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Adrenergics
Pharm 2
| Question | Answer |
|---|---|
| What neurotransmitters does Postganglionic fibers in the sympathetic nervous system release? | Postganglionic fibers in the sympathetic nervous system release norepinephrine (NE) (a few release epinephrine (Epi), and some release dopamine (DA). |
| L-dopa synthesis | L-tyrosine (from the blood) is taken up into adrenergic neurons. This is then converted to L-dopa by the action of tyrosine hydroxylase (TH) (the rate-limiting step in synthesis |
| Dopamine synthesis | L-dopa is converted into dopamine by dopa decarboxylase (DD) (l-amino acid decarboxylase). |
| norepinephrine synthesis | In norepinephrine neurons, the enzyme, dopamine β-hydroxylase (DBH) is present in the vesicles. This then catalyzes the conversion of dopamine to norepinephrine |
| epinephrine synthesis | In epinephrine neurons, a cytoplasmic enzyme, phenylethanolamine n-methyltransferase (PNMT) is present which can convert cytoplasmic norepinephrine (from re-uptake or internal release from vesicles) to epinephrine. |
| What are the other functions of Dopa decarboxylase | It is a fairly non-selective enzyme with broad substrate specificity (can also convert 5-hydroxytryptophan to 5-hydroxytryptamine. It can also convert α-methyldopa to α-methyldopamine, which can be further converted to α-methylnorepinephrine |
| What are α-methyldopamine,and α-methylnorepinephrine called | false transmitters |
| How does NE acts in feedback loop? | Cytoplasmic NE acts in feedback loop on the enzymes TH and DD to decrease excessive production. Therefore, if there is excessive NE release, there is less NE in the cytoplasm, thus less feedback, and more rapid synthesis. |
| True or false. NE re-uptake is main contributor to the NE pool (actually two pools, rapid and slow turnover pools). | True |
| True or False. In the cytoplasm, NE acts to feedback on DA production | True |
| True or False. In addition, NE in the cytoplasm of the adrenal medulla chromaffin cells is converted to EPI before packaging in vesicles | True |
| In the chromaffin cells, both EPI and NE are stored and released in the ratio of __ EPI,__NE. This is important due to the receptor specificity differences between EPI and NE. | 80%, 20% |
| where are both EPI and NE are stored and released in the ratio of 80% EPI, 20% NE. | In the chromaffin cells of the adrenal medulla |
| where are catecholemines stored? | Catecholamine storage is mainly in granular vesicles |
| These vesicles may be made | in the cell body and carried to the nerve terminal for filling, or they may be made by endocytosis (pinching off) of the nerve terminal membrane |
| NE in the granules is in a complex with | ATP (4NE:1ATP) and other proteins (neurotransmitters and neuromodulators) as well as DBH and DA. |
| Neuropeptide Y is one example of | these proteins stored with NE, and it is released with NE as a co-transmitter. |
| Two cytoplasmic pools of NE exist. They are | the fast and slow turnover pools. |
| What is the function of the fast turnover pool | The fast turnover pool is probably used as transmitter and is stored, or can be released directly from the cytoplasm |
| What is the function of the slow turnover pool | The slow turnover pool is probably a reserve pool, present in case NE levels get too low, at which time it can be utilized |
| α-methyl-p-tyrosine inhibits | TH |
| α-methyldopa inhibits | DD |
| Disulfiram (Antabuse)inhibits | DBH |
| What causes synaptic release of the neurotransmitter | Impulse traveling down neuron triggers Ca++ inflow at the nerve terminal, leading to the cascading reaction triggering exocytosis of vesicles and the synaptic release of the neurotransmitter |
| True or False, the same thing happens in adrenal chromaffin cells, but the neurotransmitter is released to blood vessels where it is picked up and transported throughout the body | True |
| What is the most important mechanism in stopping neurotransmitter action at the receptor sites | Following release, approximately 80% of NE released from neurons is retrieved by re-uptake pumps back into the cytoplasmic pool |
| How is This retrieved NE is then taken up back into vesicles | against concentration gradient |
| Which 2 mechanisms are points of potential drug attack | (1)Following release, approximately 80% of NE released from neurons is retrieved by re-uptake pumps back into the cytoplasmic pool, (2)This retrieved neurotransmitter is then taken up against concentration gradient back into vesicles |
| Some of the released neurotransmitter in the synapse can act on presynaptic α2 autoreceptors to inhibit | further release via feedback loop |
| Very small amounts of neuronally released neurotransmitter gets free to enter circulation except from | the adrenal medulla |
| True or False, Some is metabolized in the synapse before the re-uptake pumps can recycle it | True |
| The two principle enzymes responsible for the degradation of catacholamines are | monoamine oxidase (MAO), and catechol-o-methyltransferase (COMT) |
| MAO exists in two major forms | A and B |
| True or False, Type B is the most active form for metabolism of NE (DA, EPI, and 5-HT (serotonin) also) | False, Type A is the most active form for metabolism of NE (DA, EPI, and 5-HT (serotonin) also) |
| Both MAO and COMT are widely distributed in body, with MAO mainly on | the outer surface of mitochondria in sympathetic neurons (and other body cells) |
| COMT is located mainly in | the synaptic cleft (and other spaces and locations in the body) |
| The liver has a lot of --- and ---, thus rapidly metabolizing circulating catecholamines | MAO and COMT |
| α-agonist potency: | EPI > NE > DA > ISO |
| β-agonist potency: | ISO > EPI > NE > DA |
| Selective antagonists for α receptor | phenoxybenzamine |
| Selective antagonists for β receptor | propranolol |
| True or False, Pre-junctional (α2) receptors were found to be different than post-junctional (α1) | True |
| First compounds shown to have more agonist potency for α2 than α1 receptors | Clonidine |
| A ‘selective’ α2 agonist | Dexmedetomidine (Precedex) |
| True or False,Phenylephrine (Neo-Synephrine) is more potent at α1 than at α2 receptors | True |
| Selective antagonists for α1 receptors | prazosin |
| Selective antagonists for α2 | yohimbine |
| Now known that some α2 agonists act at some post-junctional sites, showing | contraction of smooth muscles, platelet aggregation, etc |
| All α2 receptors inhibit | adenyl cyclase by G protein interaction, causing a hyperpolarization |
| All α2 receptors inhibit adenyl cyclase by G protein interaction, causing a | hyperpolarization |
| α1 stimulation triggers | increased intracellular Ca++ release by activation of phospholipase C, which is also G protein mediated |
| β1 is found mainly on | cardiac tissue |
| β2 is found | everywhere else |
| β2 receptor potency: | EPI > NE |
| β1 receptor potency: | NE > EPI |
| Selective antagonists: β1 | atenolol and metoprolol |
| Selective antagonist β2 | butoxamine |
| Selective agonists: β1 | dobutamine |
| selective agonist β2 | albuterol |
| where are β3 receptor found | colon and adipose tissue |
| True or false, propranolol does act on B3 receptor to block the action of isoproterenol | False, propranolol does not act on B3 Receptor to block the action of isoproterenol |
| Properties of Norepinephrine (Levophed) | Potent vasoconstrictor and inotropic agent |
| True or False, L-isomer much more potent than d-isomer | True |
| True or False, Norepinephrine (Levophed) has More β than α activity | False, it has has More α than β activity |
| True or False, Norepinephrine (Levophed) has has More α than β activity | True |
| α activity produces | increased peripheral vascular resistance, and increased systemic blood pressure and increased coronary artery blood flow |
| Some β1 activity: in lower doses | β1 cardiac stimulatory effects are seen |
| With larger NE doses | vasoconstrictive effects (α1) are predominate cause of increased BP |
| Like other catacholamines, NE increases cAMP in cells via | β stimulation |
| NE decreases cAMP via | α stimulation |
| Which effects of NE are less than seen with EPI | Glycogenolysis, inhibition of insulin release and lipolysis |
| Reflexive vagal stimulation secondary to increased TPR and BP | slows the heart and increases stroke volume |
| Increased TPR and BP causes | Reflexive vagal stimulation which slows the heart and increases stroke volume |
| Blood flow to abdominal organs and skeletal muscle is --------, while coronary blood flow is -------- indirectly due to a stimulation | decreased, increased |
| True or False, NE Does not increase myocardial O2 consumption | True |
| How is NE normally given, onset, and duration | Normally given only via IV, with rapid onset and short (1 - 2 minute) duration |
| True or False, NE Does not cross the BBB | True |
| NE is mainly used for | shock and severe hypotension |
| Epinephrine (Adrenalin) is Administered | parenterally, via inhalation, or topically to eye |
| Epi is Used as a | cardiac stimulant and bronchodilator (anaphylactic shock) |
| True or False, other uses in asthmatics is limited now due to more selective compounds | True |
| Epi is Combined with other drugs (such as local anesthetics and topical eye preps) to | prolong action by vasoconstriction, causing slower absorption and removal of the other agent from the site |
| Epi is use in Ophthalmic as a | diagnostic aid |
| True or False, Epi is a Potent α and β agonist (non-selective adrenergic agonist) | True |
| α1 action leads to | arteriolar vasoconstriction |
| α2 stimulation leads to | decreased NE release from neurons |
| β1 stimulation leads to | increased chronotropic and inotropic activity |
| β2 stimulation leads to | arteriolar vasodilation, bronchial smooth muscle relaxation and increased glycogenolysis |
| Major therapeutic Epi effects include: | bronchodilation, cardiac stimulation, skeletal muscle vasodilation, and glycogenolysis |
| True or False, Smooth muscle effects are specific and depend on receptor density and hormonal effects | False, Smooth muscle effects are "varied" and depend on receptor density and hormonal effects |
| What is the effect of EPI on ocular pressure | It lowers intraocular pressure (wide-angle glaucoma) and causes brief mydriasis |
| Topical or local administration of EPI | constricts blood vessels (hemostasis) |
| β2 stimulation effect on mast cell | decreases mast cell histamine release |
| What are the effects of Epi on systolic and diastolic pressure | Systolic pressure usually increased (due to increased inotropy) while diastolic is decreased (vasodilation) |
| The effect of Epi on coronary artery and myocardia | It increases coronary artery vasodilation and stimulates increased myocardial O2 demand which has further local effect (via NO) to increased coronary vasodilation |
| Epi Increases the risk of arrhythmias due to | β1 activity |
| At normal doses Epi causes | some vasoconstriction, some dilation |
| At higher doses Epi causes | Mostly constriction |
| α stimulation in liver | increases gluconeogenesis and inhibits insulin release |
| β stimulation (β3) in adipose tissue causes | catabolism and increased free fatty acids in plasma |
| β2 stimulation at skeletal muscle and liver | increase glycogenolysis |
| True or False, Epi Does cross BBB well | False, Epi Does not cross BBB well |
| Duration varies with administrative route: IV | few minutes |
| IM duration | 1 - 4 hours |
| Inhalation duration | 1 - 3 hours |
| Epi Uses include | acute bronchospasm, anaphylaxis, asthma(??), cardiopulmonary resuscitation, glaucoma, surgical bleeding, ventricular fibrillation and asystole |
| What are the properties of Isoproterenol (Isuprel) | Potent bronchodilator and inotrope |
| True or False, Isuprel is a Synthetic compound similar to EPI, and is a potent α agonist (non-selective) | False, Isuprel is a Synthetic compound similar to EPI, and it is a Potent "β" agonist (non-selective) |
| True or False, Isuprel has very little α activity at therapeutic doses | True |
| The effect of Isuprel on blood flow and smooth muscles | Increases blood flow (vasodilation) and relaxes GI smooth muscles |
| Isuprel can be administered via | Oral (sublingual), inhalation and IV routes |
| Sublingual onset | 30 minutes with 1 - 2 hour duration |
| IV onset and duration | very rapid, but less than 1 hour duration |
| Inhalational duration is | 2 - 4 hours |
| Isuprel is Used for | acute bronchospasms, bradycardia, asthma, etc |
| A property of dobutamine | Parenteral inotrope |
| Dobutamine is a Selective ___ agonist (minor β2 or α effects) | β1 |
| Dobutamine stimulates | rate and contraction of heart, increasing CO |
| The effect of dobutamine on systolic and diastolic pressure | Systolic pressure is increased due to increased stroke volume, with little change in diastolic pressure |
| The effect of dobutamine on coronary blood flow and myocardia | It increases coronary blood flow and myocardial O2 demand seen |
| The difference between DA and dobutamine is | Unlike DA, does not increase NE release from sympathetic nerves |
| What is dobutamine half life | Plasma half-life approximately 2 minutes, so needs to be administered via constant IV infusion |
| Dobutamine uses include | cardiac surgery, cardiogenic shock, and heart failure |
| DA Mimics action of endogenous DA, which is a precursor of | EPI and NE |
| DA Works at DA receptors to | dilate renal arterioles and increase renal blood flow and GFR |
| At low doses, DA causes | much vasodilation in renal, mesenteric, and coronary vessels |
| At moderate doses, Da stimulates | β1 receptors, stimulating the heart (while maintaining vasodilation) |
| At high doses DA Stimulates | α receptors, increasing TPR |
| True or false DA Does not cross BBB | True |
| How is DA administered | Normally given via continuous IV infusion |
| What is DA half life | half-life ~ 2 minutes |
| DA is Used for | heart failure, shock |
| True or false, Metaproterenol (Alupent)is a synthetic compound similar in structure to isoproterenol | True |
| Metaproterenol (Alupent)More ___ selective than isoproterenol (but less than Albuterol) | β2 |
| Metaproterenol (Alupent)is Exclusively used as a | bronchodilator |
| Metaproterenol (Alupent) is used for | COPD, asthma, chronic bronchospasms |
| Albuterol (Ventolin) is a Selective ____ agonist | β2 |
| Albuterol (Ventolin)Indications | bronchospasm in patients with obstructive airway disease, asthma |
| Albuterol (Ventolin)Adverse reaction | nervousness, tremor, tachycardia, palpitations |
| Pirbuterol (Maxair)is a selective ___ agonist | β2 |
| True or False, Pirbuterol (Maxair) is Structurally similar to Albuterol | True |
| Pirbuterol (Maxair)is Used for | asthma and bronchospasms |
| Salmeterol (Serevent) is a ___ agonist | β2 |
| True or False, albuterol is Much more selective for β2 than Salmeterol (Serevent) | False, Salmeterol (Serevent)is Much more selective for β2 than albuterol |
| True or False, many β2 receptors now known to be located on the heart; Their function is unclear at present | True |
| Salmeterol (Serevent) is used For | chronic treatment of asthma (BID dosing, due to longer half-life) |
| Salmeterol (Serevent) Side effects include | tachycardia, palpitations, hypersensitivity, tremor, and headaches |
| Terbutaline (Brethine)is a ___ agonist | β2 |
| Terbutaline (Brethine) is Used for | bronchospasms and asthma, emphysema |
| Terbutaline (Brethine) Side effects include | tremor, nervousness, tachycardia, palpitations, nausea and vomiting |
| Clonidine (Catapres) is a Selective ___ agonist | α2 |
| True or False, Clonidine (Catapres) has More CNS activity than peripheral | True |
| α2 receptor stimulation in the CNS leads to | decreased sympathetic outflow, increased parasympathetic outflow |
| Clonidine (Catapres) is Indicated for | control of hypertension |
| Side effects of Clonidine (Catapres)include | dry mouth, skin irritation |
| Phenylephrine (Neosynephrine) is a ____ agonist | α |
| Phenylephrine (Neosynephrine) is used as | vasoconstrictor to maintain blood pressure during surgery, decongestant, mydriatic (without cycloplegia) |
| Phenylephrine (Neosynephrine) is contraindicated in | narrow angle glaucoma, ventricular tachycardia, aneurisms |
| Phenylephrine (Neosynephrine)Side effects include | bradycardia, decreased CO, arrhythmias, angina, dizziness, CNS excitation |
| Metaraminol (Aramine) is a parenterally administered potent vasoconstrictor | (α1) |
| Metaraminol (Aramine) is used to prevent | surgical (spinal anesthesia) hypotension and shock |
| Metaraminol (Aramine) Adverse reactions include | anxiety, cardiac arrhythmias, and hypertension |
| True or False, Methyldopa (Aldomet)Forms α-methyl NE - acts as a false transmitter - less potent than NE | True |
| Methyldopa (Aldomet) is Used to treat | hypertension |
| Methyldopa (Aldomet) is contraindicated in patients with | hepatic disease |
| Methyldopa (Aldomet) Side effects include | angina, congestive heart failure, orthostatic hypotension, bradycardia, many others |
| Cocaine inhits | amine re-uptake pump, thus causing increases stimulation (Indirect effect) |
| Cocaine also has local anesthetic effects in that it | blocks Na+ channels of nerve membranes |
| Cocaine is used for | local (topical) anesthesia of mucous membranes in mouth, laryngeal and nasal cavities |
| Cocaine side effects include | vasoconstriction, mydriasis, nervousness, respiratory failure, cardiac arrest, general CNS stimulation |
| Indirect Adrenergic Agonists | Trigger NE release |
| Amphetamine (Dexedrine)Stimulates | (1)sympathetic neurons to release neurotransmitter, (2)Also has direct post-synaptic effect (mixed action) |
| Amphetamine (Dexedrine) is Used for | Narcolepsy, ADD, obesity |
| Amphetamine (Dexedrine) is contraindicated in | any cardiovascular disease, hypertension, hyperthyroidism |
| Amphetamine (Dexedrine) Adverse reactions include: | palpitations, tachycardia, increased blood pressure, psychoses, insomnia, headaches, tremor, general CNS stimulation |
| Ephedrine Stimulates both ___ and ___ receptors | α, β |
| Ephedrine Peripheral actions are due | partly to norepinephrine release and partly to direct effect on receptors |
| Therapeutic doses of ephedrine produce mainly | relaxation of smooth muscle and, if norepinephrine stores are intact, cardiac stimulation and increased systolic and usually increased diastolic blood pressure |
| Ephedrine effect on systolic and diastolic BP | increased systolic and usually increased diastolic blood pressure |
| How is Ephedrine metabolized? | It is Metabolized to a small extent, with remainder excreted unchanged in urine |
| How is Ephedrine administered | Ephedrine is Available in oral and parenteral forms |
| True or False, Ephedrine has a fairly high abuse potential | True |
| Many reported Ephedrine cases of | cardiovascular events |
| Pseudoephedrine (Sudafed) is a Potent sympathomimetic, they possess direct____ ,____ and____ activity in addition to triggering the release of catacholamines from the nerve terminal (mixed effects) | α1, β1, β2 |
| Pseudoephedrine (Sudafed)is Used mainly for | asthma, stimulant (OTC) preps |
| Pseudoephedrine (Sudafed) is Contraindicated in | CV disease, hypertension |
| Pseudoephedrine (Sudafed) Side effects include: | CNS excitation, tremors, insomnia, nervousness, palpitations, tachycardia, cardiac arrhythmias, headache, sweating |
| True of False, Tyramine (not used clinically) is taken up into nerve terminal and converted to false transmitter that has less activity, leading to decreased sympathetic tone | True |
| Tyramine has Slight direct | α activity |
| T/F, Tyramine Also triggers release of neurotransmitter from neuron | True |
| Tyramine is Found in some foods such as | Red wine, chocolate, cheese, etc |
| Tyramine presents a potential interaction on patients taking | monoamine oxidase inhibitors |
| Other indirect adenergic antagonists are | Methamphetamine (Desoxyn), Methylphenidate ( Ritalin), and Phentermine (Adipex) , |
| α1 agonists are: | NE, EPI, DA (higher doses),Phenylephrine, Metaraminol |
| α1 agonists Effects: | Increased arterial tone, increased TPR, increased diastolic pressure, decreased heart rate (reflex), increased venous tone |
| α2 agonists are: | NE, EPI, Clonidine, α-methyldopa |
| α 2 agonists Effects: | Increased tone in large arteries, increased TPR (Post synaptic α2), increased coronary vasodilation |
| β1 agonists are: | NE, EPI, ISO, DA, Dobutamine |
| β1 agonists Effects: | Increased heart rate, increased O2 consumption, increased automaticity, conduction velocity, increased force of contraction, increased stroke volume and CO, decreased filling volume (in tachycardia), increased coronary vasodilation |
| β2 agonists are: | Albuterol, Terbutaline, EPI, ISO |
| β2 agonists Effects: | Decreased arterial tone, decreased TPR, decreased diastolic pressure, increased heart rate (reflexive) |
| Several other drug classes that possess some degree of α receptor antagonism are | neuroleptics, TCA’s, and serotonin receptor antagonists |
| Phenoxybenzamine (Dibenzyline) is ‘irreversible’due to | covalent binding |
| Phenoxybenzamine is a ____ and ____ antagonist | α1, α2 |
| Duration of Phenoxybenzamine (Dibenzyline) has a | Long lasting effects (at least three days) |
| Phenoxybenzamine (Dibenzyline) is Most effective at | smooth muscle and exocrine glands |
| Phenoxybenzamine (Dibenzyline) is Used for: | pre-op treatment of pheochromocytoma to block potential hypertensive crisis during surgery, sweating and hypertension caused by pheochromocytoma, certain vasospastic disorders, and frostbite therapy |
| Phenoxybenzamine (Dibenzyline) Side effects include: | dizziness, decreased ejaculation ability, fatigue, miosis, orthostatic hypotension, tachycardia |
| Phenoxybenzamine (Dibenzyline) Half-life is approximately | 24 hours, and the drug takes several hours after initial dosing to see effects |
| Care must be taken with other drugs given even upon cessation of therapy, as blockade may still be present for | 7 days after the last dose |
| Phenoxybenzamine (Dibenzyline) is given by | Oral dosing |
| Phentolamine (Regitine) is a ____ and ____ competitive antagonist | α1, α2 |
| T/F, Phentolamine (Regitine) has a Shorter duration of action of action than phenoxybenzamine | True |
| How is Phentolamine (Regitine) administered | by Parenteral dosing |
| Phentolamine (Regitine) is Used for: | pheochromocytoma diagnosis, pheochromocytomectomy, MAO induced hypertensive crisis, impotence |
| Phentolamine (Regitine) Side effects include: | dizziness, decreased ejaculation ability, flushing, hypotension, sinus tachycardia |
| Phentolamine (Regitine) duration | Given parenterally - short acting |
| Prazosin (Minipress) is a Selective ___ antagonist | α1 |
| Prazosin (Minipress) is used for | hypertension |
| Prazosin (Minipress)Side effects include: | dizziness, headaches, drowsiness, palpitations, tachycardia, orthostatic hypotension |
| T/F Because Prazosin (Minipress) does not block α2 receptors, there is no excessive release of NE from neurons, and less of a risk of reflexive tachycardia seen with other α blockers | True |
| Prazosin (Minipress) is Available as an | oral dose form |
| Terazosin (Hytrin) Selective ___ antagonist | α1 |
| T/F Terazosin (Hytrin)is closely related to prazosin, but less potent | True |
| In comaprison to prazosin, Terazosin (Hytrin)is | More water soluble and higher bioavailability than prazosin, and also has a longer t1/2 (12 hrs), and can be used qD |
| Terazosin (Hytrin) is used mainly for | treatment of hypertension and benign prostatic hyperplasia (BPH) |
| Terazosin (Hytrin) is Available as an | oral dose form |
| T/F Doxazosin (Cardura) is a Selective α1 antagonist,also closely related to prazosin | True |
| Give similarities and differences between Doxazosin (Cardura) and prazosin | Doxazosin (Cardura) has similar bioavailability as prazosin, but has a longer t1/2 (20 hrs), and can be used qD |
| Doxazosin (Cardura) is used mainly for treatment of | hypertension and benign prostatic hyperplasia (BPH) |
| Doxazosin (Cardura) is Available as an | oral dose form |
| Give similarities and differences between Alfuzosin (Uroxatral) and prazosin | Alfuzosin (Uroxatral) is a Selective α1 antagonist, Also closely related to prazosin,Similar bioavailability as prazosin, but with a slightly longer t1/2 (3-5 hrs) |
| Alfuzosin (Uroxatral) is Used mainly for treatment of | benign prostatic hyperplasia (BPH)- relaxes smooth muscle in bladder neck and prostate |
| Alfuzosin (Uroxatral) is Available as | an extended release oral dose form |
| T/F Tamsulosin (Flomax) is a Selective α1A antagonist (but limited α1B activity, which controls vascular smooth muscle) | True |
| T/F Tamsulosin (Flomax) is somewhat more selective at treating BPH, with little effect on blood pressure | True |
| What is the half-life of Tamsulosin (Flomax) | t1/2 of 5-10 hrs |
| How is Tamsulosin (Flomax) Metabolized | mainly by P-450 system |
| Tamsulosin (Flomax) is Available as | an oral dose form |
| Yohimbine (Yocon) is a______ anatagonist | Selective competitive α2 antagonist |
| Yohimbine (Yocon) mechanism of action | Blocks central α2 receptors leading to increased blood pressure and heart rate (decreased parasympathetic outflow, and increased sympathetic outflow), possible aphrodisiac properties, due to peripheral α2 blockade and parasympathetic override |
| Yohimbine (Yocon)Side effects include: | antidiuretic effects, CNS excitation, hypertension, tachycardia, increased motor activity, nervousness, irritability, nausea and vomiting |
| Yohimbine (Yocon) is administered by | Local injections into penile shaft to increase erections |
| Propranolol (Inderal)is the Prototype | β blocker |
| Propranolol (Inderal) is Non-selective because | it blocks both β1 and β2 receptors |
| Propranolol (Inderal) is Used for | hypertension, ‘speakers’ nerves, angina, arrhythmias, migraines, pheochromocytoma |
| Propranolol (Inderal)Has membrane stabilizing effect (local anesthetic) which | enhances its anti-arrhythmic effects (most b blockers share this property) |
| Propranolol (Inderal) is Contraindicated in | shock, bradycardia, asthma, congestive heart failure |
| Propranolol (Inderal)Side effects include: | bradycardia, congestive heart failure, hypotension, heart block, insomnia, hallucinations, bronchospasms |
| Nadolol (Corgard)is a Non-selective | β antagonist |
| Nadolol (Corgard) is used For treating | angina, hypertension |
| Nadolol (Corgard) is Contraindicated in | bradycardia, bronchial asthma, shock, heart block, myocardial infarction |
| Nadolol (Corgard)Side effects include: | bradycardia, cardiac failure, conduction disturbances, arrhythmias, dizziness, bronchospasm, diarrhea, impotence, decreased libido, blurred vision |
| Timolol (Timoptic) is a Non-selective | β antagonist |
| Timolol (Timoptic) is used For treating | hypertension, ocular hypertension (wide angle glaucoma) |
| Timolol (Timoptic) Contraindications include | asthma, COPD, bradycardia, heart failure |
| Timolol (Timoptic)Side effects include | fatigue, bradycardia, dizziness, cold hands and feet |
| Pindolol (Visken) is a Non-selective | β antagonist with some sympathetic agonist activity |
| Pindolol (Visken) is a vasodilatory β blocker | due to strong β2 agonist activity |
| T/F Pindolol (Visken) has as much bronchoconstriction as with other β2 blockers | False, Pindolol (Visken) Also not as much bronchoconstriction as with other β2 blockers |
| Pindolol (Visken is Used to treat | hypertension |
| Pindolol (Visken) Contraindications: | bradycardia, COPD, heart failure |
| Pindolol (Visken Side) effects include | fatigue, dizziness, diarrhea, cardiac failure |
| Labetalol (Normodyne) is (non-selective) | α1, β1 and β2 antagonist, Partial agonist at some β2 receptors |
| Labetalol (Normodyne) is used for treating | hypertension |
| Labetalol (Normodyne)Contraindications: | asthma, cardiac failure, severe bradycardia |
| Labetalol (Normodyne)Side effects include | postural hypotension, sweating, dizziness, nausea and vomiting, nasal stuffiness, bradycardia, impotence |
| Carvedilol (Coreg) is a nonselective | α1, β1 and β2 antagonist |
| T/F Carvedilol (Coreg) has a Higher β:α blockade than labetolol (and longer duration) | True |
| Carvedilol (Coreg) Indications: | angina, heart failure (NYHA type II and III), hypertension |
| Carvedilol (Coreg)Contraindications: | bronchospasm, emphysema, COPD, asthma, bradycardia, diabetes mellitus, heart failure (NYHA type IV), liver disease, pheochromocytoma |
| Carvedilol (Coreg) Adverse reactions: | Bronchospasm, diarrhea, dyspnea, fatigue, headaches, hypotension, peripheral edema, bradycardia, syncope |
| Metoprolol (Lopressor) is a selective | β1 antagonist |
| Metoprolol (Lopressor) is Used to treat | hypertension and angina pectoris |
| Metoprolol (Lopressor) Contraindications: | bradycardia, heartblock, shock, myocardial infarction |
| Metoprolol (Lopressor) Side effects include | dizziness, bradycardia, nightmares, congestive heart failure, peripheral edema, bronchospasms, nausea, diarrhea |
| T/F Acebutolol (Sectral) is Mostly β1 blockade, but is also a partial sympathetic agonist (non-selective) | True |
| Acebutolol (Sectral) has little CNS side effects because | Low lipid solubility |
| Acebutolol (Sectral) is Used in the reduction of | hypertension and to control ventricular arrhythmias |
| T/F Acebutolol (Sectral) Does not cause as much bronchoconstriction as non-selective β blockers, and Less likely to cause bradycardia than other β1 blockers, due to its intrinsic sympathomimetic activity | True |
| Acebutolol (Sectral) Side effects include: | alopecia, dizziness, angina, fatigue, heart failure |
| Atenolol (Tenormin) Blocks | β1 mostly |
| Atenolol (Tenormin) is Used to treat | hypertension, acute myocardial infarction, angina pectoris |
| Atenolol (Tenormin) is Contraindicated in | bradycardia, heart block, shock, cardiac failure |
| Atenolol (Tenormin) Adverse reactions include | bradycardia, dizziness, fatigue |
| Esmolol (Brevibloc) is a selective | β1 antagonist |
| Esmolol (Brevibloc) Given by | IV infusion |
| Esmolol (Brevibloc) is Used for | atrial fibrillation or flutter, paroxysmal supraventricular tachycardia |
| Esmolol (Brevibloc)Contraindications: | bronchospasms, bradycardia, shock |
| Esmolol (Brevibloc) Side effects: | AV block, cardiac arrest, hypotension, bradycardia |
| Esmolol (Brevibloc) Half-life | only a few minutes (very short duration) |
| Metyrosine (Demser) is a Inhibitor of | tyrosine hydroxylase |
| Metyrosine (Demser) is Used for | pheochromocytoma |
| Metyrosine (Demser) is Contraindicated in | hepatic disease, Parkinson's disease |
| Metyrosine (Demser) Adverse reactions include | anxiety, confusion, crystalluria, depression, Parkinsonism, salivation |
| 6-hydroxydopamine (experimental) MOA | Taken up into adrenergic nerve terminals and destroys the cells |
| 6-hydroxydopamine Stimulates | free radical production in cells, leading to cell death; Therefore, removes adrenergic neurons (chemical sympathectomy) |
| Bretylium (Bretylol) Blocks | catecholamine release from nerve terminal |
| Bretylium (Bretylol) is Used for | ventricular tachycardia, prophylaxis of ventricular fibrillation |
| Bretylium (Bretylol) Adverse reactions: | hypotension, bradycardia |
| Reserpine (Serpalan) inhibits | storage of catecholamines (and serotonin) in granules, leading to depletion; Initial effects may cause transient release |
| Reserpine (Serpalan) is Used for | hypertension, schizophrenia |
| Reserpine (Serpalan) Contraindications include: | mental depression, peptic ulcer, ulcerative colitis |
| Reserpine (Serpalan) Side effects: | vomiting, diarrhea, dry mouth, syncope, angina, many more |
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