Peripheral Receptors and Agents Acting on PNS and CNS

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Peripheral Receptors and Agents Acting on PNS and CNS
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Peripheral Receptors, Agents Acting on PNS and CNS in Pharmacology and Toxicology
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  1. Nervous system
    • primary communication and control center, functions in concert with endocrine system.  
    • Allows adaptation, maintains homeostasis, controlled by hypothalamus
  2. 3 functions of nervous system
    • sensory
    • integrative
    • motor
  3. Dif between endocrine and nervous
    NS sends electrical messages, ES sends chemical messages.
  4. Neuron
    • fundamental unit of NS.  
    • Dendrites, cell body, axon, tilodendra, myelin sheath made of schwann cells, nodes of ranvier
  5. myelin sheath
    insulation for axon, made of schwann cells.  Where there is no sheath is called a node of ranvier
  6. nodes of ranvier
    gaps between myelin sheath (schwann cells)
  7. schwann cells
    make up myelin sheath.
  8. __________carry impulses away from the nerve cell
    axons
  9. ___________carry impulses toward nerve cell
    dendrites
  10. telodendra
    • ends of axons (fray).  10,000 or more per axon.
    • Synaptic end bulbs pass nerve impulses to adjacent structure
    • Emit neurotransmitters into synapse
    • Acetylcholine, norepinephrine, dopamine, seratonin, gamma-aminobutyric acid
  11. GABA
    gamma aminobutyric acid
  12. 5 parts of a reflex arc
    • receptor
    • sensory neuron
    • center in CNS for a synapse
    • motor neuron
    • effector
  13. Cerebrum
    higher function
  14. Thalamus
    pain, relay between cerebrum and other parts of the brain
  15. hypothalamus
    • mediator of endocrine system, using the pituitary gland.  
    • Controls autonomic NS
  16. Medulla
    • with the pons, makes up the brainstem
    • connects spinal cord to brain
    • sensory and motor
    • vital, unconscious functions
  17. reticular formation
    network of nerves from the medulla upwards in the brainstem, contains the reticular activating system (RAS),  which controls wakefulness.
  18. Two divisions of nervous system
    • CNS is the control center (brain and spinal cord)
    • PNS (cranial nerves, spinal nerves, connects CNS to glands, muscles, receptors)
  19. 2 nerves of PNS
    • Afferent (out to in)
    • Efferent (in to out)
  20. 2 parts of PNS
    • Somatic NS (efferent, to skeletal muscle, voluntary)
    • Autonomic NS (efferent, CNS to cardiac muscle, smooth muscle and glands, involuntary
  21. Autonomic NS and 2 parts
    • Controls unconscious body activities (automatic and involuntary)
    • innervates smooth muscle, cardiac muscle, salivary glands and viscera
    • Parasympathetic or Sympathetic
  22. Parasympathetic NS
    • CHOLINERGIC
    • regulates energy conserving activities
    • Rest and Digest
    • Craniosacral
    • Long preganglionic, short postganglionic
  23. Sympathetic NS
    • ADRENERGIC
    • regulates energy expending activites
    • Fight or Flight
    • thoracolumbar
    • short preganglionic, long postganglionic except adrenal medulla
  24. Similarities in Sympathetic and Parasympathetic
    • both have two neurons, preganglionic synapses at ganglionic synapse with postganglionic
    • Postganglionic synapses with target tissue
    • work with mostly the same organs
  25. Exceptions to normal sympathetic/parasympathetic balance
    • sweat glands, adrenal medulla and hair follicles are only controlled by sympathetic stimulation.
    • Adrenal medulla acts as post-ganglionic neuron, accepts Ach with Nicotinic receptor.  
    • Sweat glands are stimulated by symp, but use a Muscarinic receptor.
  26. Largest ganglion
    Celiac ganglion.  Sends nerves to GI, adrenal, kidney, spleen and stomach.
  27. Heart: Para and Symp effects and receptors on SA node, AV node, Atrial and ventricular muscle.
    • SA node: symp increases HR, B1
    • para decreases HR, Muscarinic
    • AV node: symp increases conduction, B1
    • para decreases conduction, M
    • a/v muscle: symp increases force of contraction, B1
    • para decreases force of contraction, M
  28. Lungs: para and symp effects and receptors on bronchial smooth muscle and secretions
    • Smooth Muscle: symp relaxes for more air in, B2
    • para contracts for less air in, M
    • Secretions: symp inhibits for clear airways, B2
    • para stimulates to catch dirt, M
  29. Vascular smooth muscle: Parasympathetic vs sympathetic effects and receptors
    • Symp: constricts to increase blood pressure (a1) or dilates (B2).  BOTH.  
    • Para: there are receptors, we don't know what they do.  Probably muscarinic.
  30. GI system, motility and secretions: parasymp vs symp effects and receptors
    • motility: symp decreases, a1 (and more)
    • para increases, M
    • secretions: symp decreases, a1 (and more)
    • para increases, M
  31. Urinary bladder, detrusor muscle and internal urethral sphincter: symp vs parasymp effects and receptors
    • detrusor: symp relaxes, B2
    • para contracts, M
    • urethral sphincter: symp contracts, a1
    • para does nothing.
  32. Eye, pupil diameter and focal point: parasymp vs symp effects and receptors
    • pupil diameter: symp dilates (mydriasis), a1
    • para contracts (miosis), M
    • focal point: symp far, B2
    • para near, M
  33. mydriasis
    dilated pupil
  34. miosis
    constricted pupil
  35. Adrenal medulla: parasymp vs symp effects and receptors
    • symp: stimulates to release epinephrine/norepinephrine, Nicotinic.  
    • No para influence
  36. sweat glands: parasymp vs symp, effects and receptors
    • symp: stimulates, Muscarinic
    • no para influence
  37. Cholinergic
    • accepts acetylcholine.  Parasympathetic.  
    • Neuromuscular junction, autonomic ganglia (all), cardiac muscle, smooth muscle, glands except sweat glands.
  38. Nicotinic receptor
    • Cholinergic, found at adrenal medulla, autonomic ganglia, neuromuscular junction (excitatory)
    • Parasympathetic except autonomic ganglia and adrenal medulla.
  39. Muscarinic receptor
    • Cholinergic, found at heart muscle, smooth muscle, secretory glands.  Both excitatory and inhibitory.  
    • Always para, except sweat glands.
  40. Adrenergic receptors
    • Sympathetic.  Epinephrine, norepinepherine, alpha and beta, dopamine.  
    • Alphas are usually excitatory (a1, a2)
    • Beta 1 are usually excitatory, beta 2 usually inhibitory.
  41. Alpha adrenergic receptors
    • a1: constriction of spincters and arterioles, constriction of dilator muscle for pupils, constriction of urethra for increased tone.
    • a2: inhibits presynaptic neurons, constricts skeletal muscle vessels.
  42. Beta adrenergic receptors
    • B1: increases rate of conduction, BP and contractions in heart, releases renin in kidneys.  
    • B2: dilates skeletal blood vessels and bronchioles, relaxes GI smooth muscle
  43. dopaminergic adrenergic receptors
    • DILATES
    • blood vessels of kidneys
    • dilates coronary vessels of heart
    • dilates mesenteric blood vessels
  44. Which adrenergic receptor only uses Epi?
    B2.
  45. Cholinergic agents
    • stimulate receptor sites mediated by acetylcholine (parasympathetic exc, sweat and adrenal medulla)
    • Can be direct (mimic ACh) or indirect (inhibit breakdown of ACh)
  46. Clinical uses of cholinergic agents
    • diagnosis of myasthenia gravis
    • reduce IOP in glaucoma
    • stimulate GI motility
    • treat urinary retention
    • control vomiting
    • antidote for neuromuscular blockers
  47. direct cholinergic agonists
    stimulate cholinergic receptors, cause para effects (muscarinic or nicotinic)
  48. 2 phases of micturition
    • storage (sympathetic)
    • voiding (parasympathetic)
  49. Direct-acting muscarinic agonist, primary and secondary reactions
    • Primary: causes GI wall smooth muscle contraction, urinary bladder wall contractions
    • Secondary: sphincter of iris (blurry far vision), SA node of heart, Brochiolar smooth muscle cells, lacrimal, salivary, sweat, bronchial, mucosal, digestive glands
    • (Parasymp functions)
  50. Contraindication
    • any condition which makes a particular type of treatment improper
    • causes harm.
  51. Direct acting cholinergics
    acetylcholine, carbamylcholine, bethanechol
  52. Carbamylcholine
    direct acting cholinergic causing GI atony and uterine contractions in pigs
  53. bethanechol
    direct acting cholinergic causing GI atony and uterine atony
  54. Pilocarpine
    • direct acting cholinergic
    • decreases intra-ocular pressure, stimulates gland secretion.
    • For use in neurogenic KCS, activates Facial nerve (VII) to produce tears
  55. Metoclopramide
    • direct acting cholinergic
    • anti-emetic, promotes gastric motility.
  56. angle of schlemm
    aqueous humor drains from pupil from this angle, can be blocked by dilated pupil.  Pilocarpine allows to drain.
  57. atony
    no muscle tone
  58. Competitive indirect acting cholinergic agents
    temporarily occupy ACh binding site on acetylcholinesterase, which breaks down acetylcholine.  More ACh in synapse, more firing.
  59. Anticholinesterases
    • competitive indirect acting cholinergic agents
    • edrophonium, pyridostigmine, neostigmine, physostigmine
  60. toxic effects of anticholinesterases
    skeletal muscle weakness, vomiting, colic, diarrhea, bradycardia, dyspnea, respiratory paralysis, blurry distant vision, CNS depression (physostigmine only)
  61. edrophonium (tensilon)
    • reversible indirect cholinergic/anticholinesterase
    • diagnosis of myasthenia gravis.  
    • IV
    • short duration, 2-5 minutes.
  62. Pyridostigmine (mestinon)
    • reversible anticholinesterase
    • Treatment of myasthenia gravis
    • oral
    • longer acting, hours (usu BID)
  63. synechia
    • anterior and posterior lens adhered to something else in eye.  
    • anterior, lens attached to cornea by scar
    • posterior, lens attached to retina by scar
  64. What other problem comes with myasthenia gravis?
    megaesophagus
  65. myasthenia gravis
    autoimmune disease that destroys nicotinic receptors in neuromuscular junction.  Edrophonium is a great test for it (anticholinesterase), and pyridostigmine is the treatment
  66. Neostigmine
    • competitive anticholinesterase
    • used in humans for myasthenia gravis.
  67. Physostimine
    • competitive anticholinesterase
    • topical ophthalmic that decreases IOP in glaucoma or breaks down posterior synechia in horses.  Also helps in GI atony in cattle.
  68. Irreversible indirect-acting cholinergic.
    • Covalently bonds, inactivating AChE forever.  
    • Organophosphates
    • used in pesticides
  69. Cholinergic effects of irreversible anticholinesterase
    Organophosphate toxicity: Bronchoconstriction, increased salivation, lacrimation, airway secretions, digestive secretions, diarrhea, vomiting, abdominal cramping, urination, miosis, muscle tremors to paralysis, CNS toxicity including seizures.
  70. dog flea/tick on cat is an example of what?
    Organophosphate toxicity, from irreversible anticholinesterase.
  71. Cholinesterase reactivators
    • pralidoxime (2PAM, PAM)
    • breaks bonds between organophosphate and AChE.  
    • Atropine (muscarinic antagonist)
  72. agent selectivity
    • a selective agent preferably interacts with pme receptor subgroup at low plasma concentrations.  
    • As levels increase (you give more), it becomes less selective
  73. cholinergic receptor antagonist
    agent blocks effects of parasympathetic (cholinergic), so sympathetic (adrenergic) continues unopposed.
  74. If you have ciliary spasming you should apply
    muscarinic receptor antagonist.  May cause mydriasis.
  75. Treatment of cardiac arrhythmias
    Muscarinic receptor antagonist, fixes sinus bradycardia, AV block, ventricular asystole.
  76. Antidote for organophosphate toxicity
    muscarinic receptor antagonist
  77. Before and during general anesthesia, ___________used to be used, and why
    • mucarinic receptor antagonists
    • they suppress bronchial secretions, suppress salivary secretions, prevent vagal bradycardia due to vagus nerve.  
    • Can also remove vagal influence to cure AV block and fix ventricular asystole when due to excessive parasymp tone
  78. Anticholinergic effects
    sympathetic effects
  79. cholinergic effects
    parasympathetic
  80. Mechanism-based adverse effects of anticholinergics
    • predictable extensions of muscarinic receptor blockers
    • sympathetic effects like tachycardia, ileus etc 
    • Atropine goes to CNS, can cause anxiety, restlessness, disorientation
  81. Contraindications of anticholinergics
    • Not used in large animals, horses can die from ileus and ruminants get CNS toxicities and rumen stasis. 
    • tachycardia
    • GI or urinary obstruction, both physical and functional.
    • KCS
    • glaucoma
  82. anticholinergic drug examples
    • atropine
    • glycopyrrolate
  83. glycopyrrolate
    • anticholinergic
    • More polar than atropine, so less blood-brain or placental interaction
    • Less likely to cause tachycardia
    • longer duration and slower onset of effect than atropine, so not choice in emergencies, but good for C-section and anything else
  84. What to give for overdose of anticholinergic like atropine or glycopyrrolate
    anticholinesterase, ideally edrophonium.
  85. atropine
    • anticholinergic agent often used in emergencies.  Belladonna
    • Increases heart rate, dilates bronchioles, good for cardiac arrest.  
    • Contraindicated in glaucoma, heart problems, etc
  86. dysnergia
    impairment between detrusor and sphincter causing urinary retention.  Prazosin with bethanacol can help line up.
  87. sympathomimetic
    Symp NS effects, like catecholamines
  88. anticholinergic effect on bronchioles
    • Block muscarinic or parasympathetic influence, sympathetic or B2 (epinephrine) influence unopposed.
    • Bronchial smooth muscle relaxes and mucous secretion decreases. (B2)
  89. anticholinergic effect on eye
    • Block muscarinic or parasympathetic influence, sympathetic or a1/B2 (norepi or epi) influence unopposed.   
    • spincter muscle of iris contracts (mydriasis), pupil dilates (a1)
    • ciliary muscle relaxes (cycloplegia), focus is far (B2)
  90. anticholinergic effects on heart
    • Block muscarinic or parasympathetic (vagal) influence, sympathetic or B1 (norepinephrine) influence unopposed.
    • SA node increases heart rate (B1)
    • AV node increases, speeds condution (B1)
    • Atrial/Ventricular muscles contract, increasing force of contraction (B1)
  91. Chatecholamines, endogenous and synthetic
    • direct-acting adrenergic agonists (sympathomimetic).
    • Endogenous: norepinephrine, epinephrine, dopamine
    • Synthetic/exogenous: isoproterenol, dobutamine
  92. MAO
    monoamine oxidase, breaks down catecholamines
  93. endogenous catecholamine synthesis
    • Tyrosine
    • Dopa
    • Dopamine
    • Norepinephrine
    • Epinephrine
  94. Dopaminergic neurons are found (generally)
    CNS, enteric nervous system and kidney
  95. Noradrenergic neurons are found (generally)
    In CNS and PNS
  96. Epinephrine is found (generally)
    In adrenal medulla and neurons in CNS ONLY
  97. Direct-acting adrenergic receptor agonist drugs
    Interact with and activate adrenergic receptors (Alpha, Beta, Dopaminergic)
  98. A1 adrenergic receptors
    Stimulation produces smooth muscle contraction, except in GI smooth muscle cells (inhibit ACh release)
  99. B2 adrenergic receptors
    causes smooth muscle relaxation
  100. B1 adrenergic receptors
    • Stimulation produces excitatory effects in cardiac muscle
    • SA node: increases HR
    • AV node: speeds conduction
    • Ventricular muscle: increases force of contraction
  101. How NEpi and Epi interact with A and B receptors
    • Both stimulate all except B2.  
    • Only Epi stimulates B2 (relaxes smooth muscle)
  102. Direct cardiac effects of Epi and NEpi
    • SA node: increases HR
    • AV node: speeds conduction
    • Ventricular muscle: increases force of contraction
  103. Chronotropic effect
    • relates to heart rate
    • positive chronotropic effect increases HR.
    • Adrenergic agonists and anticholinergics both positive effect
    • Cholinergics and anticholinesterases have negative effect
  104. Dromotropic effect
    • Action that effects conduction of electrical velocity through AV node.
    • Adrenergic agonists and anticholinergics both positive effect
    • Cholinergics and anticholinesterases have negative effect
  105. Inotropic effect
    • Action that effects force of contraction of cardiac muscle.  
    • Adrenergic agonists and anticholinergics both positive effect
    • Cholinergics and anticholinesterases have negative effect
  106. Cardiac output
    • volume of blood leaving heart per unit time (minute)
    • CO = HR x SV
    • Increased by stimulating B1 receptors at SA node (increase HR) and B1 receptors at ventricular muscles (increase SV)
  107. stroke volume
    • volume of blood that leaves the heart per beat.  
    • Increased by stimulating B1 receptor in ventricular myocytes (adrenergic).
  108. Epinephrine at therapeutic doses stimulates what?
    a1 receptors.
  109. Peripheral Vascular Resistance
    • impediment to blood flow through systemic arteries caused by constriction of arterioles.  
    • Arterial BP = CO x PVR
    • NEpi and Epi at therapeutic doses constricts arteries to increase PVR to increase BP.
  110. Dyspnea due to bronchoconstriction
    • Epinephrine stimulates B2 receptors on airways, relaxes, bronchodilation.  
    • Atropine would also work by removing muscarinic or parasympathetic influence.
  111. Cardiac arrest
    • absense of heart sounds and pulses, generally begins with
    • Ventricular fibrillation (fluttering)
    • ventricular asystole (no pumping)
    • electromechanical dissociation (bizarre rhythm but no connected pumping).  
    • Then blood flow stops.
  112. Epinephrine
    • direct-acting adrenergic, works on a1, a2, b1 and b2.  Comes from CNS and adrenal medulla.
    • Often supplied in 1:1000 (0.1%), need to dilute to 1:10,000 (0.01%).  
    • May need refridgeration, light-sensitive.  
    • Usually give IV or IT for cardiac arrest
  113. IT administration
    double dose, mix with 2-5 ml of sterile water, pour through catheter in endotrachial tube, give 2 breaths.
  114. Dopamine
    • secreted by dopaminergic neurons in brain, enteric NS and kidney.  
    • receptors in brain, mesentery and heart.  
    • Cats kidney's DO have them, but they are a different sub-type (there used to be a question)
  115. enteric nervous system
    • GI has own nervous system, consisting of myenteric plexus and submucosal plexus
    • Provide communication between different layers of alimentary canal
    • Dopaminergic and a1, and muscarinic receptors.
  116. myenteric plexus
    • part of enteric nervous system, neurons that provide communication between longitudinal muscle and circular muscle.  
    • Contains alpha 1 and dopaminergic receptors that help it relax and muscarinic receptors to flex
  117. submucosal plexus
    • part of enteric nervous system
    • neurons providing communication between muscularis and mucosa/submucosa layers.
    • Contains a1 and dopaminergic receptors to help it relax and muscarinic receptors to flex
  118. alpha 1 receptors in GI
    • inhibit acetylcholine to cause relaxation.
    • Only non-excitatory a1 receptors.
  119. moderate dose of dopamine causes
    • dilation of mesenteric and renal arteries
    • stimulation of B1 receptors of heart (indirect by becoming NEpi) causing increased heart rate and increased force of contraction
  120. high doses of dopamine cause
    vasoconstriction, by indirectly stimulating a1 receptors.
  121. therapeutic uses of dopamine
    • Shock (moderate dose)
    • Refractory congestive heart failure (moderate dose)
    • hypotension
    • oligouric renal failure
  122. Dopamine use in shock
    • moderate dose increases blood flow to kidney and mesentery
    • increases cardiac output by increasing HR and force of contraction
  123. dopamine use in refractory congestive heart failure
    moderate doses cause increased cardiac output without increased PVR.
  124. Administration of dopamine
    • MUST be diluted in CRI, IV administered.  Use a pump, extremely small amounts so measurements must be accurate.  
    • Must stay within vein, can cause necrosis and sloughing of tissue
  125. dobutamine
    • synthetic catecholamine, B-agonist, specific to B1 at therapeutic doses.
    • Increases force of contraction more than increasing heart rate (chooses ventricles over SA node)
  126. Therapeutic uses of dobutamine
    • Shock
    • refractory congestive heart failure
    • Must be diluted in CRI, IV administrated.
  127. Isoproterenol
    • synthetic chatecholamine, B-agonist.  Stimulates B1 and B2 with no effect at a1.  
    • increases HR at SA node, conduction at AV and force of contraction in ventricles.  Powerful vasodilator in veins and airways.  
    • Little effect in kidney
  128. Uses of isoproterenol
    • complete AV block (short term until pacemaker can be installed)
    • Bronchodilator in anaphalactic shock (dangerous due to hypotension side effect)
  129. Adverse effects of Isoproterenol
    • B2 stimulation without a1 effect causes vasodilation.  No PVR causes hypotension.  
    • Though cardiac output increases (from B1 receptors), PVR decreases more so overall systemic is decreased BP
    • Kicks off baroreceptor reflex, causing reflex tachycardia
  130. Arterial baroreceptors
    • located in walls of aortic arch and carotid sinuses
    • Stretch receptors that detect BP
    • report to medulla which stimulates sympathetic or parasympathetic response to compensate
  131. Autonomic reflex arc
    Baroreceptor reflex
    arterial baroreceptors located in walls of aortic arch and carotid sinuses, feel pressure and detect blood pressure.  Report to medulla if too high or low, medulla stimulates sympathetic or parasympathetic response
  132. Reflex tachycardia
    When blood pressure drops, baroreceptor reflex causes heart rate to rise.
  133. arrhythmogenic effects of catecholemines
    • all are potentially arrhythmogenic !  
    • Epinephrine and isoproterenol are worse than dopamine and dobutamine.
  134. Do catecholamines cause hypertension or hypotension (epinephrine, dopamine, norepinephrine, isoproterenol)
    • regular dosing of epinephrine = sympathetic = hypertension
    • high-dose dopamine = a1 vasoconstriction = hypertension
    • norepinephrine = no B2 = hypertension
    • isoproterenol = B2 = hypotension
  135. strongylus vulgaris
    • parasite that migrates in intestines of a horse causing problems in blood supply.  
    • "verminous" aneurisms
    • catecholamines that cause hypertension can cause aneurisms to rupture
  136. aneurisms are contraindication for what drugs?
    Anything that causes hypertension (catecholamines)
  137. CNS effects of catecholamines
    Epinephrine and isoproterenol are most likely to cause CNS effects like fear, anxiety, restlessness, tremor and excitability.
  138. possible catecholamine/direct-acting adrenergic agonists side effects.
    • adrenergic (sympathetic) effects.
    • mydriasis
    • blurry near vision
  139. albuterol inhalation aerosol
    • B2 selective adrenergic agonist at therapeutic doses.
    • rescue drug for bronchodilation in asthma, not maintinence (will lose effect). Best as an inhalant.
    • At high doses, will stimulate B1.
  140. Inhalant drugs
    • albuterol for asthma
    • fluticazone, steroid
  141. ephedrine
    • non-catecholamine adrenergic agonist. 
    • Stimulates a and B adrenergic receptors directly and by indirectly by increasing norepi.
    • Bronchodilation and increases BP
    • Can cause arrhythmias, stroke, anxiety, excitement, restlessness and even to seizures and death.
    • Prohibited by FDA
    • AKA Ma Huang, ephedra
  142. FDA's role in supplements
    • FDA does not have authority to required approval prior to marketing.
    • Cannot remove unless proves "significant or unreasonable risk of illness or injury
  143. Phenylpropanolamine (PPA)
    • non-catecholamine adrenergic agent.
    • used to treat urinary incontinence in dogs (urethral sphincter hypotonus)
    • a1 agonist (contraction of urethral smooth muscle), b2 agonist (relaxation of detrusor muscle)
    • some anxiety, restlessness, hypertension, cardiac arrhythmias, urinary retention
    • Banned in humans for hemorrhagic strokes
  144. Prazosin
    • reversible alpha adrenergic receptor antagonist
    • Blocks a1 to relax urethral smooth muscle
    • Used to prevent urethral spasm in treatment of FLUTD
    • Can cause vasodilation and hypotension
    • dogs with reflex dyssnergia (impairment between detrusor and sphincter so do not balance)
  145. Phenoxybenzamine
    • reversible alpha adrenergic receptor antagonist
    • Block a1, vasodilation and hypotension
    • Used to prevent urethral spasm in treatment of FLUTD
  146. Alpha adrenergic receptor blockade, pharmacological effects and mechanism-based adverse effects
    • blocking a1 causes miosis and vasodilation
    • vasodilates arterioles, lowers PVR, decreases arterial BP
    • vasodilation causes blood pooling and decreased venous return upon standing. Ventricular preload decreases, cardiac output decreases, causes orthostatic hypotension, dizziness, syncope. "head rush"
  147. Alpha-adrenergic blockade effect and how it causes orthostatic hypertension
    vasodilation causes blood pooling and decreased venous return upon standing. Ventricular preload decreases, cardiac output decreases, causes orthostatic hypotension, dizziness, syncope. "head rush"
  148. sympathetic reflex arc resulting from alpha receptor blockade
    • decreased BP stimulates carotid and aortic baroreceptors, send message to medulla. Sympathetic outflow is increased, NEpi is increased, stimulates B2 and B1 (a1 blocked). Para (Ach) decreased.
    • vasodilation, reflex tachycardia
  149. acepromazine
    • alpha blocker
    • tranquilizer
    • hypotension and vasodilation (get cold from vasodilation in skin)
  150. Yohimbine
    • alpha 2 antagonist (alpha blocker)
    • antidote for xylazine toxicity (large-animal sedative)
  151. Atipamezole
    • alpha blocker
    • reversal agent for medetomidine
    • antisedan (alpha2 antagonist)
  152. propanolol
    non-selective beta blocker.  Blocks B1 and B2 adrenergic receptors, get parasympathetic response
  153. Esmolol
    cardioselective beta blocker, preferentially blocks B1 adrenergic receptor.
  154. non-selective beta blockers cause
    • decreased HR, decreased AV conduction velocity, decreased force of contraction
    • No B means vasoconstriction, increase PVR and decreased CO makes decreased BP.  Then sympathetic reflex arc kicks in
  155. Dual innervation of the iris
    • ACh at muscarinic receptors on circular smooth muscle, contraction, miosis
    • NEpi at a1 adrenergic receptors on radial smooth muscle, contraction, mydriasis
  156. Therapeutic uses of beta blockers
    • treatment of cardiac arrhythmias (usually)
    • adjunctive therapy in feline hypertherapy and tachycardia (Atenolol, B1)
    • Feline hypertrophic cardiomyopathy (Atenolol, B1)
    • Congestive heart failure (controversial, but long term decreases fibrosis and O2 demand)
    • Glaucoma (Timolol for hereditary primary glaucoma, stops non-glaucoma eye getting there)
  157. Toxic effects of non-selective beta blockers
    • immediate contraction of bronchial smooth muscle
    • cardiac arrhythmias (slowing too much, heart block, don't use in bradycardia)
    • hypotension (more decreased cardiac output, increased PVR.  More decreased cardiac output so decreased BP)

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