  42. Name the two ways to manipulation of the SNS can occur
    • 1. Agonizing directly: organic or synthetic catecholamine.
    • 2. Indirect: reduce degradation of catecholamine.
  43. Adrenergic Receptor type Alpha 1 affects WHAT and effects WHAT
    • 1. Receptor - Vascular smooth muscles
    • 2. Effect - increase IP3, DAG
  44. Adrenergic Receptor type Alpha 2 affects WHAT and effects WHAT
    • 1. Recptor - CNS
    • 2. Effects - Decrease cAMP
  45. Adrenergic Receptor type BETA 1 affects WHAT and effects WHAT
    • 1. Recptor - heart
    • 2. Effects - increase cAMP
  46. Adrenergic Receptor type BETA 2 affects WHAT and effects WHAT
    • 1. Recptor - Lungs
    • 2. Effects - increase cAMP
  47. Adrenergic Receptor type DOPAMINE affects WHAT and effects WHAT
    • 1. Recptor - renal
    • 2. Effects - increase cAMP
  48. The receptor type that increases IP3, DAG
    1. Alpha 1
  49. The receptor type that decreases cAMP
    1. Alpha 2
  50. The receptors that increase cAMP
    • 1. Beta 1
    • 2. Beta 2
    • 3. Dopamine
  51. What is meant by many drugs are "dirty"
    1. Many drugs are “dirty” – they have affinity for more then one receptor and as such cause a variety of responses
  52. Example of receptor affinity norepi vs epi
    • 1. Norepi: Equal alpha binding, B1 greater then b2
    • 2. Epi: equal alpha binding, equal beta binding
    • 3. Isoproterenol: pure beta, little to no alpha
  53. Endogenous Catecholamine's: "dirty"
    • 1. Norepinephrine (NE): a1=a2 > B1
    • 2. Epinephrine: a1=a2, b1=b2
    • 3. Dopamine: low dose=dopa, mod=dose alpha, high dose=beta
  54. Direct Acting Sympathomimetic:
    • 1. Phenylephrine – pure alpha 1 agonist
    • 2. Clonidine – pure alpha 2 agonist
  55. Sympathomimetic Drugs, Ephedrine has
    1. Mixed alpha and beta
  56. Sympathomimetic Drugs, indirect acting agents act by increasing NE in two ways, name them
    • 1. Entering nerve cells and displacing NT leads to increased concentrations (amphetamines)
    • 2. Reducing the termination of NT (MAOI)
  57. What will reduce turbulence in airways
    1. Beta 2 agonist
  58. What effect does a sympathomimetic drug have on alpha 1 receptor
    • 1. Tissue - most vascular smooth muscle (innervated) Action - contraction
    • 2. Tissue - pupillary dilator muscle - Action - contraction (dilates pupil)
    • 3. Tissue - pilomotor smooth muscle - Action - Erects hair
    • 4. Tissue - Prostate - Contraction
    • 5. Tissue - Heart - Action - Increases force of contraction
  59. What effect does a sympathomimetic drug have on alpha 2 receptor
    • 1. Tissue - Postsynaptic CNS - Action - probably multiple
    • 2. Tissue - Platelets - Action - aggregation
    • 3. Tissue - Adrenergic and Cholenergic nerve terminals - Inhibits transmitter release
    • 4. Tissue - Some vascular smooth muscle - Action - Contraction
    • 5. Tissue - Fat Cells - Action - inhibits lipolysis
  60. What effect does a sympathomimetic drug have on beta 1 receptor
    1. Tissue - Heart, juxtaglomerular cells -Action - Increases force and rate of contraction; and increases renin release
  61. What effect does a sympathomimetic drug have on beta 2 receptor
    • 1. Tissue - Respiratory, Uterine, and Vascular smooth muscle - Action - Promotes smooth muscle relaxation
    • 2. Tissue - Skeletal muscle - Action - Promotes potassium uptake
    • 2. Tissue - Human liver - Action - Activates glycogenolysis
  62. Hypotension: From Sepsis – toxins leads to vasodilation. What is the best agent for treatment? Why?
    1.
  63. Hypotension: Neurogenic –Loss of ANS control leads to loss of SVR (maybe hear rate). What is the best treatment? Why?
    1.
  64. Hypotension: Cardiogenic – loss of contractile force/pump. What is the best treatment? Why?
    • 1. Positive inotropic agent such as dopamine or dobutamine
    • 2. The goal is tissue perfusion, not blood pressure
  65. Hypotension: Hypovolemic - loss of volume. What is the best treatment? Why?
    • 1. Norepinephrine
    • 2. Phenylephrine
    • 3. Methoxamine
    • All have the the vasoconstriction properties desired
  66. Anaphylaxis: Anaphylaxis commonly causes mast cell degranulation  hypotension. Best choice? Why?
    1. Epinephrine
  67. Adrenoceptor Antagonist will have what effect
    • 1. Blockade or Antagonism of SNS receptors will reduce the outflow of the “fight or flight” response
    • 2. Reduction in NT or BLOCKADE of a receptor will cause a reduced clinical effect
  68. Adrenoceptor Antagonists duration of action is dependent on
    • 1. the half life
    • 2. clearance of the drug
  69. Alpha Antagonists, blockade of alpha 1 receptors will
    • 1. Decrease in SVR, orthostatic hypotension
    • 2. Miosis (small pupils), nasal congestion
    • 3. May see reflex tachycardia
  70. Phenoxybenzamine:
    • 1. Covalent bond with alpha 1
    • 2. Low oral bioavailability
  71. Generally, beta blockers, Beta Receptor Antagonist have
    • 1. High oral absorption
    • 2. Extensive first past effect
    • 3. Rapid distribution with large Vd.
    • 4. ½ lives approximately 3-10 hours
  72. What effects does the Beta Blockers have on the body, Pharmacodynamics: CardioVascular System:
    • 1. Reduction in BP1.
    • 2.Primarily via B1 rate control, but may also reduce renin release
  73. What effects does the Beta Blockers have on the body, Pharmacodynamics: Respiratory System:
    1. Non selective B or B2 blockers can increase bronchiolar resistance
  74. What effects does the Beta Blockers have on the body, Pharmacodynamics: Ocular:
    • 1. Reduces IOP
    • 2. Decreases aqueous humor production.
  75. Specific agents: Propranolol "prototypical drug"
    1. Non-selective drug
  76. Specific agents: Metoprolol:
    1. selective B1 greater than B2
  77. Specific agents: Labtolol:
    1. B1 > a1, may see bronchospasm. Less reflex tachycardia.

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Author:
 scoleman
ID:
 193641
Filename:
 Flashcards.txt
Updated:
 2013-01-18 23:12:48
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Pharm Exam
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Description:
Exam One Fourth Lecture
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