Comprehensive Pharmacology Exam Review

All right, well, it's 8 Eastern Time, so we'll get started. I'm Dr. Drayton, if you haven't met me before, and I've been teaching pharmacology for the university since 2016. I see a lot of the residential St. Augustine students here, so welcome back, and other folks from other campuses, welcome. We're going to do exam to review. I think I'm going to go over an hour. It's probably going to be an hour and 10 to 15 minutes. I'll try to go fast, but not so fast. You're not following. And just note in the chat, there is the link to complete your review so you can get your badge in iLearn. So make note of that. So if you would go to menti.com and use the code listed here so you can answer the questions as we go through this. And feel free to unmute, ask questions. You can put questions in the chat as well if you're more comfortable with that. But you are welcome to just turn your microphone on and ask questions. This PowerPoint will be available through iLearn if you didn't see it already there. And if you're having trouble accessing, I can email it directly to you as well. And also, I did post it on the St. Augustine. residential pharmacology course announcements today. All righty. So we're going to start by covering chapter 25, but we'll brush through all the units 5 through 14 as well. First thing we're going to talk about is the drugs to treat hyperlipidemia and coagulation issues. And I just want to just do a quick brief review of the coagulation cascade because in order to understand how these medications work, You need just a general understanding of how blood clots are formed, which you've probably seen before. So this is probably a review. So typically what happens is an endothelial wall of a blood vessel or capillary is damaged and that activates collagen and tissue factors to start the clot response. So then what happens is platelets are activated to aggregate and adhere, so to become sticky. So they form that platelet plug. And then through a series of coagulation or clotting factor chain of events, fibrinogen here is converted into fibrin that are these insoluble strands that add to the strength of the clot. So that's how the clot is formed. And we have three different drugs to treat clotting, which we'll talk about. So we'll start with our question. which type of medication is best for DVTs. So our antiplatelet, anticoagulants, or our fibrinolytics. So it would be our anticoagulants for DVTs. So the anticoagulants are our classic meds to treat blood clots, DVTs. Heparin is typically used in the hospital when someone has a DBT, reason being it has its large molecule in size, so it typically must be administered intravenously. We also do have low molecular weight heparin that can be administered subcutaneously. And the heparin will activate antithrombin, which inactivates clotting factors. And then when somebody goes home or typically used to prevent DVT, patients will take oral Coumadin or Warfarin. So this is typically utilized at home. So Warfarin interferes with vitamin K metabolism in the liver, impairing hepatic synthesis of several clotting factors in that clotting chain of event. So the issue with warfarin and Coumadin is that patients are told they have to avoid dark leafy greens. Now I know with my kids, that's not a problem. But the dark leafy greens are high in vitamin K, which will basically counteract the medication. So we want to limit those when taking this. All right. So risks. Hemorrhage is a big risk with any of these anticoagulants. medications. So blood in the urine, blood in stools are a sign that there's too much bleeding. Sudden onset of back pain or joint pain and swelling would be a concern. GI distress. And of course, we often see these skin reactions, especially when I've seen it a lot, like working in skilled nursing facilities. A lot of patients on blood thinners, their arms look like this. So we want to certainly as PTs just watch out, just try to avoid patients hitting things or skin tearing, things like that that could cause bleeding. We certainly don't want to be doing deep tissue work or instrument assisted soft tissue work with patients who are on anticoagulants. Dry needling is another. um precaution patients who are on these cervical manipulation things like that all right let's talk now about anti-platelet drugs so these inhibit that activation of the platelets that makes them sticky um generating that clot so prevent clot formation um in arteries also in veins but predominantly arteries So the most commonly used antiplatelet medication is aspirin. That's correct. So aspirin, as low a dose as 81 milligrams or a baby aspirin can help prevent MI and stroke, whereas oftentimes an adult dose of 325 milligrams will be prescribed prophylactically as well. For example, I just had ACL surgery. So I'm taking aspirin daily for a month, an adult dose to prevent DBTs. So we just talked about how they work. Again, treating, preventing DBTs, preventing MI. Certainly there's a risk of CVA, risk to livers, kidneys, GI disturbances, and CVA, of course, which type of stroke would aspirin be utilized for prevention? That's right, ischemic. So an ischemic stroke, where there's a blood clot that forms in the brain to block blood flow to the tissue, would be prevented, whereas the patient may be at higher risk for a hemorrhagic stroke. with taking anti-platelet medications. In the event of acute MI at home, it is advised that aspirin should be administered via which route? So typically, I like what everyone's thinking, sublingual, but with aspirin, typically it doesn't dissolve very well under the tongue. So normally we're just going to have an oral tablet at home that's available. And so it's advised just to chew an adult dose of aspirin to just get it in the system faster. Nice. All right, next question. Which medication is best for arterial clots, such as acute MI or ischemic strokes in the ER? Nice. Yes. Fibrinolytic agents. So this morning during class, there was a similar question and there was two options, anti-fibrinolytic and fibrinolytic agents. And fibrinolytic is the correct answer. So these facilitate the breakdown of clots. So these are the ones that need to be administered within 12 hours with acute MI or within three hours with ischemic stroke to help preserve that tissue and prevent tissue death by breaking up that clot. So these are our kinase medications. And of course, the biggest risk is cerebral hemorrhaging with these meds. So the anti-fibroanalytics are typically prescribed in the situation of somebody who has hemophilia and they're undergoing surgery because this will prevent excessive bleeding and prevent that breakdown of fibrin. Okay, we're going to move on to cholesterol meds. So which type of cholesterol should ideally be higher? Now, why is it showing the answer? Have all the answers been shown on this? Maybe it was just this one. This is correct. So the HDL. So we want the HDL to be high. So we want the HDL to be 60 or higher. That's the good cholesterol that helps reduce the arthrosclerotic plaques. We want the LDLs, ILDLs, VLDLs to be low because that is the bad cholesterol that contributes to increasing risk of stroke and heart attack. So we have statins and we have fibrates that help reduce cholesterol and lower the LDL and in some cases increase HDL. So statins have been shown basically to, you know, reduce the chance of heart attack and stroke. And they also have some cancer preventative. properties in some studies. They have anti-inflammatory, antioxidant effects. They also increase production of nitrous oxide, which is a natural occurring vasodilator. So they have a lot of great properties. However, they do cause myopathies. That's the biggest concern. And the worst case scenario would be rhabdomyolysis, where there's really a major breakdown of proteins, which can really put... big stress on the kidneys and can be life-threatening. GI distress is also another concern and kind of off the record as well. There are some newer studies looking at risk of tendinopathy with statins. So another thing to keep in mind for us as PTs. All right, now we're going to talk about benzodiazepines. So benzodiazepines increase the inhibitory effects of GABA. So what are five clinical applications for benzodiazepines? See what that residential class remembers from today. Right. So benzodiazepines are going to calm and quiet the nervous system. So they're going to help with seizures. anxiety, they're going to be muscle relaxers. They are not going to help with depression because depression, the nervous system is already calmed and quieted. And we don't want to reduce activity even more in the case of depression. General anesthesia as well. Exactly. Good. So we have sedative hypnotic. anti-anxiety, anti-epileptic, muscle relaxer, and general anesthesia. So lots of uses for these benzodiazepines. However, they're not used all the time because of some concerns with them. So what's the biggest concern with the benzodiazepines? Yes. Sedation is a concern. Biggest concern would be tolerance and dependence, for sure. Great. So tolerance and dependence are the biggest concerns. Also, these stay in the system for a long time. They have a long half-life and they also are lipid soluble. So they get stored in adipose tissue. So they stay for a long time. They cause sedation. and people can have just a residual hangover. They take it for sleeping and then the next day, they're just feeling groggy all day. Now, another thing you won't be tested on, but I do want to list it here. There was a large cohort retrospective study in people with Alzheimer's disease, and they were 50% more likely to have used benzodiazepines. And there was a link associated with how high the dose and how long the person used the dose. use the drug. So there is a link that we just want to be aware of. I mean, it's part of why these are not used as often. So sedative hypnotics and anti-anxiety drugs, again, are going to calm and quiet the nervous system. So we also, beyond the benzodiazepines, we have barbiturates. Now, barbiturates also act by increasing the inhibitory effects of GABA, but it's not fully understood how. The issue with the barbiturates is that there is a small therapeutic index. So there's a risk of overdose. And also these can be addictive. But they were used for a time as a sedative hypnotic. And we're going to revisit barbiturates when we talk about anti-seizure medications, because these are, the barbiturates are the most common medication used worldwide for seizures. So we will revisit those. So the last group of sedative hypnotics on my list for tonight are our Z drugs. So Z drugs for... insomnia and for sleep. Ambien, probably the most common. And one of our discussion questions in residential University of St. Augustine was about a patient who was wake up in the morning and he could tell that there were signs that he was eating at night, he was gaining weight and doing all these things he had no memory of. And these are complex behaviors. Patients taking sleep. Ambien have been known to sleepwalk, drive, which is quite scary, and eat. So the Z drugs are most notorious for this. And actually, my husband was in the Navy. And when he was on deployment, they gave him no-go and go pills to make it very simple. And the no-go pill was Ambien. And he called me a bunch of times. And we had conversations. He didn't remember anything that we talked about. So amnesia is also an issue too. So anxiety, I think we all know what anxiety is. So benzodiazepines are used for anxiety, but typically it's more situational scenarios. So oftentimes we have patients taking Valium, which is a benzodiazepine for if they're claustrophobic and they're going for an MRI. Okay, so what are the four main types of medications used to treat anxiety? We have one of them, benzodiazepines, we just talked about. One of our discussion questions also was which medications are, which antidepressant medications are used for anxiety. And those are our serotonin selective reuptake inhibitors and our serotonin norepinephrine reuptake inhibitors, because there is, we do have an understanding that serotonin and norepinephrine imbalances are involved in anxiety. We also have buspirone, um, Benzodiazepines, great. Somebody put beta antagonists on there too. So BZDs, Buspirone, SSRIs, and SNRIs. So Buspirone is commonly prescribed in older adults. It stimulates serotonin receptors, certainly less sedation and dependence as compared to benzodiazepines. There are some side effects. Does take a little longer to kick in. And as I mentioned, commonly used in older adults. With our younger adults, often we're using the antidepressants to address anxiety. Somebody already stole my thunder on this question, which is great. What type of cardiovascular medication is used to treat anxiety? Yes. Beta blockers, exactly. So beta blockers are also used because they're just going to block basically sympathetic input. Again, often used in situational anxiety, like somebody's going for a job interview, something like that. Okay. And then we have antipsychotics and anticonvulsive medications as well. We've talked about the adverse side effects. I just have them all in one list here for you. Let's move on to seizures. So seizures, recurrent uncontrolled cerebral excitation. So again, the goal is going to be to calm and quiet the nervous system when somebody has a seizure disorder. So we have six basically traditional agents are hydantoins, common dilantin you've probably heard of. And then last two on the list, the benzodiazepines, which we've already listed, and then the barbiturates, which I mentioned, are the... found to be very effective. They're very effective. They're also very cheap. So it is one of the most common meds prescribed worldwide. However, they're not selective. So there's a lot of side effects, issues with generalized inhibition, balance issues, ataxia, lack of coordination, um, issues with overdose, like I mentioned, and also, um, neural tube defects. So pregnant women shouldn't be taking some of these traditional agents as well, or dose may need to be lowered. And then we have our second generation agents or newer agents. So when we're comparing primary and secondary medications for seizures, primary medications are what? Are they very effective or not so effective? Are they very safe? or not very safe. So this is perfectly correct. So these are very effective, but there's lots of side effects. So they're not so safe. So the primary agents are very effective, less safe, whereas the secondary agents are safer. but not as effective. So one of the discussion questions we had in residential was, we have somebody who has a seizure disorder and the doctor wants to prescribe a second medication. They're already taking a primary agent. Do we think it's a good idea? And typically we want to avoid polypharmacy, but in this scenario, it would be good because if they can take that primary agent at a lower dose and add a secondary agent, it's going to improve basically the seizure control just from different mechanism of action and also improve the safety by lowering the dose of that primary agent. So the meds act basically by reducing the excitability in the brain by either reducing excitatory effects by increasing the inhibitory effects of GABA, or by reducing sodium and calcium entry, which is going to reduce the ability of neurons to depolarize in the central nervous system. So here's a list of our central or our second generation agents. I've got a few starred because those are also commonly used in the treatment of chronic pain as well. Certainly you don't need to know the names of these. You should know the... drug classes. So like these subclasses, the hydantoins, the imostibines, the benzodiazepines, barbiturates, these are just examples over here. You don't need to know these, but you do need to know the drug subclasses and just secondary, second generation agents. And I just list these meds just for recognition for you. Okay, so we talked about the side effects, certainly sedation and coordination. We want to watch out for those things. We certainly want to watch for signs that the person's really having some physical limitations or very sedated during therapy. For our pediatric patients, we really want to note if they have an increase in seizure frequency because they may have outgrown their medication. And in some scenarios, if the patient has been seizure-free for two years, they may be able to stop taking the medication, but it depends on the situation, of course. All right, let's move on and talk about depression. So name three amine neurotransmitters involved in depression. And sorry, this is a bit of a repeat for the residential, but... Hopefully you'll get these right this time if you didn't the first time. So serotonin, dopamine, and norepinephrine. Exactly. So those are the three neurotransmitters involved in depression. Excellent. So in depression, there's a reduction in electrical activity in the brain of somebody with depression. versus not depressed. So that's why we're not going to be prescribing something like what physicians aren't going to be prescribing, benzodiazepines, because we don't want to inhibit the brain any further. So what are the four main types of drugs used to treat depression that will affect some or all of those neurotransmitters involved? one response. There we go. Yep. So you guys have it right. So the SSRIs, SNRIs, MAO inhibitors, and the tricyclics. So, and depending on which one, it's going to affect different neurotransmitters, which I have listed here. So basically these three, these first three, there's going to be It's called a reuptake inhibition. So the neurotransmitters are released into the synaptic cleft, and then they are reabsorbed into this presynaptic neuron after they act on the postsynaptic neuron. So if we block that reuptake, it's going to leave the neurotransmitter available in that cleft to continue to act on the postsynaptic neuron. Whereas with MAO inhibitors, there's also this enzyme that breaks down the neurotransmitter. And if we block that enzyme, then it's going to block the breakdown, again, leaving more available to act on the neuron. So here's just an example of some SSRIs. Like I said, you don't need to know these drugs. You just need to know the drug class, selective serotonin, reuptake inhibitor. And with the drugs that predominantly affect serotonin, the SSRIs and the SNRIs, there is an increased risk of seizures related to serotonin syndrome. The tricyclics and the MAO inhibitors affect dopamine as well as serotonin and norepinephrine. So they're going to have more side effects. So anticholinergic effects, orthostatic hypotension, arrhythmias. So the tricyclics are some of the oldest medications. And so, of course, they're, you know, effective, but more side effects. And then we have the MAO inhibitors, which we talked about in our discussion. The issue with these is that they basically increase norepinephrine in the system and the systemic circulation as well as the CNS. And then if taken with foods that contain tyramines, such as fermented foods, that's going to cause catecholamine or norepinephrine and epinephrine release. And so in combination, these can cause a hypertensive crisis and cardiovascular symptoms. Serotonin syndrome, another concern predominantly with the SSRIs and SNRIs. symptoms, confusion, hallucination, shivering, usually reversible, but it can be fatal if left unchecked. So we want to watch for those signs. So the antidepressants are also used in the treatment of chronic pain sometimes, particularly the SSRIs and the SNRIs. And as we mentioned, also used to treat anxiety. So how long does it take for antidepressants to take effect? Correct. Two to four weeks. That's right. So there is a lag time for these to take effect. And that kind of justifies the theories that support depression. So the... down regulation theory. So there's a time lag, two to four weeks, and the depression can get worse during that time lag period. Particularly susceptible are our young adults and teens. So we really want to watch for that. There's an increased risk of suicide, particularly in that period of time. So we want to be aware and know our resources when we're treating. patients who are taking these medications or starting these medications. All right, let's talk about bipolar. So with bipolar disorder, there's episodes of manic and depressive mood swings, and it's thought to be due to an imbalance of all the neurotransmitters, serotonin, dopamine, and norepinephrine. To date, the premier treatment is lithium, which is an element. It's not degraded. It's eliminated in the... kidneys and it can accumulate rapidly in the body. So we want to know our signs of lithium toxicity. So what are the signs of lithium toxicity? Come up with a few of these signs if you can. Dizziness is definitely a concern. Metallic tastes, very good. Weakness, vomiting, nausea, dysarthria, yep, confusion. Coma definitely would be a strong indication something's going on, right? So here's our list. You guys covered a lot of them. Orthostatic hypotension is not on this list. The other concern is that with lithium toxicity, we can have possible permanent damage to the cerebellum. So we want to really watch out for this. And typically blood serum levels will be monitored with this. Let's talk about antipsychotics now. So psychosis, certainly the most severe form of mental illness. Schizophrenia is considered a form of psychosis. Most of these are due to an increase in dopamine in specific pathways in CNS, particularly the limbic system. There's other neurotransmitters involved, but dopamine is certainly the key causative factor that we can address with a pharmacology. So medications for psychosis block the D2 receptors, which are predominantly concentrated in the limbic system. So it'll be used for many forms of psychosis, schizophrenia, and also used to treat aggression and agitation with Alzheimer's disease and dementia. And I was sharing with the class today, I've got a very feisty great aunt who's in memory care and she is on an antipsychotic medication because she causes a lot of trouble in her memory care unit. She's very naughty. Um, all right. So we have traditional antipsychotics. And then we have atypical antipsychotics. So our traditional, our original strong antagonist for D2. So as you can imagine, very effective, not necessarily that safe. Whereas our atypical or newer antipsychotics are weak D2 antagonists, and they also affect serotonin. So they'll block serotonin. So there's milder side effects. Not quite as effective as the traditional agents. So common theme goes along with our anti-seizure agents as well. So what is the primary concern with those traditional agents? Yes, yes. tardive dyskinesia. I think somebody meant to write there. Tardive dyskinesia. Good one. Pseudo-Parkinsonism. Exactly. Good job. Akathisia. Yep. Very good. So yeah, it's these extra pyramidal motor side effects, which some of which you listed, akathisia, pseudoparkinsonism, and tardive dyskinesia, which is the most feared. It involves oral facial movements, grinding movements of the jaw. I mentioned to the class today, I would YouTube tardive dyskinesia example, just so you can see what it looks like. And the issue is that it can be permanent. So we really want to watch out for it. And by the time someone starts to show these oral facial movements, they've probably showed a lot of these motor side effects. This is kind of an advanced progression of the motor issues that can occur. So typically this medication will have to be tapered down or even stopped. It will have to be tapered though initially. So we certainly want to let doctor know if we're seeing the tardive dyskinesia or some of these, a change in their movement patterns. All right, we're going to move on to Parkinson's disease. So it's due to degeneration of what's creating neurons in the where. Good. So dopamine secreting neurons in the substantia nigra. So with our antipsychotic meds, we were blocking dopamine and we had movement side effects, pseudo-Parkinsonian side effects, because we were reducing dopamine in the limbic system and there was overflow to the basal ganglia and particularly the substantia nigra. With Parkinson's disease, there's degeneration of the neurons, the dopaminergic secreting neurons in the substantia nigra, which is part of the basal ganglia. Correct. I think we all know signs and symptoms, rigidity, resting tremors. We'll see these patients for falls oftentimes. So there's a lot of medications used to treat Parkinson's disease. L-DOPA is the main medication or CARBA-DOPA along with CARBA-DOPA. We have COMT inhibitors, dopamine agonists, anticholinergic drugs, MAOB inhibitors, amantadine. And the two that are starred here are starred because those two types of medication are often used in the early phases because they are, well, dopamine agonists are because they're thought to have some neuroprotective effects. Okay. So levodopa. One of the discussion questions is why don't we just give dopamine to patients who have Parkinson's disease? Dopamine does not cross the blood-brain barrier, so it's not going to get in. So it's given in the form of levodopa, which will cross the blood-brain barrier. It will be broken down by dopa decarboxylase, which is an enzyme in the body. And it will convert it to dopamine where it can act on the basal ganglia, particularly the substantia nigra. Now, without the medication carbidopa in conjunction with L-DOPA, we're going to have DOPA decarboxylase in the periphery also breaking down levodopa into dopamine. And with dopamine circulating in the systemic system. we're going to have side effects such as GI irritation, orthostatic hypotension, and other issues. So if we give carbidopa that blocks dopa decarboxylase in the periphery, it also does not cross the blood-brain barrier, so it will just act in the periphery, which will leave more levodopa to enter the central nervous system and act and reduce those systemic side effects. So the other concern is that there is a COMT enzyme that breaks down L-DOPA as well in the peripheral circulation. So COMT inhibitors, again, will block that breakdown, allowing more L-DOPA to enter and act in the cerebral tissue. So it helps reduce fluctuations in the response to L-DOPA and prolong effectiveness. Side effects, certainly GI irritation, hypotension, which I talked about. I've definitely had patients on L-DOPA that had orthostatic hypotension, even though they were taking the carbidopa as well, or L-DOPA and carbidopa in combination, which is a drug called Sinemet. Psychotropic and behavioral effects, we think about too much dopamine in the limbic system, right? It was an issue with psychosis. So by adding more dopamine to the brain, we can have those behavioral side effects, dyskinesias or abnormal movements, freezing gait. Another thing to keep in mind is this end-of-dose akinesia. So as we get to the end of that L-DOPA dosing, the patient may have more freezing and rigidity. This certainly can be resolved by providing the patient with an extended release form of Sinemet or maybe changing their dosage. There's also another issue called on-off phenomena. And L-DOPA, because of this just irregular absorbency of it in the system, patients may experience good benefit of the L-DOPA in a single dose, and then it'll stop working for a little, and then suddenly it'll just start working again for a little bit longer. So the erratic absorption is an issue. The other concern is there's a diminished response with long-term use. We're not sure whether... Patients are getting a tolerance to the drug. So we try to delay administration of the drug. It also may be partially due to just progression of Parkinson's disease. Those neurons that are degenerating can no longer compensate. Sometimes patients are put on a drug holiday. They'll take a little time off from the L-DOPA and they'll take a dopamine agonist or another medication. to help with the symptoms during that period. So we mentioned dopamine agonists, which cross the blood-brain barrier and directly will stimulate the dopamine receptors. These have a longer half life. Dosing is very predictable. Like I mentioned, they can be used in the initial treatment. Certainly, there's a lot of side effects because we're stimulating dopamine receptors everywhere. So there'll be orthostatic hypotension, nausea, vomiting, and then all the central effects as well. There's other medications that I've listed here for your reference. I'm not going to go into detail about those just for time purposes, but I would breeze through this when you're reviewing the PowerPoint. Okay, next question. Your 10 o'clock, I don't know why it's showing the answer and then I have to hit enter. I'm sorry about that. Your 10 o'clock patient with PT is prescribed Sinemet, which is levodopa and carbidopa in a single tablet. When should you advise them to take the Sinemet to maximize their performance during PT sessions? Yes, and you guys got it correct. Very good. So typically you want to take the meds and... hour before. So typically 30 to 60 minutes prior to therapy, because there is evidence that PT treatment with the medication will improve outcomes more than just taking the medication alone in Parkinson's disease. So there's a synergistic effect here. Certainly Like I mentioned earlier today, we want to make sure, though, we may want to see the patient once or twice when they are in between doses so we can help them with compensatory strategies to deal with the freezing and the rigidity. We also really want to keep in mind that we need to monitor for movement changes and also watch out for that orthostatic hypotension. So taking vitals, pausing. before the patient starts ambulating when you're getting them from sit to stand. Okay, I'm going to move on to general anesthetics. So goal with general anesthetics, we want them to kick in fast. We want the skeletal muscle to relax. We want to inhibit, withdraw reflex and autonomic reflexes. We want to easily be able to adjust the dosage. We want minimal toxic effects. And we want rapid, uneventful recovery, of course. And we probably don't want anyone to remember what happened. So as general anesthetic dose increases, there's these stages that patients go through. So first, you feel amazing for a second. And then there's this moment of delirium, which we want that to be very brief. We don't want people to become combative on the operating table. And then the patient achieves surgical anesthesia where they're unconscious and they don't have sensation. We want to limit medullary paralysis. We don't want to shut down the respiratory and cardiovascular centers typically. So there's a lot of different routes of administration, inhaled gas routes, and then we have IV anesthetics as well. So why are patients often given IV anesthetics followed by inhaled anesthetics when undergoing surgery? And this was also a discussion question. So onset, which one kicks in faster? Right, you guys got it. So the IV is going to kick in faster. So that way we can limit that stage two delirium. So we'll get the patient in that stage three phase rapidly. And then why are patients often converted to inhaled anesthetic once they're in that stage three? So difficult to adjust dosage, easier to adjust dosage. Now I would say IV and inhaled both. pretty easy to adjust the dosage. However, the inhaled anesthetics are easier to adjust the dosage and also easier to withdraw the dosing at the end of the surgery. So easier to adjust with inhaled anesthetics. Good. So certainly considerations, which I know we've talked about before, the anesthetic. typically is lipid soluble. So it can be stored in the adipose tissue. So that's why you get your patient up then after that surgery, total knee surgery, and you try to get them up walking and you walk them a couple of feet. And fortunately you've got that wheelchair right behind them. So when they're like, Ooh, I don't feel so good. I feel woozy. You can have them sit right down. And that's because sometimes that anesthetic starts to come out of the system as you get them up and moving. So we want to watch for that. Just be aware. So these act different ways. So you can review that some increased inhibition, some decreased excitation. All right, we're going to move on to local anesthetics. So these work by inhibiting sodium channels of neuronal axons. So they're going to block that depolarization or that signal being sent through the nerve. conducting that sensory information. So certainly we're going to lack residual effects. There's not going to be that post-op confusion that we have with general anesthesia, less recovery time, and minimal systemic effects. So somebody having a dental procedure, oftentimes they're just going to do a local anesthetic injection in the mouth. And then there is a delay before it kicks in. And sometimes we don't always get full numbing effects, right? So those are some of the cons of the medication. But there's a delay, typically 10 minutes with a dental procedure. So these often end in cane or lidocanes. There is a concern that if these are spread systemically, they can inhibit. respiratory control, which is called LAST. And typically this is treated with an emulsion of lipid compounds. So we want to watch for that. So I told students earlier today, I had a pain pump, which I don't know if I have it here, but I had a pain pump after my ACL surgery. I had two and a half weeks ago. And the sheet that I got with it basically said, you know, if you have difficulty breathing. or shortness of breath, call 911 and turn off your pain pump, by the way, because of this risk of last. Okay, why is epinephrine administered simultaneously at times with the local anesthetic? So we want to think what epinephrine will do. Yes, yes. So epinephrine will cause vasoconstriction. It will prevent vasodilation, which will reduce bleeding in an area that maybe we're trying to suture or physicians making a surgical incision. So we don't want a lot of bleeding in the area. And also it will help keep that anesthetic local because of that vasoconstriction. Excellent. So there's a lot of different administration routes. Topical anesthetic. I know when my daughters have dental work, they have like a little gel they'll put on their gums before they administer the shot. Fluorimethane spray when I was a new PT. People had like a spray and stretch and it was a fluoromethane numbing spray that you would spray on the muscle and then stretch it. Kind of ridiculous. But anyway, we don't use it anymore. Transdermal patch, lidocaine patches. Often we have patients with these patches on. We have peripheral nerve blocks and central neural blockades. I'm sorry for the repeat residential class, but after my surgery, I had one of these. pain pumps. There was a little button here I could press to get some of that local anesthetic. It was some sort of cane medication. I can't remember the name of it, but it ended in cane. And then every three hours, there was medication delivered. And the little catheter went into some sensory nerve, nerve ending or nerves that innervated my knee. I didn't have to take narcotics for the first three days post-operatively, whereas 20 years ago when I had ACL surgery, I did. I had to take a lot of narcotics initially. So it worked really well. And I was telling them I got a cross body bag with it that held the pain pump. So I was feeling pretty good after my surgery. Okay. So we also have epidural local anesthetic. Um, so the epidural basically is injected between the vertebral column and the dura matter. Um, and you hear all these horror stories about women who are going in labor and they get their epidural and it only, um, reduces pain on half their body. So there, sometimes there's not full coverage. I had an epidural and it worked wonders for me. Um, so Okay, we have also caudal block, which is basically an epidural injection into the sacral hiatus. And then we have spinal nerve blocks. So with the spinal nerve block, the medication is inserted into that subarachnoid space or intrathecal area. So intrathecal injection. So this will be used for local anesthetic and intrathecal injection is also used with the baclofen. pump muscle relaxant. So if somebody's getting a baclofen pump, the catheter actually is going to sit right in that intrathecal space below the level of the spinal cord injury. Okay, we have sympathetic blockades and beer blocks. So with the beer block, you need a tourniquet. It's into a peripheral vein. So procedure has to be under two hours. I mean, I think this is often like uh rarely used but for a limb procedure all right let's move on to muscle relaxants and um there's been a lot of repeat for the residentials so you know i won't be offended if you if you leave the chat or stay for another review you do that much better on the test um so muscle relaxants are used to normalize muscle excitability with and the goal is to not decrease muscle function. However, this is a concern. We need to understand the difference between spasticity versus muscle spasm because some medications treat spasm, some treat spasticity. So my first question to you is muscle spasm as compared to spasticity. Which of the following is true for muscle spasm, which is not true for muscle spasm? And I can tell those St. Augustine residential students were paying attention today. You guys nailed it. So muscle spasm is due to local tissue inflammation or damage. So muscle spasm, we think about our acute lumbar strain, our orthopedic patients. So there's increased tension in that muscle or increased tone because of different inflammatory mediators that are irritating that area and causing the muscle to tighten up or increase tone. Also could be due to peripheral nerve root irritation. So in the case of, for example, a herniated disc or a disc issue. I also think about it as kind of like nature's splint where the muscles just tighten just to hold something where it is as a protective mechanism. So with spasticity, it's typically due to a supraspinal. inhibition from the spinal cord and the central nervous system. So it's due to pathology in the CNS or spinal cord. And there's hyper excitability of the muscle stretch reflex with spasticity, which is clonus. So if we quick stretch that muscle, there's a hyper excitability of that reflex, and we're going to get the clonus. So we have drugs to treat muscle spasm. We have benzodiazepines, such as diazepam or Valium-X, again, to increase the inhibitory effects of GABA. So of course, sedation, dependence, and tolerance will be an issue. So it's not really a long-term solution. And then we have our central acting antispasm drugs. Now, the mechanism of action of these is not fully understood. The thought is they inhibit polysynaptic. epileptic reflex pathways that in conjunction help reduce that increase in tone or flow to the alpha motor neuron. These cause a lot of sedation. So oftentimes our outpatient ortho population will complain of just sleepiness on these medications. So they might just take it at night and not take it during the day. So flexoril, soma are common medications in this category. All right, so now we're going to look at the anti-spasticity drugs. So you do need to know these drugs in this left-hand column. So these are all the ones to treat spasticity. So let's start with baclofen. So baclofen is a GABA agonist, so it's going to increase those inhibitory effects. commonly used due to spinal cord lesions, not as effective in CVA and CP, particularly due to just the administration route. If you have to take it orally, it really causes a lot of drowsiness. And another thing to note here, it can cause muscle weakness too. So often with our spinal cord injured population, as I mentioned. they might be put on a baclofen pump, which will deliver the medication directly below the level of the spinal cord injury to act very locally to reduce the systemic effects. And there was a great case example of this in your text. Also, just to note, certainly with intrathecal baclofen pumps, the pump is surgically, or the catheter is surgically implanted. Um, the, the pump can malfunction. Um, we want to make sure it's working because abrupt withdrawal of black flint, backflint can cause seizures and all sorts of problems. It is kind of a dangerous situation. So we want to make sure the pump is functioning well. Um, we have dantrolene sodium. This is the only one that acts directly on the muscle. So it inhibits calcium release from the sarcoplasmic reticulum. And if you remember, the calcium then allows for the actin and myosin binding in the muscle tissue. So it's used to treat all forms of spasticity. It's taken orally. Muscle weakness is a concern because it does act directly on the muscle and liver toxicity as well. Often used for CP. CVA, CVAs, things like that, sometimes used with spinal cord injury as well. So then we have our benzodiazepines. And I think, you know, we've covered that enough. And then let's move on to Botox. So Botox inhibits acetylcholine release at the neuromuscular junction. So it acts on the neuromuscular junction, not on the muscle the way dantrolene sodium does. But it will be a local injection into the muscle tissue that's involved. So used, of course, cosmetically, used for migraines, used for muscle dystonias, torticollis. I'm sorry for the repeat residential class, but I did have a stroke patient in inpatient rehab who we used Botox on. She had had a stroke and had a lot of extensor tone. And. She was meniscus with ambulation because her extensor tone affected her upper cervicals. So she was stuck like this when she was walking because of that tone. And she had a hard time seeing the horizon. So the physician ended up injecting Botox into her suboccipitals. So then she could get her head in neutral position. And she went from meniscus to supervision just with those Botox injections. And she was able to go home and live with her husband, which was great. So issue there, of course, you would have to go back and get the injection typically every three months. They administer the Botox injections because it does wear off. There is a risk of an immune response where your body will generate antibodies to the Botox. If that's the case, Botox really isn't going to be effective for that patient. All right, we're going to move on to opioids. So opioids provide pain relief by interfering with substance P-mediated transmission of painful sensations. So these are our narcotics. So narcotics are sourced naturally from opium poppies. We also have semi-synthetic, which are sourced from the opium poppy and then chemically modified, such as heroin. And then we have synthetic, so our tablets typically form. Certainly notoriety due to their potential for addiction. So which opioid receptor in particular is involved with addiction and respiratory depression? Nice work. Mu, correct. So mu is involved with respiratory depression and addiction. Next question, which receptor type is involved with sedation and psychotic effects? Kappa, correct. Correct. Very good. So kappa is involved. with sedation and psychotic effects. We're not quite done. I just ran out of slides on this presentation. So I've just got to switch over real quick. Hold up one second. Yeah. And I just have a couple more slides and then we'll be done. So opioid receptors, we have um, Mu, which is involved in respiratory depression and most addictive, the kappa, psychotic effects. And then we have delta. Delta is involved with growth hormone release and dopamine release. Dopamine inhibit dopamine release. So it'll block dopamine from being released. So if we think about opioids and naturally... occurring opioids. So our endogenous opioids, we have endorphins and keflins and dynorphins that are naturally released in the body in response to tissue injury, to control inflammation and pain, also involved in various other systems. So in response to eating or drinking, we think about endorphins when we think about that runner's high after we exercise. And then we have our exogenous opioids. So these are the medications, the external medications. So all three of these receptors are going to provide analgesic effects. Keep that in mind. So opioids, medications are described basically based on their affinity for mu. So we have strong agonists that have a strong affinity for mu. So these, of course, are going to be most notorious for causing addiction issues and also respiratory depression. So morphine, typically that's prescribed with severe pain, end of life, somebody who's on hospice or just very severe pain. We have fentanyl, another medication used for severe pain, also for anesthesia. And then methadone. Why is methadone bold? Methadone is bold because this is the medication that's used to treat addiction. So why would we use a strong agonist to treat it? addiction. The reason is because even though it's a strong agonist, it has less withdrawal symptoms. So as somebody is getting weaned off the methadone, they'll have less withdrawal symptoms. We have mild to moderate agonists like our hydrocodone, oxycodone. So after my surgery, I was prescribed oxycodone, which thanks to that pain pump, I really didn't need to take it very much. And then... Percocet is oxycodone in combination with acetaminophen, and that's to help try to spare opioid use. And then we have our mixed agonist antagonists. So these have a high affinity for kappa. So they'll bind to kappa, but they'll block mu. So there's less addictive issues with the mixed agonist antagonists. But... If we think about what kappa is involved in, there are going to be more psychotropic effects, hallucinations, things like that. So then we have our antagonists. These are our life-saving medications in the case of opioid overdose. So these basically will block all opioid receptors and they'll actually displace opioids from that mu receptor. So naloxone or Narcan, oftentimes it's a nasal spray and it acts very rapidly. And if you've ever seen it, the patient is very grumpy when they wake up. So there's a lot of different administration routes for these medications. They're distributed through all the tissues, metabolized in the liver, excreted in the kidneys, physical withdrawal. Typically lasts five days. And of course, tolerance and physical dependence are major issues with these medications. So let's go over the indications. So pain, very common indication for these medications. Addiction, methadone is often prescribed to treat addiction. Diarrhea. So we all probably know these opioids cause... Pause. major constipation and after surgery and narcotics, we're giving birth to the bowling ball, basically. So these can be used to treat diarrhea. They would be used for severe diarrhea because there's certainly alternatives for mild diarrhea. But in the case of severe diarrhea, they may be used. Cough suppressant, codeine is a common one prescribed to suppress cough. We think about these as a common one. repressing that respiratory system, and then anesthesia. So how do these act? Number one, they have spinal effects. So they inhibit painful signals from the dorsal horn in the midbrain. Basically, they allow descending pain pathways to transmit inhibitory signals to the dorsal horn, which will decrease transmission of pain stimuli to the brain. And then they also act by blocking the pain nerve endings in the periphery. So they act in three different ways to reduce pain. Certainly, if you're treating patients on narcotics, you want to consider they might be sleepy, confused, a little slow. They might be feeling really good and talkative. Anticipate orthostatic hypotension. respiratory depression. So we want to watch the respiratory rate, O2 sats, especially if they have a comorbidity that involves lung disease. GI distress may be an issue and that constipation that we talked about. So often stool softeners and laxatives are prescribed in conjunction. And of course, PT is one of the best ways to promote peristalsis. So we'll be hanging out by the bathroom. So we want to make sure that if somebody has a lot of pain, for example, somebody with a really traumatic injury that's in a lot of pain or say a rotator cuff repair that's fresh and you're doing passive range of motion, they may want to take that narcotic an hour before therapy. So the pain is under control once you're treating them. We talked about dependency and tolerance. The other thing we really need to educate our patients. that when they stop taking these medicines, they're probably going to feel more aches and pains initially due to that physical withdrawal. So probably they're going to need to take something when they're getting off these meds, such as Tylenol is often, or acetaminophen is often prescribed. Often need to wean off the meds, needs to be a plan to start and stop, typically not meant for maintenance therapies. And of course, we as PTs can provide lots of pain management alternatives beyond using opioids. That's one of our roles. All right. So I'm going to stay here for questions. Make sure you go to the chat and you'll see the link to record your attendance for this particular presentation. And thanks for joining in and participating. Thank you. My pleasure. Thank you. Thank you. Putting that link. I don't see the link in the chat. You don't see the link in the chat? No, ma'am. Huh. Okay. Let me repost it. Okay. Maybe I posted it too early. See if you see it now. Oh, yeah. It came through. Okay. What about, did you say that you posted these slides somewhere? Yeah, they should be in iLearn. Barbara should have posted them. Okay. I'll check there. And if, I mean, if you want as well, you can always just. put your email address in the chat and I can send it directly to you too. Okay. Thank you. I got you, Michaela and Haley. And David, did you get my email, Dr. Drayton? I put it in the chat. My name is Melissa. I don't know. Melissa, I see you. Yep. I will send it to you too. And David too. Yeah. Thank you so much. I appreciate it. Thank you

I think I'm going to go over an hour. It's probably going to be an hour and 10 to 15 minutes. I'll try to go fast, but not so fast. You're not following.

And just note in the chat, there is the link to complete your review so you can get your badge in iLearn. So make note of that. So if you would go to menti.com and use the code listed here so you can answer the questions as we go through this. And feel free to unmute, ask questions.

You can put questions in the chat as well if you're more comfortable with that. But you are welcome to just turn your microphone on and ask questions. This PowerPoint will be available through iLearn if you didn't see it already there. And if you're having trouble accessing, I can email it directly to you as well. And also, I did post it on the St. Augustine.

residential pharmacology course announcements today. All righty. So we're going to start by covering chapter 25, but we'll brush through all the units 5 through 14 as well. First thing we're going to talk about is the drugs to treat hyperlipidemia and coagulation issues. And I just want to just do a quick brief review of the coagulation cascade because in order to understand how these medications work, You need just a general understanding of how blood clots are formed, which you've probably seen before.

So this is probably a review. So typically what happens is an endothelial wall of a blood vessel or capillary is damaged and that activates collagen and tissue factors to start the clot response. So then what happens is platelets are activated to aggregate and adhere, so to become sticky.

So they form that platelet plug. And then through a series of coagulation or clotting factor chain of events, fibrinogen here is converted into fibrin that are these insoluble strands that add to the strength of the clot. So that's how the clot is formed.

And we have three different drugs to treat clotting, which we'll talk about. So we'll start with our question. which type of medication is best for DVTs.

So our antiplatelet, anticoagulants, or our fibrinolytics. So it would be our anticoagulants for DVTs. So the anticoagulants are our classic meds to treat blood clots, DVTs.

Heparin is typically used in the hospital when someone has a DBT, reason being it has its large molecule in size, so it typically must be administered intravenously. We also do have low molecular weight heparin that can be administered subcutaneously. And the heparin will activate antithrombin, which inactivates clotting factors. And then when somebody goes home or typically used to prevent DVT, patients will take oral Coumadin or Warfarin. So this is typically utilized at home.

So Warfarin interferes with vitamin K metabolism in the liver, impairing hepatic synthesis of several clotting factors in that clotting chain of event. So the issue with warfarin and Coumadin is that patients are told they have to avoid dark leafy greens. Now I know with my kids, that's not a problem.

But the dark leafy greens are high in vitamin K, which will basically counteract the medication. So we want to limit those when taking this. All right. So risks.

Hemorrhage is a big risk with any of these anticoagulants. medications. So blood in the urine, blood in stools are a sign that there's too much bleeding.

Sudden onset of back pain or joint pain and swelling would be a concern. GI distress. And of course, we often see these skin reactions, especially when I've seen it a lot, like working in skilled nursing facilities.

A lot of patients on blood thinners, their arms look like this. So we want to certainly as PTs just watch out, just try to avoid patients hitting things or skin tearing, things like that that could cause bleeding. We certainly don't want to be doing deep tissue work or instrument assisted soft tissue work with patients who are on anticoagulants.

Dry needling is another. um precaution patients who are on these cervical manipulation things like that all right let's talk now about anti-platelet drugs so these inhibit that activation of the platelets that makes them sticky um generating that clot so prevent clot formation um in arteries also in veins but predominantly arteries So the most commonly used antiplatelet medication is aspirin. That's correct.

So aspirin, as low a dose as 81 milligrams or a baby aspirin can help prevent MI and stroke, whereas oftentimes an adult dose of 325 milligrams will be prescribed prophylactically as well. For example, I just had ACL surgery. So I'm taking aspirin daily for a month, an adult dose to prevent DBTs.

So we just talked about how they work. Again, treating, preventing DBTs, preventing MI. Certainly there's a risk of CVA, risk to livers, kidneys, GI disturbances, and CVA, of course, which type of stroke would aspirin be utilized for prevention? That's right, ischemic. So an ischemic stroke, where there's a blood clot that forms in the brain to block blood flow to the tissue, would be prevented, whereas the patient may be at higher risk for a hemorrhagic stroke.

with taking anti-platelet medications. In the event of acute MI at home, it is advised that aspirin should be administered via which route? So typically, I like what everyone's thinking, sublingual, but with aspirin, typically it doesn't dissolve very well under the tongue.

So normally we're just going to have an oral tablet at home that's available. And so it's advised just to chew an adult dose of aspirin to just get it in the system faster. Nice. All right, next question.

Which medication is best for arterial clots, such as acute MI or ischemic strokes in the ER? Nice. Yes.

Fibrinolytic agents. So this morning during class, there was a similar question and there was two options, anti-fibrinolytic and fibrinolytic agents. And fibrinolytic is the correct answer. So these facilitate the breakdown of clots. So these are the ones that need to be administered within 12 hours with acute MI or within three hours with ischemic stroke to help preserve that tissue and prevent tissue death by breaking up that clot.

So these are our kinase medications. And of course, the biggest risk is cerebral hemorrhaging with these meds. So the anti-fibroanalytics are typically prescribed in the situation of somebody who has hemophilia and they're undergoing surgery because this will prevent excessive bleeding and prevent that breakdown of fibrin. Okay, we're going to move on to cholesterol meds. So which type of cholesterol should ideally be higher?

Now, why is it showing the answer? Have all the answers been shown on this? Maybe it was just this one.

This is correct. So the HDL. So we want the HDL to be high. So we want the HDL to be 60 or higher.

That's the good cholesterol that helps reduce the arthrosclerotic plaques. We want the LDLs, ILDLs, VLDLs to be low because that is the bad cholesterol that contributes to increasing risk of stroke and heart attack. So we have statins and we have fibrates that help reduce cholesterol and lower the LDL and in some cases increase HDL. So statins have been shown basically to, you know, reduce the chance of heart attack and stroke. And they also have some cancer preventative.

properties in some studies. They have anti-inflammatory, antioxidant effects. They also increase production of nitrous oxide, which is a natural occurring vasodilator.

So they have a lot of great properties. However, they do cause myopathies. That's the biggest concern. And the worst case scenario would be rhabdomyolysis, where there's really a major breakdown of proteins, which can really put... big stress on the kidneys and can be life-threatening.

GI distress is also another concern and kind of off the record as well. There are some newer studies looking at risk of tendinopathy with statins. So another thing to keep in mind for us as PTs.

All right, now we're going to talk about benzodiazepines. So benzodiazepines increase the inhibitory effects of GABA. So what are five clinical applications for benzodiazepines? See what that residential class remembers from today.

Right. So benzodiazepines are going to calm and quiet the nervous system. So they're going to help with seizures. anxiety, they're going to be muscle relaxers. They are not going to help with depression because depression, the nervous system is already calmed and quieted.

And we don't want to reduce activity even more in the case of depression. General anesthesia as well. Exactly.

Good. So we have sedative hypnotic. anti-anxiety, anti-epileptic, muscle relaxer, and general anesthesia. So lots of uses for these benzodiazepines.

However, they're not used all the time because of some concerns with them. So what's the biggest concern with the benzodiazepines? Yes.

Sedation is a concern. Biggest concern would be tolerance and dependence, for sure. Great.

So tolerance and dependence are the biggest concerns. Also, these stay in the system for a long time. They have a long half-life and they also are lipid soluble.

So they get stored in adipose tissue. So they stay for a long time. They cause sedation.

and people can have just a residual hangover. They take it for sleeping and then the next day, they're just feeling groggy all day. Now, another thing you won't be tested on, but I do want to list it here.

There was a large cohort retrospective study in people with Alzheimer's disease, and they were 50% more likely to have used benzodiazepines. And there was a link associated with how high the dose and how long the person used the dose. use the drug. So there is a link that we just want to be aware of. I mean, it's part of why these are not used as often.

So sedative hypnotics and anti-anxiety drugs, again, are going to calm and quiet the nervous system. So we also, beyond the benzodiazepines, we have barbiturates. Now, barbiturates also act by increasing the inhibitory effects of GABA, but it's not fully understood how. The issue with the barbiturates is that there is a small therapeutic index.

So there's a risk of overdose. And also these can be addictive. But they were used for a time as a sedative hypnotic.

And we're going to revisit barbiturates when we talk about anti-seizure medications, because these are, the barbiturates are the most common medication used worldwide for seizures. So we will revisit those. So the last group of sedative hypnotics on my list for tonight are our Z drugs.

So Z drugs for... insomnia and for sleep. Ambien, probably the most common. And one of our discussion questions in residential University of St. Augustine was about a patient who was wake up in the morning and he could tell that there were signs that he was eating at night, he was gaining weight and doing all these things he had no memory of. And these are complex behaviors.

Patients taking sleep. Ambien have been known to sleepwalk, drive, which is quite scary, and eat. So the Z drugs are most notorious for this.

And actually, my husband was in the Navy. And when he was on deployment, they gave him no-go and go pills to make it very simple. And the no-go pill was Ambien.

And he called me a bunch of times. And we had conversations. He didn't remember anything that we talked about. So amnesia is also an issue too.

So anxiety, I think we all know what anxiety is. So benzodiazepines are used for anxiety, but typically it's more situational scenarios. So oftentimes we have patients taking Valium, which is a benzodiazepine for if they're claustrophobic and they're going for an MRI. Okay, so what are the four main types of medications used to treat anxiety? We have one of them, benzodiazepines, we just talked about.

One of our discussion questions also was which medications are, which antidepressant medications are used for anxiety. And those are our serotonin selective reuptake inhibitors and our serotonin norepinephrine reuptake inhibitors, because there is, we do have an understanding that serotonin and norepinephrine imbalances are involved in anxiety. We also have buspirone, um, Benzodiazepines, great.

Somebody put beta antagonists on there too. So BZDs, Buspirone, SSRIs, and SNRIs. So Buspirone is commonly prescribed in older adults.

It stimulates serotonin receptors, certainly less sedation and dependence as compared to benzodiazepines. There are some side effects. Does take a little longer to kick in.

And as I mentioned, commonly used in older adults. With our younger adults, often we're using the antidepressants to address anxiety. Somebody already stole my thunder on this question, which is great. What type of cardiovascular medication is used to treat anxiety?

Yes. Beta blockers, exactly. So beta blockers are also used because they're just going to block basically sympathetic input. Again, often used in situational anxiety, like somebody's going for a job interview, something like that.

Okay. And then we have antipsychotics and anticonvulsive medications as well. We've talked about the adverse side effects. I just have them all in one list here for you.

Let's move on to seizures. So seizures, recurrent uncontrolled cerebral excitation. So again, the goal is going to be to calm and quiet the nervous system when somebody has a seizure disorder.

So we have six basically traditional agents are hydantoins, common dilantin you've probably heard of. And then last two on the list, the benzodiazepines, which we've already listed, and then the barbiturates, which I mentioned, are the... found to be very effective. They're very effective. They're also very cheap.

So it is one of the most common meds prescribed worldwide. However, they're not selective. So there's a lot of side effects, issues with generalized inhibition, balance issues, ataxia, lack of coordination, um, issues with overdose, like I mentioned, and also, um, neural tube defects. So pregnant women shouldn't be taking some of these traditional agents as well, or dose may need to be lowered. And then we have our second generation agents or newer agents.

So when we're comparing primary and secondary medications for seizures, primary medications are what? Are they very effective or not so effective? Are they very safe?

or not very safe. So this is perfectly correct. So these are very effective, but there's lots of side effects. So they're not so safe.

So the primary agents are very effective, less safe, whereas the secondary agents are safer. but not as effective. So one of the discussion questions we had in residential was, we have somebody who has a seizure disorder and the doctor wants to prescribe a second medication. They're already taking a primary agent. Do we think it's a good idea?

And typically we want to avoid polypharmacy, but in this scenario, it would be good because if they can take that primary agent at a lower dose and add a secondary agent, it's going to improve basically the seizure control just from different mechanism of action and also improve the safety by lowering the dose of that primary agent. So the meds act basically by reducing the excitability in the brain by either reducing excitatory effects by increasing the inhibitory effects of GABA, or by reducing sodium and calcium entry, which is going to reduce the ability of neurons to depolarize in the central nervous system. So here's a list of our central or our second generation agents. I've got a few starred because those are also commonly used in the treatment of chronic pain as well.

Certainly you don't need to know the names of these. You should know the... drug classes.

So like these subclasses, the hydantoins, the imostibines, the benzodiazepines, barbiturates, these are just examples over here. You don't need to know these, but you do need to know the drug subclasses and just secondary, second generation agents. And I just list these meds just for recognition for you.

Okay, so we talked about the side effects, certainly sedation and coordination. We want to watch out for those things. We certainly want to watch for signs that the person's really having some physical limitations or very sedated during therapy. For our pediatric patients, we really want to note if they have an increase in seizure frequency because they may have outgrown their medication.

And in some scenarios, if the patient has been seizure-free for two years, they may be able to stop taking the medication, but it depends on the situation, of course. All right, let's move on and talk about depression. So name three amine neurotransmitters involved in depression.

And sorry, this is a bit of a repeat for the residential, but... Hopefully you'll get these right this time if you didn't the first time. So serotonin, dopamine, and norepinephrine. Exactly.

So those are the three neurotransmitters involved in depression. Excellent. So in depression, there's a reduction in electrical activity in the brain of somebody with depression. versus not depressed.

So that's why we're not going to be prescribing something like what physicians aren't going to be prescribing, benzodiazepines, because we don't want to inhibit the brain any further. So what are the four main types of drugs used to treat depression that will affect some or all of those neurotransmitters involved? one response.

There we go. Yep. So you guys have it right.

So the SSRIs, SNRIs, MAO inhibitors, and the tricyclics. So, and depending on which one, it's going to affect different neurotransmitters, which I have listed here. So basically these three, these first three, there's going to be It's called a reuptake inhibition. So the neurotransmitters are released into the synaptic cleft, and then they are reabsorbed into this presynaptic neuron after they act on the postsynaptic neuron.

So if we block that reuptake, it's going to leave the neurotransmitter available in that cleft to continue to act on the postsynaptic neuron. Whereas with MAO inhibitors, there's also this enzyme that breaks down the neurotransmitter. And if we block that enzyme, then it's going to block the breakdown, again, leaving more available to act on the neuron. So here's just an example of some SSRIs.

Like I said, you don't need to know these drugs. You just need to know the drug class, selective serotonin, reuptake inhibitor. And with the drugs that predominantly affect serotonin, the SSRIs and the SNRIs, there is an increased risk of seizures related to serotonin syndrome.

The tricyclics and the MAO inhibitors affect dopamine as well as serotonin and norepinephrine. So they're going to have more side effects. So anticholinergic effects, orthostatic hypotension, arrhythmias. So the tricyclics are some of the oldest medications. And so, of course, they're, you know, effective, but more side effects.

And then we have the MAO inhibitors, which we talked about in our discussion. The issue with these is that they basically increase norepinephrine in the system and the systemic circulation as well as the CNS. And then if taken with foods that contain tyramines, such as fermented foods, that's going to cause catecholamine or norepinephrine and epinephrine release.

And so in combination, these can cause a hypertensive crisis and cardiovascular symptoms. Serotonin syndrome, another concern predominantly with the SSRIs and SNRIs. symptoms, confusion, hallucination, shivering, usually reversible, but it can be fatal if left unchecked. So we want to watch for those signs. So the antidepressants are also used in the treatment of chronic pain sometimes, particularly the SSRIs and the SNRIs.

And as we mentioned, also used to treat anxiety. So how long does it take for antidepressants to take effect? Correct.

Two to four weeks. That's right. So there is a lag time for these to take effect.

And that kind of justifies the theories that support depression. So the... down regulation theory.

So there's a time lag, two to four weeks, and the depression can get worse during that time lag period. Particularly susceptible are our young adults and teens. So we really want to watch for that. There's an increased risk of suicide, particularly in that period of time.

So we want to be aware and know our resources when we're treating. patients who are taking these medications or starting these medications. All right, let's talk about bipolar.

So with bipolar disorder, there's episodes of manic and depressive mood swings, and it's thought to be due to an imbalance of all the neurotransmitters, serotonin, dopamine, and norepinephrine. To date, the premier treatment is lithium, which is an element. It's not degraded.

It's eliminated in the... kidneys and it can accumulate rapidly in the body. So we want to know our signs of lithium toxicity. So what are the signs of lithium toxicity? Come up with a few of these signs if you can.

Dizziness is definitely a concern. Metallic tastes, very good. Weakness, vomiting, nausea, dysarthria, yep, confusion. Coma definitely would be a strong indication something's going on, right? So here's our list.

You guys covered a lot of them. Orthostatic hypotension is not on this list. The other concern is that with lithium toxicity, we can have possible permanent damage to the cerebellum.

So we want to really watch out for this. And typically blood serum levels will be monitored with this. Let's talk about antipsychotics now. So psychosis, certainly the most severe form of mental illness.

Schizophrenia is considered a form of psychosis. Most of these are due to an increase in dopamine in specific pathways in CNS, particularly the limbic system. There's other neurotransmitters involved, but dopamine is certainly the key causative factor that we can address with a pharmacology. So medications for psychosis block the D2 receptors, which are predominantly concentrated in the limbic system.

So it'll be used for many forms of psychosis, schizophrenia, and also used to treat aggression and agitation with Alzheimer's disease and dementia. And I was sharing with the class today, I've got a very feisty great aunt who's in memory care and she is on an antipsychotic medication because she causes a lot of trouble in her memory care unit. She's very naughty.

Um, all right. So we have traditional antipsychotics. And then we have atypical antipsychotics. So our traditional, our original strong antagonist for D2.

So as you can imagine, very effective, not necessarily that safe. Whereas our atypical or newer antipsychotics are weak D2 antagonists, and they also affect serotonin. So they'll block serotonin. So there's milder side effects.

Not quite as effective as the traditional agents. So common theme goes along with our anti-seizure agents as well. So what is the primary concern with those traditional agents?

Yes, yes. tardive dyskinesia. I think somebody meant to write there. Tardive dyskinesia.

Good one. Pseudo-Parkinsonism. Exactly. Good job.

Akathisia. Yep. Very good.

So yeah, it's these extra pyramidal motor side effects, which some of which you listed, akathisia, pseudoparkinsonism, and tardive dyskinesia, which is the most feared. It involves oral facial movements, grinding movements of the jaw. I mentioned to the class today, I would YouTube tardive dyskinesia example, just so you can see what it looks like.

And the issue is that it can be permanent. So we really want to watch out for it. And by the time someone starts to show these oral facial movements, they've probably showed a lot of these motor side effects. This is kind of an advanced progression of the motor issues that can occur.

So typically this medication will have to be tapered down or even stopped. It will have to be tapered though initially. So we certainly want to let doctor know if we're seeing the tardive dyskinesia or some of these, a change in their movement patterns. All right, we're going to move on to Parkinson's disease. So it's due to degeneration of what's creating neurons in the where.

Good. So dopamine secreting neurons in the substantia nigra. So with our antipsychotic meds, we were blocking dopamine and we had movement side effects, pseudo-Parkinsonian side effects, because we were reducing dopamine in the limbic system and there was overflow to the basal ganglia and particularly the substantia nigra. With Parkinson's disease, there's degeneration of the neurons, the dopaminergic secreting neurons in the substantia nigra, which is part of the basal ganglia.

Correct. I think we all know signs and symptoms, rigidity, resting tremors. We'll see these patients for falls oftentimes.

So there's a lot of medications used to treat Parkinson's disease. L-DOPA is the main medication or CARBA-DOPA along with CARBA-DOPA. We have COMT inhibitors, dopamine agonists, anticholinergic drugs, MAOB inhibitors, amantadine. And the two that are starred here are starred because those two types of medication are often used in the early phases because they are, well, dopamine agonists are because they're thought to have some neuroprotective effects.

Okay. So levodopa. One of the discussion questions is why don't we just give dopamine to patients who have Parkinson's disease? Dopamine does not cross the blood-brain barrier, so it's not going to get in.

So it's given in the form of levodopa, which will cross the blood-brain barrier. It will be broken down by dopa decarboxylase, which is an enzyme in the body. And it will convert it to dopamine where it can act on the basal ganglia, particularly the substantia nigra.

Now, without the medication carbidopa in conjunction with L-DOPA, we're going to have DOPA decarboxylase in the periphery also breaking down levodopa into dopamine. And with dopamine circulating in the systemic system. we're going to have side effects such as GI irritation, orthostatic hypotension, and other issues.

So if we give carbidopa that blocks dopa decarboxylase in the periphery, it also does not cross the blood-brain barrier, so it will just act in the periphery, which will leave more levodopa to enter the central nervous system and act and reduce those systemic side effects. So the other concern is that there is a COMT enzyme that breaks down L-DOPA as well in the peripheral circulation. So COMT inhibitors, again, will block that breakdown, allowing more L-DOPA to enter and act in the cerebral tissue. So it helps reduce fluctuations in the response to L-DOPA and prolong effectiveness. Side effects, certainly GI irritation, hypotension, which I talked about.

I've definitely had patients on L-DOPA that had orthostatic hypotension, even though they were taking the carbidopa as well, or L-DOPA and carbidopa in combination, which is a drug called Sinemet. Psychotropic and behavioral effects, we think about too much dopamine in the limbic system, right? It was an issue with psychosis.

So by adding more dopamine to the brain, we can have those behavioral side effects, dyskinesias or abnormal movements, freezing gait. Another thing to keep in mind is this end-of-dose akinesia. So as we get to the end of that L-DOPA dosing, the patient may have more freezing and rigidity. This certainly can be resolved by providing the patient with an extended release form of Sinemet or maybe changing their dosage.

There's also another issue called on-off phenomena. And L-DOPA, because of this just irregular absorbency of it in the system, patients may experience good benefit of the L-DOPA in a single dose, and then it'll stop working for a little, and then suddenly it'll just start working again for a little bit longer. So the erratic absorption is an issue. The other concern is there's a diminished response with long-term use. We're not sure whether...

Patients are getting a tolerance to the drug. So we try to delay administration of the drug. It also may be partially due to just progression of Parkinson's disease.

Those neurons that are degenerating can no longer compensate. Sometimes patients are put on a drug holiday. They'll take a little time off from the L-DOPA and they'll take a dopamine agonist or another medication. to help with the symptoms during that period. So we mentioned dopamine agonists, which cross the blood-brain barrier and directly will stimulate the dopamine receptors.

These have a longer half life. Dosing is very predictable. Like I mentioned, they can be used in the initial treatment.

Certainly, there's a lot of side effects because we're stimulating dopamine receptors everywhere. So there'll be orthostatic hypotension, nausea, vomiting, and then all the central effects as well. There's other medications that I've listed here for your reference.

I'm not going to go into detail about those just for time purposes, but I would breeze through this when you're reviewing the PowerPoint. Okay, next question. Your 10 o'clock, I don't know why it's showing the answer and then I have to hit enter.

I'm sorry about that. Your 10 o'clock patient with PT is prescribed Sinemet, which is levodopa and carbidopa in a single tablet. When should you advise them to take the Sinemet to maximize their performance during PT sessions? Yes, and you guys got it correct. Very good.

So typically you want to take the meds and... hour before. So typically 30 to 60 minutes prior to therapy, because there is evidence that PT treatment with the medication will improve outcomes more than just taking the medication alone in Parkinson's disease. So there's a synergistic effect here. Certainly Like I mentioned earlier today, we want to make sure, though, we may want to see the patient once or twice when they are in between doses so we can help them with compensatory strategies to deal with the freezing and the rigidity.

We also really want to keep in mind that we need to monitor for movement changes and also watch out for that orthostatic hypotension. So taking vitals, pausing. before the patient starts ambulating when you're getting them from sit to stand.

Okay, I'm going to move on to general anesthetics. So goal with general anesthetics, we want them to kick in fast. We want the skeletal muscle to relax. We want to inhibit, withdraw reflex and autonomic reflexes. We want to easily be able to adjust the dosage.

We want minimal toxic effects. And we want rapid, uneventful recovery, of course. And we probably don't want anyone to remember what happened.

So as general anesthetic dose increases, there's these stages that patients go through. So first, you feel amazing for a second. And then there's this moment of delirium, which we want that to be very brief. We don't want people to become combative on the operating table. And then the patient achieves surgical anesthesia where they're unconscious and they don't have sensation.

We want to limit medullary paralysis. We don't want to shut down the respiratory and cardiovascular centers typically. So there's a lot of different routes of administration, inhaled gas routes, and then we have IV anesthetics as well.

So why are patients often given IV anesthetics followed by inhaled anesthetics when undergoing surgery? And this was also a discussion question. So onset, which one kicks in faster?

Right, you guys got it. So the IV is going to kick in faster. So that way we can limit that stage two delirium.

So we'll get the patient in that stage three phase rapidly. And then why are patients often converted to inhaled anesthetic once they're in that stage three? So difficult to adjust dosage, easier to adjust dosage. Now I would say IV and inhaled both. pretty easy to adjust the dosage.

However, the inhaled anesthetics are easier to adjust the dosage and also easier to withdraw the dosing at the end of the surgery. So easier to adjust with inhaled anesthetics. Good. So certainly considerations, which I know we've talked about before, the anesthetic.

typically is lipid soluble. So it can be stored in the adipose tissue. So that's why you get your patient up then after that surgery, total knee surgery, and you try to get them up walking and you walk them a couple of feet.

And fortunately you've got that wheelchair right behind them. So when they're like, Ooh, I don't feel so good. I feel woozy.

You can have them sit right down. And that's because sometimes that anesthetic starts to come out of the system as you get them up and moving. So we want to watch for that. Just be aware. So these act different ways.

So you can review that some increased inhibition, some decreased excitation. All right, we're going to move on to local anesthetics. So these work by inhibiting sodium channels of neuronal axons. So they're going to block that depolarization or that signal being sent through the nerve.

conducting that sensory information. So certainly we're going to lack residual effects. There's not going to be that post-op confusion that we have with general anesthesia, less recovery time, and minimal systemic effects. So somebody having a dental procedure, oftentimes they're just going to do a local anesthetic injection in the mouth. And then there is a delay before it kicks in.

And sometimes we don't always get full numbing effects, right? So those are some of the cons of the medication. But there's a delay, typically 10 minutes with a dental procedure.

So these often end in cane or lidocanes. There is a concern that if these are spread systemically, they can inhibit. respiratory control, which is called LAST. And typically this is treated with an emulsion of lipid compounds.

So we want to watch for that. So I told students earlier today, I had a pain pump, which I don't know if I have it here, but I had a pain pump after my ACL surgery. I had two and a half weeks ago. And the sheet that I got with it basically said, you know, if you have difficulty breathing.

or shortness of breath, call 911 and turn off your pain pump, by the way, because of this risk of last. Okay, why is epinephrine administered simultaneously at times with the local anesthetic? So we want to think what epinephrine will do.

Yes, yes. So epinephrine will cause vasoconstriction. It will prevent vasodilation, which will reduce bleeding in an area that maybe we're trying to suture or physicians making a surgical incision. So we don't want a lot of bleeding in the area.

And also it will help keep that anesthetic local because of that vasoconstriction. Excellent. So there's a lot of different administration routes.

Topical anesthetic. I know when my daughters have dental work, they have like a little gel they'll put on their gums before they administer the shot. Fluorimethane spray when I was a new PT. People had like a spray and stretch and it was a fluoromethane numbing spray that you would spray on the muscle and then stretch it.

Kind of ridiculous. But anyway, we don't use it anymore. Transdermal patch, lidocaine patches.

Often we have patients with these patches on. We have peripheral nerve blocks and central neural blockades. I'm sorry for the repeat residential class, but after my surgery, I had one of these. pain pumps. There was a little button here I could press to get some of that local anesthetic.

It was some sort of cane medication. I can't remember the name of it, but it ended in cane. And then every three hours, there was medication delivered.

And the little catheter went into some sensory nerve, nerve ending or nerves that innervated my knee. I didn't have to take narcotics for the first three days post-operatively, whereas 20 years ago when I had ACL surgery, I did. I had to take a lot of narcotics initially. So it worked really well.

And I was telling them I got a cross body bag with it that held the pain pump. So I was feeling pretty good after my surgery. Okay.

So we also have epidural local anesthetic. Um, so the epidural basically is injected between the vertebral column and the dura matter. Um, and you hear all these horror stories about women who are going in labor and they get their epidural and it only, um, reduces pain on half their body.

So there, sometimes there's not full coverage. I had an epidural and it worked wonders for me. Um, so Okay, we have also caudal block, which is basically an epidural injection into the sacral hiatus.

And then we have spinal nerve blocks. So with the spinal nerve block, the medication is inserted into that subarachnoid space or intrathecal area. So intrathecal injection.

So this will be used for local anesthetic and intrathecal injection is also used with the baclofen. pump muscle relaxant. So if somebody's getting a baclofen pump, the catheter actually is going to sit right in that intrathecal space below the level of the spinal cord injury. Okay, we have sympathetic blockades and beer blocks. So with the beer block, you need a tourniquet.

It's into a peripheral vein. So procedure has to be under two hours. I mean, I think this is often like uh rarely used but for a limb procedure all right let's move on to muscle relaxants and um there's been a lot of repeat for the residentials so you know i won't be offended if you if you leave the chat or stay for another review you do that much better on the test um so muscle relaxants are used to normalize muscle excitability with and the goal is to not decrease muscle function. However, this is a concern.

We need to understand the difference between spasticity versus muscle spasm because some medications treat spasm, some treat spasticity. So my first question to you is muscle spasm as compared to spasticity. Which of the following is true for muscle spasm, which is not true for muscle spasm? And I can tell those St. Augustine residential students were paying attention today. You guys nailed it.

So muscle spasm is due to local tissue inflammation or damage. So muscle spasm, we think about our acute lumbar strain, our orthopedic patients. So there's increased tension in that muscle or increased tone because of different inflammatory mediators that are irritating that area and causing the muscle to tighten up or increase tone. Also could be due to peripheral nerve root irritation. So in the case of, for example, a herniated disc or a disc issue.

I also think about it as kind of like nature's splint where the muscles just tighten just to hold something where it is as a protective mechanism. So with spasticity, it's typically due to a supraspinal. inhibition from the spinal cord and the central nervous system. So it's due to pathology in the CNS or spinal cord. And there's hyper excitability of the muscle stretch reflex with spasticity, which is clonus.

So if we quick stretch that muscle, there's a hyper excitability of that reflex, and we're going to get the clonus. So we have drugs to treat muscle spasm. We have benzodiazepines, such as diazepam or Valium-X, again, to increase the inhibitory effects of GABA.

So of course, sedation, dependence, and tolerance will be an issue. So it's not really a long-term solution. And then we have our central acting antispasm drugs.

Now, the mechanism of action of these is not fully understood. The thought is they inhibit polysynaptic. epileptic reflex pathways that in conjunction help reduce that increase in tone or flow to the alpha motor neuron.

These cause a lot of sedation. So oftentimes our outpatient ortho population will complain of just sleepiness on these medications. So they might just take it at night and not take it during the day.

So flexoril, soma are common medications in this category. All right, so now we're going to look at the anti-spasticity drugs. So you do need to know these drugs in this left-hand column.

So these are all the ones to treat spasticity. So let's start with baclofen. So baclofen is a GABA agonist, so it's going to increase those inhibitory effects.

commonly used due to spinal cord lesions, not as effective in CVA and CP, particularly due to just the administration route. If you have to take it orally, it really causes a lot of drowsiness. And another thing to note here, it can cause muscle weakness too.

So often with our spinal cord injured population, as I mentioned. they might be put on a baclofen pump, which will deliver the medication directly below the level of the spinal cord injury to act very locally to reduce the systemic effects. And there was a great case example of this in your text.

Also, just to note, certainly with intrathecal baclofen pumps, the pump is surgically, or the catheter is surgically implanted. Um, the, the pump can malfunction. Um, we want to make sure it's working because abrupt withdrawal of black flint, backflint can cause seizures and all sorts of problems.

It is kind of a dangerous situation. So we want to make sure the pump is functioning well. Um, we have dantrolene sodium.

This is the only one that acts directly on the muscle. So it inhibits calcium release from the sarcoplasmic reticulum. And if you remember, the calcium then allows for the actin and myosin binding in the muscle tissue. So it's used to treat all forms of spasticity. It's taken orally.

Muscle weakness is a concern because it does act directly on the muscle and liver toxicity as well. Often used for CP. CVA, CVAs, things like that, sometimes used with spinal cord injury as well. So then we have our benzodiazepines. And I think, you know, we've covered that enough.

And then let's move on to Botox. So Botox inhibits acetylcholine release at the neuromuscular junction. So it acts on the neuromuscular junction, not on the muscle the way dantrolene sodium does. But it will be a local injection into the muscle tissue that's involved.

So used, of course, cosmetically, used for migraines, used for muscle dystonias, torticollis. I'm sorry for the repeat residential class, but I did have a stroke patient in inpatient rehab who we used Botox on. She had had a stroke and had a lot of extensor tone. And.

She was meniscus with ambulation because her extensor tone affected her upper cervicals. So she was stuck like this when she was walking because of that tone. And she had a hard time seeing the horizon.

So the physician ended up injecting Botox into her suboccipitals. So then she could get her head in neutral position. And she went from meniscus to supervision just with those Botox injections. And she was able to go home and live with her husband, which was great. So issue there, of course, you would have to go back and get the injection typically every three months.

They administer the Botox injections because it does wear off. There is a risk of an immune response where your body will generate antibodies to the Botox. If that's the case, Botox really isn't going to be effective for that patient.

All right, we're going to move on to opioids. So opioids provide pain relief by interfering with substance P-mediated transmission of painful sensations. So these are our narcotics. So narcotics are sourced naturally from opium poppies.

We also have semi-synthetic, which are sourced from the opium poppy and then chemically modified, such as heroin. And then we have synthetic, so our tablets typically form. Certainly notoriety due to their potential for addiction. So which opioid receptor in particular is involved with addiction and respiratory depression?

Nice work. Mu, correct. So mu is involved with respiratory depression and addiction.

Next question, which receptor type is involved with sedation and psychotic effects? Kappa, correct. Correct. Very good. So kappa is involved.

with sedation and psychotic effects. We're not quite done. I just ran out of slides on this presentation. So I've just got to switch over real quick. Hold up one second.

Yeah. And I just have a couple more slides and then we'll be done. So opioid receptors, we have um, Mu, which is involved in respiratory depression and most addictive, the kappa, psychotic effects.

And then we have delta. Delta is involved with growth hormone release and dopamine release. Dopamine inhibit dopamine release. So it'll block dopamine from being released. So if we think about opioids and naturally...

occurring opioids. So our endogenous opioids, we have endorphins and keflins and dynorphins that are naturally released in the body in response to tissue injury, to control inflammation and pain, also involved in various other systems. So in response to eating or drinking, we think about endorphins when we think about that runner's high after we exercise.

And then we have our exogenous opioids. So these are the medications, the external medications. So all three of these receptors are going to provide analgesic effects. Keep that in mind.

So opioids, medications are described basically based on their affinity for mu. So we have strong agonists that have a strong affinity for mu. So these, of course, are going to be most notorious for causing addiction issues and also respiratory depression. So morphine, typically that's prescribed with severe pain, end of life, somebody who's on hospice or just very severe pain.

We have fentanyl, another medication used for severe pain, also for anesthesia. And then methadone. Why is methadone bold?

Methadone is bold because this is the medication that's used to treat addiction. So why would we use a strong agonist to treat it? addiction.

The reason is because even though it's a strong agonist, it has less withdrawal symptoms. So as somebody is getting weaned off the methadone, they'll have less withdrawal symptoms. We have mild to moderate agonists like our hydrocodone, oxycodone.

So after my surgery, I was prescribed oxycodone, which thanks to that pain pump, I really didn't need to take it very much. And then... Percocet is oxycodone in combination with acetaminophen, and that's to help try to spare opioid use.

And then we have our mixed agonist antagonists. So these have a high affinity for kappa. So they'll bind to kappa, but they'll block mu. So there's less addictive issues with the mixed agonist antagonists. But...

If we think about what kappa is involved in, there are going to be more psychotropic effects, hallucinations, things like that. So then we have our antagonists. These are our life-saving medications in the case of opioid overdose.

So these basically will block all opioid receptors and they'll actually displace opioids from that mu receptor. So naloxone or Narcan, oftentimes it's a nasal spray and it acts very rapidly. And if you've ever seen it, the patient is very grumpy when they wake up.

So there's a lot of different administration routes for these medications. They're distributed through all the tissues, metabolized in the liver, excreted in the kidneys, physical withdrawal. Typically lasts five days. And of course, tolerance and physical dependence are major issues with these medications.

So let's go over the indications. So pain, very common indication for these medications. Addiction, methadone is often prescribed to treat addiction.

Diarrhea. So we all probably know these opioids cause... Pause. major constipation and after surgery and narcotics, we're giving birth to the bowling ball, basically. So these can be used to treat diarrhea.

They would be used for severe diarrhea because there's certainly alternatives for mild diarrhea. But in the case of severe diarrhea, they may be used. Cough suppressant, codeine is a common one prescribed to suppress cough. We think about these as a common one. repressing that respiratory system, and then anesthesia.

So how do these act? Number one, they have spinal effects. So they inhibit painful signals from the dorsal horn in the midbrain. Basically, they allow descending pain pathways to transmit inhibitory signals to the dorsal horn, which will decrease transmission of pain stimuli to the brain.

And then they also act by blocking the pain nerve endings in the periphery. So they act in three different ways to reduce pain. Certainly, if you're treating patients on narcotics, you want to consider they might be sleepy, confused, a little slow.

They might be feeling really good and talkative. Anticipate orthostatic hypotension. respiratory depression. So we want to watch the respiratory rate, O2 sats, especially if they have a comorbidity that involves lung disease.

GI distress may be an issue and that constipation that we talked about. So often stool softeners and laxatives are prescribed in conjunction. And of course, PT is one of the best ways to promote peristalsis. So we'll be hanging out by the bathroom. So we want to make sure that if somebody has a lot of pain, for example, somebody with a really traumatic injury that's in a lot of pain or say a rotator cuff repair that's fresh and you're doing passive range of motion, they may want to take that narcotic an hour before therapy.

So the pain is under control once you're treating them. We talked about dependency and tolerance. The other thing we really need to educate our patients. that when they stop taking these medicines, they're probably going to feel more aches and pains initially due to that physical withdrawal. So probably they're going to need to take something when they're getting off these meds, such as Tylenol is often, or acetaminophen is often prescribed.

Often need to wean off the meds, needs to be a plan to start and stop, typically not meant for maintenance therapies. And of course, we as PTs can provide lots of pain management alternatives beyond using opioids. That's one of our roles.

All right. So I'm going to stay here for questions. Make sure you go to the chat and you'll see the link to record your attendance for this particular presentation. And thanks for joining in and participating.

Thank you. My pleasure. Thank you.

Thank you. Putting that link. I don't see the link in the chat. You don't see the link in the chat? No, ma'am.

Huh. Okay. Let me repost it. Okay. Maybe I posted it too early.

See if you see it now. Oh, yeah. It came through.

Okay. What about, did you say that you posted these slides somewhere? Yeah, they should be in iLearn.

Barbara should have posted them. Okay. I'll check there. And if, I mean, if you want as well, you can always just. put your email address in the chat and I can send it directly to you too.

Okay. Thank you. I got you, Michaela and Haley.

And David, did you get my email, Dr. Drayton? I put it in the chat. My name is Melissa.

I don't know. Melissa, I see you. Yep. I will send it to you too.

And David too. Yeah. Thank you so much.

I appreciate it. Thank you

Transcript for:Comprehensive Pharmacology Exam Review

Transcript for:
Comprehensive Pharmacology Exam Review