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174 Cards in this Set
- Front
- Back
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What NT and receptor are used in the synapse between the pre and post ganglions of the PS and SNS?
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NT: ACh
Receptor: Nn |
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NT and receptor at the post-ganglionic synapse of PS?
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NT: ACh
Receptor: M |
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NT and receptor at the post-ganglionic synapse of SNS on smooth muscle?
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NT: NE
Receptor: α & β |
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NT and receptor at the post-ganglionic synapse of SNS on sweat gland?
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NT: ACh
Receptor: M |
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NT and receptor of a somatic motor neuron?
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NT: ACh
Receptor: Nm (only 1 neuron) |
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What is the precursor to NE?
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Tyrosine
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What is the main mechanism for NE inactivation in a sympathetic synapse?
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uptake by the norepinephrine transporter (NET) on the pre-synaptic varicosity
-inside it is either reused or degraded by MAO |
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Where is NE converted to Epi and by what enzyme
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In the Adrenal Medulla by PNMT
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Relative sympathetic receptor affinity for NE and EPI
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NE α1=α2 β1>>β2
EPI α1=α2 β1=β2 |
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What 2 receptors are found on blood vessels?
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α1 and β2
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What does low dose EPI do to blood vessels?
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Activates β2 receptors causing vasodilation and decreased PVR
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Main mechanism for the inactivation of ACh?
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acetylcholinesterase (AChE) in the synaptic cleft
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3 locations for a N receptor
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skeletal m., parasympathetic and sympathetic ganglia
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Gs (G-protein)
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s for stimulate
(activates adenylyl cyclase) |
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Gi (G-protein)
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i for inhibits
(inhibits adenylyl cyclase) |
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Gq (G-protein)
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activated Phospholipase Cβ
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What is interesting with regard to β2 receptors and their G-protein?
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β2 receptors are coupled with Gs protiens with cause stimulate but ultimitely cause relaxation
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Where are β1 receptors found and what is the result of activation?
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heart: inc. HR, inc. force of contraction
kidney: renin release |
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Where are β2 receptors found and what is the result of activation?
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smooth m.: relaxation
liver: glycogenolysis, gluconeogenesis |
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Where are β3 receptors found and what is the result of activation?
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lipolysis
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What is the mechanism of activation for nicotinic receptors?
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ligand gated ion channel
(note: not G-protein) -> results in depolarization |
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Where are M3 receptors found?
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smooth muscle and secretory glands
-> cause contraction/ secretion ->Gq |
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Where are M2 receptors found?
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heart
-> causes decreased activity -> Gi |
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What happens to the permeabitlity of K+ upon ligand binding to M3?
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increase permeability of K+ which results in hyperpolarization -> longer to reach threshold
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What happens to receptor number upon chronic exposure to an antagonist?
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receptor up-regulate
(issue when drug is taken away) |
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What happens to receptor number upon chronic exposure to an agonist?
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receptor down-regulation
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What is the effect of PS stimulation of the iris sphincter smooth muscle?
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contraction and constriction (miosis)
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What is the effect of sympathetic stimuation of the iris radial smooth muscle?
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contraction and dilation (mydriasis)
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What is the effect of PS stimulation to the ciliary muscle?
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contraction of the ciliary m. -> unflatten the lens -> accomodation for near vision
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How does the ciliary muscle allow for far vision?
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relation of the ciliary muscle -> flattening the lens
(note: no ANS stimulation needed for this) |
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What are the PS and S receptors found on bronchial smooth muscle?
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M3 and β2
(note: β2 receptors have no innervation, rather react to circulating EPI) |
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What receptors are on the bronchial glands?
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M3
-cause secretion |
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PS stimulation to the lungs causes bronchoconstriction or bronchodilation?
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bronchoconstriction
(M3 receptors) |
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3 effects of parasympathetic stimulation to the GI system
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1. gastric secretions
2. relax sphincter 3. contraction - increase tone and motility |
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2 effects of sympathetic stimulation of the GI system
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1. contract sphincter
2. relaxation - decrease tone and motiltiy |
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What would be used to stop gastric secretions?
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muscarinic antagonist
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Describe parasympathetic stimulation to the bladder
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Micturation
-contraction of the detrusor m. -relaxation of the trigone m. |
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Describe sympathetic stimulation to the bladder
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Urinary retention
-relax detrusor m. (β2) -contract trigone m. (α1) |
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Describe the effect of ACh within the lumen of a blood vessel on the endothelial cell?
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ACh binds to M3 receptor -> endothelial cell releases NO -> NO activates guanylyl cyclase in smooth m.
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3 examples of blood vessels innervated by parasympathetic nerves?
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-erectile tissue
-salivary glands -GI glands |
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What sympathetic receptor is more prevalent on blood vessels to liver/skeletal m.?
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β2 -> vasodilation
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What sympathetic receptor is more prevelant on blood vessels to the rest of the body other than liver/skeletal m.?
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α1 -> vasoconstriction
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3 effects of parasympathetic stimulation to the heart
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1. decrease HR
2. decrease force of contraction 3. decrease conduction velocity |
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3 effects of sympathetic stimulation to the heart
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1. increase HR
2. increase conduction velocity 3. increase force of contraction (atria and ventricles) -> β1 receptors |
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Does isoproterenol have more affinity for β or α receptors?
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β
β=β>>>>>α |
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What 2 secretory glands are innervated by parasympathetics?
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salivary and nasopharyngeal glands
-> secretion M3 |
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Describe sympathetic innervation of sweat glands
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2 types
-thermoregulatory sweating - M3 -palms of hands - α1 |
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Describe sympathetic innervation to a fall cell
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NE -> β3 -> lypolysis to provide energy
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Describe the effect of low plasma glucose on the adrenal medulla and liver and skeletal m. cells
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low plasma glucose -> causes release of EPI from adrenal medulla -> EPI activate β2 receptors on liver and skeletal m. -> glycogenolysis and gluconeogenesis
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How does sympathetic stimulation cause a decrease in insulin release?
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Sympathetic innervation to α2 receptor
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How does sympathetics cause an increase in insulin release?
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circulating EPI activates β2 receptors
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How does sympathetics cause renin release?
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sympathetic innervation to β1 receptors on the kidney causing an increase in renin release
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EPI activation of β2 receptors shift K (into or out) of the cell.
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into the cell
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Would a β2 agonist be used to treat hyperkalemia or hypokalemia?
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hyperkalemia
-bring K into the cell |
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What does overstimulation of skeletal m. due to EPI cause?
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tremors
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Adrenalin
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epinephrine
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Which receptor on blood vessels has a greater sensitivity for EPI?
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β2
-> at low dose of EPI vessel will vasodilate and decrease PVR |
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What does high dose of EPI do the PVR in blood vessels?
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causes increased PVR due to the amount of α1 receptors compared to β2
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Dipivefrin
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-prodrug converted into epinephrine
-topical, opthalmic agent |
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Dopamine
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-activates dopamine, β1, α receptors
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Phenylephrine
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α1 selective agonist
-sudafed PE |
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Dipivefrin
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-prodrug converted into epinephrine
-topical, opthalmic agent |
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Xylometazoline
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α1 selective agonist
-nasal |
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Dopamine
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-activates dopamine, β1, α receptors
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Phenylephrine
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α1 selective agonist
-sudafed PE |
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Oxymetazoline
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α1 selective agonist
-also activated α2 -nasal |
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Xylometazoline
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α1 selective agonist
-nasal |
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Oxymetazoline
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α1 selective agonist
-also activated α2 -nasal |
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Midodrine
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α1 selective agonist
-oral -orthostatic hypertension |
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Brimonidine and Aprachonidine
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α2 selective agonist
-topical -eye (glaucoma) |
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Isoproterenol
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non-selective β agonist
-parenteral |
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Dobutamine
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(+) isomer - β1 agonist, α1 antagonist
(-) isomer - α1 agonist -parenteral |
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β2 selective agonist (3)
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-Albuterol
-Metaproterenol -Pirbuterol (inhalation, some oral) |
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Terbutaline
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β2 selective agonist
-oral/parenteral |
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Salmeterol, Formoterol, Arformoterol
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β2 selective agonist
-inhalation |
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Drug for hemorrhage from a minor cut
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EPI
-activate α1 receptor -> vasoconstrict blood vessels in the area |
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What is the difference btwn Phenylephrine and Xylometazoline and Oxymetazoline
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Phenylephrine has a short 1/2 life (4 hrs)
Xylometazoline and Oxymetazoline have a long duration of action (overnight) |
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Describe rebound nasal congestion
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down regulation of α1 receptors with chronic use of nasal decongestant -> in absence of drug NE has low affinity for α1 receptors -> nasal congestion
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Describe the reactions of Anaphylaxis and the effects of EPI
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Angioedema -> α1 constrict capillary beds
Bronchoconstriction -> β2 bronchodilation Pruritus, Urticaria -> β suppress release of mediators from mast cells Hypotension -> α1 β1 raise BP |
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How does Phenylephrine correct paroxysmal supraventricular tachycardia?
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-convert arrhythemia to NSR
-PE (α1 agonist) causes vasoconstriction -> increase BP -> decrease firing of baroreceptor -> decrease HR and decrease conduction |
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How does Phenylephrine effect hypotension?
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activates α1 receptors that cause vasoconstriciton leading to an increase in BP
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3 locations of dopamine receptors and effects of activation
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1. renal vasculature -> vasodilation, increase renal blood flow
2. β1 receptos -> increase CO and BP 3. α1 receptors -> increase PVR and BP |
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3 drugs to treat shock (hypovolumic, cardiogenic, distributive)
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dopamine, dobutamine, NE
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Drug to treat AV Block
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EPI, isoproterenol
β1 agonist, increase AV conduction |
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Drug to treat Ventricular fibrillation/ Pulseless ventricular tachycardia
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EPI
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Short acting drugs for Asthma/COPD
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albuterol, metaproterenol, pirbuterol, terbutaline
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Long acting drugs for Asthma/COPD
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salmeterol, formoterol, arformoterol
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Drug to stop premature labor
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Terbutaline
-activation of β2 receptors cause uterine smooth muscle relaxation -> stop uterine contractions |
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What drug is used to dilate the pupil?
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Phenylephrine
-α1 agonist -contraction of the iris radial smooth muscle -dilation without cycloplegia (paralysis of the ciliary m.) |
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Adverse effects from α adrenergic activation
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-reduced peripheral blood flow (α1 on blood vessels)
-excessive contraction of blood vessels at infusion site (ischemia/necrosis) -rebound nasal congestion -mydriasis (dilation of pupils) |
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Adverse effects from β1 adrenergic activation
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β1 receptors on the heart
-increase HR (palpitations, tachycardia, cardiac arrhythmias) -increase force of contraction -> increase work load -> angina |
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Adverse effects from β2 adrenergic activation
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-hyperglycemia (β2 receptor activation on the liver stimulates glycogenolysis)
-tremor (over activation of skeletal m.) |
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Contraindications of direct acting adrenomimetics
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-cardiovasuclar disease
-hyperthyroidism -diabetes |
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4 indirect acting adrenomimetics
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-Tyramine
-Amphetamine -Methylphenidate -Atomoxetine (last 3 CNS stimulants and/or used for ADHD) |
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Tyramine
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NOT A DRUG
-comes from gut bacteria and fermented food -normally is metabolized in the liver by MAO -if not... found in blood and promotes release of NE from sympathetic nerve terminal |
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2 mixed acting adrenomimetic agents
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Ephedrine, Psudoepedrine
-release NE from the nerve terminal and activate both α and β -cross the blood/brian barrier |
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Approved uses from Ephedrine
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Asthma, COPD, nasal congestion
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Adverse effects of Ephedrine
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-cardiovascular (excessive stimulation of the heart)
-CNS (insomnia, nervousness, anxiety) |
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Actions of Pseudophedrine
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-directly activates α and to a lesser extent β receptors
-release NE from nerve terminal -less CNS effects than ephedrine -nasal decongestant |
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α1 selective antagonist, reversible
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all end in -osin
-Prazosin -Terazosin -Doxazosin -Tamsulosin -Alfuzosin -Silodosin |
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Non-selective α antagonist, reversible
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Phentolamine
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Non-selective α antagonist, non-reversible
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Phenoxybenzamine
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3 α antagonists used to treat hypertension
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Prazosin, Terazosin, Doxazosin
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2 α antagonist used to treat Pheochromocytoma
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Phentolamine, Phenoxybenzamine
(both α1 blockers) -goal is to reduce the BP caused by an increase in EPI in the system due to a tumor on the Adrenal Medulla |
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6 α antagonist used to treat Benign Prostatic Hyperplasia (BPH)
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Prazosin, Terazosin, Doxazosin, Tamsulosin, Alfuzosin, Silodosin
-increases urine flow by blocking α1 receptors and relaxing smooth m. in the base of bladder and the prostate |
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3 α antagonist used to treat Raynaud's disease
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Raynaud's disease: cold induced vasospasm in fingers and toes
Prazosin, Terazosin, Doxazosin -block the α1 receptors on fingers and toes -> maintain circulation |
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What is the 1st dose effect with regard to orthostatic hypotension?
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With the 1st dose of the α antagonist medication profound orthostatic hypotension with syncope is observed (also occurs when increase dose)
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What is the mechanism for orthostatic hypotension with regard to α antagonist
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Prazosin inhibits the α1 receptors on blood vessels -> no vasoconstriction -> blood pools in the veins -> decrease CO -> hypotension with syncope
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How does Prazosin (α antagonist) cause reflex tachycardia?
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Prazosin blocks the α1 receptors on the blood vessels -> decreased BP -> stimulate baroreceptors -> reflex tachycardia
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6 Non-selective, competitive, reversible β receptor antagonists
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Propranolol, Nadolol, Timolol, Pindolol, Carteolol, Levobunolol
(all end in olol) |
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6 β1 selective, competitive, reversible β receptor antagonist
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Metoprolol, Atenolol, Acebutolol, Betaxolol, Bisoprolol, Esmolol
(all end in olol and begin with BEAM) |
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What cardiovascular diseases are treated with β receptor antagonists?
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Hypertension, Ischemia, Arrhythmias, MI, Heart failure
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Are β antagonists used to treat Pheochromocytoma?
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Yes in conjunction with α blocker
(Pheochromocytoma - excessive EPI and NE release caused by adrenal tumor) |
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What is typically used to treat migraines?
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β receptor antagonists
-used only to prevent rather than treat (prophylactic) |
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What is used to prevent Esophageal variceal bleeding?
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non-selective β blockers
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Describe the adverse effects of β receptor antagonist with regard to the heart
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inhibition of β1 receptors on the heart lead to bradycardia, AV block, decreased contractile force => hypotension and heart failure
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What 2 β receptor antagonists are able to cross the blood brain barrier and cause adverse effects?
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Propranolol and Metoprolol
-cause: nightmares, lassitdue, mental depression, insomnia |
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What is the issue with having your diabetic pt on β receptor antagonists?
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hypoglycemia activates the sympathetic NS to release EPI to act on the liver (glycogenolysis, gluconeogenesis) and heart (inc. HR)
-> eliminate these responses |
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Why are both non-selective and β1 selective blockers contraindicated in a pt with asthma?
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non-selective: block the β2 receptors on the lungs -> bronchoconstriciton
(β1 selective lose their selectivity at higher doses) |
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What happens when a pt with peripheral vascular disease is on a β receptor antagonist?
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unopposed vasoconstriction
-no β2 activity |
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Describe rebound hypertension with regard to β receptor antagonists
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chronic therapy up regulates β receptors
abrupt withdrawal from β blocker causes rebound hypertension, nervousness, tachycardia, angina |
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6 direct acting muscarinic agonists
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Acetylcholine, Bethanechol, Pilocarpine, Carbachol, Cevimeline
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Upon activation of M receptors...
heart, blood vessels, ciliary body, iris sphincter, GI tract, bladder |
Heart- decrease HR
Blood vessels - vasodilate via NO Ciliary muscle - contraction/near vision Iris sphincter - miosis GI tract - increase activity Bladder - micturition |
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2 therapeutic uses of Bethanechol
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muscarinic agonist
1. post operative abdominal distension and urinary retention 2. neurogenic atony of the urinary bladder with retention (non-obstructive retention) |
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Therapeutic uses for Pilocarpine, both topical and oral
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muscarinic agonist
Topical: miotic, open angle glaucoma, narrow angle glaucoma Oral: Sjogren's syndrome, radiation induced dry mouth |
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Therapeutic use of Cevimeline
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muscarinic agonist
-newer drug from Sjogren's syndrome (autoimmune disorder against moisture producing gland) |
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Is Muscarine a drug?
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No, present in mushrooms
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Adverse effects of direct acting muscarinic agonists with regard to salivary glands, sweat glands, GI tract, Stomach
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salivary gland - salivation
sweat glands - sweating GI tract - intestinal cramps/NVD stomach - aggravate ulcer |
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Adverse effects of direct acting muscarinic agonists with regard to CV system
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blood vessels - dilation (via NO)
heart - bradycardia -> reflex tachycardia |
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How do direct acting muscarinic agonists adversely affect the lungs and eye
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Lungs: bronchoconstriction (difficulty breathing/asthma attack)
Eyes: near vision and miosis |
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Reversible AChE inhibitors
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Physostigmine, Neostigmine, Edrophonium, Edrophonium + Atropine, Pyridostigmine
Work in the CNS: Donepezil, Tacrine, Rivastigmine, Galantamine |
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What drug would be used or an overdose of a muscarinic blocker?
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Physostigmine
(note: it is lipid soluble and can cause severe adverse effect -> only used when absolutely needed) |
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2 topical uses from Physostigmine
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miotic (constriction of the pupil) and treatment of glaucoma
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Which would be used for postoperative urinary retention and abdominal distension (Neostigmine or Pyridostigmine)
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Neostigmine
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Which 2 drugs could be used to treat Myasthenia gravis and why?
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Pryidostigmine and Neostigmine
-they are non-lipid soluble and are more selective in the neuromuscular junction |
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Drug used as a diagnostic test for myasthenia gravis
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Edrophonium (analog of neostigmine)
-shorter acting, 3-4 minutes -IV only |
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Name 2 irreversible AChE inhibitor therapeutic agents
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Echothiophate [+ charged, not volatile, used over DFP]
Diisoprophyl flourophosphate (DFP) [high lipid solubility, volatile] -only given topically on the eye |
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3 irreversible AChE inhibitor insecticides
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Tetraethyl pyrophosphate (TEPP), Parathion, Melathion
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3 Nerve Gases
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Sarin, Soman, Tabun
(irreversible AChE inhibitors) |
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Which insecticide is used to treat head lice?
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Melathion
-low dermal absorption |
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Toxicity of irreversible AChE inhibitors
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Malathion < Parthion <<<< Sarin (nerve gas, micogram dose)
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3 adverse effects of AChE inhibitors
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1. lens opacities
2. chronic neurotoxicity 3. cholinergic crisis |
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Differentiate Neostigmine, Physostigmine, Organophosphates with regard to reversibility and ability to cross the BBB
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Neostigmine: reversible and does not cross BBB
Physostigmine: reversible but does cross the BBB Organophosphates: irreversible and crosses the BBB |
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What drug is used to treat a Cholinergic crisis?
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Atropine: muscarinic blocker
(remember it does not act on the Nicotinic receptors in the skeletal m. Neuromuscular junction) Pralidoxime: cholinesterase reactivator (NMJ, used only for organophosphate poisoning) |
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7 non-depolarizing neuromuscular blocking agents
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Tubocuraine, Atracurium, Cisatracurium, Mivacurium, Pancuronium, Rocuronium, Vecuronium
-all have curoni in the name |
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1 depolarizing neuromuscular blocking agent
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Succinylcholine
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Sequence of paralysis with non-depolarizing neuromuscular blockers
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eyes, face, limbs, abdominal, intercostals, diaphragm
(small m. first, recover is the reverse order) |
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How would you reverse the effects of a non-depolarizing neuromuscular blocker
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AChE inhibitor
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3 characteristics of all neuromuscular blockers
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1. do not enter the CNS
2. do not affect sensory neurons 3. are not anesthetic or analgesic |
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Describe phase I block of Succinylcholine
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-acts as ACh to depolarize the cell
-resistant to AChE -> repetitive excitation that may elicit fasciculations -depolarization block that leads to flaccid paralysis |
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Describe phase II block of Succinylcholine
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continuous exposure causes re-polarization of the receptor which resembles desensitization
-difficult for the receptor to be depolarized again |
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Which is short acting agent and which a long acting agent (Pancuronium & Succinylcholine)
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Succinylcholine - short 1/2 life, 5 minutes
Pancuronium - long 1/2 life, 120-180 minutes |
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Adverse effects of non-depolarizing neuromuscular blockers
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-histamine release - really bad for asthmatics
-block autonomic ganglia - vasodilation, hypotension, tachacardia -block muscarinic receptor - tachacardia |
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Describe the adverse effects of Succinylcholine with respect to hyperkalemia
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In pts with denervation supersensitivity upon exposure to Succinylcholine there is a large efflux of potassium resulting in hyperkalemia -> cardiac arrest =(
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Describe the adverse effects of Succinylcholine with regard to Malignant hyperthermia
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causes an excessive release of calcium from the SR -> potentially fatal
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List of Muscarinic Antagonists
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Atropine, Scopolamine, Tropicamide, Cyclopentolate, Ipratropium bromide, Tiotropium bromide, Tolterodine, Fesoterodine, Oxybutynin chloride, Darifenacin HBr, Solifenacin, Trospium Chloride
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What 3 drugs are used to achieve Mydriasis and cycloplegia
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Tropicamide (short duration)
Atropine and Scopolamine (long duration) |
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What are 2 methods for treating acute rhinitis
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1. muscarinic antagonist - get rid of snot
2. alpha agonist - constrict blood vessels |
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What are the differences between Ipratropium bromide and Tiotropium bromide for the treatment of Asthma/COPD?
|
Ipratropium - short duration of action, usually given 4x/day
Tiotropium - longer duration of action, once a day (both inhaled muscarinic antagonists -> inhibit bronchoconstriction) |
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Which is more lipid soluble Atropine or Ipratropium bromide
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Atropine
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Which preoperative drug has more sedative and amnesia effects (Atropine or Scopolamine)
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Scopolamine > Atropine
-a much higher dose of atropine is needed -both result in less oral secretions |
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How are muscarinic antagonists used to treat hyperactive carotid sinus syndrome?
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inhibit the excessive PS stimulation to the heart -> stopping bradycardia and AV block -> guy with very tight tie does not have an episode of syncope =)
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What is used to treat motion sickness
|
Scopolamine
-put behind the ear -inhibit stimulation of the vomit center in the medulla, which has M receptors |
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Does atropine effect ventricular arrthymias?
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No, because there aren't any M receptors on the ventricles
-able to act on the AV node |
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Main agents used to treat urinary incontinence due to detrusor overactivity
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Tolterodine, Oxybutynin Chloride, Darifenacin, Solifenacin, Trospium Chloride
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List the order of severity of adverse effects of mucarinic antagonists with regard to the CNS
(Atropine, Scopolamine, Ipratropium) |
Scopolamine > Atropine >>>> Ipratropium (does not cross the BBB)
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When is it not appropriate to use Muscarinic antagonists
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pt with narrow angle glaucoma
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What produces Aqueous Humor in the eye?
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Ciliary Body
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2 ways to treat open angle glaucoma
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1. decrease aqueous humor production -> β antagonist to decrease production or α2 agonist to decrease production
2. clear the trabecular meshwork -> α2 agonist |
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2 α2 agonists used to treat open angle glaucoma
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Brimonidine and Apraclonidine
(both end in nidine) |
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What type of drug is used to open the hole within the trabecular meshwork of open angle glaucoma
|
Muscarinic agonist
-contraction of the ciliary m. -Pilocarpine |
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What is the first choice for treatment of open angle glaucoma
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beta blocker
-then alpha agonists, EPI, and cholinomimetrics |
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Describe the Cholinomimetics used for Glaucoma
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Muscarinic agonists (Pilocarpine, Carbachol)
Reversible Acetylcholinesterase Inhibitors (Physostigmine( Irreversible Acetylcholinesterase Inhibitors (Echothiophate) -preferably used in that order |
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Is Pilocarpine used for Narrow Angle Glaucoma
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yes, contract the iris sphincter m. -> move iris out of the way
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