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We wait for a couple more people to come through. I'm just going to say a couple of words about, about me, me, which is the organization through which we are delivering its talk. Um So medic is a charity that I started when I was in fifth year of medical school. So that's probably about five or six years ago now. Um So for those of you who haven't come across it before, essentially how it works is we produce various me resources. We try and make it, you know, as affordable as possible and from the various subscription fees, we eventually raise enough money to do some sort of product abroad. So they normally focus on either public health or education related initiatives. So for example, in the top right corner, we built a 75,000 L rainwater catchment tank in Kenya. We've delivered stethoscopes to med schools in Uganda and Kenya as well and done various other projects as well. So essentially by supporting me medic, by using our resources, you enable us to do these kinds of projects abroad, which is a really a nice sort of full circle moment really. So I'm just going to quickly introduce myself as well before cracking on with the questions. My name is Laz. I was at Imperial until 2020. So I think the finally is now I probably the last year that was at med school at the same time as me, which is a slightly scary thought. I'm an acs anesthetics trainee at the moment based in London in East London. I've defected over to the Bart side of London. And if you do need to contact me, then feel free to email me, email address is on there. Or else you can just contact me on linkedin or Instagram or whatever is most convenient to you guys. Um So just going to put this up there nice and early as well. So I've basically gone through all the meme resources. I've looked at the UK MLA curriculum and just made some to be honest, fairly minor changes because I know they've rebranded, it, made a new name, made it standardized. However, realistically, medicine hasn't changed an awful lot. It's all going to be a similar sort of content. So there's a huge amount of resources on there, which is very cheaply available. It literally costs you 2 lbs 99 per month and all of that will be going towards our products abroad as well. So if you think that will be helpful for you, then please do take a look and subscribe. And so in terms of how I'm gonna do this, I appreciate those 50 spas. Um I don't want to take loads and loads of your time on a Thursday evening. So I'm just going to go through it fairly quickly just highlighting the key points for you to consider. I'm not going to bother reading out the entire SB each time because you've seen all of these. Uh I'm just going to go through the answers and, and, and basically why it is the correct answer if you have any questions, I just recommend noting down the question number and basically the main thing that you had a problem with and then at the end, we'll go through it all together rather than starting and stopping constantly. So I hope that sounds all right to you guys. And let's crack on with question one. So question one essentially is focusing on a patient who has what sounds like stable angina, very, very common presentation in primary care. And generally speaking, the first investigation that's done or that a GP would refer to is a CT angiogram. So in the past, it would be things like stress echoes and stress ecgs. However, if you think about it, in terms of the logistics, that's quite, quite a time consuming and logistically awkward thing to do to get someone on a treadmill with an ECG and see if there is any ischemic changes. Whereas CT CT Coronary angiograms or CT CAS as they are called, are much more straightforward. It's just a specialized type of CT scan where you can visualize the coronary arteries non invasively and basically triage these patients in terms of how likely they are to need an intervention or how bad their coronary artery disease is. So basically long story short, stable angina main investigation is a CT coronary angiogram, moving on to question two. So this is a kind of interesting one, a lot of the time people see chest pain, they see high drop and they think this is an mi however, in this circumstance, the main point to bear in mind is that they've described the pain as being severe, central chest pain radiating through to the back. So that in itself should make you concerned about a possible aortic dissection. Adding to that there's a big BP differential between the two arms. This is one of those things that comes up a lot in exams. But to be honest, in real life, you know, I've asked for that investigation to be done. But how often that's been useful is a different question altogether. But it's certainly something to bear in mind. If they mention that there is a BP differential, there's tearing chest pain going through to the back. You should think about an aortic dissection. The important thing to add is that with an aortic dissection, you basically just get the tunica intima peeling off like basically just wall paper being stripped off the wall. The issue is that, that creates this false lumen which prevents blood from flowing in a certain direction. So, aortic dissections can progress along the aorta distally or it can actually progress proximately as well. So the important point with this spa is that sometimes you can get aortic dissections that progress proximately. It actually gets so far as the aortic root and it can actually affect the aortic valve itself. And if you remember immediately behind the cusps of the aortic valve are the ostia for the coronary vessels as well. So basically, if you get this wallpaper tearing, tearing off, coming down close to the valve, it can actually lead to occlusion of one of those coronary blood vessels, coronary arteries that's coming out of the proximal aorta. If that were to happen, you are essentially sort of mimicking an mi it's not caused by a blood clot. It's caused by a dissection. But if you get proximal progression of an aortic dissection that involves the coronary arteries, it can cause an mi basically on top of that. So that's what's happened in this case. It's gone down what looks like the right coronary artery. It's caused an mi as well because it's a dissection that has progressed proximately. That was quite a long spiel. But my main point is chest pain. Think about aortic dissection even if someone has a high drop. Just think is it possible that the high drop isn't from a thrombus within one of the coronary arteries. But it is in fact, because of the propagation of the dissection moving on, we've got a patient who basically sounds like they're in pulmonary edema secondary to heart failure. And that's all confirmed by the chest X ray findings of widespread alveolar shadowing upper lobe diversion. It's all the stuff. And so they've already initiated treatment. They basically told you, you know, we actually know what the diagnosis is. They've got ischemic heart disease, they've got po edema, we've given them two doses of iomide, nothing much has changed. The next thing that you can do from a medical point of view, and this is actually a really good topic to know. Well, when you're a in FF one because it's so common, you see people in like acute heart failure so often and being able to keep your cool and just figure out what to do is, is really important. And the other thing I'd actually, I was about to make a point about how am Sam likes this topic. But I've realized you guys are doing a standardized exam now anyway. So if you've given Theresa, my, the next thing that you can do medically is a nitrate infusion. So, nitrate infusion, that means a nitrate like GTN like glycerol trinitrate, you think of that in terms of the spray. But in fact, you can give it as an infusion as well. So the main reason that works is that it's a really, really good venodilator. So it helps dilate the big vessel, bigger big veins in your body, which essentially reduces the venous return to the heart. And hence, it essentially takes the strain off the struggling floppy, full heart and helps it pump a bit more effectively. So, main points to consider are if there's a coupon redeemer flusemide is the first thing you give nitrates provided their BP can handle. It is the second thing you should consider from a medical point of view, right. Moving on, there's a patient who's become acutely breathless, um basically has a very high oxygen requirement and is in fast. Af so af again, very very important and common medical issue that you see on the wards all the time. And by extension, it is very common in exams as well. And I'm certain it's going to come up in some form in the UK MLA. The main thing to remember with AF management is that step one is to consider, are they hemodynamically unstable or are there any adverse features? So in this case, I would say there is a very obvious adverse feature which is the fact that they are needing 15 L of oxygen and they are only saturating at 88% and they are breathing at 34 per minute with widespread in spirit crepitations. So as for the adverse features or hemodia instability, the main things to watch out for which may require DC cardioversion are first of all, if their BP is absolutely tanking. So if their heart is beating so fast that it has no time to fill enough to be able to pump enough blood out of it, then it means that you need to just DC cardio vet them other adverse features are if there is any evidence of myocardial ischemia. So if they have this sort of crippling chest pain, maybe the, maybe the ECG shows some evidence of ischemia as well on top of it, then you might consider ec cardioversion. And then another really important one is if they've developed heart failure, essentially because if you think about it for the heart to function, it needs time to fill and then it needs to pump effectively. In this case, if you're going at 190 BPM and your atria are just fluttering about, you're not going to be able to fill that ventricle enough to be able to maintain a decent cardiac output. And as a consequence, blood is going to backlog into the lungs, leak into the airspaces and cause pulmonary edema. So dey cardioversion should be considered in this case. Another question about af just to draw the point home. Um An issue with af in a chronic sense is that you do run the risk of forming clots. If the blood isn't circulating through your heart effectively, all those clotting factors is bump against each other. They activate each other unintentionally and they can lead to the formation of clots and subsequently strokes. So basically, the chads mas score is used to gauge whether someone would benefit from anticoagulation because the risk of them having a stroke due to their af is high that should be balanced with the orbit score usually, which is basically the risk of anticoagulation. A patient. So again, that's a, that's a common topic worth committing that to memory. Um So we have got a patient who's a poorly controlled asthmatic come in with an acute exacerbation. Again, very common topic. They've given the oxygen, they've given some nebulizers. What do you do next? So basically, the next step in this circumstance would be to give some magnesium. So acute asthma attacks. Again, you'll see that all the time, especially if you do any jobs in a and the first thing to do is make sure they're not hypoxic. They aren't always give some nebulizers. So salbutamol or ippi and then magnesium is a really good way of also bronchodilating them as well. And it's one of those drugs that is generally quite safe as well. There's not really much harm in giving magnesium. Um Moving on to question seven. So we've got someone who's had a very long history of shortness of breath and been complaining of some joint aches. It's all a little bit chronic nonspecific and they've done this chest X ray. So, the main feature here is the bilateral hilar lymphadenopathy. So, sarcoidosis is a condition in which you get these non caseating granulomas forming in various tissues. Most commonly the lungs. I'm not entirely sure why it happens, but it is something that can lead to this chronic breathlessness. It can lead to interstitial lung disease. And it is one of those things that is disproportionately represented in exams just because it's quite a good topic to write questions about. The main thing with sarcoidosis is most of the time it affects the lungs, chronic breathlessness, bilateral hilar lymphadenopathy, and perhaps some generalized constitutional upsets like having a dry cough, joint aches, etc question eight. So we have got a patient whose similar sort of context, actually, two year history of worsening shortness of breath, it's a dry cough, really limiting their exercise. Inhalers have not worked. You used to be a coal miner. This is a very, very classical buzzword type spa. But in this circumstance, the best investigation is a high resolution chest ct ct chest. So obviously, a lot of the time these patients will have chest x rays first. However, this question is asking what's the imaging modality that's most likely to be useful essentially in this scenario. So, interstitial lung disease refers to diseases that affect the tissue of the lungs itself. So it doesn't affect the airways per se. It affects the actual tissues in between. And what's being described here is pneumoconiosis. So one point I'd like to make this is one of those slightly niche points that will help you access some of the sort of higher tier marks in the exam is the difference between extrinsic allergic alveolitis and pneumoconiosis. So those are two terms that med student a lot of the time get very confused about. All I'll say is both of these conditions fall under the umbrella of interstitial lung disease, meaning that it affects the interstitial, not the airways. The main distinction between the two is that pneumoconiosis is caused by inorganic allergens. So for example, coal dust or silica or asbestos. So stuff that isn't alive, basically, whereas extrinsic allergic alveolitis is the range of diseases that have slightly weird names like bird fanciers, lung and farmer's lung and stuff like that. So that's all caused by organic allergens like bird droppings or whatever. So that's the main distinction, but they manifest in similar ways. But this the point of this SBA is that HRCT is the best investigation for suspected interstitial lung disease. So we have got someone who's presented with a cough, productive, yellow sputum. Everything else looks pretty ok. Essentially, this patient is has a pneumonia but with a low curb score and hence, they can just go home with some amoxicillin and then they should be fine. So please do have a look at the pneumonia guidelines according to my CKs, it's definitely worth knowing about and how to interpret Kerb 65. Um question 10. So we have got someone with a tender swelling in their calf and the Doppler revealed a DVT and most importantly, they had an ACL repair done just four weeks ago. So the point of this question is basically testing your understanding of anticoagulation for DVTs, what should be used and how long should it be for? So, at present, the guidelines suggest using a DOAC just because it's obviously much easier to administer than a low molecular weight heparin. And it's either, so it's three months if there's a clear precipitant. So in this case, there is a clear precipitant, they've just had some major orthopedic surgery. So three months will suffice and you can be fairly confident that you know why they had a DVT if this happened completely out of the blue and you have no idea why, then the patient should definitely have anticoagulation for at least six months. And in that time, some investigations need to take place to figure out why has this happened? Do they have an underlying cancer? Do they have some sort of factor 5 L in some sort of procoagulant condition? Um or, or is it again just, just, just sporadic and inexplicable? So, in so in those people, they will need anticoagulation for longer whilst you figure out if there is a precipitant, but here, clear precipitant use a DOAC three months, right? So if someone has presented with right sided chest pain, shortness of breath, CTPA shows that they are the right segmental pulmonary embolism and which of the following parameters are useful in determining the severity of this p. So this is a slightly trickier question, but it's actually quite a good one to know because again, it's one of those things that relatively few people would get. Right. So in this circumstance, the answer is troponin. So obviously, a lot of the time you associate troponin with being an mi type blood test to request. But in fact, with big peas, if you think about it, the right side of the heart is pumping blood out into the pulmonary circulation. If you suddenly have a big clot within the pulmonary circulation, it essentially causes back pressure on the right heart. If there is back pressure on the right heart, it causes an increased demand on the right heart muscle. And sometimes you may find that the blood supply to the right heart is insufficient to meet that demand. And hence you get ischemia which causes a rise in the troponin. So basically, in people with a really big P that's causing right heart strain, a troponin and actually even a BNP are useful blood tests to factor in because it can basically give you an idea of how bad this P is. So once you start working, you, you'll realize that pes are one of those really strange diagnoses that sometimes it might sound like someone has a bond or pe but it isn't. And then some people they seem all right and then they have a massive pe it really is quite hard to say for certain clinically if someone has a pe or not. And it's really important to have these objective measures, to be able to paint a picture and figure out how much is this p affecting someone. So, basically troponin is really useful in that context. Question, 12 patients from Bariatric Clinic, morbidly obese drinks 12 units of alcohol per week most likely cause is non alcoholic, fatty liver disease. So this is one of those things that to be honest, I don't remember learning about it an awful lot at med school. But since then, literally, even in the last five years, it's been become, I think the main cause of liver disease or cirrhosis in the UK. And so basically, what you'll see this all the time as well when you review patients blood blood test results and it's useful to know because you won't freak out about it if you see it. But essentially non alcoholic fatty liver disease due to the deposit, the deposition of fat around the liver, much like what happens in alcoholics. But the reason it happens is actually largely driven by, by diet and metabolic diseases like type two diabetes. So it typically causes a bit of a transaminitis where your alt will go up a little bit. So again, it can cause the same long term effects like cirrhosis. So it does require management most often in the form of diet and exercise advice. Really? Right. Question 13 basically patient with the back of alcohol, excess vomiting, lots, cirrhotic or esophageal varices, which of the following has a prognostic benefit. So the answer to this question is cefTRIAXone. So if you think about what an upper gi bleed is, it's sort of like having a wound, like an open wound in your gi tract. And the gi tract is famously not sterile. So that's part of the reason why antibiotics are factored in because I remember when I was learning about upper gi bleeds, I was like, why exactly do we give antibiotics? And I never really got a clear answer to that, but apparently it has, it has been proven based on data that people who get antibiotics have improved outcomes in the long term. And it's thought to be due to the fact that there is some translocation of bacteria into the circulation when someone has an upper G bleed. It's a part of the obviously upper ger bleed management at approach, dealing with the hemodynamic side of things, giving blood if need be and correcting any coagulopathy. But one other big aspect is giving ceftrixone, basically give you some sort of antibiotic. It may not necessarily be cataract. Um Right. So sho has a needle stick injury and basically, uh what's that? So the patient has a hepatitis B serology done. Um This can seem like a really complicated topic, but it isn't actually that hard to wrap your head around. So this is let me just click. This is an example of previous Hepatitis B infection. I'm just gonna move past this because I could easily spend 10 minutes talking about hepatitis B serology. Um There is a video on exactly this topic in the Me Emetic Bank. Um And I would recommend just reading the explanation to this question as well when it's sent round just because I think that will be a better use of everyone's time, but just give it, give it a good 5, 10 minutes for you to actually sit down, understand what's going on and make sense of it and it will stick with you for life, right? Got a 14 year old with intermittent diarrhea. And basically the main findings are that they are B12 and folate deficient. They are iron deficient and they've got a normocytic anemia. So that's a very, very classic picture of someone with celiac disease. And the reason it's normocytic is because something that's malabsorptive, you wouldn't absorb B12 and folate, which typically cause a macrocytic anemia and you may not absorb iron very well, which causes a microcytic anemia. And hence those two things sort of push the MCV in opposite directions resulting in actually a normocytic anemia. And the main blood test that you send off is anti tissue transglutaminase antibody, which is meant to be pretty sensitive for celiac disease. And then ultimately, they probably will end up having an OGD and biopsy 54 man back on cirrhosis and HEP C has this set of bloods. What's the main abnormality? So, there are two aspects of this question. So first of all, you can see that the patient is hyperkalemic and hyponatremic and the main drugs that would do that of the option. There are spironolactone which is an aldosterone antagonist and aMILoride which blocks one of the sodium channels in the collecting duct. So the main point though is that spironolactone is something that's typically used in people who have chronic liver disease aMILoride is relatively rarely used. But the main thing to remember, spironolactone is it's an aldosterone antagonist. So basically, whatever aldosterone does, it'll do the opposite of. So it'll cause potassium to go up, sodium to come down and it'll probably as a consequence, drop the BP. Um Rice moving on her biochem team is called about this patient who has essentially had a worsening AKI. Um And what are we saying here? So fine. So basically, what do we do in this circumstance? So this is another important point to bear in mind is that sometimes you may think that people sometimes say that flusemide is nephrotoxic or don't give frusemide to someone has an AKI. I would argue that it's very, very much dependent on the context because for example, in this case, this is someone who basically seems to have quite a dodgy heart which doesn't seem to be pumping particularly effectively. If that dodgy heart gets really full of fluid and gets overstretched, it's not going to be able to pump particularly effectively. So that classically leads to peripheral edema. When blood backlogs towards the ankles, it can lead to pulmonary edema in the case of left sided failure where it backlogs into, into the lungs. And also if it's not filling properly and it's not pumping properly, the perfusion of the organs is also going to be inadequate. So that's why people can develop akis when they are fluid overloaded from a heart failure perspective. So I hope that makes some physiological sense. But in these circumstances, you need to really try and figure out what's going on on the whole because in this patient, I'd say the main issue is that they are a little bit fluid overloaded and they need a bit of offloading to get that heart into a comfortable state where it can pump effectively enough to perfuse the kidneys a bit better. So that's one slightly nuanced topic. I'd like to introduce to you guys because a lot of the time people see an AKI and they think it's definitely prerenal, I'm going to give loads of fluid, but that is not going to necessarily help things all the time, especially in patients with heart failure, right? Moving on. Um So this is a patient who is clearly confused, has all kinds of medical comorbidities and they have this quite bad hyponatremia. I imagine the imperial people who are on here will be quite familiar with the hyponatremia because we get taught a lot of endo but essentially in this case, the cause is Ssadh. So that's usually considered a euvolemic cause of hypernatremia which is due to inadequate inappropriate secretion of ADH. So the main, the main point I'm focusing on here is how to interpret serum osmolality and urine sodium. So first of all, if you have a low sodium, you do the urine osmolality to make sure it's a true result because sometimes you can get other things that confound the sodium results like people being super hyperglycemic. So in this case, you're like, ok, fair enough. This is a true hyponatremia. The urine sodium is really useful because it basically tells you whether um the kidneys are trying to hold on to sodium or is it trying to hold on to water too much? So, in this circumstance, um the number 20 is sort of your cut off point. So generally speaking, if someone has a urine sodium over sorry under 20 it suggests that the kidney is actually trying to hold on to sodium as much as possible and absorb more water. It suggests that it's a hypovolemic cause of hyponatremia because if your intravascular fluid volume is quite depleted, your kidneys are one of the main organs to try and compensate for that. So what it's going to do is basically, it's going to think, gosh, we don't have enough fluid, we need some fluid back how do I do that? I'm going to absorb or retain as much sodium as possible. There's going to be barely any sodium in the urine. And with that sodium comes a lot of water and hopefully that'll replenish the fluid volume. In this case, you can see that there is quite a bit of sodium in the urine which suggests that there is a lot of water being absorbed inappropriately. So main point is if the urine sodium is over 20 consider ih if it's under 20 consider prerenal or hypervolemic causes of hypernatremia. Right. Moving on, we have a patient with a new AKI and you've had a look at the drug chart again, a very common occurrence in F one which of these do cross off. So, Metformin is a very, very, almost all of you will certainly do this at some point in the next next year or year and a half. Metformin very commonly used for type two diabetes. Of course, the issue is that it is really excreted and it can accumulate in patients with AKI and also in the short term missing Metformin for a couple of days, it probably not going to make much of a difference. So normally you tend to either cross it off or you reduce the dose if they've got a new AKI, right question. 24 7 CD um basically has a pe um they, they've had a pee and then incidentally you do the bloods and you see that the calcium is sky high. So with any calcium related issue, the main thing you want to check is the PTH. So whenever there's a calcium problem check, the PTH is the next step and then Vitamin D is also useful to check. But to be honest, everyone is so chronically Vitamin D deficient that it's not always that helpful. But in this circumstance, you can see they've got a high calcium and they've got a low pth. So, in fact, the parathyroid gland is responding completely appropriately and reducing its output, which suggests that the calcium is coming from elsewhere. And a lot of the time in that circumstance, unfortunately, it is due to malignancy and that fits with the vignette, which is someone with an unexplained P. So, the mechanism by which malignancy can lead to hypercalcemia is multifactorial bone metastases, just destroying the bone and releasing calcium into the circulation is one fairly obvious way in which it happens. But then there are also some cancers I think it's is it squamous cell carcinoma. Um There are some cancers which produce PTH related peptide. It's sort of like a variant of PTH, which basically has the same effect and it can drive your calcium up. So basically high calcium, low pth consider malignancy, 55 year old currently being treated for AKI and you get this blood test result again, very common on call situation. What do you do? You give 10 units of actrapid at 100 m of 20% dextrose. So the actrapid. So one of the sort of in some sense off target effects of insulin is that it does also drive potassium into cells, which is useful in the short term. And then obviously in this circumstance, you are using the insulin purely to drive the potassium into cells. You are not using it to lower the blood glucose. So you need something to balance off the blood glucose, lowering effects of the insulin. So you give 100 meals of 20% glucose. There might be some slight variations to that. So sometimes I think you can give, I think it's 200 M or 10% glucose or something like that. There might be some slight variations, but basically for hyperkalaemia, you only really need 10 units of actrapid and you generally give about 100 MS or 20% glucose. 500 ml of 5% is a bit pointless. That's quite a big bag for no reason and you certainly wouldn't be giving 50 units. Um moving on 51 year old, very drowsy at home. Um and basically diabetic and have been a little bit unwell before that. So what do you do in this circumstance? So you can see from the bloods that the ph is totally fine, that's important. Glucose is very high, lactate is quite high, but the ketones are normal as well. So this complication is, is a hyperosmolar hyperglycemic state or HHS, I'm just going to very briefly talk about this because I think people get confused about this all the time. So HS is a complication of type two diabetes. So in type two diabetes, people are still producing insulin. So it's not that their pancreas has just completely gone bust. They are still producing some insulin. It's just that all their tissues are very resistant to it. So it doesn't have the same glucose lowering effect that it used to remember that insulin has two effects, it lowers glucose, but it also switches off ketone production. So those are two different responses. So in people with type two diabetes, the insulin may not be enough to suppress the glucose. However, even a small amount of insulin will be fine at suppressing the ketones. So what happens in this circumstance is that their glucose goes up and up and up, but their ketones stay quite low. So the main issue is that these people get very dehydrated because imagine if your circulating blood glucose concentration is 35 you're going to be peeing buckets constantly, you're not going to be able to keep up with that and you end up getting super super dehydrated, especially if this has been triggered by you just being generally unwell and out of sorts before that. So these people need a massive amount of fluid. So there is a calculation you can apply to figure out exactly how much you should give. But generally speaking, it's about 3 to 6 L within the 1st 12 hours of their admission. Sounds like a lot, but they really do need it. So that's just a point about HHS Management. Please do look into that and the guidelines are actually really, really clear. Uh Moving on, painful, sore on the right foot basically is well demarcated. It's very tender and that's suggestive of an arterial ulcer. Venous ulcers are usually poorly demarcated in the gata area. They don't tend to be quite as painful. So, ulcers are fairly easy questions if you know the brin, right, a 51 year old, lots of po at home after falling off a ladder. So basically, this is an extradural hemorrhage. So with extradural hemorrhages, you have this sort of convex appearance and because they are acute, the blood is bright white. So that's because basically, when you have an acute bleed, the iron within the hemoglobin, I think that's what causes it to be radiolucent. It's basically like having metal on the CT scanner and that's why it appears bright white. Uh So basically acute um acute loss of consciousness after head injury. Uh and they've got a convex bulge on the CT, that's an extra dal hemorrhage. So we have got a 31 year old with confusion and seizures, they've had an LP. So what's actually most likely to be causing it? So if we first look at the actual results that we've got we can see that they are the high white cell count. We can see it's mainly lymphocytes that's useful because that suggests that it's more likely to be viral or perhaps TB, the glucose is basically more than half the serum glucose concentration. So it doesn't seem like it's bacterial and the protein is high. So basically with viral meningitis or encephalitis, in this case, you get a high white cell count that's primarily lymphocytes. The glucose doesn't seem to be that low in the CSF and the protein will be high. And ultimately, even without the CSF results, HSV is the most common cause of viral encephalitis. So we have got a patient with Crohn's disease who has quite bad Crohn's disease by the sounds of it has had more and more flares and they have a blood test. So the blood test is showing quite a few abnormalities to be fair. They've got, they've had some sort of inflammatory response to the flare. They've got microcytic anemia, probably due to the chronic disease, they've got a bit of an AKI as well. And the main finding I'd say in this circumstance is asking various renal questions is that the urine PCR is very, very high. So the urine PCR being high is essentially suggestive of some sort of nephrotic syndrome going on. And in patients with chronic disease, it's important to consider amyloidosis. So, again, briefly about amyloidosis, it's a condition in which you get abnormal proteins accumulating in various tissues across the body. Most notably, the kidneys and the accumulation of those proteins in the glomeruli basically makes it extremely leaky. So you get protein in the urine in industrial quantities and you end up getting nephrotic where you become edematous, hyper albuminemic etc. Um what causes amyloidosis? There's two main categories. One of them is in the context of people with multiple myeloma. All of those um antibodies essentially that they produce can clump together and form amyloid proteins which then get deposited in various places. The second is in people with chronic chronic disease of any form. So, if you remember in terms of acute phase proteins, we mainly focus on CRP. There's also an acute phase protein called serum amyloid A. So that's a protein that basically gets up regulated whenever you are in an inflammatory state. The issue is that people with Crohn's disease who've had it since they were 14 are basically in a chronically inflamed state. So all of these proteins clump together get stuck in various tissues like the kidneys and cause problems. Um Right, I've got a 71 year olds. Uh basically, it sounds like they've got a cap um and they need some empirical cover for gram positive organisms. And importantly, they have an anaphylactic reaction to amoxicillin. So it may immediately from that point, you can basically just screen the options for anything that's related to amoxicillin, which is basically a betalactam class. And the main one is cefTRIAXone. So to be honest, there are certain circumstances in which someone may have had some sort of allergic reaction to penicillin. But you're like, you know what I'm going to, it doesn't sound like it's likely to be anaphylaxis. I'm just going to take the hit and give, give her cephalosporin because the cross reactivity I think is only like 10 to 15%. However, in this circumstance, there's no real need, there's other options available. So, Tiopronin is, what's the class? It's a glycopeptide antibiotic that's effective at targeting gram positive organisms. Antibiotics are again, quite a confusing topic to wrap your head around when you're at med school, especially because I think you get taught, you're taught by microbiologists, you obviously know an insane amount about these topics. But in fact, for the purposes of F one F two, you just need to have a basic understanding of the classes and the categories and what to use in which situation. So if you do subscribe to me Emetic bank, there's a video that I basically dedicated to understanding antibiotics in a way that makes sense plane and grandpa don't cover right. So here we have someone with shortness of breath um seems to be quite chronic chest X ray was equivocal. So they did a CT scan and essentially what we have here is idiopathic pulmonary fibrosis. So this is a classical picture where you get this kind of honeycomb pattern. So you can see that you can still see the airspaces. It's just that the bits in between the airspaces, the interstitial is thickened and fibrotic. Hence why it appears so clearly on a CT scan. So that's again, going back to one of the earlier questions. It's something to consider in people with chronic shortness of breath who don't have any evidence of airways disease like COPD. It's important to consider diagnoses like idiopathic pulmonary fibrosis. Moving on as an 86 year old metastatic prostate cancer. A me has been having seizures, rationalized medications are anticipator. So this is first of all asking about anticipatory medications very commonly comes up. These are medications that you give when someone is approaching the end of life and you've acknowledged that they are approaching the end of life, you're not doing anything to change. That course, you're just trying to keep them comfortable. And then there's a set of four or five medications that are quite often used because in fact, the symptoms of dying are relatively stereotyped. So, Glycerone and bromide, I'll just go through the options first. Glycopro and bromide is something that can help dry secretions because you, you seem to get quite a lot of secretions in your, in your chest, which can make the breathing quite noisy when you in your last days. Haloperidol is good for nausea. Midazolam is good for the anxiety and agitation and things like morphine and oxyCODONE is good for the for pain as well. So the main thing to bear in mind is that in a lot of these circumstances, they'll, especially if you use online systems, they'll be like an order set which basically requests all the, all the antispas medications in one go in. Someone who has Parkinson's disease, you really don't want to be giving them any sort of dopamine antagonist. So avoid things like aloperidol because all that's going to do is make them extremely rigid in their final days. So that's something to bear in mind. Parkinson's disease, avoid things that block dopamine. So we have a jaundiced patient who has a background of vs colitis and the ultrasound shows dilated common bile duct um and lots of gallstones. So all of this sounds like bad news. Um and which tumor marker should you request? So, in this circumstance, it will be ca 19 9. So that's a tumor marker that's associated with pancreatic cancer and cholangiocarcinoma. And this question is probably hinting more towards the cholangiocarcinoma end of the spectrum. The reason being that one of the main complications or associations of osr of colitis is that patients can develop primary sclerosing cholangitis as well, which is an autoimmune condition that obliterates your bile ducts and your bile ducts being chronically inflamed, just like any other tissue being chronically inflamed can result in dyskaryotic changes in the cells and eventually lead to cancer. So basically, this is something that can happen to patients who have a background of as a sequence of events have a background of vascular colitis. It can be associated with primary sclerosing cholangitis and that in turn can lead to cholangiocarcinoma. The question stem itself is fairly, fairly one dimensional. It's basically just asking about tumor markers just to go briefly through the other options. Alpha fetoprotein is associated with testicular cancer and liver cancer. LDH is quite nonspecific but a lot of the time it's used for things like lymphomas cea is used for colorectal cancer. Ca 125 for ovarian cancer and ca 19 9 is for pancreatic and cholangiocarcinoma. Um impressed with myself remembering that because I did not think I had the ano um Right. Moving on. So surgical options, we've got someone who's gone to the Colorectal cancer clinic. Um and they've got a tumor at the rectosigmoid junction. It's by the sounds of it, it's a small tumor, no nodes involved, no metastases. So, what do you do? So this question is basically mainly focusing on the fact that it's a localized tumor. And where is it? It's the rectosigmoid junction. So an anterior resection is a procedure where they basically remove the upper part of the rectum and the lower part of the sigmoid colon. And it usually means that you can just tie the loose ends together and maintain the continence. This should not be confused with an abdominoperineal resection. So that's the other type of operation that is used for rectal tumors but this is used for lower lying rectal tumors where it's a bit too low to be able to salvage any distal part of the gi tract. And hence, you essentially take, take, remove everything from the anus up to some point along the sigmoid colon and you bring out a stoma. So again, there's a video on procedures and stomas, it's worth knowing the stuff because it's not particularly hard to grasp. You just kind of need to see some diagrams and then it will be in your head forever. 74 year old Urology clinic, big prostate gland, keen to avoid surgery and opt for medical management. Very common occurrence. Tamsulosin is an alpha blocker which helps relax the smooth muscle around the prosthetic urethra and basically can relieve quite a lot of these symptoms and avoid surgery or at least delay surgery for some of these patients. The other class of medications that is used for the same reason is five alpha reductase inhibitors which are basically prevent the conversion of testosterone, I think into dihydrotestosterone or basically a more potent form of testosterone that promotes prostate growth. And an example of that class of drug is Finasteride. So you'll see lots of elderly men who are on tamsulosin and Finasteride. This question, I got to discard it because when I was going through this again, I realized that they've recently changed the management guidelines for new authorities. And I'm not going to go through that question because it's not applicable. The main thing I will say is that this is the new guideline for pneumothorax management. The interventions themselves are basically the same. It's either needle aspiration, it's either chest drain or it's nothing slash follow up. However, the reason for intervening is a little bit different. I've included this in the, in the explanations document which I think I've already shared with, with the team that ran this event. So I would recommend just having a look at this flow chart in your own time and making sense of it. It it does, it's fairly easy to follow uh some lots of water, right? A 71 year old man has acute on chronic urinary retention has a background of BPH has not had surgical intervention and you've just stuck a 14 French catheter in what's the most important thing to monitor. So that's another really important point is urine output. So there will be plenty of times I'm sure in the next year where someone is in retention, you put a catheter in and you feel like a legend, you walk off. In fact, in those patients, it's really important to monitor their urine output for the first couple of hours and really stress that to the nurses as well. The reason being that people who are in chronic retention, they can get basically hydronephrosis all the way up to their kidneys and that hydronephrosis washes out the concentrating capabilities of the renal medulla So instead of having this nice gradient between the between the filtrate within the tubule and the interstitium around it, you basically get no gradient at all. And hence nothing really is reabsorbed and it all just floods out. So there are some specific numbers which I really can't remember off the top of my head in terms of what is considered post obstructive diuresis. But it is just really important that after someone is catheterized, who has been in chronic retention, you keep an eye on the urine output. So it's not talking about the residual volume. So if you stick your cats in and immediately a liter comes out, that's not what it's talking about. It's talking about once that initial bit is decompressed, are the kidneys suddenly starting to hose out loads of fluid and off the top of my head. I think it's a number like 200 M is considered the cut off for post obstructed diuresis. At which point the patient is at risk of becoming profoundly dehydrated. So they do normally need some fluids as well to try and achieve a decent fluid balance. So again, there's going to be more detail about this in the explanation in the written explanation, right, 41 year old, persistent dysphasia seems to come and go at times. What's the most likely diagnosis is achalasia? So, achalasia is a, is a condition in which you get um basically failure of appropriate relaxation of the lower esophageal sphincter and it's barely hit and miss. So it's not something that's there all the time, but you can essentially sort of have flares of it where you notice that every now and then something seems to get stuck. So it's an important differential to consider alongside things like esophageal malignancy. Uh, right. So, here we have a 61 year old abdominal distension, uh, has two previous operations on his abdomen, which is an appendix and a gallbladder. And essentially the main point to note is that he does have distended loops of small bowel. The way you know that it's small bowel is that you have these lines, these white lines going all the way across which are called valvular conveners. And if you were to measure it, it would be over three centimeters in diameter and typically with small bowel obstruction, it tends to be in the center of the image, so to speak, rather than around the edge. Um In terms of what's caused it, they've had two operations in the past. What's the most common cause of small bowel obstruction? It's adhesions, right. A seven year old, um admitted after stoma failed CTS request, it's more about obstruction due to adhesions in the left upper quadrant obstruction does not, does not appear to be caused by the parasal hernia. So, basically, again, common surgical case, this is the type of thing that you will be expected to have to deal with as an F one obviously you're not going to do the operation, but you can at least kind of sort the patient out in the meantime. So this is where I'd like to make a very clear distinction. So people, people, most people have heard about this whole drip and suck thing where you give IV fluids and you aspirate from the NG tube. But one thing that some of you, if you haven't necessarily spent a whole lot of time in surgical places will realize is there's basically two different types of NG tube. An NG tube we normally refer to is a feeding NG tube. However, in this circumstance, you're not, you're certainly not giving anything down the NG tube. You're actually trying to decompress that obstruction because the issue with someone having a bowel obstruction is that if, if things aren't going further down, it's all going to sort of build up and come upwards. And a cataclysmic thing that can happen in this circumstance, which does happen is that people can basically vomit, aspirate into their lungs become extremely unwell and die. So especially if patients are really uncomfortable, they're vomiting. It's really important to put a RS tube in aspirate any stomach contents and basically attach a bag to that Riles tube. So that anything that does come up to their stomach has an easy route out that avoids them having to vomit it up. So drip and up means IV fluids insert a Riles tube, which is basically a really fat NG tube that's not used for feeding. It's used for taking stuff out of the stomach. Right. 53 year old gen clinic. Two week wait, uh, what was it had? Diarrhea, mixed with bright red blood, lost this much weight? So this, I have to admit is a pretty old school type of question that I've written. It must have been a while ago that I wrote it. But essentially there's this theory that there is that based on the relationship between blood and stool, you can figure out where the tumor is. Obviously nowadays, you do a CT scan or a colonoscopy. But in case there is the old old school question, the theory is that if it's mixed together, it's more likely to be proximal. If it's coated around a fairly formed stool, then it's more likely to be distal 41 year olds, basically routine blood test. And there's an abnormality. The main abnormalities that the platelet count is very low. What's the next most appropriate thing to request? So this is a blood film. So again, this will happen in the hospital as well, platelets can clump together and give a falsely low result when the machine automatically counts it. So in that circumstance, you request, you call the lab, you ask them to do a blood film and they may say, yeah, actually don't worry about it. All the platelets come together, it's probably just a false result. So that's one thing to always consider in patients who have isolated and otherwise unexplained thrombocytopenia. Right? You've got a 35 year old in agony, urine dip is positive for blood and leucocytes. What you request. It's a non contrast CT kub. So it's a pretty, it's a very convenient investigation because it's a relatively low radiation dose and it needs to be non contrast because the vast majority of urinary tract calculi are radio lucent. So there's no point you filling the entire urinary tract, all of that, all of that system with bright white contrast, if the thing that you are trying to see is white. So non contrast, CTK is a gold standard investigation for urinary tract calculi, right? Last 10 questions, plow through um 41 year olds, breathlessness and change in the color of their eyes. Um And the blood test results show the following HB is very, very low. MCV is quite high platelets seem all right white cells seem all right and reticulocyte percentage is high. So if you saw this, if you ignore the background and everything, the main thing you should be thinking is ok. So the bone marrow is trying to make amends for something, the HB is low. Clearly, there is some loss of red blood cells somewhere. However, the bone marrow is fine, the bone marrow is healthy, it's actually doing an appropriate response to what's going on here. So given that the patient is jaundiced as well, the yellow tinge is the other thing you need to factor in. So this sounds like it could be hemolytic anemia. So, hemolytic anemia just means um a condition in which you become anemic due to reduced survival of red blood cells. So that can be because for example, you've got malaria and the malaria is destroying all your red blood cells. It could be because for whatever reason, you've started producing antibodies against your own red blood cells and it's, it's making, it's destroying all of them. Um It's just an umbrella term, there's lots of different causes. Um But that's something to consider in anyone who is anemic and jaundiced and has a high reticulocyte count. A direct antiglobulin test is basically a test for autoimmune hemolytic anemia. It basically looks to see whether there are antibodies coating the red blood cells, right. So there's a 21 year old squash player positive Lachman test and the MRI confirms that they've unfortunately got an ACL injury. What do they use to repair it? So most of the time it's a semi tendinosis tendon. I think they can use a graceless tendon or the patella tendon as well. But this is one of those fairly classic Ortho questions. Not much more to say about this, to be honest, but that's the, that's the answer. Another question. 7175 year old came into the fall has previously fractured their hip. What is this device here? So this is a dynamic hip screw. So that's something that's used for for neck of feur fractures. And it has a very distinctive appearance on X ray imaging. So again, NF management, clinically, very important topic can get a little bit confusing. There is a video that explains exactly in which circumstance they use these different options like total hip replacements, hemiarthroplasty, etc, et cetera. Uh right. Uh 48 year old uh cholecystitis review, how is still spiking temperatures? LFT S remain deranged with a significantly raised serum bilirubin concentration. So this should really be ringing alarm bells for you because this patient has already has evidence of an infection within their biliary tree. However, now their LFTs are kicking off and they are continuing to spike temperatures. So this suggests that they are developing an ascending cholangitis. Um So the issue here is that they've got some sort of something causing an obstruction, well, a gallstone causing an obstruction to bile flow. And that system is infected literally anywhere in your body. If you have a tube that's blocked and whatever proximal to that is infected, the management of that is draining it. So think about an infection obstructed urinary tract. You do a nephrostomy or something, you basically need to decompress it somehow. The same applies to the biliary tree. Given that this patient is septic and unwell, they've got an infected and obstruction, biliary tree, they need to have that drained and the best way to achieve that in the first instance to stabilize the patient, get control of the source of the infection is percutaneous drainage. A 37 year olds, a patient with a background of got needle track marks on their, on their arms has previously injected heroin and a murmur is heard upon a saltation. Again. There's a very classic question, perhaps a little bit old school again. But the point is that with infective endocarditis, there's sort of two different camps of patients who have infective endocarditis. There's the ones who have dodgy valves and because their valves are dodgy, they get infected by otherwise fairly benign bacteria. So classically, it's patients who have rheumatic heart disease, they have some sort of mitral valve defect and the fat and by extension, when their mitral valve is abnormal, it means that certain fairly innocuous bacteria from their gi tract or from the oral cavity will stick and cause a vegetation. That's one camp of, of infective endocarditis. The other camp is when there are people who get exposed to very, very nasty sticky bacteria which basically latch on to the first obstacle that comes across and creates an infection. So this typically refers to people who are intravenous drug users who may not necessarily clean their skin particularly well before injecting. And hence, they can introduce nasty sticky bacteria like staph aureus into the bloodstream. So if you think about it, it's into the venous side of the circulation. The first irregularity really that these veins will come across is the tricuspid valve. So that's, that's a classic picture. Obviously, I'm not sure a quite how relevant this is any more because obviously these patients get echoes and various things pretty quickly. But classically, patients who inject drugs run the risk of introducing staph aureus into their venous circulation. The first valve they come across is the tricuspid valve and hence, they are at increased risk of developing tricuspid valve endocarditis. The only reason I included that is because that definitely came up in one of my med school exams quite a few years back, right? 67 year olds back on CKD um dose for hemodialysis three times per week. Uh So what's the main abnormality? Obviously, the creatinine is high but not much higher than usual. Um Everything else looks all right, except for the fact that the calcium is quite low. And remember what I mentioned earlier whenever you look at a calcium, look at the PTH. And in this case, you can see that the PTH is actually totally appropriate. So this is secondary hyperparathyroidism. So I think hyperparathyroidism can be taught a bit a bit confusingly sometimes because secondary hyperparathyroidism makes it sound like it's a diagnosis like it's pathological, but it's not, it's completely physiological. This patient is hypocalcemic because their kidneys don't work properly. And hence, they don't do the whole process of activating Vitamin D as it should. And hence Vitamin D being one of the main drivers of calcium in your body. If that isn't activated by the kidneys, it means that your calcium levels are going to start dropping when your calcium starts dropping. You have one other mechanism of trying to bring that up and that's your parathyroid hormone. So, a completely appropriate response in that circumstance is for the parathyroid gland to start start producing more PTH to try and drive the calcium up. I'm just going to briefly mention what tertiary hyperparathyroidism is in that case. So we've just talked about second parathyroidism. So let's imagine the same patient a few, few years further down the line, they come into clinic and their calcium is, I don't know like um like 3.5 or something and their PTH is still high. So with tertiary hyperparathyroidism, essentially, what happens is that this overworked parathyroid gland suddenly just develops a mind of its own and starts producing shed loads of PTH and not responding to feedback anymore. So that's why the calcium actually becomes high rather than staying within a normal range. Oh, right, 13 boy nephrotic syndrome has to be started on prednisoLONE. What's the other big risk? And this is venous from embolism. So with minimal change disease, you basically have damage to the podocyte foot processes, which basically makes the glomeruli much, much leaker to proteins. So you get loads of protein in the urine. And if you think about which proteins leak out, you get clotting factors leaking out. But actually disproportionately, you get lots of antithrombin three leaking out. So, antithrombin three is one of the main anticoagulant, intrinsic anticoagulant mechanisms within your body. So, if you leak out a lot of antithrombin three, it means that of the various procoagulant and anticoagulant substances that you produce endogenously, which normally maintain a fairly harmonious balance, preventing your blood from becoming too sticky or too thin. If you suddenly lose a lot of the antithrombin three, your blood is just going to be a bit too sticky, full stop. So that means that they are at increased risk of VTE and that needs to be managed accordingly. Right. Last three questions. See, my voice holds out. Um, 71 year old has had a sty ejection fraction of 35% which of the following has a prognostic benefit. So there's the pillars of heart failure management. And another point I want to make is, please do remember there's a very clear distinction between someone who's in acute heart failure where they've got pulmonary edema, they're hypertensive etc versus someone who has chronic heart failure. So, in acute heart failure, it's all about offloading the patient usually by giving frusemide, by giving nitrates by giving CPAP if need be. Whereas in chronic heart failure, when they're stable, it's all about giving medications that improve the health and remodeling of the heart. So the class of medications that are important in, in the in or rather have a prognostic benefit in chronic heart failure are beta blockers, like bisoprolol ace inhibitors, like Ramipril, sometimes things like spironolactone as well. And they, there's also all sorts of various new medications as well, which tend to be used quite a lot. So SGLT two inhibitors like dapagliflozin. And then there's various, what's the word angiotensin receptor blocker slash neprilysin inhibitors like secure Valsartan, which you will come across. But the main ones to remember are ace inhibitors and beta blockers. Those tend to be the two staple ones that they are started on. And then with more specialist input, they might be on things like dabrosin and secure Valsartan. What um intractable itch didn't respond to antihistamines and this is the LFT S. So again, we sort of touched on this topic earlier. Um they've got a background of vas colitis and one of the associates of V colitis is primary sclerosing cholangitis, which is just to remind you autoimmune obliterative condition which affects the bile ducts causes basically narrowings within the, within the biliary flow. And that leads to this obstructive picture. And this process can in turn result in cholangiocarcinoma. So the main point to see here is that it's the two sort of biliary LFTs. So ALP and GGT, which are raised, although over time, you can also get a derangement in uh the, the transaminases as well. Finally, final question, we have a 49 year old, increasingly breathless on the surgical ward, had an uncomplicated orthopedic surgery procedure recovering well, seems all right on the whole, but has a new option requirement of 4 L per minute. Everything else seems all right. He did ad dimer. It doesn't seem to be bad. Chest X ray also doesn't, doesn't look too bad, just some opacification in the, in the right um lower lobe. So in this, this is again, very, very common. It's introducing you to the topic of atelectasis. So, atelectasis is something that again, I really can't remember being taught about this whilst at med school. But basically your lungs need to have a reasonable circulation of air for it to remain open. Um And if it doesn't get air, it kind of snaps shut and hence you lose surface area for gas exchange. So imagine someone has just had a big operation there, basically hunched over in bed, they're in pain, they're breathing quite shallowly. It means that the bases of their lungs aren't actually expanding particularly well and air isn't circulating through them particularly well. So that can lead to these airways just collapsing in on themselves. So, you know, you absorb, you extract the oxygen from it, but there's no fresh supply coming in. So these airways collapse in on themselves. And over time, you do get a reasonable loss of surface area for gas exchange and, and that's called atelectasis. Simple solution. You just do some chest physio with them. You basically encourage them to do some deep breathing. You can give them this incentive spirometer thing, which looks like a, I don't know how to describe it. It looks like a shisha pipe basically. But you take deep breaths to try and open up those lungs. And then the physios can also come and do some stretches and exercises and breathing drills and things to try and improve that as well. So it's definitely an important diagnosis to consider. It's very common and it avoids you giving antibiotics to everyone who has got some crackles on a chest X ray, right? So that's, that is everything. Um Sorry, I rattled through that pretty fast, but I did want to try and be as efficient as possible just for your sakes. Um I'm more than happy to answer whatever questions you may have and I think there's a, there's a feedback form as well for you guys to fill out if you want to. Um And that's it. Thank you very much for joining. Thank you so much. We have lots of questions in the chart as well. Oh, sure. Sorry, I didn't even see that. Let me just have a uh I can't seem to see the chat as the main issue. I can read them out for you. Yes, please. Ok. So question six. Yeah, hold on, let me, yeah, go ahead. Sorry. Why would you not give steroids before advancing to magnesium sulfate? Yeah. Good question. I think it's based on the option of steroids that I gave you in the first place. Yeah, basically the, the steroids, you're completely right. You would give prednisoLONE or maybe hydrocortisone. You absolutely categorically will not give methylprednisolone, methylprednisolone is like the domes of, of steroids. It's something that you only use for things like giant cell arthritis or MS flares. Um It's exceptionally potent. It is not something you'd use for an asthma attack. So good question. But, um, and steroids, you would give the circumstance. you just would not be giving me without bread. So of the of the options available. Magnesium sulfate is the right one. OK. Question one, we have, what's the difference between outpatient angiogram and CT angiogram in this case? Fair enough. II should probably word that a bit more clearly. When I said outpatient angiogram, I was talking more an invasive angiogram. So when you um because you can do routine invasive angiograms where someone gets an appointment, they go to the, whichever center does it and they have the catheter stuck in through their radial artery into their coronary arteries and they get an angiogram done where they can stent vessels as well. So that's a really good point. I will change that now just to make it clearer because that, that was a bit a bit ambiguous. Um But yeah. OK. Question 11. We have what PC two would be useful um slash change at all? NPE, sorry. Say again. What was the question? What PCO two would be useful slash change at all in P so I wouldn't really focus too much on the PCO Two in someone with AP, because PCO two is mainly driven by your minute ventilation. It's basically how, like, essentially you can still get rid of a lot of carbon dioxide whilst part of your lung is out of action. So with a pe, you can have essentially, let's say a whole lobe of your lung is knocked out. Um It's not participating in gas exchange because there's no perfusion that in itself makes you hypoxic that makes you breathe faster. And when you breathe faster, you are just ventilating the rest of your lung much quicker and you're siphoning off the carbon dioxide. So you would actually expect someone who is breathing fast to have a low PCO two. So that isn't particularly useful in the context of a of AP. OK. And then for this question, would the troponin be as elevated as in? And am I? Um that's a, that's a difficult question to answer because I've seen, I've seen patients with NSTE who have a drop of, I don't know, like 100. And then I've seen some patients with who have a drop of like 12,000. So drops like the actual number itself is kind of immaterial. It's more to do with. Is it, is it new? Is it a trend? Is it going upwards? So I wouldn't say there's a certain number that I can attribute to it. Question 12 is there an alt ast ratio for non alcoholic fatty liver disease? That's a good question as far as I'm aware. No. So the thing that II learned from med school exams is that the ast to alt ratio, I think of 2 to 1 was more strongly associated with alcoholic liver disease. I'm not, I'm not personally aware of any ast alt ratios for non alcoholic fatty liver disease, but it's worth looking that up. And then also why is ALP also raised? Uh So you can just get, you basically can just get like a certain other um abnormalities as well. So, so in this circumstance, II, think I did that just to try and get you to focus on the necessary part of it if that makes sense. So, so with this type of condition, you can, you can get some slight, slightly abnormal alps and things as well. However, the most, I'd say the most striking abnormality in this circumstance is the fact that the alt is very raised. There isn't really anything to suggest that they have gallstones just because like they may do. But I wouldn't say that that's enough to explain the alt basically altogether. I think non alcoholic liver disease better explains the fact that they have this transaminitis and they can have a little bit of an ALP rise as well. Question 16, why not aMILoride as it's also a potassium sparing diuretic? So that's a good question. And aMILoride can cause a high potassium. The main thing is that in someone who has got chronic liver disease, that's unlikely they are basically unlikely to be on aMILoride. So the main diuretic that they use for someone with chronic liver disease is spironolactone aMILoride. I've only really seen, used a handful of times and that's usually to balance off the effect that another diuretic has on potassium. So for example, if they are on various other diuretics like frusemide or some sort of thiazide, which makes them hypokalaemic. I've seen patients being put on aMILoride to balance off the hyperkalaemia if that makes sense. So the main point, this is kind of twofold and it's a completely fair question, what causes hyperkalaemia of these options? It's only spironolactone and aMILoride given the circumstances, which drug is the patient more likely to be on? It's spironolactone. OK. Question 17. Would you mind just elaborating the clues that the patient is in fluid overload? Um Sure. So to be fair, that's, that's a completely fair criticism because II do think it's, it's probably not giving you quite enough information to say for certain that their heart is overloaded. Um I think the main issue is that the patient does have um a background of quite significant heart disease. So that's a completely fair point. I do think it probably does need a little bit more bulking out and just to just to be fairly certain that it is fluid overload that's causing it but uh but either way, I think the most important thing to remember is that patients who have dodgy hearts can have poor perfusion because their ventricle is being stretched a little bit too much. It's all to do with the whole Frank Starling law where the stretch of the ventricle leads to improved contractility up to a certain point beyond which it starts to decrease. So the idea is that by basically offloading the patient, reducing the venous return to the right side of the heart, it gets the stretch of the heart muscle to a better position where it's able to contract a bit harder. So in response to that question, I think that's completely fair enough. I don't think there is actually enough. That's um aside from the extensive heart disease background, it is a little bit difficult to decipher this spa. And I think there should be a few more clues to suggest that they are probably a bit fluid overloaded. Ok. Question 19. Could you also stop atorvastatin due to muscle side effects as she's had a long life? Uh That's uh that's fair enough. But I would say in this context, the more important thing too, that's a really good, that's a really good observation. So you probably would. But to be honest, I think like statins cause a degree of rhabdo in a sort of idiosyncratic way. And I don't think it would necessarily make things that much worse in the short term. And I think in this circumstance, a more important thing to withhold is the Metformin given that they have a new AKI. So again, that's actually a really fair point. That's not something I'd considered. And I probably will actually change that answer option just to save confusion, but it might be well done for spotting that question. 20. Why is her Vitamin D high 20? So I think that was mainly just to illustrate the point that Vitamin D levels are notoriously inaccurate or they are a bit hard to interpret. Like you can interpret it when it's, when it's, when it's extremely low. But you very rarely get people with very high Vitamin D and something that's 57. You really wouldn't think twice about it. So it's basically to illustrate the point that a Vitamin D assay isn't particularly accurate or reliable. It's sort of like almost like a binary test really? Because a lot of people have extremely low vitamin Ds in which case, you know, for certain that they are Vitamin D deficient. Ok. Question 21 isn't 20% for hyperglycemia? Why not go 5%? Uh, 20 sorry, it was 21. Is it 21? Yeah. Sure. Question was, why not give 5%. Yeah. So on the whole, all the guidelines that I've ever seen has been, I don't think 5% I don't think 100 MS or 5% would cut it. I've never seen 500 MS or 5% being used just because you do need to introduce insulin pretty quickly. So it's usually given over about 10 minutes or something. And the issue with doing this is that I don't think it would respond to the insulin bolus quite as quickly. So, generally, speaking of all the places I've worked, this has been the, um, the prescription that's used for hyperkalaemia. The only exception is in places like I, you can give them like 50% Dextros and stuff without too much, too much trouble. But usually it's 10 units and 100 M of 20% just because that's enough glucose to make sure you don't become hypoglycemic. And honestly, no one is going to be harmed by 20% glucose anyway. And it's a smaller volume of fluid. So it's usually easier to administer in question 23. How would a pressure so present? So I wouldn't say I'd say that that's one diagnosis you're basically never going to be making yourself because it's usually something that, um, that the nurses pick up a lot of the time. So whether you're working in Ed or in a hospital is usually when nurses are doing the sort of personal hygiene side of things or moving the patient around, they notice that there's sores on their bottom or whatever. The main thing to know about pressure sores is that it's, as you can imagine, it occurs at points of points of contact. So bony provinces, especially when people are quite emaciated, they can get sacral sores because that's the bit of bit of their body that they are lying on. Most of the time can happen on their elbows, their ankles anywhere where it's bony and it's in contact with the bed or chair or wherever they've been, you can get a pressure sore, but they look very different and there's a whole grading system for pressure sores. But to be totally honest, that's much more sort of a nursing and tissue viability thing. And it's not something that I've ever really had to personally deal with an awful lot except for deciding if it's infected or not. In question. 30. Can you get cholangiocarcinoma from UC without initially getting PSA, I'm sure you can. Yeah, just the same way that I suppose anyone can get, can get cholangiocarcinoma. Um But I think it's, I think if that were to happen a lot of the time, I imagine you'd probably guess that maybe you did have a degree of PSC just because I think my understanding is that ulcer colitis is associated with primary sclerosing cholangitis. I don't think it has an independent association with um cholangiocarcinoma. But I think that's a, that's a, that's just a bit of nuance there. Um But, but your main point is, is associated with PSC. Question 31 why not Hartman's as this? Also, this removes the sigmoid and rectum two. So the issue with the fair point, the issue with Hartmann's is that it, you bring out a colic colostomy and you leave a rectal stump. So Hartmann's is generally an emergency procedure. It's not something that tends to be done electively. So it's usually in conditions like let's say you have a big tumor in your sigmoid colon which is causing an obstruction and you present in bowel obstruction or you have a volvulus or you have a diverticular preparation in that area. It's something that's done under suboptimal conditions where you just need to get rid of the bit that's affected, you bring out a stoma and you let everything settle down. So, in someone who is otherwise completely fine, I'm certain that they wouldn't be keen to just have a stoma for no reason. In which case, an anti resection is more appropriate. So your heart's, it tends to be more of an emergency operation. In question 33. What would the answer be in line with the current guidelines? Say again, what would the answer be in line with the current guidelines? That's a good question. I actually didn't. Um uh chest pain, breathlessness playing rugby, not desaturating symptomatic. Yes. High risk characteristics. No, safe to intervene. Uh So that's, I think safe to intervene is based on how big it is and whether it's like whether it's amenable to aspiration and what's the main. Yeah. So basically you can't really answer that question because you don't really know this section of it. You don't know whether they, they are fairly comfortable with it. They'd rather avoid the. So essentially you can't really answer the question based on the new guidelines. I would just recommend just having a really solid look through this, um, this guideline just to make sure that you're familiar with how it works. Ok. And question 38 why isn't blood in the stool from the cecum dark Melina, whereas from the sigma is bright red. So sorry, what was it? Say that again? So why isn't blood in, in the store from the cecum do like Melina? Right? Ok. I would say that I think it requires a little bit more digestion than just that to, to cause it to go dark. So normally you get dark blood from it being in the upper gi tract. So basically anything from basically anything from the start of the Jejunum upwards that has sufficient time along a huge length of small bowel to become digested and mix with all kinds of stomach acids and bile and stuff and have that malonic appearance. Whereas a lot of stuff that's in the colon tends to be quite fresh and question 40. Um Did you say most kidney stones are radiolucent? Yes. Yes. Except for like certain subsets like cystine stones or something. I can't remember the details of that. But um but most are radiolucent which is why noncontrast CT KUB S are are are recommended and question 44 is percutaneous drainage the same as the RCP here. Uh No, it isn't. So ERCP is an endoscopic. So the e is endoscopic. Um so that's not percutaneous. That's literally stick a stick a probe through the mouth. Um Percutaneous means. So you can do um stuff like percutaneous transhepatic cholangiogram or PTC S. It's probably worth writing that down and just looking at a diagram of it. Um But essentially that's a procedure done by interventional radiologists where they, I don't know which form of imaging. I imagine the CT, but basically under imaging guidance, they can stick a drain directly into the common bile duct and drain that system. So there are two main things that can be done. It's a cholecystostomy, not a cholecystectomy, a cholecystostomy. And that's when you literally stick a stick a drain through the skin into the gallbladder and allow the bile to flow backwards out of that. Or you can do a percutaneous transhepatic cholangiogram and stent. And that's when you basically go through the skin through the liver into the, I think it's the hepatic duct or the common bile duct and you stick a drain in there. So that all of that bile that's got stuck there can drain outwards. And then he says, why would her inflammatory markers normalize if she's developing ascending cholangitis? That's a good question. That's a good question and, and to be fair, it can lag a little bit as well. So, so you can sometimes get a get an infection and actually like a couple of days later, your CRP manifests. So that's a fair point. But I wouldn't base it just on the inflammatory markers. There's enough stuff here to make you very concerned that you don't need the inflammatory markers. They're spiking temperatures. Um, and abdomen has this hard mass in the right upper quadrant, which is potentially the gallbladder and basically the bilirubin concentration has gone sky high. So all of that together suggests that there is some sort of congestion to their bilary tree. You don't really need the inflammatory markers to be able to be concerned about what's going on. And then for this question, still, um, investigation is not needed prior to drainage. They will need a, a CT scan of some form, but that's it really. So I think investigations wise, that's probably all that they would need is a CT scan just to demonstrate the fact that it is struct or an ultrasound scan if the sufficient personnel are around and then could, could this not be an? Absolutely. It could also be an, er, either way they would need drainage of that because there's no way in which an, er, is going to resolve itself without, without having to actually remove it. Basically, in question 50 how would you distinguish atelectasis from fat embolism in this case, from, from a pea, from a fat embolism? Oh, fat embolism. First of all, is extremely rare. Uh, it tends to happen a little bit, a little bit more acutely and, and basically fat embolism. Um, it's a bit of a misnomer because people associate fat embolism with being something that, um, like presents a bit like a pe but like, it's a bit of fat that gets stuck in a blood vessel and causes obstruction to the pulmonary circulation. It's not that at all, essentially fat is just super, super stimulating to all the various enzymes and clotting back to the various things in your blood. So, fat embolism when completely fair point because it is something that the complication of orthopedic surgery because the fat in the bone marrow can sometimes leak into the circulation. The issue with fat embolism is that you've developed this massive inflammatory response. So it isn't like a pe where people just get a bit breathless or whatever people develop this horrendous inflammatory response because there's this very, very stimulating bit of fat going through your circulation and your entire inflammatory response is activated to an extreme level. So I would, I would definitely read up on the topic of fat embolism, but it's exceptionally rare and it presents in quite a different way. Ok. We have a handoff. I don't know if someone wants, hi, sorry. Um I just want to ask for a question 44 if it was an empyema. Is, is that the, so is having the percutaneous drain the way to manage it or at what stage would you consider doing a cholecystectomy. Uh Sorry, it's 44 was it? Yeah. So let's say this was, I mean, I know it's not clear but let's say if this was a, so I'd say the main reason why I'd be concerned about this being so of the two diagnoses, the main reason I'd be more concerned about the um ascending cholangitis side of things is also the fact that the bilirubin concentration is going sky high as well. You can get that with an empyema as well. Um However, I would say it's probably more likely in the context of um of ascending cholangitis in terms of if it is an empyema, what would they do to manage it? So a lot of the time they do, they can just do a percutaneous drainage. To be totally honest, I'm not 100% sure at what point they would decide to do a cholecystectomy. Um I doubt they'd do a laparotomy. I don't think changing the antibiotics are necessarily going to make much of a difference and it's not going to be an Mr CP and it's, I would say it's unlikely to be a lap cholecystectomy for something like an empyema just because you don't want to accidentally spill all of this pus into the abdomen. So I think of the answer options available. It's it's still going to be percutaneous drainage in the context of an empyema. I hope that answers your question. Thank you. We have a few more questions. Sure. Um Question 38. Can you please repeat why? It's um I know it's in the 3838. This is a really old school. I think I need to get this one. Basically, the idea is that so basically with your stools, they are very, very liquid up until they get to the cecum in the cecum. And from that point onwards, it starts to dry up. The purpose of your colon is to absorb the water, make it a little bit more solid and formed. So if you think about that journey, it goes from being quite liquid in the cecum to being quite solid in the sigmoid colon and rectum. So if you've got some bleeding at the start, that's all going to mix in with the liquid stool and then eventually that's going to become, well, it might not become particularly formed ever. Just because the fact that you have blood involved, the blood mixed in means that it's not able to form a solid stool quite as well. If you have some bleeding near the sigmoid colon, first of all, you might just have some blood coming out on its own without any stool or you'll find that the stool is perfectly formed, but it's got some streaks of blood on the outside. So the idea is basically saying in that sort of conveyor belt process where it goes from being liquid to being solid. Where are you inputting the blood and how would that mixture manifest in terms of clinical features and question six, why not methylprednisolone? Yeah. So just to reiterate the point. So methylprednisolone is a super, super potent steroid. It's never, never used for asthma. It's only used for quite aggressive inflammatory conditions like giant cell arthritis, MS flares and things like that. So I put that in as a distractor on purpose, prednisoLONE perfectly fine. You would definitely get that. But I didn't put that answer in because that would also be correct. Methylprednisolone is far too potent. A steroid to use for an asthma attack. And question 20 how does a malignancy cause? Pe that's a good, good question. So basically malignancies in general, they, they cause various, I think there's lots of different mechanisms. I think it depends on what type of cancer it is. But there is a very strong link between having some sort of active malignancy and being hypercoagulable. I don't know precisely what mechanism it is. And I imagine, to be honest, I imagine it's a variety of different mechanisms depending on the cancer, but it must be something sort of humorally mediated. So the cancer cells might produce something which increases the production of your clotting factors or makes you just generally more procoagulant. So I wouldn't worry about the mechanism because I don't think there is a single mechanism. Just know that if someone has a pa you really do need to think, do they have some sort of underlying cancer. And question 16, why is it not bend 16? So benzthiazide would ordinarily cause a hypokalemia as well. So that's the main reason it wouldn't necessarily cause a hyperkalemia. That's the main, main point. So the two drugs that could cause hyperkalaemia are spironolactone and I because they are potassium sparing diuretics in question 39. Why is it blood film? 39. Uh So 30 I imagine that's the thrombocytopenia question. Yeah. So basically, this patient is otherwise fine. The blood test, the only abnormality is a low platelet count. Um Basically one very common reason that the printout or the the the number on the platelet count is low is because the platelets have just clumped together. So it doesn't mean that they're just, it's just an error of the whole like sort of sampling process. Um So it doesn't mean that there's anything wrong with the platelets or that there's not enough of them. It just means that when the machine was counting it, some of the platelets had clumped together and hence they were counted as one instead of 100 or whatever. So basically, the blood film allows you to look at the, look at the blood cells and see that. Oh, actually, you know what these platelets all clumped together. So this isn't a true thrombocytopenia. It's a false thrombocytopenia due to the fact that these platelets are clumped together. So that's the reason you'd request a blood film in question three, we have nice IV nitrate is only used in acute heart failure if concomitant a severe hypertension or recursion aortic or mitral valve disease. So what is the indication in this case? So in this case, I would say that. So I would um to be honest, that's I've not seen that specific. So sorry, it says only use it for severe might get hypertension or am I fine? Um That's a bit of a tricky one because in this circumstance, you would absolutely 100% give a nitrate infusion just because I mean, fair enough about the BP, you wouldn't give it if their BP is like teetering. However, if their BP is stable, they don't need to be critically hypertensive to have it. But it is just a second medical option that you can use when you don't have any other options available at the time. And given the options available, I would say that is the most appropriate one. So the the the guidelines that you just mentioned, there's a few different things on there to be fair. Like none of this, none of that is mentioned here. However, of the options available, you need to do something about it because they are still on 15 L per minute. And the only option of these ones which can improve things is a nitrate infusion. So you don't have enough to work with at this point in time to know if they are having an mi or anything like that. You've just got to take action because they are in Florida pulmonary edema and they haven't responded to two dose of famide. So I would say irrespective of that point, I mean, fair enough that there's a guideline on that, but some of those guideline points you can't actually answer at this stage in this patient's journey. And hence, hence, II do think the most appropriate thing to do would be a nitrate infusion. Certainly wouldn't be any of the others. OK. And question 26 FSGS is associated with autoimmune conditions. So can, can it not be this? Uh Let me um I would say it's probably less likely because FSGS are normally associated with. Um I didn't really associate with autoimmune conditions quite as much as I associate with things like HIV and obesity so that I'm not 100% sure about. But generally speaking, in someone who's got, who's got chronic inflammatory disease, regular flares and is proteinuric, I would head towards amyloidosis as the most likely diagnosis. So it's worth having you look to see which one is more likely in chronic inflammation. But on the whole, I've always learned chronic inflammation has been more strongly associated with amyloidosis due to the due to the accumulation of that serum amyloid A protein. OK. And question 38 aren't the sigmoid and rectum more distal than the cecum? So if it's bright red, why isn't it one of these. Yeah. So that, that's basically the same, same point as before. I think you can still get pretty bright, you can get pretty bright red blood from anywhere in the colon. So it tends to be dark, you know, like black mic like that kind of classical description when it's upper gi so there's, there's several meters of small intestine between, between like a peptic ulcer bleeding and the cecum. And in fact, the colon is a relatively short stretch of bowel compared to the small bowel. So you can, so blood that comes out in the cecum doesn't actually spend that long in the gi tract before it comes out of the entire system. And it's not really undergoing digestion. It's just the water is just being extracted from the contents of the large bowel. So basically the kind of black, dark digested blood is more associated with the upper gi tract. And you can just get relatively fresh blood from any point within the colon. And for the same question, how would you differentiate between sigmoid and rectal cancer that I think would be pretty difficult? I don't think there's going to be any, I suppose the only way in which you probably could differentiate is if you did a Dre and you felt a mass, I don't think you'd be able to necessarily distinguish it based on the, based on the description alone. OK. And for question three, how many doses of furosemide? Can you give before moving on to the nitrate. So generally speaking again, I'm not 100% sure if there is a guideline on this, but a lot of the time you would just give two doses of 40 MGI V. Um It kind of depends on the context, to be totally honest because you can have patients who are normally on, I don't know, 40 mg BD or flusemide at home in which case they are going to need a higher dose anyway. So it requires a little bit of, little bit of, I don't know, just factoring in the context with the patient. But on the whole, I'd say two doses of IVO flusemide would be the first thing that I do. And then after that, if the BP allows it, then a nitrate infusion would be a good way of trying to again reduce that preload on the right side of the heart. And then if that's all failing, then it would be a case of progressing to CPAP. Ok. That's all the questions. Ok. Sure. Then. No.