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Data Interpretation & Drug Monitoring - Dr Hong

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Summary

This on-demand teaching session is relevant to medical professionals and is designed to help with learning how to interpret blood test results and act on them. Attendees will learn the major blood tests and how to recognize when a number is off. Attendees will also learn how to recognize infections, anemia, GI bleeds, electrolyte abnormalities and other common issues seen in medical practice. Through engaging real-world scenarios, attendees will gain valuable insight into data interpretation and drug monitoring.

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Description

Welcome to the eleventh of 12 sessions prepared by AMSA England for the Prescribing Safety Assessment 2022-23. This course will be covering difficult topics and exam techniques on how to best prepare yourselves for the PSA exam.

This session will be hosted by Dr Sa-Bin Hong, who will be covering data interpretation, what to look out for, and how to avoid losing easy marks when answering these questions.

Then in the second half, Dr Sa-Bin Hong will be covering drug monitoring questions, the common question topics, and what level of monitoring is adequate for the different scenarios.

Learning objectives

  1. Understand how a full blood count is used to identify signs of infection.
  2. Recognize abnormal white cell counts and the likely cause in various scenarios.
  3. Describe the mechanisms of how various types of anemia arise.
  4. Demonstrate knowledge of electrolyte imbalances, paying particular attention to sodium levels.
  5. Identify the indications for additional blood tests and interpret the results in order to diagnose and treat patient conditions.
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

right. Can everyone hear me? I can. I'll just appreciate a great leave. You can just stay in the chat. You can see. I want to see, uh, the camera is off. That's because, uh, I don't really have that much of a staple into the connection and environment. Um, yeah. I'll try to speak a little bit louder. Can you guys see the slides? Anyone see the slides? Mhm. Let me see. Okay. Is this any better? The sand wise, uh, just re uploaded the slides. Um, Okay, now you guys can see right, So let's get started. Um, thanks for joining us. Uh, bright and early morning on a Saturday morning. Um, yeah. Sorry about that. Sorry about the background noise. Just in a cafe at the moment. So Right. So, yeah, My name is Salome Hong. I'm, uh, Foundation. You're one trainee currently in east of England, and I'll be going through data interpretation and, uh, drug monitoring after after this month. Okay, so just a bit of an overview. So I think the structure for the talk today will focus on the major blood tests you'll be ordering as an f I one or any sort of, um, clerking doctors and patient coming in through the through the door or routine blood tests that will, um, be asking for us and patient's and how to interpret those results. And, um, and how to act on it. Um uh, critical. Uh um, So you guys are all final years, so I wouldn't argue with exact numbers. I think recognizing which number is off, Um, when you're given with a series of blood test results is the easy part. Um, you will be given reference ranges. And if it's not sort of, um, written in the question itself, there's always a tap on your of the right hand corner that you can open up. And that should give you all the reference ranges for pretty much all the tests that you can. Um, imagine so things like phobia can use the knees elope. TFC. So we'll be there. Um, a B G values, um, as well. Um, so I won't be sort of going into detail, uh, or giving you a long list of numbers that just repeat of our time. Okay, So just to start off with So, um, one of the first things that literally all the person is coming through the door will be, uh, full blood counts. And one of the things first things that we noticed the white cell count. So highway Selcan quite obviously sign an infection, although it can be can falsely raised in quite a few different scenarios. So all the common causes are raised. One cell can without infections, background of the, uh, patient's on, uh, or on steroids. So if you check your drug history and they're taking prep listener, then you would expect the white cell to be a little bit under rates sides. So, um, see, if the patient's taking long term steroids, especially high dose steroids, then I wouldn't be too learned about what's account of 12. Now, if the same patient presented with a white cell count of 24 that's a different story. But as a general rule of thumb, high white cell count is a, uh, infectious marker and, um, patient's presenting with high well sell college as well as, um, rates crps and uh, and you go examine the patient. They're unwell. Federal, You know they're dropping their BP. They're not producing any urine. Then the first thing that should be on your mind is is this patient septic? So, um, usually you get a breakdown of white cell counts. So what? Two things that you would need to look at on a day to day basis as well for the purposes of PS exact is neutrophil accounts. So if you have a raised neutrophil count that shows this most likely a material infection, um, viral infections can cause both high left side count and lower lip side cancer. It's not as useful when getting like a snapshot picture of the patient. So, um, usually most of the questions will test you on how whether you can identify high white account on the basis of a neutrophilia uh, now low ones accounts, especially looking at neutrophils should ring some alarm bells for a minute strictly. Um, and I put in a question, um, next flight. So I think I'll explain. So So a 68 year old male, um, as a background of bowel cancer with distant minutes presents to e. D. Acutely unwell with fever, vomiting, your general dates. He completed his first course of chemotherapy last week, and on the examination, the patient's tech kidney cardia and, uh, now you take some bloods and white cells are very low at 1.4 with a neutrophil count of 0.1. So he practically has no neutrophil count. What should he do? I'll give you going a couple of minutes to think about. Uh, yeah. Okay. Okay. I feel free to to pop your answers on the chat, go through them to get there anything. Good night. So one person says I be Taz. Oh, my God. Okay, excellent. So it looks like you guys will be safe f once. So? So, if you're suspecting what What are you suspecting this case? So someone who has completed their course of chemotherapy comes in with really new know neutral fields with systemic symptoms. Um, the first thing on your mind should be a neutropenia. Sepsis. Now, it'll be good to have an awareness of other drugs that can cause neutropenic sepsis. Methotrexate is one drug that p s a loves to test you guys on, so make sure you know, um what? How? Um, methotrexate can cause neutropenic, sepsis and other side effect profiles like it's a fully antagonist, so you can cause low folic levels as well. But going back to this patient. So especially for chemotherapy patient's if they present with neutropenia and septic picture. Um, one thing they should never, ever do is wait for, um, even a blood count. Um, just don't wait for anything. If you're suspecting sepsis, start them on broad spectrum and politics. So, um, usually check with your trust guidelines. But in my trust, it is IV taxing. For apply Q. D s um, aggressive flu resuscitation could be, um, another answer. But the most appropriate answer in this case would be IV tassan because there's no mentioned about the patient being hypertensive. So that is not the most Well, it will be done as part of your sepsis. Six. But it is not the most common sensitive, um, objective that is need to that will need to be reached. Okay, so that's that moving on to your the rest of your full of accounts. So, um, on the day debate basis, the couple of things that you should definitely look at is the pages HB. And once you have an idea of what's going on with your HB, especially if they're anemic, you look at their MCV to get a better idea of what's going on to say. I always found this little bit difficult in terms of iron deficiency anemia. So iron deficiency can cause both macro microcytic and normocytic anemia. So think about it. This way, though. The mechanism how you get iron deficiency anemia is that, um, with say, for instance, would prolong bleed like an upper giant lead. You have a constant laws of, uh, hemoglobin, and the body is having to constantly reproduce that hemoglobin using, uh, using up your, um, iron, uh, storage inside the body. So eventually, the body runs low on those those iron so which can be protected by ferritin levels. And then you get microtechnique me A. Because the body just doesn't have, you know, um, iron to make proper red blood cells so they end up making smaller ones. Now, in the case of an acute blood loss, so say, if someone came and stabbed me in the back right now and it started losing a lot of blood, um, the body doesn't have time to react to that with increased urethra praecis, so the body doesn't even have time to use up the iron storage. So in that case, you just get a dilution of, uh, of hemoglobin. Especially if the patient has, um, just received aggressive fluids of station in the e d. Um, other things to be aware of. So in case a macrocytic and email the most common things that you would look at our things like following and B 12 deficiency, especially if they're on drugs that, um, antagonize full late. So things like methotrexate like mentioned. So if you have a patient presenting with macrocytic anemia, um, and they're taking methotrexate, then stopping methotrexate, if it is tolerated, could be an option. So another thing that you would need to look at is the LFTs. So can anyone tell me why LFTs would be relevant? Especially, um, in a patient with Microsoft anemia? What would you be most interested in? Um, looking at LFTs? Uh, sorry. Um uh, please. Using these. Hola, uh, relevant. Uh, anyone? Any guesses? Yeah. Okay, um, I'll just move on. So, in terms of using these, um, if you look at the rock wall criteria for, uh, a GI bleed, One of the key component is a raised Yuri account. So when you have, um, blood, that is being digested through your digestive tract. Um, you got to raise your ear. So if you have a patient presenting with microcytic anemia with iron deficiency and you do use an ease, their kidneys are fine at the moment. But you have an isolated raised urea. Then that would sort of, um, strengthen your your differential, Um, your top differential being, uh, upper GI bleed. And that would be you would need to consider an order in, uh urgent o g d to identify and clip the bleeding. Okay, right. Use Annie's, um, so if you order using these so you get a wide variety of things, So you start with Sarah. Seldom levels passing levels. You get your your area, you get your crept in, and then the system will automatically calculate the egfr for you. Um, and that's really the gist of using these. Um, sometimes they add on additional things like these false paper. It's not really regularly tested. So starting with the two main electrolytes that we're interested in, so high sodium, high sodium count, um, and low sodium counts can cause it can be caused by different things. I'll start with the low sodium so low sodium. When someone presents with low sodium, you go and assess their fluid status. So if they're fluid overloaded or or the IV Olynyk port there hyperkalemic Okay, yes. So, firstly, it's not automatically on the use and ease. It is added on, and usually it is part of bone profile rather than you, um, use the knees. So another thing that you would need to look at when you have a patient with low serum sodium is, um uh, urine, osmolality ceremonies, morality and, uh, urine sodium count. So if you have someone with low sodium and then urine osmolality is high with a high sodium count, then you're you know, where a patient, including the sodium, sodium. So you look at their, um, egfr look at their renal function and think about more of a renal cause of losing the sodium. They're euvolemic um, the top cause will be s I e. H. So, um, you go down your top differential of things that can cause s I d SIADH. And if they're hyperbole, make that becomes a little bit, um, complicated because ideally, the management for low sodium is giving them more sodium, obviously. But you cannot really give them aggressive fluids. Um, because they're already hyperbole. Nick's. So, um, if there if they have low sodium. But if their food overloaded, then this is something that you need to ask your senior about. And, um, they'll need to be started on the hypertonic saline, but at a very slow rate. So I've covered sodium um, in my previous lectures, Um, how to replace the sodium in different cases. But one big rule of thumb for both sodium and potassium is that you're never supposed to correct them rapidly. So take your time with correcting the sodium and correcting the potassium. And, uh, if you do it rapidly in case of sodium, you have the risk of central point, uh, my appliances or cerebral edema, so just bear those in mind. So if you if you come across any question that says rapid infusion, I've hypertonic saline or rapid infusion of kcl, you automatically No, that's not the correct answer on the P S. A. Uh right so high potassium count is usually caused by things like, uh, sparring the left hand. So your potassium sparing direct IX, um, alongside with multiple other things. Quite a few different causes, but sort of on the wards in patient's and, um, a acute setting. So, uh, no. Um, so quantum myelin mildly. And the little nice is, and cerebral edema are not the same thing. So CPM it cause when you have, uh, low sodium county corrected too quickly and sort of big dimas the high sodium and then give them too much fluids. And then you get, um, hypotonic, um, sort of fluid because you already have a high sodium count. So rushing into the body and then you get a pulling of the fluid inside the inside the brain so you end up with cerebral email. Okay, uh, high potassiums who give things like calcium gluconate. Um, insulin. Um, I think there are some newer drugs that are being discussed. Um, but they're not in the guidelines yet, but each sort of treatment option comes with different risk factors. So I think in terms of high potassium, especially with E. C g. Changes, um, the safest thing to do with start them on dextrose, um, and insulin so that you know, you don't have a crazy high blood would coast and then, um, sell beautiful nips and then call for senior support. Um, low potassium, on the other hand, has entirely those dependents. So, um, just a mildly low potassium can be corrected with oral, huh? Sorry. Potassium. So sand. Okay, Um, one thing that I've noticed about students, um, and like, well, I'm like myself, and I was sort of learning about sand. Okay, Was that you know, if you're adding potassium to patient, so you could You're thinking about all those scary side effects, like, um, arrhythmias and And, um, you think you'll be quite, you know, risky for driving sand. Okay. Without senior guidance. But if you think about if you can if you look at the amount of potassium, actually including the sand. Okay, it's basically giving a patient a banana. So, um, I mean, I guess bananas taste a little bit better than sand. Okay, But, um, my point being is that sand okay is quite safe to give is unless you're like giving them a crazy amount. So just go with the the sand. Okay, The amount. That is the dosage that is recommended on the B n f or the trust guidelines. And it really shouldn't cause any issues um, other ways of dealing with low potassium We can discuss in the next question. So here we go. So you have a 62 year old gentleman. He has me an inpatient for decomp decompensated. Um, congestive cardiac failure on the cardiology ward. He has been started on high dose furosemide confusion. So if you think back to your pre clinical times frozen mind, it shuts down your triple. Um, transporters in the distal, convoluted tubule. So what it does, it'll chuck out pretty much all the electrolytes. But what you're most worried about is potassium in this case. And lo and behold, um, use unease that shows that he does have a little potassium. Say feel free. Um, to look up the potassium reference ranges you would do in the in the normal exam. And tell me what? How you would manage this patient. So options being you would stop the frozen might, which I guess we'll take care of the potassium issue. Um, rapid kcl infusion. Prescribe sand. Okay, check stool charts and vomiting because they're spirinolactone. Give them a bolus of 500 mils of part mints, or just leave them be. I'll give you another 33 minutes if you think about it and feel free to pop your answers. All right. Any takers? So, uh uh. Okay. Okay. You have one person saying, see one person saying be okay, Right. So I'm glad nobody went for stopping frozen mide. Um, your cardiology colleagues would hate you if you start stopping frozen wide for using these, um, deranged using these? Um, um, yeah, that's why there are fights between nephrologists and cardiologists. So there was a really funny incident that I'll share with you later on in the second half. Electric. So you don't stop the furosemide Because this patient has, um, decompensated ccf, Meaning he has his vastly fluid overloaded with fluids, um, in the leg, in the legs and more importantly, in the lungs. So stopping frozen might in this case, can cause something called a flash pulmonary edema. So that's when you're entirely, um pretty much fills up with edematous fluid, and you can get acute desaturation of the patient. Um, you get crazy. Um, often saturations like 70%. 60%. And it happens quite quickly. That's why it's called a flash Pulmonary edema. So stopping froze more in this case would not be an option. Um, rapid kcl infusion. Um so remember, potassium IV potassium is never ever ever given rapidly should given. Give it very slowly at a low, quite a diluted. Um, dosage. Um, the correct answer here is see, so you prescribe some standard K. So you first look at potassium 2.9. So it the reference range the lower end of reference range is dependent, dependent on the trust, Um, in our trust of 3.3. So it's not a massive decline, and there's no mention that patient is having any symptoms or no e c g changes. So just giving him some sand. Okay, it's fine. Um, the reason why you want to check for stool chart or vomiting is, uh, if the patient is losing potassium through vomiting or through diarrhea, then that's another issue that we need to investigate and deal with, um, spirit of lacto OK for potassium. Okay, So spironolactone is, uh, potassium sparing diuretic so it doesn't cause the patient po or the potassium, so it can actually be used to increase the serum potassium level and patient's with the potassium polos of farm under heart mints can technically be a right answer because it does have some, um, pass him in it. But, um, Hartman has been sort of kind treated so that it would meet the electrolyte requirement for a normal, healthy human being. Um, not undergoing any any procedures, not having any additional insult such as this in this case, Frozen might. So while it would sort of top part potassium a little bit, it wouldn't really change much in terms of this patient, because this patient is on the high dose froze mind infusion and a tiny bit of potassium given the heart mints would be peed out for the next few hours and no action required. In this case, it's just unsafe. Thanks very much. Right? OK, renal function. So one key thing to keep in mind is that AKI, by definition, is defined by sarin. Creston. So, um, so I can't remember the exact figure off the top of my head, but it's an acute incline of more than 25 million miles per liter, or more than 1.5 from the patient's baseline. So you can't really say the patient has AKI based off of one using these results. You need to know the patient's background because a lot of the patient's especially elderly ones, they'll have chronic kidney disease and their baseline kidney function will depend on the individual. So if their baseline, um se e egfr was 40 and it goes down to 35 you wouldn't consider that an AKI. You just say, Oh, if he has CKD has gotten just a bit worse Now if a young and fit person like you guys usually would have would expect to have an egfr of over 90. And now if you came into E d and then you were found to have an egfr. 40 then that's a big A key I and that would need to be investigated. So again, egfr is a dynamic figure. Um, if you in case of, say, pre Reno, um uh, a k I if you give them decent amount of fluids and increase the increase the profusion of the kidneys, then you can see sort of like a transient increase of Egypt for following that which is sometimes used to, uh when you need an urgent CT scan with contrast. And you know you're worried about contrast, um induced uh, nephrotoxicity um we sometimes give them a little bit more aggressive fluids to talk them up and then get their Egypt for up so that they can tolerate the contrast. Little bit better. Can we calculate the baseline creatinine? Um, so correction in can be influenced by a lot of different factors. Um, so if the patient is quite big and muscular, they're they're expected to, you know, have a high baseline cracks in If you know, even if a normal dude, um, you know, it doesn't really work out, Usually suddenly decides to go to the gym, you know, lift the weight. You would expect a increased creatinine, so it's really difficult to calculate the baseline creatinine. Um, I think if you're talking about creatinine clearance, that's a different issue. So, um, if you go into mg kelt, that's a really useful calculator to, um, to calculate creatinine clearance clearance. So you put in their serum creatinine levels, their body weight, their gender and then spits out their creatinine clearance, uh, which you would need to know for certain medication. So, um, things like, say, prospector and geopolitics, Um, things like meropenem. Um, you would need to adjust their dosage depending on their craft in clearance. So if they're the renal function is so poor. Say, if the creatinine clearance comes back at 17, instead of giving it giving the normal dose eight hours give half does 12 hourly. So that kind of thing. Okay, so one another thing that you need to know about, um, you Erian Kratt in, in, in, in terms of renal function is that three renal causes of a K. I tend to cause a rise in your area, predominantly, whereas most of the other things like post renal and intrinsic causes Well, you're looking at creating your eyes predominantly. Now, this is a rule of thumb. It doesn't really always work this way. But, um, it's something that you could keep on your mind when you're examining a patient or you're seeing a patient trying to determine what's the cause of the E. K. I obviously you need to use this in conjunction with the clinical picture and the history. Yeah, Okay, so let's check if you guys have been paying attention. So 79 year old gentleman presents to the e. D. With epigastric pain. Uh, has been ongoing for five days. Uh, blood test show microcytic anemia. So low HB with low MCV with raise your re account. He is a known boozer. Give you guys a couple of minutes. What's your top differential for? This gentleman should be quite straightforward. So give you guys just a couple minutes and then we'll crack on. So please put your answers in. Okay, So one person thought this is a is a facial bleed secondary to cirrhosis. I'll accept the answer. But, um, it's quite interesting how you went straight to cirrhosis. Um, it could be caused by cirrhosis. So, um, just to add on to that So any liver pathology's or trans cirrhosis or HCC in your case would lead to, uh, portal systemic hypertension. So you get various is, um, appearing sort of around the body. So one thing's think things like anal varices or, in this case, it's a facial. Various is, and these can tear quite easily, and you end up with the opportunity bleed and things to look out for or microcytic anemia. Ray Syria, As I explained, because HB, when it gets digested, turns into urea because a high urea count another common sign, uh, symptom that you need to look out for is Molina So black tarry stool really smelly. Um, if you come across it once, You know what Molina is, um will be quite difficult to forget what Molina smells like. And but in this case, it doesn't necessarily have to be cirrhosis. So if this patient somehow magically had normal, um, LFTs, then I wouldn't sort of, uh, upper gi believe would still be on my top differential, because, um, upper GI bleeds can be caused by many different things. For instance, what do people do when they drink a lot of alcohol? Uh, when they have a hangover, next morning, they vomit, and you keep on vomiting. And, uh, you get Mallory Weiss tears. So that's another way. Another, more straightforward way of getting an upper GI bleed due to E T O h. Access. All right, um, I think we're about halfway through. So if anyone has any questions so far, just feel free to pop it in the chat. I'll give you guys one minute and then Okay. Uh oh. Sorry. So, um, upper joint lead. Um, so it depends on how bad the anemia is. Obviously, the patient is me Nick, you think about transfusion? So different trusts have different guidelines. So for our trust is, um, under 70 if they're symptomatic and, uh, above 80 if they have a c s so transfuse, um, you'd want to resuscitate them if they require resuscitation and urgent, urgent o g d referral, um, to identify the cause of the bleed and ideally, stop the bleed using O g D. Um, things like Charlie press in or something called the sun stock and black and took a break. And more true, can you use so SP to is basically a really thick N g tube that you shut down the nose because all the way down the esophagus and then it's sort you can blow it up inside. It's like a balloon and compresses against the esophageal wall, essentially sort of providing him oh, Stasis. But these are all interim measures, and the ultimate management would be an urgent o t. G. All right, Right. So next question, um, this is actually a real life scenario that I've seen on the wards, um, a little bit, um, different kind of scenario for from because I I didn't really mention about vancomycin and um, how to monitor that? So, which I will I will be going into more detail about maximizing gente my zing that my next part of the lecture. But I thought it would be quite useful to have this question in here. So 72 year old female admitted with orbital fractures and facial cellulitis around the area has been commenced on IV vancomycin as per trust trust guidelines. Now, um, there was a prescription error. Um, and the patient was given an obscenely high dose of IV vancomycin. Uh, trough level taken just before the next dose comes back at 51.3. So have a search. Um, either on TNF. So I'll suggest the B n f. Because you won't have access to the regular internet during the exam. So have a look on DNF. Look at the trough level guidelines the normal range. And think about what would you do in this case? In terms of in All right, any takers have given you some extra time because I understand that you guys need to read through the b n f entries, and, you know, figure out what's the trough level target. Okay. Oh, okay. Right OK, so in the interest of time, so crack on so trough level um, reference range for vancomycin is usually 10 to 15. Um, for sort of normal usage in terms of severe infections is 15 to 20 so you can see that a trough 50 51.3 is very high, and it's definitely can cause toxicity. So with maximizing what you're worried about is, um, net for toxicity. So you need to monitor their use any so dearly. Use these for the next week or so. Um, and another thing with vancomycin and gentamicin to, uh so bank agenda, um, they both cause audio toxicity. So, um, one thing is you need to check for their hearing. So if there are any changes in their sense of hearing, um, and if you do on sort of like bets are examination, then you refer them on to audiology testing. Another thing is you want to check the patient's gait. So there there's any additional state instability, instability if Joe Romberg's test, you know, heel to toe tandem, walking all the whole um, state assessment and sort of fact. Find out if there are any problems with the balance Um, thankfully, in this case, um, she didn't have any, uh, used any changes. Her egfr was completely fine. Um, she didn't have any changes in her sense of hearing, but she was a little bit more unstable. So she was referred on for neurological testing. Um, yeah, and she was transferred to a different world. So I don't know what's happened to her. I hope she's alright. And most importantly, in this case, um, not so much relevant for your P s s. But once you start working is your duty of candor. So it doesn't matter if you're the one prescribed the vancomycin. Um, um, so they would need to be seen by neurology consultant. And they'll, um they'll probably decide what to do on words. Sorry, I don't have a better answer than that. Uh oh, yes, obviously, yes. So start the vancomycin. If it hasn't been stopped already. Yes. And, uh, as I was saying, um, you do have a duty of candor. So, um, it doesn't matter if you were the one who prescribed it. You go to the patient, tell them what happened, apologize. And if they so wish to do so, then you give them directions to Police Department, right? Another question. So 66 year old meal with a background of essential hypertension is brought in by ambulance following up fall and long life. So another sort of real life tips. So when a patient comes around or four think about the potential causes of the false, so it could be orthostatic. It could be cardiogenic. So, um, if it's cardiogenic you're thinking about maybe, um, you know, take stenosis or heart failure with reduced ejection fraction, you know, lead to a very poor profusion. It could sometimes be steps is related, or it could be mechanical fall. So sometimes just tripping over stuff. Um, it could be neurological and yeah, so just try to think of, uh, sort of system systematic way of going through the causes of falls because you'll be seeing a lot of full patient's once you start working on that. So, yeah, brought in by ambulance following a full and long line. So the patient has been underground for a long time, so that that tells you a couple of things. Um, one thing is, you don't know when the patient has suffered the fall. Um, and Nobody was there to watch the fall. And the patient didn't regain consciousness right after fall. Right? So the patient is confused with bruise marks, alongs, flank and thigh. On examination, the patient is normal. Pensive doesn't have any focal neurology. And there are no signs of fractures. Blood results show of creating high knees level of 5000. That is very high. She takes amlodipine and atorvastatin. Amlodipine dose has been increased five days prior to mission by his G P. What would be the most appropriate? Um, of course of Axion for this patient, give it another couple of minutes and then throw through the answers together. All right. Um, what do you guys think? Uh huh. Okay, yes. So I think from the picture here is quite clear that, you know, the patient has had a, uh right. Okay, So the patient has had rhabdomyolysis as a result of long life. So would you do A B, C and D? Are you talking about a B, C D u? Or, like, the answer choices here? Okay, so let's look at answer choices. Um, so I the flu for this, um, I wouldn't really do much good in this case because the patient is already normotensive. Um, so you could consider, uh, eight hourly IV fluid. So the reason why I wouldn't do an IV fluid boulders Because, um, you don't know how the kidneys are reacting to wrap the minuses, Remember, Wrapped oh can cause AKI as well. And with the CK level of 5000, there's a very high risk of this patient developing ai. So giving this patient of fluid boulders Um, yeah, maybe 250 or 500 would be okay, but there is a chance that you might flu related patient and worse in the e k I. So, yes, eight hourly IV fluids could be a an answer. But the most appropriate answer in this case is see So, yes, you would give eight hourly i fluids because you want to get rid of that, um, creating clinics in the in the systems, but more urgent. Uh, thing to do is stopping the tour a statin because remember, atorvastatin can cause rhabdomyolysis as well, and with a patient that has already sort of suffered rhabdomyolysis and recovering from it. If you keep giving them towards statin, you can make it worse and eventually keep them. Um, AKI, even if they weren't in a K I previously, um, so the next part of C is timeframe loaded pain following an ls bp. So, um so I know in this case, it says the patient is more intensive, but you need to see for orthostatic drop. And that is unfortunately, um, orthostatic job is one of the side effects of most, um, anti hypertensive drug drugs. So if you do have a positive job over the static drop of more than 25 millimeters of, um, h g um, in the systolic BP, then you titrate, uh, your antihypertensive. Now, if the patient is cannot be titrated due to other issues say the patient's sort of resting BP is too high or, you know, the patient is not an anti hypertensives, and you still get a longstanding BP. Then you think you're not. You need to think things start thinking about more about neurological causes. Um, so things that affect your sympathetic nervous system. And in a lot of these cases, um, the patient can be started on this drug called Mid drawing, which increases your sympathetic drive and sort of allows your body to phase a constrict when you move from a sitting or lying position to a standing position and allow you to retain that BP and hopefully prevent you from passing out. And yeah, you would observe overnight. But obviously you need to deal with CK of 5001st if you just submit them and observe. Um, that's pretty much medical insurgence and same thing with discharge home with safety 19 vice, right? So I'll quickly go through LFTs. So if you have a one off race, Billy, Ruben and A S T or a L T is normal that that that tells you there's probably nothing wrong with with liver. Now it is. LFTs are kind of a funny thing, so you can have sort of list of answers. So, you know, if the Billy Ruben is raised is probably this and then, like if conjugated bilirubin is raised, it's probably that, but it is. What did you do? L. Sbp to check for orthostatic job. So in the last question, eight hourly food is also a right answer. But the most appropriate answer is the third option because you're you're thinking of any patient on anti hypertensive that comes in with a full. Um, you do a line and standing BP because all antihypertensives can cause orthostatic job. So that is one of the most likely reason for the whole in the great place. Okay, looks right. So going back to LFTs? Yeah. So it's a bit of a gray area, and obviously, if you're in doubt, it's always good to, um, ask your senior, um, after help from the gastrology team. Yeah, so going back to the slide. So sort of like an isolated race bilirubin. It can be hemolysis. So if you think back to your pre clinical times again when you have, um, you have red blood cells that circulate around it gets broken down in the sling. Once it has reached the 120 days of its lifespan and then one is broken down. It is conjugated to it has changed. Uh, it is excreted as, um as Billy Ruben. So if you have more, um, breakdown, the red blood cells happening, you get raised, Billy Ruben, and you can also get splenomegaly. And once you have those two, then you get John Doe's quite a picture and Yes. A patient with, um low HB, um, in large spleen and the race Bolivar bid with normal otherwise normal LFTs. Then you're most likely think about small icis. Now, if you have changes in the S d l t s the transaminases then, um, you know that there's something going on. Deliver itself. Now you get you Look at the S D l P L T ratio. If a s t is high, Um, that is most likely alcoholic related. If the a L t is high, then it's most likely borrow. But this is more of a rule of thumb. It doesn't always work this way, but it is something to guide your, um, sort of list of differentials when you do come across a patient with grace deliver been and, uh, the range of FTS. Okay, so post a partic, um, is quite an interesting one. So AOP is a very, very nonspecific, um, biomarkers. So it can be raised in bone disease. It can be raised in, um, issues with with with your biliary tree. So in terms of yes, so a S T will be high compared to a l T. But it's not like a definite tive diagnosis. You need to take a full history. Most importantly, yeah. So going back to, um, posthepatic obstructive causes. Um, so a L P is usually raised in terms. Um, in the context of LFTs, that usually means there's something wrong with the bile duct. So it could be an intrahepatic duct. Or it could be extra patrick duct, um, any sort of, uh, pathology. And within the biliary tree, all the way leading up to the sphincter of oddi that were connects to the rest of the the digestive tract can cause a raised, uh, L t L P Sorry. Another, um lft biomarker that looks at your biliary pathology is your gamma GT. So like I mentioned, AARP is quite unspecific. So it is always nice to look at look at it together with your gamma GT. And if you have raised AOP as well as the rays Gamma GT that it tells you pretty much that it is an extra pathetic posthepatic sort of obstructive kind of picture. Um, so some causes of obstructive picture can can be things like stones. Um, so cholangiocarcinoma you don't really see very often this country. Um, it is usually caused by, um, PSC. Um but it is quite rare. Um, but it is more sort of like an endemic in the Southeast Asian Southeast Asian regions because of the liver flutes that live in the area and consumed actively by the local population. And another thing that you need to think about is, um, head of the pancreas tumor. So those things can grow and compress on the on the biliary tree. So if you think about the anatomy, um, so your your bile does come out from liver, your cystic duct joins up, and then it sort of wraps around the head of the pancreas before draining into this victor OD into your duodenum. So if you have a tumor on the got to head, then as it grows, it will sort of it's very easy for it to, um, uh, sort of put some pressure on your bile ducts and cause obstructive kind of picture. If you're still unsure with AARP and Gamma GT, Um, one thing you could do is ask for a split the bilirubin, so don't ask for it. Your bilirubin will be recorded as a total bilirubin. Now, if you ask for a spill. It bilirubin. You get a breakdown of that bill? A revenge showing conjugated uncomplicated. So if you think about it logically, um, if you have pre op a tick or intrahepatic issues, um, that's meddling either with the amount of bilirubin produced in the first place. Or, um, in the case of Enterp a tick, um, you have, um, you have an issue with the liver's ability to congregate the bilirubin, so you would expect a rise in unconjugated bilirubin. But in the case, post Patek causes, um, the bilirubin has already gone past the liver metabolism. So most of the vial and there would be conjugated. So that is another way of differentiating between different causes of your, uh, lft arrangement. So it's just a little okay, so quite an interesting question. So 46 year old male otherwise fit and well presents to e. D with jaundice after drinking quite heavily last night. So another real life tip, um, be very, very precise and accurate when you take alcoholic history. Um, you know, if the patient might tell you Oh, I just drink casually on the weekends. Nothing too crazy. That can mean something. Very different to you. And, you know, from what the patient actually intends, Like a bottle of vodka on a Sunday might be a casual drink for the patient, whereas obviously for, you know, people for normal people, that would be considered quite excessive. So don't just write it off as social drinking, minimal drinking. Be quite specific, Um, and actually understand. Oh, how many units are they taking in a typical week, Right. So this chap, otherwise been healthy, Had some heavy drinks last night, suddenly becomes jaundiced, Doesn't have any fevers. He's completely stable, Doesn't have any work organomegaly. And the only thing that's raised is total. Bolivar been, I'll give you going three minutes for this one because it's something that, if you know about this condition, that you'll get it right quite easily. You don't have to do some searching, so I'll give you some time. All right. Any ideas? People? He says things. One person thinking, so I'll call the hepatitis. Okay, fair enough. Okay. I'll just give you guys the answer before I give you guys the answer. Any French speakers here, OK, doesn't seem like there are any French speakers. So, um, this patient most likely has a condition called Gilbert or the as a French called It's A It's a French physician. So is Gilbert. But like, yeah, so it's a it's a genetic condition. Um, uh, that causes a deficiency of, uh, enzyme called u D P G T. That converts your, um uh your bilirubin, um, has a role in Congregation of bilirubin. So when you do have, um, Gilbert, Um and you have low u u D p g t levels. Um, the liver is just very bad at metabolizing bilirubin. And you get a high level bilirubin, um, with no other uh, arrangements in your LFTs. So it is quite common for these patient's to be completely fit and well, and then they go out for a drink or any sort of even minor, um, hepatic insult with cause, uh, jaundice. So John doesn't itself is quite harmless. It wouldn't really cause any any sort of long term issues unless you get really, really crazy high levels of bilirubin where you're worried about connectors and sort of like your logical, um, issues. But most patient's with you there will live on their life just knowing that they have Joubert's and they will go. Biello. They have a drink or two. Um, they'll be a voice not to drink so much because obviously their ability to metabolize um, the alcohol is much impaired compared to normal people, but in this case, there's nothing to worry about. Um, in terms of managing his patient, um, just maybe some fluids if they require, um encourage oral intake and, um, even discharge with safety netting. And, um maybe arrange for outpatient, um, genetic testing to see, um, if he actually has the genes for Gilbert's. So, uh, all right, I'll in the interest of tile just briefly touch on the TFTs. Uh, for Gilbert. So it is u D P g t is, um, has involved is it? It is involved in the congregation of liver. Been. So it'll be unconjugated bilirubin that's raised Yes, right. So TFT So, um, patient on levothyroxine, um, you if they come in with symptoms, um, either hyper or hypo thyroid thyroidism. Then you do a TFT, especially looking at the TSH. So think about it This way is TSH is thyroid stimulating hormone. So if the TSH flow basically your brain is telling the patient's brain is telling the thyroid. Dude, you're working too hard. Chill out. So that happens when you have too much. 3334 Circulating the in the system. So when you have a very low TSH of saying 0.4 then you know we've over titrated with the new thyroxin now on the other side, you have raised TSH. Then the brain is basically finding thyroid's. Hey, you're slacking. You do possible for some weight. So in this case, you will need to apply Treat the the virus and Kirby muscle, um, as a number of different, uh, side effect profiles, namely things like neutropenic sepsis and a gra Newell cytosis. Um, but in terms of this lecture, um, just bear in mind there are two ways of using carbimazole so it can be too concentrated in terms of like parathyroidism. It can be used to sort of regulate the level of thyroxine and the blood. Or you could sort of give a much larger dose of carbimazole completely block out your patient's sort of intrinsic thyroxin produced production and replace that with medication levothyroxine. Uh, I can't and some brief, um, things about a BGs. So if you get If you're getting confused about metabolic and respiratory alkalosis, um, acidosis. Just think about it this way. Um, carbon dioxide Okay, so blocked and replace so personally presents with hypothyroidism. So there are two ways you can use carbimazole to sort of limit how much dioxin is being produced by the patient's thyroid glands. That's one way another way is you give them a very large those carbimazole. They'll essentially shut down the patient's thyroid glands, and then you you replace the thyroxin that's not being produced by the glands with medication. So it's just two ways of managing, um, hyperthyroidism with carpet muscle. All right, Um, the interesting time. Sorry thing I'll have to press on. So ABGs, if you're getting confused about respiratory and metabolic alkalosis diagnosis, just key principles, remember? So carbon dioxide in your blood is acidic by nature. It turns into carbonic acid, so it causes your blood to be acidic. Now to contract that the body, the kidneys, um, sort of start retaining more bicarbonate, which is basic by definition. So, um, you have a patient that's breathing very fast. The patient's pretty probably breeding off a lot of the carbon dioxide in the systems. The level of carbon dioxide in the blood goes down, so there's less less acid in the blood. So the patient becomes Alka Logic. So, um, get respiratory alkalosis iss. On the other hand, if the patient is short of breath, not really perfusing that well, um not really being bent ventilated that Well, there's not much oxygen exchange happening. Um, and more importantly, the patient starts accumulating carbon dioxide than you get, um, acidosis on the basis of respiratory cons. So you get respiratory alkalosis, and the body will try to compensate for that by sort of retaining more by cards and right So Taiwan respiratory failure and talk to respiratory failure. Um, they tend to make it a little bit too complicated. Basically, you look at the patient's oxygen um P 02 levels. If the P 02 level is here and you think that's down, then you have type one respiratory failure. If the P CO2 results are high, that's type two respiratory failure that you commonly see in COPD Patient's, where they retain carbon dioxide over chronic period. And so, for type one respiratory failure, the management is CPAP, so you just need to push more oxygen into their lungs to basically oxygen, Then better. But in terms of trying to respiratory failure, getting an oxygen into the body as well as getting rid of rid of that carbon dioxide is equally important. So you need a bypass Athay. So bi pap pushes air in and pulls the air back out into your lungs. So by pushing the air in, you get more oxygen. And then by pulling the air out, you ate with the carbon dioxide exchange as well, right? I think that is the end of my lecture. I think, um, I didn't mean to have, like, a 15 minutes break, but I can see that we have massive you overrun. So I think I'll give you some couple of minutes to stretch your legs, and, uh, we'll crack on with the next one. Okay? Yeah. So feel free to grab a drink. Um, use the toilet, stretch your legs, Uh, start quarter past 10. All right. So I just know that wasn't much of a break, But in the interest of time, I think we need to press on. So drug monitoring. So, um, there's not much content to be covered. Um, sort of like less structure content. So I think I'll sort of case by case basis where I go through some key drugs that often come up on the P s A. Or you'll see quite often being used in the wards or, you know, patient being prescribed. And, uh, again, I'll sort of pair them up them up with some real life tips. Then, um, we've got some questions at the end, so yeah, and bear with me. If these slides are a bit drier than usual, I usually try to put in some more, um, fun things like memes and, uh, interactive things. But, uh, my shift has been quite dreadful right lately, and, uh, just didn't have the mental capacity to do that, right? So some top tips for this section So it's not a major section of the PS PSA. There's not much, many points associated with it. So I wouldn't really sort of waste too much time advising this topic particularly, um, if you sort of study the other areas, especially the prescribing section, then you should be automatically be ready to answer these questions. Um, so instead of sort of trying to remember the exact climbing, like exact climbing for the monitoring requirements. Just try to remember the major, um, those warring side effects for each drug and the monitoring choir requirements should be based on those major side effect profiles, so it should sort of logically follow if you remember the major common side effects. Another useful thing is remember where the medication is metabolized and excreted, so whether it's pathetic metabolism or whether it's renally excreted or fecal excreted that kind of things. So you know, if, for instance, things like medications that are freakley excreted and the patient has constipation or, um, yeah, constipation or, uh, reduced gastric motility, then you you'd expect the medication to hang around and system much longer. So things like that, right? Oh, and remember, your enzyme inducers and inhibitors. So these are the drugs? Well, not just drugs. Anything that can influence your C Y. P Um uh, two fifties, Uh, that metabolizes most of the, uh, medication. So I think there's a very handy, uh, pneumonic that everyone uses that devices. Yeah. So, um, if you haven't heard of it before, um, have a look through that and trying to sort of keep most of it in your memory for the exam, because at least be able to recognize them when it comes up in the questions. Um, uh, yeah, so right crack on. So, statins, you need to know their baseline. Lft. Um, yeah, in the morning, I'll I can let me see. I can add it to the slide before I send it out. Um, there's a very neat, uh, like a table. That sort of shows everything. Um, yeah. I'll add it to the the slides before I send it to Leo to be just to read it out. All right. So, statins, um, are metabolized, um, primarily in the liver. And also, it's created equally. Although there is a degree of renal agreements, uh, excretion as well, but the majority of it is being is treated, uh, equally so. You need to know their LFTs that start and then monitor, uh, three months and 12 months start since starting the, uh, statin treatment. So again, there's no need to memorize a three month 12 month. Um, LFTs. Just remember, statins, they deal with, um, cholesterol. Now, where does cholesterol metabolism metabolism happen? That happens and deliver so statins mess with something in the liver. So you want to know whether your liver is doing fine before you start them on statins. Now, another thing that I've mentioned in the previous lecture statins can cause wrap My analysis and just generalized muscle pain is a very common side effect of statins. So if the patient has had some unexplained muscle pain or known to have rapid virus is if you need to do a CK level before you start them with statins, so lithium so you need to monitor them quite closely. Um, when you start them on therapy. But once they've been established on their sort of routine, the regimen then doesn't really require that much of a close monitoring per se. Say, give the dose of lithium and then you wait 12 hours and then you take a sample and then you check what the sample is doing, and then you titrate accordingly. So obviously, if you are, if if it's not an acute presentation, um, and you're thinking more about maintenance dosage, you're trying to sort of keep that on the lower side. Um, but obviously an acute presentation of say, something like mania then you want to be sort of closer to the one million more people eater, uh, want to shape, right? So, methotrexate, it's, uh it's one of the favorites on P s A. S. Um, I could guarantee you, um, every year you take the p s. A. There's a question of, uh, series of questions about methotrexate. So really, no. This drug inside and out. Um, it's useful. Quite a few different things. It's an essence, uh, immunosuppressant as well as, uh, call it antagonist so it will suppress your immune system's. So So you would need to monitor your full blood count, especially your white cell count. Um, and and it's a full night antagonist. So things like macrocytic anemia um, any neuropathies and especially the patient's, uh, planning on getting pregnant doesn't matter if the male side or the female signs taking methotrexate. Um, you need to counsel them appropriately. Tell them you cannot get pregnant long. They're on methotrexate believe they need to be off methotrexate before six months before trying to conceive. Um, another thing is, if the patient is on methotrexate is always a good idea to start them on folic SLL for folic um, replacement That will help with the, uh, anti folic, uh, tendencies of methotrexate. So one sort of real life tip is that when a patient presents, um, comes into E. D. And you're the first doctor to clerk them, and you see methotrexate and they're unwell. Um, have neutropenic sepsis as a high priority on your differentials list. Yeah, sure. Uh, yoga room is a bit of a funny one, so it can be used for rhythm control and af patient's, um, but it needs to be used with caution. So when you start them on, the new drug is always a good idea to put the patient on cardio monitor because it amiodarone itself can cause them arrhythmia. So there's always too. It's a good idea to hook them up on cardiac monitor and monitor them across accordingly. So important sort of flight effect profile is to keep keep inside your head. So corneal deposits. Yeah, it can happen, but not as important. More important is the thyroid dysfunction, So any odor messes up with the eye. Oh, iodine, um, metabolism in your body so it can cause hypo and hyper thyroidism and on the B N F I believe it. They're both listed as common and very common side effects. So you would expect to see quite a few deranged thyroid function tests when you have a patient on long term and my odra Uh um, another thing is Pepto toxicity. So monitor your LFTs and especially pulmonary toxicity. So check your chest X ray before you start them on it. And if someone comes in with, um, hemoptysis iss and they've been amiodarone, think about pulmonary hemorrhage, take a chest X ray and refer urgently to respiratory team. Uh, so I think we can talk about talk about carbimazole in the previous lectures. So it is used for hyperthyroidism, so it inhibits, um, thyroxine produced production in your thorough glands. Um, it can be used in two different regimes. So it can be either used to titrate down the level of thyroxin being produced by the patient's thyroid glands. Or it can be used as a block and replace regime where high dose of crept Mosul is given so that the patient's and thyroid glands pretty much shuts down. And then you replace the lost thyroxin with levothyroxine. Um, it doesn't really require monitoring as per the B n F guidelines. But if you have a patient on carbon muscle and then you see some deranged blood test, then carbon muscle is one of the first things that you would suspect might be causing, um, things like a granular cytosis. So if you have sort of across the board low white cell count, then you need to start thinking about Oh, is this carbimazole causing a Granules granular cytosis. Okay, Yeah, a lot. Right. Antipsychotics. So you have things like uti prolongation so that you need to be watching f for hyperprolactinemia is a common side effects. So if the patient especially male patient's if they come in with gyneco mice, India or, um, any nipple discharge is than to think about changing or reducing or stopping antipsychotics and lipid disorders as well as waking are common. Um, side effect profiles for antipsychotics. Um, most notably, things like olanzapine land on olanzapine is known to be quite, uh, quite prevalent in causing weight gain. Um, one of the way I remember this was olanzapine starts with their own quite round. So, uh, patient's on olanzapine. The patient's become round. Not the nicest way of remembering it. but it worked for me. Alright. Digoxin is a very tricky drug to utilize. One thing that you need to remember is that before you start them with the jocks in, you need to check you the knees. If the patient's, um, potassium is low especially, you know, just below the reference range that you can treat with oral. Um, sand. Okay. You need to correct that before you start them on the Johnson, because even a trace hypoglycemia can called adjusting to succeed toxicity. Um, if you're interested in the mechanism, how hyperkalemia can cause jobs and toxicity. I came. I'm more than happy to go through it. Um, after the lecture, if you if you're curious about that, send it, send, you send me an email and then I can go through it together with you. Um, I think in the interest of time, I don't think I'll have the time to go through. It is quite a complex process, but just remember, hypochelemia can cause the Jackson toxicity. It doesn't really affect the serum. Um, concentration of jokes in It just increases the Jackson activity in the myocardium and, uh, same with amiodarone. If you're starting someone with Jackson, it can cause arrhythmias as well. So it is a good idea to, um, place them on cardio monitor. So common patient's that get started on digoxin or patients with atrial fibrillation. But they have heart failure with reduced ejection fraction. So if you give them something like bisoprolol, which will slow down the heart, which you do want in, um uh, A F But it will also reduce the cardio output and can send them into cardiogenic shock, which you don't want to do. So Digoxin slows down the heart heart rate as well. But it is an inotrope, which means it increases cardio, Um, contractility. So while it slows down, the heart gets the heart to pump harder, so sort of allowing you to maintain the cardio open as best as possible. Right? So I think I've talked about bank and 10 before, So banking eyes and gentle my zing, they're used for a variety of different things. Um, for my from my experience, a lot of people have been started on bank and gents because they had, um, susceptible, um infective endocarditis with, say, like a prosthetic valve or algae group asset route abscess. That kind of thing. Uh, so these are very strong antibiotics and with a very serious profile, uh, side effect profile. So things like ultra toxicity it can cause, um, egg granular cytosis and neutropenia. Although it's not as prevalent as things like methotrexate or or carbon is, uh, and they're both, um, renal excreted and can cause a k i s And, uh, when they're overdosed. So do check your user knees before you start them on Either flank and gent monitor using these two about the treatment. And this is more done through, um, sort of primary care setting. But it's always good to think about checking their hearing, especially if they've been overdosed, like in the case that I've told you about. Yeah. Uh huh. Oh, did I skip one? Okay. Sodium Valparaiso. A. Um, it's another mood stabilizer, so you can constant deranged LFTs and pancreatitis at the same time. Um, so before you start them on, sodium, uh, Valprol bake, you need to check your LFTs and monitor LFTs throughout the treatment. Um, another most important thing is the absolute contra indication of the patient is, um is pregnant or, you know, even of child bearing age. So if it's a women of childbearing age, you really need to think about other alternatives and come back to soldier. Develop a rate if you really don't have any other options and even then you need to start them with adequate specialist guidance. Do right. ACE inhibitor is a bit of a funny one. Um, there is a question later on regarding ace inhibitors that, um, yeah, but one thing is that it can cause a k I It can be nephrotoxic. So if you have a patient coming with a K I and then there are any centimeters that needs to be stopped now patient with CKD it's a bit of a different issue, so I'll cover the end of question later on. And another thing that ace inhibitors do is you can cause hyperkalemia. So I understand that it can be a little bit confusing because you have, um, loop dietex like frozen, my causing hypokalemia and then you have a sin emitters causing hyperkalemia. So just if you think about how ace inhibitors work that it becomes sort of you can sort of logically follow while you get hypokalemia with ace inhibitors, so ace inhibitors um, inhibit. In essence, the NGO run an angiotensin industrial system. So the rats system. So what's at the what's the end product of the running angiotensin industrial system of the Austrian? Right. So what does the industrial do? It helps you retain sodium and keep your BP up. Now, a days inhibitors sort of shut down this well, inhibit that system right in the middle. So you get less industrial activity, so you get less salt retention so well, less sodium retention. So you have less, um, sodium, which is n a plus coming into the body. So in order to maintain home your spaces, you need to check out something a positive ion in exchange. So sorry, it's the other way around. So you have less, um, sold retention. You're losing more sodium. So in order to compensate for that, um, you need to start retaining other iron, other positive ions. So the ace limiters end up getting more potassium ions to be retained in the system. Now, that is not the exact mechanism. How this how this happens. But if you think about it that way, it's sort of it for for my case. I think It helps me sort of think about this logically, and then sort of memorize it better. So right. So going back to a senator's, um so it can cause a k I. So it's always a good idea to monitor. Use the knees. Um, right, right. So, diabetic drugs, the reason why I put this in red is because it has some serious side effect profiles. So metformin is the first line that people get start started on after they've tried. Um, dietary and lifestyle changes so it can cause lasting, as those is a patient comes in with, uh, increased respiratory, um, sort of rate, you know, either to kidney, and then you do a blood gas. It shows high lactate. Um, the one of the most, uh, probable corporate is metformin of the patient is diabetic. A couple of things I want to point out. So things like sulfonylurea in acute care setting. Um, if the patient comes to a hypoglycemia, then, um, that, um, that you need to investigate further. So, um, same thing with insulin. So, um, if you think about how the treatment pathway for type two diabetics, they are started on diet and exercise and then they get put on metformin and then they get put on geo therapy. So metformin plus really any of the following five and then when? When that doesn't work, they get started on insulin. So, you know, when you have time to diabetic on insulin, then they had really a lot of trouble managing their blood sugar levels. So if the patient's on on cellphone urea or if they're on um uh, insulin as a type two diabetic, then keep an eye out for hypoglycemia. Ask the nurses, um, to check their bmd's regularly. Um, I think another very important thing that I need to mention is F g L2 t two inhibitors. So things like empagliflozin mean, uh, that gleeful seen. It's just yeah, so So these are diabetic drugs that allow basically cause you to pee out all the excess glucose in the body. So you are expected to have glucose area, and then you have glucose in the urine. You get more frequent UTI s. But more importantly, um, it is quite common to see patient's ending up in D. K with SGLT two inhibitors. So when you have a patient on saying empagliflozin mean, and, you know, they come in with after pain, vomiting, maybe even confusion. Then you need to start thinking about D K A. And start the appropriate protocol. Another thing is, um, they need to be stopped in acute illness. So if they are in patient for any sort of infection, any sort of operation procedure that they need to be stopped and then ideally with endocrinology or, um, diabetic specialist nurse input, they would need to be started on an alternative treatment. Um, another just interesting bit of fact about SGLT two inhibitors. They're now being used for the treatment of heart failure. So just quite a two different mechanisms of how they prognosis and heart really patient's. But just bear in mind. Um, there are patient's, um, that uses, uh, that type of, uh, closing. So we call that data, um, for for the treatment of cardiac failure. Right loop, diuretic. So frozen. Might, um right now I'm currently on a cardiology ward. So, um, yeah, we use them day to day every day. They and they say it is quite common. Um, very common, in fact, to, uh, patient's end up in a k. I especially if they're on high dose IV furosemide. So common dosage wise, you start them on, like, 40 mg once daily and then, you know, they come in with decompensated CCF. They get started on IV frozen might doesn't cut it. They get put put on IV infusion giving, trying to 40 mg over 24 hours, 300 mg over 24 hours. And like I mentioned, can cause hypochelemia. So you need to keep a very close eye on using these. So that means daily use the knees. So, as you can see, um, our nephrology colleagues don't really like, um, people being on frozen white, especially on high doses. So it's not uncommon to have a bit of a dispute or more more of a friendly discussion amongst the cardiologists and nephrologist regarding, um, what comes first, we need to think about AKI first. What we need to treat this massive cardio failure. So, yeah, just a bit of an interesting news article from there. Uh, so in the U. S. Apparently, uh, a nephrologist punched, uh, cardiologist during an eye to ward round and, uh, was charged with assault because apparently the, um, the cardiologist was going behind the nephrologist back and kept restarting the first month when he told them it couldn't be started again. Uh um, Other loop diuretics to be aware of or things like rheumatoid say rheumatoid has a higher by availability. It is better tolerated. Um, renally, But it is also more potent. Say 1 mg. I'm just thinking off the top of my head, 1 mg of dimensionality equals 2 40 mg of froze might. But don't quote me on the exact figures, but so yeah, so the maximum dose is 2 mg b d. I believe so, which is would translate to 80 mg b d for frozen void. But even until now, for some reason, um, I'm not entirely sure why, but cardiologist seem to prefer, um, starting the patient or frozen like first. And then if that is not tolerated, they get switched onto Burma tonight. Um, yeah, just, uh okay, So first question is, can you give a senate bitters to a CKD patient? So have a think about it. Feel free to pop it in the chat. Excellent. So, yes, ace inhibitors are actually indicated in chronic CKD patient's. Mm. Uh, diabetics can cause a K I s, um actually don't know how unsure about the exact mechanism of how the diuretics can cause a K I s I believe it might be due to hyper hyper profusion of the other America glow mer align because you're obviously pumping away all the fluids, so get less profusion of the glow Marylise. So you can cause acute drop of G f r. But that's just off the top of my head. I wouldn't Yeah, I'm not really sure about the exact mechanism. Sorry about that. Okay, So going back to eight limiters and CKD patient's so ace inhibitor is what they do is it constricts the different vessels from the kidneys, and then it lowers the resistance in the renal arteries so it actually enhances kidney perfusion. So if you're thinking about increasing, um, kidney perfusion um, ace inhibitor is definitely indicated in terms of CKD. Now, that means you're giving more blood flow to the kidneys that could already be slightly damaged. Now you push them a little bit over the edge and you send them into a K I. So when you get a patient on on asymmetry, ear's, you know, with a background of CKD and then they present with a K on CKD. Then you need you need to stop these limiters because that's going to make the e k worse. Eee different with e Uh, Okay, okay. All right. Second question. 84 year old female background of congestive cardiac failure came with increased shortness. Spread was an exertion. She didn't have any chest pain. E c g didn't have any changes. Japan It was negative on examination. Patient is sitting up the bed. She is short of breath, but I didn't have any cyanosis. Cab refill. Time is less than 22 seconds. Moist membranes with JVP Raised heart sounds one and two with no add sounds Chest off saltation shows by basal crackles Pity edema up to mid shins. What medication would you start this lady on and what you need to monitor? It's quite a straightforward one. So I'll give you a couple minutes to think about it, and then we'll go through the answer. Uh oh. Sorry. I got distracted by a dog, Right? Surely give you the answers. Any any takers? Okay, right. Let's right. Let's go through it together. So this is a classic classic picture of decompensated CCF, causing fluid overload in in the lungs and legs. So so when you have a listen to their back, it'll sound crisp like really crisp, like someone's like crunching a bag of crisp and you examine their legs. Um, you often see pitting edema, uh, missions all the way up to the knees, depending on the patient. So, as you can pretty much tell the first medication that you need to start this patient on would be frozen mind so looked automatic. So you need to look at they're using these first. So if they're egfr is fine, then you can start them on quite high dose. So and in this patient she is still short of breath. So I would start her on IV furosemide because as a quicker um, course of Axion, and it's more potent and high as a higher bio availability as well. Um, just some real life tips for prescribing first might when you actually start working. Um, it's not very nice to give for his might at night. Um, you'll keep a patient awake going to the toilet, so try to even if you're giving the BD trying to give them in the morning or before midday at the latest, right? Another sort of separate question regarding this is how do you know? First, mod is working. So you prescribe some pros mind for a patient, and the patient says, Oh, Doctor, I've been going to the toilet all day like keeping out stuff. Does that tell you it's working? What do you need to do just off the top of your head? Um, just just shout it out into chat. Very good. Check weight. Daily weights. Excellent. Oh, you guys are Yeah, already to work. All right, so daily weights are a good thing, but just based on the presentation, uh, loop diuretics when they actually work, it causes a sudden bout of diaries. Diaries is and then it's not supposed to cause, like a prolonged diaries is continuing on for the whole day. So if the patient tells you Oh, Doctor, I took the pill in the morning and then I went to the hole there, like, three times during the during the morning. And then I peed out like a lot of fluids that, you know, the probiotics are working. But if you tell them oh, I took a pill in the morning. Been going, you know, to hold that for the whole day. And even until the night then you know, frusemide that you've prescribed is subclinical. And the patient is just going to toilet because of the subclinical effects of the frozen might, plus being fluid overloaded in the first place. So, in that case, just increase the first my dosage, and you're supposed to see, like, about of diversities. Um, that starts shortly after you've given it and doesn't sort of stay prolonged. Yeah. So just going back to daily weights for this kind of patient's with decompensate CCF, um, common sort of starting management would be, um, So diaries diuresis. So you started, like, frozen mind. You check daily weights, you put them on 1.5 liters. Flu restrictions. You asked for a strict input output chart and daily use the knees. All right, You ready? All right. Say next question. 87 year old says on medical assessment unit found to have non valvular atrial tribulation started on rivaroxaban 20 mg daily. Yeah, give me one minute for this one. It's quite a straightforward one. Um, I'll be quite worried if you get this wrong. Um, so to fair, all the answers could be sort of correct. Suffered be. So aspirin is not contraindicated. While order of rock band. Obviously, you need to monitor the monitor the bit more closer for signs of bleeding. But the most appropriate answer here would be if there are any signs of bruising or spontaneous bleeding that needs to come in for medical attention because she has been started on a dose pack, which makes her more likely to bleed about E um, rivaroxaban should ideally be taken at night. So it's not a requirement per se, and you wouldn't be tested on on in your P s A. But, um, it is good practice to prescribe anti coagulation. Um uh or antiplatelets or especially things like low molecular, low molecular weight heparin that the patient will be placed on for DVT perplexes while they're inpatient. It's good to prescribe that night or evening because if you think about it when our patient's most likely more, more susceptible to from both, this day is when they are sedentary, they're not moving around or mobilizing. So throughout the day the patient will be moved around, you know, they'll be going to toilet, you know, mobilizing around in the wards, you know they'll be moved to for doctors to examine, You know, for Oct at nighttime, they're sleeping. So there's not much movement, so they're more likely to get thrombosis. So it is not a requirement, but it's sort of good practice to prescribe these things, to be taken at night while they're impatient. Obviously, if you're talking about someone elderly, can't really expect them to remember everything. So just ask them to take it at the same time, some at some time during the day that they found most convenient. Yeah, All right, Uh, two more questions. Then we are done. So 63 year old male, four days post hemicolectomy reduce the water intake and then so you can't be prescribed back of normalcy line over eight hours, which is a standard for normal sized adults. How would you want to perform dehydration? What is the most appropriate or most important, um, criteria that you would need to serve prayer in mind? These are all well, most of these are good ways of monitoring for dehydration, but one is the most sensitive. All right, guys. So in the interest of time. Um, so the the answer here is the urine output. So skin trigger mucous membranes, JVP are all things that you sort of monitor as well, Especially when you're examining the patient day to day, but sort of most immediate. Um, change when the patient becomes dehydrated, is the change in urine output. So, um, in this case, um, if you're really worried about dehydration, that is a good idea to actually catheterize the patient. And, uh, that will be they'll give you the most accurate, um, measure of your amount, but yes. Lastly, so 85 year old meal nursing home residents can comes into e. D with malaise rigors lower up the pain. He has a background of a stroke, Um, and also has a long term catheter af uh, mitral regurg and bph medications wise, he's on warfarin. Um, it takes simvastatin, um, and total cultural the in tartrate. Now he's found to be in your oh, sepsis and prescribed, uh, super Fluxus in 500 mg 12 hourly. So how would you monitor this patient to assess whether this is working or not? So all right, let's go through the answers together, So blood cultures sounds sort of intuitive, but blood cultures, if you think about it, takes about 72 hours to come back. So it's really inappropriate to use that as monitoring purposes. Um, they're more used to guide your initial antibiotics choice when the patient comes in, um, with your sensitivities. But in terms of thinking whether this is actually working, it would take a little bit too, too long of the delay would be too much to use for monitoring purposes. Catherine urine specimen sounds also sounds quite likely, but catheters are quite contaminated by nature. So you take a capsule example, you would You're bound to grow something, and more often than not, when you do send it off for M C. N s, you'll show, um, heavy mixture of, um, bacterial growth. Um, likely contaminants. Urine dipstick for protein, urea and blood. Um, so especially blood. Uh, you can expect to have, uh, you materia even after the complete resolution of the symptoms, it can persist for a couple of days to a week. Same thing with Lucas eyes and nitrates. So nitrites especially stick around for a couple of days after the resolution of symptoms. So to have an idea of whether this antibiotic therapy is working, the best option is resolution of acute symptoms to ask them. Oh, like, are you still getting the stinging sensation or burning sensation when you pass urine? You know, things like that, any sort of super pubic pain, and also one of her for systemic symptoms, like, uh, yes. So rigors fevers. Um, confusion. All right. I think that is it. Um exactly. Yeah. I don't think we have time for questions. So if you guys have any additional questions, I'm more than happy to take them. Um, if you just pop pop me an email, um, I'll just go through the first slide. So if you have any questions about this lecture or the previous one, feel free to send an email across. Oh, and just about your answer. Check infection markers. So white cells can be a good sign to monitor. But you're thinking about crps. Crps tend to lag slightly behind white cells so you could see a decline of white cell, um, white cell count right after an aquatic therapy. But crps tend to stay up even a couple of days after all, right, Question three. Okay. Oh, Question three is D Any severe or spontaneous bruising? Seek medical attention, like, All right, um, thank you very much for attending a talk, guys. And, uh, you guys have a good weekend. Uh