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Pharmacology 2 - Sympathomimetics

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  1. 1The first step in the synthesis of NE from starts with?tyrosine
  2. 2What is the rate-limiting step of NE synthesis, name the enzyme?Tyrosine is catalyzed by tyrosine hydroxylase to make DOPA
  3. 3α1 & β1 receptors are in a different location than α2 and β2, which one needs a higher concentration due to its distance from the synapse?α2 & β2
  4. 4What group of compounds does norepinephrine belong to?Catecholamines
  5. 5What does the adrenal medulla do NE?makes epi from NE
  6. 6The adrenal medulla makes more epi than NE with the exception of what location?Pheochromocytoma cells
  7. 7What drug can inhibit tyrosine hydroxylase at the pheochromocytomas?Metyrosine
  8. 8What are the two locations of receptors called on the postsynaptic adrenergic area?Intrasynaptic and extrasynaptic
  9. 9Since α2 & β2 are relatively remote from nerve endings releasing NE, they are considered?Extrasynaptic receptors
  10. 10Since α2& β2 are considered extrasynaptic receptors they are not activated by NE released from nerve endings, rather they are activated byCirculating catecholamines
  11. 11Which type of α & β are more prevalent?α1 & β1
  12. 12By what release of NE are α1& β1mostly activated by? What type of receptor are they?NE released by nerve endings; intrasynaptic
  13. 13α1& β1 can be activated by circulating NE (or other catecholamines) but they require?Higher concentrations of such catecholamines than that required to activate extrasynaptic α2& β2
  14. 14Why are higher concentrations of needed to activate α1& β1 by circulating catecholamines?narrowness of synaptic space and power of reuptake pump in the synapse
  15. 15The reuptake pump at the synapse can take up?Epi and NE
  16. 16What do normal amounts of Epi look like?Low amounts
  17. 17What type of enzyme inactivates Epi and NE into deaminated metabolites after it is taken up?Monoamine Oxidase (MAO)
  18. 18What type of enzyme inactivates epi and NE into "o-methylated" (metanephrine) metabolites?Catechol-o-methyl transferase (COMT)
  19. 19The Vanillymandelic acid (VMA) metabolites were catalyzed by?MAO and COMT because it has been deaminated and o-methylated
  20. 20High urine levels of metanephrine and VMA are indicative of?Pheochromocytoma (more NE being produced so more metabolites are present)
  21. 21A person taking MAO inhibitors will likely experience more intense effects of what type of drug?Sympathomimetic drugs
  22. 22What is the largest vasculature bed?Skeletal muscle vasculature
  23. 23What happens to the eye with parasympathetic? (2)Pupillary constriction (Miosis); contraction of ciliary muscle (to accomadate near vision)
  24. 24What happens to the eye with sympathetic? Which receptor (2)?Pupillary dilation (mydriasis) α1; increase of ciliary aqueous humor β2
  25. 25What does the parasympathetic system do to the secretions of the body, specifically saliva?Increases secretions; copious watery saliva
  26. 26What does the sympathetic system do to saliva, name receptors?slight increase in saliva with drying α,β
  27. 27What does the parasympathetic system do to the heart?decrease rate, contractility, automaticity, and conduction velocity (mostly decrease rate)
  28. 28What does the sympathetic system do to the heart? Name the receptors.Increase rate, contractility, automaticity, and conduction velocity, mostly increases contractility; β1,β2 used for all
  29. 29What do blood vessels do with the parasympathetic system and how?Dilation; nitric-oxide mediated vasodilation on the endothelial cells
  30. 30What does the sympathetic system do to the blood vessels of the mucosa, saliva, skin, and splenic? what receptors?constrict α1 and α2
  31. 31What does the sympathetic system do to blood vessels of skeletal muscle? What receptors?constriction α1 and dilation β2
  32. 32What are the different reactions in the lungs when the sympathetic and parasympathetic nerves stimulate? What receptors?Sympathetic: relaxation β2; parasympathetic: constriction
  33. 33What does the sympathetic system do to the GI tract? Which receptors?Relaxation ( decrease moltility), α1β1α2β2
  34. 34What does the parasympathetic system do to the GI tract?Increase motility and spasms
  35. 35What does the sympathetic system do to the urinary bladder wall? Which receptors? Spincter and prostate? which receptors?Relaxation β1, β3; Contraction α1
  36. 36What does the parasympathetic do to the bladder wall and sphincter?constriction and relaxation, respectively
  37. 37What does the kidney JG cells do with the sympathetic system? Which receptorsIncrease renin secretions β1 (BP control)
  38. 38What does the sympathetic system do to the uterus? which receptor?Contraction α1, relaxation β2
  39. 39What do male sex organs do differently in sympathetic and parasympathetic? Add receptor for sympatheticS: Ejaculation α1, P: erection
  40. 40What does the sympathetic system do for the liver? What receptors?increase glucose output β2
  41. 41What does the sympathetic system do for the fat cells? What receptors?increase fatty acid output β1
  42. 42What do pilomotor muscles do with sympathetic? What receptors?Contraction α1
  43. 43What do the skin sweat glands do with sympathetic? What receptors?secretion; muscarinic
  44. 44At normal resting level, what is sympathetic nerve activity measured at?10-20 % of max use
  45. 45Why is sympathetic nerve needed at resting levels ?To help maintain critical body function at optimum levels like arterial BP and body temp
  46. 46What can lead to a fall in sympathetic nervous activity from brain to cardiovascular organ and what does it result?total spinal anesthesia; fall in arterial pressure
  47. 47What can restore BP after total spinal anesthesia?IV infusion of NE
  48. 48Why do the centers in the brain adjust from one moment to the next?In an attempt to hold bodily functions like arterial BP and body temp constant
  49. 49What do brain centers use to determine changesSensory (afferent) neurons like baroreceptors and thermoreceptors
  50. 50Where are the baroreceptors that sense small but significant changes in arterial BP?In the walls of arteries and aortic arch
  51. 51What are cardiac baroreceptors sensing?Changes produced by gravity during changes in posture
  52. 52Where do baroreceptors initiate changes to?Changes in autonomic neural outflow from CNS vasomotor centers to sympathetic vessels and sympathetic and parasympathetic heart
  53. 53Where and where are baroreceptors important?Important when preventing venous pooling of blood during orthostasis
  54. 54What is orthostasis?assumption of upright posture after sitting and reclining for a time
  55. 55What are baroreceptors doing during orthostasis and what are they trying to prevent?Maintaining arterial perfusion pressure constant to vital vascular beds like cerebral to prevent dizziness and fainting
  56. 56Larger changes in neural outflow (like hemorrhaging) will result inlarger changes in BP
  57. 57What are the thermoreceptors regulating?Body temperature in the face of changes in outside temp
  58. 58How do thermoreceptors regulate?Redistribute sympathetic nervous activity to vessels near the surface of the body or the vessels in the inner core in an attempt to shift blood one way or the other
  59. 59When thermoreceptors face cold weather, the brain also tells the adrenal medulla to?Put out more epi to increase glucose output from the hepatic cells and more free fatty acid output from fat cell for thermogenesis
  60. 60What other times will the adrenal medulla secrete more epi?Excercise and hypoglycemia
  61. 61What will increase in the heart with more epi in the blood?heart rate
  62. 62What is considered a cause of Raynaud's disease (cold blue fingers)?an abnormally excessive sympathetic NE response to cold stress
  63. 63What type of receptors does epinephrine stimulate?most α&β, nearly alike
  64. 64What type of receptors would standard low IV Epi affect the most?Extrasynaptic α2 & β2
  65. 65What will low IV Epi do? What will happen to mean arterial pressure?Decrease diastolic and only increase systolic, pulse pressure and heart rate; MAP remains unchanged
  66. 66What other receptors will be reached with higher IV ratesIntrasynaptic α1 & β1 recpetors
  67. 67What will high rates of Epi increase?pulse pressure, diastolic pressure and mean pressure
  68. 68What is the sympathomimetic directly acting against Epi used for?In high dose for circulatory shock
  69. 69What specific circulatory shock does epi treat? Why is it used?Anaphylactic shock to help treat bronchospasm and circulatory collapse
  70. 70What is sympathomimetic directly acting epi use to treat in asthma patientstreatment of bronchoconstriction
  71. 71What dose of sympathomimetic directly acting epi used? What receptor is being treated for stimulationLow dose; bronchial β2
  72. 72What life-threatening event is sympathomimetic is epi used for? What is it targeting? What dose?Cardiac arrest; cardiac β and vascular α; high dose
  73. 73When does treatment with high dose epi stop for AV block bradycardia stop?Until pacer is inserted
  74. 74When bradycardia is not from AV block it is treated with? It does not increase? Stimulates mostly?Low doses of epi; does not increase mean arterial pressure; stimulation of SA node
  75. 75Epi is sometimes mixed with local anesthetics because- it prolongs their action at local sites
    - minimizes systematic toxicity
    - minimizes local bleeding
  76. 76What kind of local concentrations are required to stimulate all vascular α receptors?high local concentrations
  77. 77What receptors can NE stimulate? Which receptor is the least stimulated?α&β but less so β2
  78. 78What do low and high rates of infusion of sympathomimetic NE do to all pressure measure? Which is least affected by low does of NE?increases all pressures, less so pulse pressurre at low NE
  79. 79At higher doses of NE what happens to HR?Reflexively decreases HR (less predictable the higher the dose)
  80. 80NE is used mainly for its effects onvascular αn receptors
  81. 81What kind of shock is NE used to treat? target?Cardiogenic, neurogenic, and certain septic shock (cardiac β1 and vascular α)
  82. 82What certain conditions would NE be used for septic shock? Target?early phase of septic shock especially if the shock persists after adequate fluid volume replacement ; vascular α
  83. 83Why is NE used for spinal anesthesia?support of BP
  84. 84What function could NE serve when mixed with local anesthesia but is not practiced?to prolong actions at sites of injection
  85. 85What receptors are stimulated by directly acting sympathomimetic Isoproterenol?stimulates β and not α
  86. 86What is decrease at high and low levels of Isoproterenol?Decrease diastolic and mean pressures
  87. 87What is increased high and low levels of isoproterenolincreases pulse pressure and heart rate, possibly more at high levels but it is hard to predict
  88. 88What is Isopreternal no longer used for in asthma?as a bronchodilator
  89. 89What rare use isoproterenol used for?bradyarrhythmia refractory
  90. 90Isoproterenol is also used as a pharmacological provocation to assist?Tilt table test for diagnosis of unexplained syncopes
  91. 91What happens to BP and HR as more NE is added?BP rises and HR decreases
  92. 92What happens to BP and HR as more Isoproterenol is added?BP declines and HR rises as a reflex
  93. 93Mathematically, what is systolic pressure?Diastolic and pulse pressure
  94. 94What does pulse pressure reflect?left ventricular cardiac contractility
  95. 95What does diastolic pressure reflect?Total peripheral arterial vascular resistance
  96. 96What is the mean pressure?A rough average of systolic and diastolic
  97. 97What is heart rate controlled by?Baroreflexes and direct stimulation of receptors in SA node
  98. 98What receptors does dopamine stimulate in the order of most stimulated?D receptors > β1 > α1 >> all others
  99. 99At low doses, what can dopamine stimulate?D receptors in splanchnic regions like GI and renal arterial smooth muscle
  100. 100At intermediates doses, what can dopamine stimulate?β1 receptors
  101. 101At high doses, what can dopamine stimulateα1 receptors
  102. 102Where does dopamine increase blood flow to at low doses?GI and Kidney
  103. 103At intermediate doses, what stimulation of β1 receptors do?Stimulation of contractility and rate
  104. 104Stimulation of α1 at high does of Dopamine (DA) cause?Mean arterial BP rise because of overall increase in total peripheral vascular resistance
  105. 105What forms of shock is dopamine used for?Cardiogenic, neurogenic and early or late phases of septic shock
  106. 106What types of patient use dopamine when they are refractory to other forms of therapy?CHF
  107. 107If patients are unresponsive to other forms of bradycardia treatment what can they use?Dopamine
  108. 108What sympathomimetic is a selective β1 agonist but affects both D receptors?Dobutamine
  109. 109Describe the mix of DobutamineMix of two stereoisomers, one is an α1 agonist and the other a potent β1 agonist plus α1 antagonist
  110. 110Dobutamine's β1 selectivity does what?Increase cardiac contractility largely and less increase in rate
  111. 111Because of dobutamine's increase in contractility what happensincrease in cardiac output and pulse pressure without an increase in diastolic and mean BP at therapeutic doses
  112. 112What treatment is Dobutamine used for?CHF and cardiogenic (late phase septic shock)
  113. 113Dobutamine is also used to stimulate the heart duringemergence from surgery on the heart
  114. 114Which sympathomimetics are selective β2 agonist?Albuterol, metaproterenol, pirbuterol, salmeterol and tertabutaline
  115. 115What are selective β2 agonist function?"bronchodilators"/ rescue inhalers --> relax bronchohial smooth muscle
  116. 116What disease are selective β2 agonist used to treat?COPD/ asthmatics with bronchoconstriction
  117. 117What do β2 agonist prevent that is exercise induced?Bronchospasms
  118. 118How can β2 agonists be brought into the body?Oral (preventative), IV and Inhaled (rescue)
  119. 119Terbutaline (β2 agonist) is also used in premature labor to? Why is it not used for long periods?Mediate uterine relaxation; high risk cardiovascular side effects with prolong use
  120. 120Which sympathomimetics are used as highly selective β3 agonist?Mirabegron & Solabegron
  121. 121What are selective β3 agonist used to treat?treatment of overactive bladder by relaxing detrusor (bladder wall) smooth muscle
  122. 122What are the sympathomimetics α1 agonists?phenylephrine and Midodrine
  123. 123Where are α 1 receptor mainly? What do they cause?Smooth muscle & blood vessel, used to increase BP
  124. 124What does α1 agonist phenylephrine cause when given via IV?Increases diastolic and mean BP with more reflex bradycardia
  125. 125Why does NE cause less reflex bradycardia then phenylephrine?Stimulation of β1 receptor in SA node oppose too much bradycardia
  126. 126When is IV phenylephrine used to maintain diastolic and mean BPDuring neurogenic shock, if DBP falls too low during therapeutic spinal anesthesia
  127. 127What is non-cardiac uses does IV phenylephrine have?hemorrhoids, nasal congestion and as a mydriatic agent
  128. 128Rarely IV phenylephrine is used to treat what?Supraventricular tachycardia
  129. 129What types of preparations are available for phenylephrine? Which is badly absorbed?Oral, topical, IV, spray; oral has poor absorptions
  130. 130Midodrine is another α1 drug why is different from phenylephrine?Better absorbed then phenylephrine because its ability to cross the GI tract better
  131. 131Midodrine is able to treat what problems?Orthostatic hypotensive systems and urinary incontinence due to loose sphincter
  132. 132Why is cocaine considered an indirect acting sympathomimetic drug?it inhibits the reuptake of NE leaving more available in the synapse for whatever receptors
  133. 133What are some beneficial sympathomimetics effect of cocaine?local anesthetic agent (for mucous membranes) and local vasoconstrictor at the site of local injection
  134. 134On rare occasions, cocaine may be used for?pain relief and reducing epistaxis while doing intubation of the trachea through the nose
  135. 135Why are pseudoephedrine and ephedrine considered indirect sympathomimetics and "mixed agonist"?The stimulation release of NE from sympathomimetic nerve endings nerve w/o action potentials may also stimulate adrenergic receptors directly
  136. 136What is pseudoephedrine mainly used for and why?Nasal and bronchial congestions because it promotes nasal and sinus drainage
  137. 137Why are Amphetamines, methamphetamine, and methylphenidate considered indirect sympathomimetics?They stimulate the release of catecholamine from sympathetic and central nerve endings
  138. 138In general pharmacokinetic considerations, α1,β2, β3 direct acting agonist and indirect acting drugs are?Readily absorbed and said to be therapeutically active after oral administrations and may last for hours in term of durations
  139. 139Which indirect acting sympathomimetics is not readily absorbed?Cocaine can cross GI very slowly
  140. 140Which β2 agonist has a very long durationSalmeterol
  141. 141Which sympathomimetics must be given parenterally (IV)?Cocaine and other directly acting agonists (E, NE, Isoproterenol, DA, Dobutamine)
  142. 142How long do the effects of cocaine and other direct acting agonist last if given by IV? What can make it last longer? ExampleLast a few minutes; Epi pen
  143. 143What is a major problem with sympathomimetic drugs? Why?Tolerance will long term use (so they need more to feel effects) bc adrenegic receptors are notorious for down regulation (reduced response to stimulus) when exposed too long to too much agonist
  144. 144For what types of treatments does tolerance normally occur?CHF (DA or Dobutamine) Chronic nasal congestion (pseudoephedrine), bronchoconstriction (selective β2 agonist)
  145. 145When original symptoms reoccur after stopping the medication that stopping medication that a patient has a tolerance is called?Rebound phenomena
  146. 146Why are side effects happening in sympathomimeticsextension of therapeutic effects (too much of a good thing becomes a bad thing) and lack of receptor selectivity
  147. 147With higher doses there are more?SIde effects
  148. 148Side effect that is related to treating depressed cardiac contractility after an acute MI with β agonistMore O2 deficiency, tachycardia, and arrhythmia
  149. 149Side effect related to treating hypotension with NE is?Severe hypertension
  150. 150When would sympathomimetics cause local dermal tissue necrosisWhen an injection intended for IV delivery of a large amount of α agonist misses the mark and ends up in the surrounding superficial tissue (massive local skin vasoconstriction)
  151. 151Side effect associated with treating incontinence or hypotensive system midodrine stimulate α1 receptors and causepiloerection and retention
  152. 152Using terbutaline prevent premature labor may cause?marked tachycardia in mother and fetus because of lack of sufficient receptor selectivity
  153. 153Inhaling albuterol for asthma may cause what due to insufficient receptor selectivitymarked tachyarrhythmias
  154. 154What is a side effect of using DA to increase renal blood flow?It will do the opposite and decrease renal blood flow
  155. 155Which type of sympathomimetic is more likely to enter the brain? Which is less likely?Indirect acting; direct acting
  156. 156What are the side effects of entering CNS?Insomnia, anxiety, convulsions, agitations, and hallucinations
  157. 157List Epi at therapeutic vs at high doses?Therapeutic- Systolic is up/ mean is same (only B1 activated)/ Diastolic is down
    High doses - (all receptors stimulated) all pressure increase
  158. 158—

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Der Nutzer hat seine Fachbereichs-Information gelöscht. Karteikarten am Pharmacology 2 - Sympathomimetics , erstellt von Gelöschter Nutzer am 21/10/2017.
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  • Erstellt von Jen Orellana · 19 Okt 2017
  • Kopiert von Jen Orellana · 21 Okt 2017
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