Hey everyone, nurse Mike here from simple nursing.com. Today we're diving into neurological drugs covering the mustnow medications for your enclelex and nursing exams. And guess what? There are over 19 study guides, one for each medication that'll pop up in the top right corner as we break them down. And for simple nursing members, get ready to grab your memory packed colorful study guides included in your membership. Now, let's log it in. First up is our anti-convulsant phenitoin given for long-term protection against seizures like with patients with epilepsy and other long-term chronic seizure disorders. Now the key word here is long-term so it lasts longer in the body and patients can get very toxic. So the memory trick is we call phenitoin phenito toxic since like most toxic drugs the max range is 20 and that's the number to know for the enclelex. So the big key points to write down is 10 to 20 is the therapeutic range. So below 10 we have to report to the HCP since there's a huge seizure risk and over 20 we hold as well and notify the HCP because of the huge toxicity risk. Now like any toxic drug we do routine blood tests. So question banks love to ask blood level monitored routinely. So that's usually the correct answer. Now we do this to check the therapeutic range of the drug as well as to monitor liver function since any drug that can cause toxicity can also affect the liver heavily. So the hessi mentions we hold the med for levels higher than 20. So remember guys over 20 is very toxic and we take the medication at the same time daily because of the narrow therapeutic index. Now, that's a really big key word. Same time every day for drugs with a narrow therapeutic range. Now, the next key point is toxicity. The early signs to report to the HCP. These are the big ENLEX tips. So, write this down. At taxia, or basically an unsteady gate or gate disturbance, as well as hand tremor and slurred speech or having trouble forming sentences. So just think fenny towan is fenny toxic. You can't talk and you can't walk. So fenny talk or fenny walk if you're fenny toxic. Now for the other adverse effects the key word here is suicidal ideiations and skin rash that are new and painful. These are typically priority since it could indicate Steven Johnson syndrome. So we report these to the HCP immediately. Now some expected side effects. We expect to have brada cardia and hypotension. Since it's a CNS depressant, we expect to have low and slow vitals. Now the big key point here is gingerval hyperplasia. Huge anklelex tip. Fancy words for overgrowth of gum tissue around the teeth resulting in big gums that bleed very easily. Again, this is to be expected. So we don't stop the drug for this. 40% of students got this wrong and wanted to stop the drug for this. So guys, remember don't stop. Big gums are completely normal. So we teach the patients good dental hygiene with a soft bristle toothbrush. The big thing here is soft toothbrush and regular dentist visits and follow-up visits. So ATI says that you teach patients to inform the dentist that they're taking phenito and the hessi mentions perform or assist with oral care every shift and a skin rash and fatigue and dysmia are priority. Remember any type of skin rash could mean Steven Johnson syndrome very deadly. Now the Kaplan mentions statements requiring immediate intervention. So, I noticed a rash on my stomach last week. Again, deadly Steven Johnson syndrome. And the second point mentioned was lately I find myself thinking about driving off a cliff. Definitely not normal. We need immediate intervention here. So, as far as patient teaching here, switching gears, there's no oral contraceptives. So, fenyitoin deactivates the pill leading to accidental pregnancies. So, we teach patients to use alternative birth control like an IUD and there's no stopping abruptly. This typically goes for any drug that's acting on the brain. And we take folic acid, calcium, and vitamin D since this drug decreases folic acid absorption and decreases bone density. So, the Kaplan mentions this in a very interesting way. Encourage foods such as milk, cantaloupe, and kale. Now all these foods are high in folate and vitamin D. And they had a second question that mentions requires further teaching when the patient states if I start having adverse effects I will stop taking this medication immediately. Guys that's a big no no. We never stop abruptly or immediately. We always taper off. Now, as far as administration, one question bank stresses the importance of phenitoin with tube feedings, stating it can decrease the absorption as well as cause seizures. So, big key word here, stop tube feedings 1 to two hours before and after administration. This was mentioned multiple times as a priority since tube feedings can interfere with the absorption and decrease phenotonin effectiveness. So guys, we always administer the medication correctly. So for two feedings, we flush with 30 to 50 mls of tap water before and after the drug is given. And then normal saline is not required. So tap water is okay. Now, as far as IV administration, we always flush the IV with normal saline before and after giving this drug. Now, lastly, don't let the enclelex trick you here. So here's three points that students usually get tripped up on. So again, gums typically bleed and that's to be expected because of the overgrowth of the gum tissue, but not the face. So there's no need to use an electric shaver. And secondly, there's no metallic taste. That's typically for metronidadazzle. 30% of students chose this as an expected side effect. And lastly, there's no photosensitivity. 50% of students wanted to think that phenito caused photosensitivity and wear sunglasses outside. But guys, no, that's not the case here. For everything you need to know to pass the enclelex, make sure to check out our enclelex review lecture series and live cram sessions. Now our second drug for anti-convulsants is levator given to prevent and treat seizures for those that are at high risk like those following a brain tumor or surgery or trauma on the brain which can increase intercraanial pressure. This is often preferred over phenitoin due to the minimal drugtorug interactions. Now the big common side effects like phenotin it's a CNS depressant so we get a low and slow body with drowsiness and fatigue. Now the major adverse effects just like phenito we get the double s's here suicidal thoughts and Steven Johnson syndrome. So we report any key words like new anxiety new agitation depression or even mood changes. And for Steven Johnson's we report rash, blistering and even muscle joint pain and even conjunctivitis. Now the big key point is for the patient teaching in terms of driving. So we have to get permission from the HCP and follow transportation department guidelines since this drug can cause drowsiness and fatigue which is common in the first 4 to 6 weeks when starting the medication. So guys, don't let the enclelex trick you. Always be sure to get driving permissions. Now for the big chonerics, we have neostigmine and pydostigmine. These are given to patients with MG that myostinius gravis. These clients get too dry and in result lack mobility and lack the strength to move since they have tons of muscle cramping. So we call my estenius gravis dry estenius gravity since the lack of strength and mobility like a big weight is weighing on them. Now this is sort of like a tin man from Wizard of Oz who needs to be lubed up to move. So clients in the same way get so dry that they can't see, pee, spit or poop and even move. So we basically get massive antiolinergic effects with myastinius gravis dry estenius. So with neastigmine this drug helps to lube up the body with secretions. So the memory trick just think stigmine or stigmine secretions are mine with the stigmines and so the body gets super wet and wild. Now the big side effect to note is this drug can work too well and add too much secretions with the stigmines causing a huge flood of fluid inside the body. It's kind of like secretion faucets are held wide open. So the patient gets wet and wild like a water park. Yoohoo. Now this is called a cononergic crisis. Basically crisis is a secretion crisis with a colonergic crisis. We see lots of C, lots of P, lots of spit and lots of sh poop. So basically an increase in pupil constriction. We get a lot of tears called lacrimmation. Salivation, we have drooling and sweating, we have diapharesis. And as far as poop, we get a lot of diarrhea and even some nausea and vomiting. Now to stop this colonergic crisis and to turn off these secretions, we just give an antiolineric. just think it's anti-seretion with an antiolonergic. So the antidote to know is atropene the most famous antiolineric here. So just think atropene ends in tropene or tropine. So think you can't pee with the tropene. These anticolinergics work by turning off the PNS that rest and digest to stop the secretions and turn on the SNS that fight and flight which makes the heart rate go crazy high. Now what did the Hessie have to say about the stigmines? Well, the first thing they had to say was we anticipate the drug to treat this myastinous gravis is neostigmi and secondly a patient being managed for myastinic crisis develops asthma we have to decrease or discontinue this pyradio stigmi. Now you have to be thinking to yourself why though? Well just think about the patho here. Asthmatics we have bronco constriction very tight lungs. The last thing we really want is wet and wild lungs. So we want to turn off that faucet and discontinue the wet. Now the last two points that Hessie mentions is a patient with antiolinergic toxicity, we give phospho stigmine. So it works both ways here. If we have too much dry with an atropine, we give the wet secretions in the stigmines. Now the last point here was medication effectiveness of a stigmine. So absence of muscle cramps and adequate vision without diplopia. So just think of the main tin man from the wizard of oz. We want our patients to get lubed up and walk around without muscle cramps and have more movement as well as correct vision here. Now the ATI had mentioned about adverse effects. We get pupil constriction difficult with visual accommodations as well as atropene is given for colonric crisis caused by excessive amounts of neostigmine. And lastly the Kaplan states that client with pyidio stigmine having salivation lacrimmation and urination we notify the hcp since all these things screams a colonergic crisis. So all those secretions. So guys just remember for your exams stigmines or stigmines cause too much secretions from all that cold andurgic effects. Now let's start with the migraine medications. We have sumotan given to treat migraines and cluster headaches by causing vasoc constriction inside the cerebral blood vessels. Basically the blood vessels in the brain. Now you can probably already guess that vasoc constricting in the brain vessels can cause some serious dangerous situations. So with any drug we always ask ourselves what's the worst case scenario or basically what kills this patient first. In this case we're already thinking a clot in the brain aka a stroke or even a clot in the heart since it can cause vasoc constriction all over the body. So the big contraindication with sumo tripan is we can't give it to patients with CAD that coronary artery disease with already narrowed heart vessels and we can't give it to uncontrolled hypertension due to the vasoc constriction properties this could cause hypertension crisis angina and even an MI now the key point to write down is we screen for history of uncontrolled hypertension and we have to report it to the provider. Now even ATI mentioned we have to teach the patient to report anggina or coronary vasospasms. So this medication again can cause constriction in the blood vessel worsening hypertension and worsening anggina. Now our second migraine drug is irerogatamine. Now it works very similarly to sumotryptan by constricting the cerebral blood vessels. So once again we see the same type of side effects here. So ATI mentioned the indication is for migraine headaches and we teach the patient to take one tablet immediately at the onset of headaches and the Hessie mentions the priority finding is pale extremities. So that's really the biggest key word there. Any type of pale body means we have a lack of perfusion. So guys just look at these key words for the enclelex. So pale body lack of profusion in this case it could be a clot from too much vasoc constriction. So we have to instruct the patient to go seek medical attention immediately based on this finding. Now for the big Parkinson's drugs we have carbodopa and leodopa. Guys this is the number one drug to know for the neurossection mentioned heavily in all the question banks. So to simplify this immensely before diving into this drug, let's recap the pathophysiology real quick. So Parkinson's disease, we have low dopamine and high acetylcholine with the formation of abnormal protein clusters called Louis bodies in the brain. This results in clients getting jittery movements like muscle tremors, muscle rigidity, and a lot of slow start and stop motions like a shuffling gate and even pin rolling of the fingers and other unsteady movements. These movements are known as brady kinesisia. So the memory trick we use for Parkinson's just think of a park in Parkinson's. Technically there's no dope allowed in the park like no drugs kind of allowed in the park. So there's no dopamine in Parkinson's. And for the signs and symptoms, it's kind of like parking a car with Parkinson's for the first time. So a lot of jittery movements, starting and stopping motions like you're pushing the brake in breaksia for bradicinesia. So just think if you have low dopamine, this means low movement and more dopa means more movement. That's why we say you can't jump rope if you don't got dope. Or you can think you want to jump rope well you need to get more dope. So we give leodopa which leaves the dopamine inside the brain and carbodopa which prevents the breakdown of leodopa allowing the body to use it more. So just say to yourself carbodopa conserves more dopamine and leodopa leaves more dopamine in the brain. Now the hessi mentioned two things about levodopa. It's the main drug for Parkinson's treatment and it's a dopamine precursor. Now for adverse effects, we get hallucinations known as psychosis as well as orthostatic hypotension. That dizziness upon standing resulting in falls. So we have to teach our patients those slow position changes. Now as far as administration, we start at a low dose to prevent those big adverse effects. And since prolonged use can lead to toxicity, we have to start slow. Now, the first sign of toxicity is disynesia, which is spontaneous or involuntary movement, kind of like ticks. So, just think to yourself, if we got too much dopamine, we have too much movement here. So, we get face or eyelid twitching, even tongue protrusions, and face grimacing. We have to report this to the HCP since it's not normal. Typically, it means that the patient is toxic. Now, for the key points for patient teaching, this drug has a slow onset, typically taking 2 to 6 weeks to become fully effective. So, typically this is true for any type of drug that's acting on the brain. It starts slow. And the second thing is slow position changes from that orthostatic hypotension. And the last point here is red and brown urine, sweat, and saliva is completely normal. So discoloration is normal. Huge ENLEX tip there. This is completely normal and doesn't need to be reported to the HCP or provider. Now for the big no nos that are not normal here. Big one to write down is no high protein meals. That's the biggest ankle tip. So protein interferes with the absorption of leodopa. So just think if you're on leodopa and carbodopa, you have to leave the protein with leodopa and just carve it up with carbodopa. Now the second point here is not elimination of tremors or rigidity. We're only decreasing this big tip. So, as a general test strategy, no drugs acting on neurotransmitters in the brain or even hormones for that matter will ever 100%ly cure the patient. So, these typically are lifelong drugs. So, be very careful with words like cure or eliminate. They usually indicate that this drug will 100% resolve the disease, which it does not. Now, lastly, we never stop abruptly. This could cause a crisis where we have complete loss of movement. So remember, if the drug takes a few weeks to kick in, well then it takes a few weeks to taper off, too. Now, here's an interesting side note to switch gears. MAIs in combination with this drug actually enhance the effectiveness. So, the Hessie mentions two things. MAOI is the anti-depressant enhances efficacy basically effectiveness and sleene and MAI is used in adjunct treatment with carbodopa and leodopa. Now the last point here is how do you evaluate the medication effectiveness or basically how do we know the medication is working for the patient. Again just think here if you can jump rope then you got enough dope. So the key word is improvement in spontaneous movement. This indicates that it's effective for bradyinesisia and Kaplan mentioned carbodopa and leodopa medication is effective when the family member says my husband can walk around the yard. And the second thing they mentioned was effectiveness. The client is more ambulatory or basically meaning they can walk around. Now lastly, don't let the enclelex trick you. This medication does not help with memory. Typically, that's Denazipil for Alzheimer's patients, but we'll cover that in a moment. So again, to drive home the key points, the two biggest ENLEX tips to know for your exams for leodopa and carbodopa. Remember, leave the protein with leodopa since protein can block absorption and you can't jump rope if you got no dope. So remember more dopamine equals more improvement with movement. Now for antiolinerics we have benzropene and atropene given for a lot of different reasons from speeding up the heart rate to turning off secretions in a colonergic crisis. So the big thing here is don't get tricked. Anti-olonergics are anti-seretions. We get really dry. So just think tropines we have no P with a tropene. So all anticolinergics we can't see, can't pee, can't spit and can't poop. Nowonerics lead to more secretions. So we get really wet like stigmines which we call stigmines the secretion drugs. So guys just remember those things and you won't get tricked. Now tropine ending drugs are given to neurological patients mainly to treat the tremors like with clients with Parkinson's where we have too much secretions from that aceticoline and it's even given to help tremors in extra parameal side effects basically with antiscychotic medications. So the key word here is tremors. So just think the tea in tropines we give to treat the tea for tremors in neuropatients. Now the mechanism of action is pretty simple. It does this by drying up the body kind of like flicking a light switch. It turns off the vagus nerve that's connected to the PNS the parasympathetic nervous system that rest and digest. So we get no more secretions for that digestion and salivation. This allows the SNS, the sympathetic nervous system, our fight and flight to be turned on in full force. So again, we're turning off the PNS and turning on that SNS, that stress nervous system, that sympathetic nervous system, which activates the vital organs, shooting up the heart rate and making the body really dry. So think you get real dry with a tropine. Or just say you can't pee with a tropeen. It just puts your heart rate really high like on top of a pine tree with a tropine. Now the key words to focus on once again it's given to treat those extra parameal side effects like donia and even Parkinson's tremors like that bradicinesia specifically muscle rigidity and shuffling gate remember tropine treats the tremors like bradicinesia and that donia those abnormal movements of the face neck and trunk now don't let the enclelex trick you here No, it does not treat signs and symptoms of psychosis like delusions. We're only treating the tremors here. Again, the T and tropine. Just think T for tremor treatment. Now, the next key points are for contraindications. We do not give antiolinergics to any client who's already dry or who has fluid retention since this can make the condition worse. Now one question bank stressed the important point when to give atropene. So atropene may precipitate acute glycom. So clients with glycom you have to notify the hcp and we can't give it. And lastly no BPH patients that benign prostate hypertrophy or even urinary retention patients. The most serious thing is we have to notify the HCP again for any urinary retention. So the memory trick we use is BPH a big prostate that holds back urine. No antiolinurgics are given to these three patients. Now lastly Hessie mentions this in terms of patient teaching. So first teaching the patient to notify the HCP if you develop urinary retention. Secondly, this medication can reduce the ability to sweat, so don't overheat. And lastly, sit or stand up slowly to prevent that ladedness. So guys, just remember here once again, you get really dry with a tropine. So no pee, no C, no spit, and no poop. Want more tips and tricks to pass your exams? Join our simple nursing membership for exit prep lectures and access to over 8,000 questions built to take your studying to the next level. Now for osmotic diuretics, we have manitol given to decrease cerebral edema with ICP that incraanial pressure like with patients with head injuries and swelling in the brain with menitis and it's even given for increased ocular pressure for glycom emergencies. So the memory trick we use is manitol. Think man it hurts or man ICP hurts in the head or basically man my eyes hurt for manitol. So the ATI mentions we give manitol for increased ICP and we assess the level of consciousness every hour. And the hessi mentions four key points for manitol. It's used to decrease ICP. For IV administration, it cannot be given PO. And one of the main side effects is edema, which begins 30 to 60 minutes after administration. Okay, you're probably thinking, hold up here. This is really interesting. Why would a diuretic, which drains fluid from the body to the body, why would it cause edema or fluid retention? Well, the mechanism of action is it works by draining fluid out of the cell into the vascular spaces. So swollen brain cells that have all that pressure causing the ICP get drained. So all that fluid gets drained into the blood vessels which can put the body in fluid volume overload. This leads to classic heart failure signs and symptoms like peripheral edema, fluid in the extremities and even pulmonary edema, fluid in the lungs. So naturally a big side effect is heart failure. So think HF for heart failure. We get HF for heavy fluid all over the body. Now ATI mentions this when talking about manitol. You monitor for signs and symptoms of heart failure specifically basilary cracks or basically crackles inside the bases of the lungs as well as pulmonary edema that fluid in the lungs. Now that's why the patho is so important here. So thanks for watching this entire video to understand all of it. Now the next drug class is neuromuscular blocking agents. We have citacoline and in this drug class we also have two other drugs pancurium and cycurium. But out of all of these the big focus is on cetaoline. It was the only drug mentioned four times in different quiz banks. Now these drugs are given to paralyze the body before ET tube intubation as well as mechanical ventilation typically for those who are difficult to intubate like before general anesthesia or even in emergency situations. Now the Hessie mentions this is used to facilitate mechanical ventilation and it produces deep muscle relaxation. Now those are big terms for exams and the enclelex. Now for the scary part. This drug only paralyzes the body but does not sedate the patient. So patients are wide awake here. So we have a huge risk for respiratory arrest since the diaphragm that muscle that helps us breathe is now paralyzed. And again it only paralyzes the body. It does not sedate the brain. So the patients can still feel pain. So talk about a horror film. It's like being trapped in your own body during surgery. You can feel everything since you have no loss of consciousness. That's why we always have to sedate with the benzoazipene while giving this drug. So the hessi says we must give sedation and the primary result of this drug is flaccid paralysis not loss of consciousness. So it goes sedation first like mazzylam or benzo ending in pam and lamb then cetaoline and then third immediate intubation. Now for the deadly adverse effects that are always on the enclelex and exit exams. Here we have malignant hyperothermia better known as MH. This is a life-threatening muscle abnormality from general anesthesia or cetylcholine. So the patho is really simple here. Calcium is released from the muscles when aesthetic is administered causing muscles to contract and become rigid. This increases oxygen demand and metabolism which results in dangerously high body temperatures. Hence the name MH malignant hyperothermia very hot body. So simply remember MH as the acronym MH M for muscle rigidity and H for hot. The immediate intervention here is to notify the HCP first. Then secondly we administer or prepare to administer muscle relaxins like dantine and then very last we give oxygen and cooling measures. So the Hessie actually asked a question about this. After administration of cetaoline, the patient experiences a high fever and muscle rigidity. The correct answer was to prepare IV dantrillene. Now 60% of the students got this question wrong. So again remember we notify the HCP first. Then we also prepare dantrilline for malignant hyperothermia. And lastly we use cooling measures. Now our last big key point comes in the peroperative nursing care. The biggest thing and the priority here is to screen for high-risk MH. So three key points to write down. Prior reaction to general anesthesia is the most critical here. We want to know if the patient has had a reaction before we give the anesthesia. Secondly, blood relatives with significant reaction to general anesthesia usually means that the patient will have a reaction. And then lastly, the alcoholics as mentioned by the Hessie typically have a high risk for reacting in MH. Now, these are the priorities above all else for this drug. So, please commit these three to memory since these three came up multiple times on various question banks as the highest risk for that deadly malignant hyperothermia. Let's dive into some top missed enclelex questions pulled straight from our simple nursing enlex question bank created by the experts who actually wrote the exam. So first question here, which nursing actions are appropriate for the nurse preparing to administer venitoin via nasogastric or NG tube? Select all that apply. Okay, so before looking at the options, let's break this down. The questions asking the appropriate nursing actions when giving phenito via that NG tube. The key word there is NG tube or nasogastric tube. So before looking at the options, we're just thinking of a few things we know about the drug. So we know fyentoin is phentoxic since it lasts a long time to prevent seizures. And the NG tube we have to flush with water before and after we give really any drug. And specifically for this drug, you have to stop feeding tube at least 1 to 2 hours before and after giving the medication. So now for the options. Option number one is correct. We do hold tube feedings at least 1 hour prior to the administration of phenitoin. So the key word there is holding at least an hour before and after giving. Now option two flush the nasogastric tube with 30 mls of tap water before and after administration. Yes guys we always flush with tap water before and after. Now, this one could have been tricky since some of you guys thought that sterile water is needed for an NG tube, which it's not. Tap water is perfectly fine. Now, option three is incorrect. Monitor the blood pressure and heart rate every 15 minutes for 2 hours after the administration. So, technically, no, this is not needed to monitor the hard stuff since it's a long-term medication. So, it takes a long time to kick in here. Now option four, monitor liver function tests on a regular basis for patients taking phenitoin. Yes, phenitoin is phenitoxic. So any toxic drug can be toxic to the liver. Now lastly, administer phenitoin at the onset of new seizure activity. So no, this is a long acting drug. So during seizures we have to give a faster acting drug like a benzo ending in pam and lamb like elpraza lamb. Okay, next question. Which adverse effects of phenito should the nurse immediately report to the provider? Select all that apply. Okay, let's break this down. This question is asking for the adverse effects of phenito to report immediately. So this is a priority question. We're looking for the most deadly adverse effects here. So before looking at the options, think what do you know about phenito which we call fenny toxic? Well, the biggest thing is the therapeutic range. 20 is maximum should be between 10 and 20. Second thing is the suicidal risk as well as the rash which obviously are not good. And the earliest signs of toxicity is a taxia and slurred speech. That inability to walk and talk with that fenny toxin. You can't fenny walk it and you can't fenny talk it. Okay, so option number one here, this one's correct. New reports feeling of unsteadiness when ambulating or basically walking around. Yes, the key word there is new and unsteady gate which indicates a taxia or that difficulty walking. Option two is also correct. The appearance of a new rash on the patient's chest. Yes, any type of new rash. The key word is we need to report this because it could be the deadly Steven Johnson syndrome. Now, option three, report feelings of hopelessness and apathetic. Yes, these are big risks for suicidal risk. And the last two options are also correct here. A morning fentinto level of 26 is technically toxic. Remember the range is between 10 and maximum of 20. And lastly, difficulty forming words or sentences. Yes, fenny toxic means fenny talking. So having difficulty forming words or sentences or even slurred speech. This is an early sign of toxicity. Now the next question here, the health care provider has prescribed four milligrams of cetaoline to be administered IV push during a rapid sequence inhabation. Which is the nurse's priority action when preparing to administer this medication? All right, that was a big question. So let's break this down. The question's asking for priority action when giving citacoline. So since this question's asking for a priority action, we always have to think what kills the patient first. So before looking at the options, we're just thinking loss of life as well as loss of limb. So we know that cetylcholine what kills the fastest is malignant hyperothermia. So we have to screen for those three criteria. a prior reaction to general anesthesia, blood relatives with significant reaction to that general anesthesia, as well as alcoholics as mentioned by the Hessie. So, option number one is incorrect. Check the patient's core body temperature. Guys, that's not the main priority here. Now, option two is correct. Ask the patient about a history of alcohol abuse. Yes, we always screen for alcoholism. The key is to anticipate the deadly malignant hyperothermia. Now, option three was a little bit tricky. Prepare a dose of mazzylam as prescribed for sedation. Now, this one's really close as a distractor. So, yes, we do give benzo for sedation, but it does not come before screening for those deadly adverse effects. And option number four, also incorrect. Ensuring a non-rebreather mask is at the bedside prior to administration. So oxygen is not the biggest priority here when we're faced with deadly adverse effects. Now the last question here, which instructions should the nurse include in the plan of care for a patient newly prescribed carbodopa and leave a for the treatment of Parkinson disease? Select all that apply. Okay, let's break this down. The questions asking for the plan of care for the key term newly prescribed carbodopa and leodopa. So before looking at the options, we're thinking a few things that we know about this drug. So number one, leave a we have to leave the protein since it decreases the absorption of this drug. And two, leave a leaves more dopamine inside the brain. So the side note is any drug that acts on the neurotransmitters, the dopamine inside the brain typically affects balance and typically takes a long time to kick in. So now let's look at the options here. Option number one, if you don't notice improvements in your symptoms within one week, notify the provider. This is big time incorrect. Any drug that acts on the brain usually takes a few weeks. So specifically leodopa takes about 2 to 6 weeks to kick in typically any neurotransmitter guys. So put that in your back pocket for the anti-depressant section. Now option two when going from sitting to standing position be sure to change your position slowly. Yes, again typically any brain drugs affecting balance we have to do slow position changes. And option three, it's a good idea to remove any clutter from your home that could cause you to trip and fall. Well, of course. So, yes, it's correct. Preventing falls with Parkinson's, that unsteady gate, and those shuffling feet. And option number four, call your provider if you notice your urine change to a slightly reddish color. This was pretty tricky, but no, it's incorrect. Colored urine is normal. And lastly, option number five. We avoid eating meals that contain large amounts of protein while taking this medication. Yes, this is correct. Leave Adopa. You leave those high protein meals. Thanks for watching. Did you know you can unlock beautifully handcrafted study guides packed with key points and memory tricks from all our videos? Plus, you'll get access to over 1,200 exclusive videos not on YouTube, all neatly organized by nursing school topic to make that complex nursing knowledge actually stick. You'll also gain thousands of practice questions written by current professors and actual ENLEX writers. So, for access to all this and more, click right up here or visit simple nursing.com. And don't forget to subscribe to our YouTube channel. Happy studying and we'll see you in the next videos.