Transcript for:
Pharmacology - Adrenergic Agonists

hello this is Professor Jim Hoffman and welcome to nursing 1721 pharmacology for nursing topic four is covering the autonomic nervous system drug classes so in this video we're going to start with topic 4A and we're going to look at the adrenergic Agonist so as you look at your reading guide um this video will cover the first five of the learning objectives so we're going to be looking at non-selective adrenergic Agonist Alpha One Agonist Alpha two agonists beta one Agonist and beta 2 Agonist your reading sections are listed in the second column again in your digital copy of the learning objectives just use the hyperlinks to go to your chapter readings I would also encourage you as another resource for this topic would be to go back to uh section 4. let me find it here real quick 4.2 in the text it's the autonomic nervous system Basics it was a list of information for the in topic three when we're looking at some physiological pathophysiological Basics and towards the end of that section is a nice summary of the autonomic nervous systems as far as Agonist antagonists uh the effects that we would expect to see so again keep that in mind topic 4.2 in the text as you begin your information on the different drug classes there's a tool I want you to make make you aware of and I will make copies of it for the various classes and put into canvas so you can use them if you choose to but in the nursing program at Rhodes State you're going to hear reference to the acronym cap RN Kappa RN is just a way of looking at how we gather information on on the drugs that we're administering in our clinical setting so when you're doing drug research for any of your clinical classes each class will have some sort of a format or model or tool to do your data collection on the drugs you'll be giving and they all follow the cap RN model so we're looking at capar and we're looking at C is for classification so that's the breakdown of our content for this course is we'll look at individual classifications and we'll be focusing on the pharmacologic which is looking at what are the pharmacodynamics of the class that result in the effect but classification can also be therapeutic now a way of distinguishing the two um you might be looking at a therapeutic class or anti-hypertensives or medications that help bring down blood pressure pharmacologic classifications would break down that therapeutic into more specific pharmacodynamic type classes so for an anti-hyper intensive drug we could be looking at diuretics because they're going to bring fluid down and lower blood pressure we could look at ACE inhibitors that we'll talk about later on or we could look at beta blockers so again the therapeutic is usually more of a broad classification and within that there are going to be a number of pharmacologic classifications our Focus will be on those pharmacologic classifications that's the C a stands for actions and that's just another way of saying the pharmacodynamics where in the body does the drug work and what does it do at those locations in the body P is for purposes or these would be the applications the indications for the drug use so what would this drug class where would we see it being used reactions includes any a side effects adverse effects any interactions with food or drugs any of those types of things so we're looking at things that impact or that we need to be aware of when we're looking at a drug class cautions contraindications those types of things would all fall under reactions then finally there's nursing implications and nursing implications are what assessments do we need to be doing what interventions might we might we be prepared to do what teaching items would be appropriate for that particular drug class so again cap RN is just a way of assembling your information I will put copies blank copies for the different classifications in each Topic in that section of the modules in canvas so you can use them if you'd like to um again it would be maybe helpful for you in your clinical classes if you start a collection of cap RNs so when you get into your clinical situations and you're looking at a drug once you identify the class you may have all of your information already assembled on the cap RN and you just transfer that over to the tool that you're using for that course so let's get started looking at the first class and we're going to start out with ADD adrenergic agonists so again adrenergic and sympathetic are the same terms so we're looking at autonomic nervous system we're looking at fight or flight responses and you're going to see drugs described as either adrenergic or sympathetic and then the other terms are going to be Agonist or you might see the suffix mimetic so a sympathomimetic is the same as an adrenergic Agonist or a sympathetic Agonist the terms are going to be are interchangeable I'm going to be looking at a concept of selective versus non-selective again you want to remember that there's multiple sites in the adrenergic system we're going to look at those on the next slide and some drugs are selective in that they only or primarily work at one particular site some are non-selective which means they can work on multiple sites we have to be aware of not just the primary use that we're seeing for the drug at one site but what are the secondary effects we're seeing in another site of the other concept is catecholamines these are the neurotransmitters or the chemicals that naturally produce this adrenergic agonistic response in the body our catecholamines for the adrenergic or sympathetic side are norepinephrine and epinephrine primarily but also dopamine and serotonin would be another two that are going to be working as adrenergic Agnes throughout the body so again these are the neurotransmitters one phrase I didn't put up here and it'll be mentioned when we're looking at some interactions are drugs that affect Mao Mao is monoamine oxidase monoamine oxidase is the enzyme that breaks down the catecholamines in the body so Mao is going to be an adrenergic inhibitor the catecholamines the norepinephrine epinephrine or dopamine are produced in the body they go to the sites they produce the responses at the sites the monoamine oxidase is an enzyme that's naturally produced in the body that starts um destroying those enzymes or those like catecholamines uh to help basically keep us from always being at a high level so it's just part of a natural process of a negative feedback loop or to keep us in balance so when we talk about some drugs later on in the psych um section we're going to talk about monoamine oxidase inhibitors so those are going to be drugs that inhibit that monoamine oxidase so if we inhibit the enzyme that breaks down catecholamines we're going to end up with a net increase in the catecholamines at the site bring that up again when we're looking at some interactions here a little bit but just remember catecholamines are neurotransmitters that's going to be epinephrine norepinephrine and dopamine then we have the adrenergic inhibitor and that's going to be the monoamine oxidase or Mao that's going to break down those catecholamines and bring that response lower that sympathetic response or adrenergic response so again just real quick reminder on receptor sites Alpha One when stimulate we're looking at vasoconstriction and pupil dilation and muscle relaxation of the bladder so if the bladder muscle relaxes it we're going to have urinary retention so these are when these sites are stimulated these would be normal sympathetic responses or in drug terms it's going to be agonistic responses beta 1 we're looking at the heart so we're looking increased heart rate increased contractility and we're also looking at some involvement with the kidneys particularly in the um encouraging or stimulating the release of renin which activates the renin Angiotensin aldosterone system and the final result of that as far as cardiovascular remember is to increase our blood pressure by giving us some vasoconstriction from Angiotensin II but also releasing aldosterone which is going to cause us to retain sodium and fluid so a primary effector to look at beta1 is the heart but just remembered also is going to have impact on the kidney beta 2 our primary site is going to be in the lungs and we're going to look for bronchodilation in the uterus we end up with muscle we create muscle relaxation and there's a secondary or smaller effect in the liver which is going to increase the production of blood sugar from stored glycogen so again beta 2 we're looking primarily usually at bronchodilation but we need to realize it's going to start having some impact on blood sugar because it's going to increase this production of blood sugar from stored materials then Alpha 2 separated out it is sort of an outlier when we're looking at the adrenergic system again it's a pathetic response we usually think of increasing heart rate and blood pressure altitude doesn't work out in the periphery out in the extremities out in the muscles and the blood vessels throughout the body it works within the central nervous system in the brain and it actually works to inhibit norepinephrine release so Alpha 2 when it stimulate actually causes vasodilation and decreased blood pressure so again it's an outlier it's not the normal fight or flight response we would expect but it is um a site that responds to or is involved with the release of the catecholamines so again Alpha two going to be that sort of counter-intuitive response of vasodilation decrease blood pressure so the first class we want to look at first pharmacologic class is the non-selective adrenergic Agonist and the text uses epinephrine as a model or prototype for this class so again when you're looking at your drugs and doing your research it's going to give you the individual drug name but it's also going to tell you what kind of which class it belongs to you know it looks often as well usually lists pharmacological class it will also list the therapeutic class as well so the actions that we're looking at with the non-selective adrenergic agonists are that they're going to mimic the actions of norepinephrine and the epinephrine the catecholamines or the dopamine so a non-selective means it's going to stimulate both alpha 1 and both of the beta sites beta 1 and beta 2. so it's going to give us the full fight or flight response we're going to get vasoconstriction we're going to get the increased heart rate contractility we're going to get bronchodilation so when we're looking at some of the uses of epinephrine one is the severe allergic reactions the anaphylactic Reactions where we have bronchoconstriction where we have the beginnings of shock going on we want all of these responses and we want them very quickly so a non-selective adrenergic Agnes Agonist is going to be held uh indicated so acute bronchospasm we use it during cardiac resuscitation when the heart muscle just needs to be stimulated for that contractility it's also have an impact on conduction in the heart so it's basically a jump start type medication the last one listed under purposes a local injection to control superficial bleeding so we're really looking at a very localized alpha-1 response here and just knowing we'll have some of the secondary beta one and beta 2 responsive it's going to be injected subcutaneously around a cut before suturing quite often causes that vasoconstriction so we end up limiting the amount of blood coming to the site to allow for the suturing to take place and cuts down on the swelling that type of thing but it's local it's going to be a short-lived type thing but particularly helpful during a suturing of a surface cut so our reactions our reactions are usually the result of um excess expected actions we want it to we get it quite often to help raise blood pressure the reaction can be that high blood pressure can continue to rise and create a hypertensive crisis it will speed the heart up um but if we're using it for something other than that specific type thing we run a risk of increasing heart rate increasing cardiac workload and causing potential damage to the heart so again it's taking those normal effects and taking them to the extreme some contraindications your text talks about some specific sites our fingers our toes some areas that have a very extensive microvascular area that if we constrict those areas we end up creating blood flow oxygenation and nutrition risk to local sites so there's some specific local sites where we want to either not use epinephrine specifically at those sites or be very cautious in doing it now the narrow angle glaucoma is a contraindication glaucoma is an increased pressure on the on the eyeball and it's caused by fluid buildup when we do a nonce non-selective or an adrenergic Agonist that causes pupil dilation that dilation of the pupil actually blocks off some of the drainage sites or drainage system of the surface of the eye and it increases that pressure so that's why it's going to be a contraindication for the certain adrenergic agonists including the non-selective so narrow angle glaucoma that pupil dilation creates more problems elderly just in general we want to use all medications with those level of caution because they don't metabolize the medication so if we have some natural decline in liver function or renal function and these Agonist non-selective agonists are not metabolized not eliminated we're going to start building up higher levels and having um these adverse and side effects that can be damaging for the elderly and we want to be cautious in cardiovascular disease because we're putting a lot of stress particularly on the heart as well as on the blood blood vessels as far as increasing blood pressure but particularly on the heart we're increasing its workload and if we already have some cardiovascular disease we can aggravate that condition through the use of these medications we have to be very cautious so some of our nursing considerations for the non-selective is we are going to again really focus on Vital Signs and cardiovascular status in our assessments if we're giving an IV we want to monitor the IV site if this this medication leaks out of the IV site we're going to get a lot of local vasoconstriction which may end up causing tissue injury and tissue death in the area a patient teaching along with telling and teaching the patients watch out for these expected signs and side effects and the expected desired effects another teaching area will be on how to administer the medication so again one of our one of the big uses for epinephrine in particular is an anaphylactic shock or potential anaphylactic shock situations so when the people are aware that they have this hypersensitivity to whatever their stimulus is they may be prescribed an EpiPen the EpiPen is a pre-filled syringe with epinephrine in it and designed for self-administration emergency situation so that would be a primary teaching for individuals who have a hypersensitivity that could lead to anaphylaxis on how to effectively use their EpiPen next we want to move to the Alpha One Agonist so we're looking at a selective adrenergic agus now pseudoephedrine is our main prototype for this class that has trade name of Sudafed phenylephrine has also historically been looked at its pseudoephedrine has some crossover to the beta sites as well so it's not totally selective but it's highly selective to Alpha One phenylephrine has been looked at as being more Alpha One selective so it doesn't have some of that carryover you may have seen some things in the news recently there's some research that's been looked at over the last several years that phenylephrine may not be quite as effective as what we've thought it was in the past so you may see some changes on its use in even in the next several months as far as some over counter drugs so again the actions of an alpha-1 Agonist is the selective stimulation of Alpha One sites and the main thing we're looking at is vasoconstriction if you go back to the other the slide at the beginning of the presentation you see some of the other areas where alpha one is going to have a response but usually we're looking at the vasoconstriction um so we're going to be using this especially for upper respiratory infections symptom relief because when we get to congestion the swelling the sinus drainage those are all a result of inflammatory response that part the key thing in inflammatory response is increased blood flow to a site and increase permeability so if we can do vasoconstriction at those sites we'd cut back on that blood flow the constriction is also going to help as a permeability issues so we're going to have less swelling and less secretions so this is where we're usually going to see the sites as a the uses of the Alpha One Agonist primarily is going to be in this upper respiratory illness situation now some reactions again are just the result of the Alpha One having impact in other places so we're taking it primarily for a local response in the upper respiratory the sinuses that area we also have to be aware that the Alpha One sites are also out in the arteries in the blood uh um cardiovascular system so we're going to see increased blood pressure it has an impact on the bladder it's going to cause the bladder wall muscle to relax we're going to have urinary retention it's also going to cause some constriction of the sphincter and also in males the prostate so that's going to also contribute to urinary retention alpha one is going to cause some jitteriness some difficulty sleeping this becomes an area where contraindications includes that MAOI the monoamine oxidase inhibitor inhibitor drug class because again remember Mao is the adrenergic inhibitor or it's purpose of the initial enzyme is to break down these catecholamines if I'm taking an MAOI MAO inhibitor drug class which is going to be one of our psych drugs um that is going to result in naturally increasing the amount of catecholamine so if I've got that natural increase in catecholamines out of the receptor sites and then I'm taking alpha-1 Agonist on top of it I'm running the risk of going in put of the individual going into hypertensive crisis um again it's going to have that alpha one response of the pupil dilation so the narrow angle glaucoma again is an issue and because it's impacting the prostate if we have an individual with a large prostate and then we further constrict the prostate we're going to increase the urinary retention issues for those individuals so from a nursing consideration standpoint we want to monitor blood pressures that's our primary site we're going to see effect then we're going to watch for these side effects these reaction type things for the patients we need to make sure they're aware of their medications including their over-the-counter because the Alpha One agonists the pseudoephedrine phenylephrine are quite often found in over-the-counter drugs in patients may not be thinking about looking at their other medications against or over count over-the-counter medications and may not be aware of the side effects of those combinations so again part of our patient teaching is just making them aware that there are potential effects and that they have a full list of medications including these over-the-counters foreign again remember Alpha 2 is an outlier its actions happen within the central nervous system in the brain and it actually doesn't mean inhibition of the sympathetic nervous system by inhibiting the release of norepinephrine and the main thing we see from it is decreased vascular resistance or some vasodilation so it's going to decrease blood pressure so again it is a sympathetic or adrenergic Agonist but it is not a typical fight or flight is actually the opposite of what we would expect so we're going to use it in hypertension it also has some uses in ADHD to sort of inhibit some sympathetic stimulation in the brain so our reactions these would be normal side effects they could become adverse effects if they become extreme we're going to get that hypotension from the vasodilation and we're going to have some impact on the norepinephrine going into the hearts we're going to get some bradycardia it's uh again cutting back on stimulation in the brain so we're going to have a feeling of sedation we have a real concern with this drug class and a couple others if we stop it abruptly the things that we're trying to treat are going to come back very quickly and more severe so that would be rebound hypertension so if we're taking the clonidine to lower our blood pressure and we don't wean It Off or slowly taper down the doses we're taking we can end up with extremely high hypertension as a rebound reaction so our consideration Center monitor blood pressure primarily teaching is going to make the patients aware of what are the signs and symptoms of orthostatic hypotension which is a natural side effect from this they don't want to combine it with alcohol because we get two responses in the brain they're both looking at sedating or slowing responses down and we want to make sure they're compliant with the dosing schedule they take it routinely so they can maintain an appropriate level they take it at the same time of the day each day again we want to maintain a maintain the therapeutic levels within the bloodstream next we're going to look at beta1 Agonist and dobutamine is a prototype resist class and with beta 1 we're looking at beta 1 specific so we're looking they've primarily focus on beta 1 sites the one that we're most often concerned with or focused on is the heart so again remember in the chest is where we're going to find our primary oxides of action for beta size we have one heart in our chest so we use beta one sites there on beta 2 we have two lungs of our hearts when we talk about beta two Agnes we're agonists we're going to look primarily at effects on the lung so beta 1 again we're looking as hard so we're going to look at increased heart rate increase force of contraction or contractility we're also going to see an increase in the conduction speed within the heart so the signal is going from the SA node to the AV node and out down through the purkinje fibers is going to be increased by stimulation of the beta 1 sites so beta 1 Diagon is such that stovine is gonna help in all those areas so our purpose is usually going to be used in case of a heart failure where we want to increase that strength of the heart we have to use some caution with the fact if we increase the heart rate as well we're increasing the workload so it's a balancing act was a heart failure um but for early stages of heart failure from fluid loss that type of thing these are going to be extremely helpful cardiogenic shock is where we're going to see it as well when we're getting low blood pressure because of decreased cardiac function we want to increase that cardiac function and the activated one Agnes will do that for us so some of our reactions are going to be the side effects just going higher than what we want so we are going to get a rapid increase in heart rate and blood pressure so we need a monitor that doesn't put us into a danger situation it's going to create that increased workload on the heart is going to cause an increased need for oxygen so we're going to see some labored breathing as a side effect The increased workload of the heart and that increased stimulation of the conduction system may actually cause chest pain and some hard irregularities that are going to be felt as palpitations may have some dizziness going on from this increased stimulation so our consideration is going to monitor the ECG Vital Signs heart rate and blood pressure particularly in critical care settings we're going to monitor cardiac output we're also going to be watching urinary output um to make sure that our fluid balances are saying are staying where we need them to be our teaching really ties into making sure the patients understand what these potential side and adverse effects are that they can recognize them if they're taking these medications at home and they can report them as early as possible before the levels become high enough to become dangerous the next class then we're going to move to the beta 2 Agonist to albuterol is our prototype for that so again stimulate beta 2 sites we're looking primarily in the lungs but there are other sites too so go back to that early slide from this presentation to see what other areas we're going to see effects so we're looking for bronchodilation there will be some bleed over that's probably not the best term some crossover into beta one site so we will see some secondary cardiac stimulation so the beta 2 agonists are selective to Beta 2 but they're not purely selective they may have some crossover into beta 1 sites so we're going to use these particularly with COPD and asthma situations where we have constrictions of bronchioles and so we're going to use these as bronchodilators so our reactions it's possible for individuals to develop hypersensitivity so we will get um may end up getting some almost counterintuitive responses we want bronchodilation but with hypersensitivity our body may go into overreaction actually get a bronchospasm type too it's going to be rare but we have to watch for it we are going to get those natural secondary effects of increased heart rate and blood pressure so if we have a patient with a cardiac function issues already a history of Mi or a history of hypertension we need to be aware that using the albuterol The beta-2 Agonist is going to aggravate those situations or uh be a cause for concern our nursing considerations then are Vital Signs particularly the respiratory related Vital Signs going to be listening for lung sounds to see if the bronchoconstriction is being eased as a result of the treatment so we can measure the effectiveness of the treatment uh often this class is administered through inhalers so in order to give it time to work and not to um overdue the circulating levels of the medication we want to make sure that after an inhalation um treatment is done that the individual knows to wait at least two minutes before they do the next round of inhalations so if they have an order for two Puffs as needed they can do their two Puffs but they don't want to do another two Puffs for at least two minutes preferably a little bit longer to make sure they can see what the effects were teaching is going to involve the use of a spacer it's going to help improve effectiveness of drug delivery so it's going to be a teaching tool that you'll be encountering and the other things we want to look at is that Administration technique especially with these inhalers that they're compliant that they use them only when they need them and that they are recognizing reporting those side and adverse effects so those are the classes that you need to be looking at under the adrenergic Agonist our next topic then we'll move to the adrenergic antagonist