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Yeah. So Hello, everyone. Welcome. Thank you all for coming tonight. My name is Lucy, and I'm part of the National Surgical Mentorship Society team. We'd like to give you a warm welcome today to the third of the MRCS party Crash course lecture series. Um, we are monitoring the chat, so feel free to ask any questions. And you have throughout the talk before I hand over my head quickly. Like to go over what, uh, SMS or national surgical mentorship Society is all about. So we have a, um, zone two fold. Firstly, we look to match mentors and mentees together. We put them from all over the country to help prepare students for their future career in surgery. And secondly, we want to adequately train surgeons. So from ct 12, s t eight to become successful mentors through a pre made virtual course, Um, the courses done on a rolling basis so you can enroll as a mentor omentum throughout the year and you'll be matched up accordingly. The benefits of becoming a mental, um, there's quite a few of them, but just a list of a couple of you we want to cultivate professional skills and teaching communication organization and leadership. Um, and this will help you a professional development of future colleagues while you strengthen your CV and develop self reflective techniques. Uh, sign up links on how to get involved on the screen in front of you, and we'll also post them on the chat along the way. Um, at the end of the talk, I'll remind you again. But please don't forget to fill out the feedback forms. We will provide a certificate and to look out for future series is or future lectures on the instagram page. So without further ado, I'd like to give a warm welcome to today's speaker, Doctor Hadippa here, who is qualified as a pharmacist and a doctor. Um, and he's recently finished F two and is currently working as an S H O in trauma and orthopedics. Um, so you take it away, please. Thank you. Hi, everyone. Welcome. We'll go straight into the questions. So basically, today is about physiology that will help towards the MRCS exam that you have in September. So the first question that we've got here is we've got a 75 year old lady who was found to be hypercalcemic and is diagnosed with multiple myeloma. What would you typically see on a Skull X ray? So the questions are there with the answers. 80. And I'll let you guys pick can actually see any answers. Sorry, I can read them out. So we've got 8% of gone with a No one's gone for B or C, 33% e and then 58% for D. So majority of comedy, which is the right answer. So I'm sure you've seen this to a medical before, is sometimes referred to as a raindrop skull or pepper pot skull. Um, and it occurs in approximately 70% of cases, so multiple myeloma is a cancer of the plasma cells. Affecting multiple areas of the body usually affects the actual skeleton and the four main features that that we referred to with the pneumonic crab. So calcium is normally elevated. They normally present with renal failure, anemia and bone lesions and bone pain. So quite a lot of people in hospital get myeloma screen. So in 2016, nice update updated their guidelines. So anybody with the age over 60 with persistent back pain or bony pain with unexplained features should get investigated for having a myeloma screen. So in this initial investigations, there's a pneumonic called Blip. So you want to do Bench Jones protein so you're an electrophoresis serum free light chain assay, serum, immunoglobulin and serum protein electrophoresis as well. Main management with multiple myeloma is either chemotherapy, bone marrow transplant or you can use bisphosphonates because it suppresses osteoclastic activity. So, question, too. We've got a 69 year old man who attends his GP practice with a history of back pain and loss of height over the past few years. His blood results are followed, followed. They're so the corrected calcium is 2.8, so it's slightly elevated. Phosphate is not 0.9 and P. T. H is 7.8 and give you a couple of minutes Just to think of the most likely cause for this case. We've got all the answers in, and we've got a few people have gone for a something e and 53% for D. Okay, so may need people to get secondary hyperparathyroidism. So the answer is actually primary hyperparathyroidism. So we'll just go over that. So this is from the EMR CS So what we know in primary hyper hyper parathyroidism is you get an elevated P T. H and elevated calcium and normally low phosphate as well. So we'll just go through the differences between the primary secondary and tertiary hyper parathyroidism in primary hyperparathyroidism. What you normally get is a solitary adenoma, and this is what causes your P T H to be elevated. PT. It's usually reacts towards the vitamin D levels in the body. Um, depending on if your vitamin D level is low or high, so as you can see in secondary hyperparathyroidism. Usually this is because you get chronic renal disease, so you're not actually activating any colleague calciferol in your body properly. Your P T H levels will be quite high in that in that level, too. But your vitamin D level is low and your calcium is actually normal, and sometimes it might be low, but most likely it's normal in tertiary hyper parathyroidism. This usually occurs when your renal function has improved after chronic renal failure. So, for example, you've had a kidney transplant. However, because you've got hyperplasia in your parathyroid glands are still reactive, so they secrete high levels of P t h And what you normally do in the treatment for that is you just play catch up over a year. If not, then they surgically need to be managed. Okay, so question three, a 70 year old man presents as a trauma call. The E d. Consultant decides to test your physiology and ask you what percentage of the total body volume is made up by trans cellular fluid. So we've got the answers there, let you guys pick. Yeah. So it looks like you split the field a bit more here. So no one's gone for a got one for be a couple for C, and then 41% for D and 33% 40. Okay, so the one for be whoever you were, correct part of the back. And this can be quite difficult concept. I normally just remember this with the diagram here that I've got with the male and female there. So these values here are normally representative of a 70 kg mail. Um, there's no hard and fast way of learning this. I think the way I kind of remember it is just fill it down to this diagram here with the mail and just split it off that way and see where it goes from there. 3% is Tran Cellular. Okay, so question for which of the following is not seen when a patient's ICP continues to rise and results, results and Koning So let's go for a TUI again. See what everyone thinks. Okay, so so far I've got 80% of gone B and a few answers for C and D Perfect. That's great. So, yeah, be tachycardia is normally not seen. So So you may have heard of this the majority of the Monterey Kelly doctrine. It's basically talking about the cranium is a fixed solid wall or fixed solid bone, and the components in it are restricted. They all live within an equilibrium. So on average, intracranial volume in an adult is 1700 mils and and when one shifts down, the other will shift up in the diagram shown here on the right. Um, what we normally say is that the brain auto regulates its blood supply. So as the ICP rises, the systemic circulation will display changes to try and meet the perfusion needs of the brain. Usually this will involve hypertension as I see rises further and the brain will be compressed. And that's when you start seeing your cranial nerve. Palsy is in there as well. When the cardiac center is involved, the Brady Brady cardio will normally developed. So you might have heard of Cushing's Triad, where you get widening of the pulse pressure, respiratory changes and bradycardia. Okay, just another question. I don't know if anyone wants to use the chat, but when does the Monroe Kelly doctor and not apply in the subset of patients? You know, if you can type in. If not, I'll just let you know. So who wouldn't this concept apply to? I'm not sure if you can see the chat. We've got one answer infer with neonate. Yeah, so neonate, You know, small infant, just because of the presence of the fentanyl and the future lines, and we'll slowly close up. Then it will apply as they get older. The perfect Okay, question five. An 80 year old woman undergoes a total hip replacement. Which of the following hormones is least likely to be released in increased quantities following the procedure? Okay, so a bit more uncertainty here, 45% think D and then 25. Think a and 25 think d be sorry. Okay, so the correct answer is the So we'll go through wise the table here. And basically it's your normal stress response that you get with this. So the stress response to surgery is characterized by increased secretion of the pituitary hormones and activation on the sympathetic nervous system and the changes in the pituitary secretion of secondary effects on hormone secretion from target organs as well. So, for example, you get the increase release of the called Contrave in releasing hormone, um from the pituitary, which stimulates quarters of release as well and and then cortisol secretion from the adrenal cortex. You get vasopressin and that's secreted from the posterior pituitary, and that has obviously its effects on the kidneys and in the pancreas you get glucagon released and insulin secretion would most likely be diminished as well. This is what I think of post surgery. Most people have a high or dysregulated bms. Uh, the overall metabolic effect in the hormonal changes is an increase cattle bolic effect in the body which mobilizes substrates to provide energy sources. And so I think of like a starvation phase. So the way I think of it is just a normal stress response. Okay, so this questions about warfarin. So which factors are directly affected by warfarin? Okay, so half of them think be something, see? And if you've got a perfect So yeah, he's the correct one. And let's find out why. So it's also a blood clotting cascade. Really? This is like a complex diagram that most people like wrote learn. I go for this one. So just about the coagulation cascade, we'll just go through it. I think it's easier if you understand it rather than wrote learning it. And it helps future when you're assessing patients as well. So the intrinsic pathway is here in red, um and this is activated by surface damage and then you've got the explains it pathway here. This is trauma and inflammation. Um, it's important to know which gotten factors are involved in which side. So both pathways go down to the common pathway. And your first, you know, factor is factor 10 here, and the way I think of explains it pathway is three plus seven equals 10 and then your intrinsic pathway intrinsic pathway has also got tissue factor, So tissue factor is factor three. They're both synonymous with each other. Um, in the diagram as well you can see. Like I said, both pathways go to the common pathway activated Factor 10 allows the formation of prothrombin to thrombin there as well. And you use cofactors. You cofactors the factor five and that's activated by calcium. Okay, that ultimately leads to clot formation. A PTT is activated thromboplastin time, which is known as P t. T as well. So just here and the way that I remember is play table tennis inside. So P t. T is to do with the intrinsic pathway and then PT is play play tennis outside. So it's extrinsic if that makes sense. But use your own know Monix, try not to learn just other people's. So the vitamin K dependent factors are to 79 10 and protein C. Uh, warfarin inhibits vitamin K reductase. Therefore, these are affected. Um, so warfarin inhibits the extrinsic intrinsic and the common pathway as well. Okay, so protein C and protein s and they're actually balanced with with the other clotting factors. So protein C and protein s, they are procoagulant So warfarin is a program in the 1st 48 hours when you actually give it to a patient. Um, so that's because it actually acts on protein C and protein s first, and then it acts on the remaining tissue factors afterwards after the 48 hours. That's why you normally get bridging with flexing. Okay. A 60 year old man is admitted to I t u following an r t a. Whilst in I t u, his urine output drops and his kidney function deteriorates. What factor would point towards pre renal uremia over acute tubular necrosis? Bit more uncertainty. So we've got mostly CS, but a few A and D. Okay, so the main answer is, Well, the only answer is a and we'll go through. Why? So the main thing with pre renal I think this diagram is quite good on the right here. So prerenal, if you think of it, your kidneys aren't getting perfused. When it's acute tubular necrosis, your actual kidneys are not functioning at all because there is inside the kidneys that are messed up. The main things that do this the drugs, toxins and prolonged hypertension in the form of being the most important of drugs and toxins. That's what causes acute necrosis. So a question hint. There would be anything to do with drugs or toxins most like in a younger patient or someone over older having an overdose or something like that. The the question was asking about your in sodium. So if your sodium is obviously re absorbed in the kidneys, if you're not reabsorbing sodium, your your brain is going to have more sodium in it, so it's going to be more concentrated. That's that's why the answer to the question was, your sodium less than 20. The other main thing is, if people have picked, you know, lack of response to a fluid challenge. Fluid actually helps in pre renal, but in, uh, in acute tumor necrosis fluid kills because you can't filter out. So essentially your body is overloaded and drowning. If you're giving fluid to in acute tumor necrosis, hopefully that makes sense. So we've got a 45 year old alcoholic, alcoholic patient who presents with severe pancreatitis, admitted to I t U 72 hour later, he's a hypoxic and confused portable chest X rays performed, which reveals a uniform classification of both lung fields. His pulmonary artery wedge pressure is 12. What is the most likely diagnosis? It's quite a few hints in the first line, so so far everyone's gone for D Good. Okay, So if it's di do, does anyone know what is the main reason for hypoxemia in this condition as well? They can write in the chart, Uh, someone coming with reduced diffusion. Yeah. So when you get diffuse lung injury, um, it's associated with loss of surfactant and increase the last days from the neutrophils results in fluid accumulation. So reduce diffusion, which is the main reason for the hypoxemia well done. So our definition wise you want, you've got bilateral Hormonial infiltrates severe hypoxemia and the absence of cardiogenic shock. So the pony wedge pressure is normally less than 18, um, causes. They can have direct causes, which is the pneumonia or indirect causes. So sepsis, trauma, pancreatitis, D i. C. Or liver failure. Clinical features. You get acute dyspnea and hypoxemia hours two days after the actual initial insult, multi organ failure as well and rising venture ventilatory pressures management. You want to treat the underlying cause. Antibiotics if they're needed, negative fluid balance so encoded a lot of people had would develop odds. Normally, do a fluid restriction on them. Recruitment maneuver. So prone Ventilation, Mechanical ventilation Using low tidal pressure's higher title. Pressure's about because they cause lung injury. Um, next question. So the question now a young patient who's an IV d'you is having an echocardiogram for suspected infective endocarditis. Which phase of the cardiac cycle is associated with closure of the tricuspid valve. Okay, so so far I've got mostly A's with a handful of B C and E. Yeah, so it's, I see also volumetric contraction, and we've got this beautiful diagram. So with those diagram, and so it always shows the right side left. So it always shows the left side right side to just lower pressure. So it's, um, you know, match to this. So as most people right, I won't go through it in particular. But what we'll go through is the It's a volumetric contraction phase. So what you get there is the ventricular pressure's increase as the ventricles contract mitral and aortic valve are shut. So the volume in the ventricle stays the same whilst the ventricle contracts. And that's why it's called Isovolumetric. contraction, ventricular pressure's increase and cause the aortic valve to open there as well. And this is just something you've got to go through, and it's better to understand it, step by step. So starting off from this historic phrase and going to end of diastolic and and that's normally one heartbeat there as well. Okay, question 10. A 14 year old girl, unfortunately, suffers from an anaphylactic reaction after unknown the eating nuts in the hospital meal she has been treated with 2.5 mg of I am. Um, let's hope that's adrenaline and is being monitored on the pediatric ward. Which of the following is the most likely responsible for her initial reaction? Okay, so everyone's gone quickly for C cake. Yeah, I g So the gallon Coombs classification here. So you've got four types there. Hopefully, most people know the pneumonic so acid at the top a c t i d. And then you got e g t. Which kind of goes through on which type of reaction is so type one anaphylactic and the mediators i g So, yeah, good to know. Good to know, for dermological reactions as well. Okay. A 72 year old woman with known COPD is in the recovery area post operatively and receives 28% oxygen via a mask. And a BG reveals the following. So the Ph 7.2 p 02. 12.1 p CO2 is 10. What is the most likely cause of these findings? Yeah. Okay, so, uh, it was changing. So 50% of Gandhi and then a few for all the other answers. Okay, Sure. So, yeah, this is the correct one. So this is the correct one. And so the reason why supplemental oxygen, So most likely this patient receive too much oxygen and what's happened? Supplemental oxygen removes COPD patients hypoxic drive causing hyperventilation which causes higher carbon dioxide level's apnea. And ultimately they get into respiratory failure if you don't stop their oxygen delivery or reduce it. Yeah. And now to the woman with a background of emphysema is receiving 28% oxygen via a mask and has the following a BG finding. So ph is 7.29 p 02 is 6.2 PCO to is April 1. Bicarb is 36 base excess is plus five. What is the most likely diagnosis. Okay, so if you really fast answers for D, um, and then a couple of people have gone a Okay, Good, Yeah, partially, because it's not resolved yet. PCO to is 8.1, and we can see that the bicarbonate base excess is high. So it's partially compensated, but not all the way there yet. So I thought I'd just go through, you know, the M A. L s trainings. They've given a five step approach to a PG. I think this might throw people off, so I don't want to go through it too much because everyone at this stage would have their own kind of way of going through an ABG. Always remember, how is the patient Clinically are the hypoxemic? Um is the patient acidotic or Alka Logic? What's happening to the peace? P CO2. And then what's the bicarb and base level saying there as well? Okay, so question 13. An elderly lady is confused in the recovery room after right hemicolectomy. Her background includes type two diabetes, hypertension, I H D COPD and bilateral total knee replacement. She is on 28% oxygen as well under a BG revealed the following So you got ph of 7.27 p 02 of 6.8 p, CO2 of 8.7 and a bicarb of 28. What is the most likely diagnosis? So the answer is coming in quite fast for E. Yeah, perfect Type two respiratory failure. Just remember type two p 02 PCO to both messed up. Okay, 14. A 24 year old man is septic in recess. After presenting with a rigid abdominal, CT reveals a perforated appendix. His BP is 92 58 his heart rate is 110 and ABG reveals the following. So the Ph is 7.26 p 02 is 7.3 p, CO2 is 7.1 and bicarb is 17. What is the most likely diagnosis? Bit less confident this time. So split the field between B and E with a handful of the D. Okay, so we've got a mixed one. The main reason why it's a mixed one is because it's acidotic, so you know that it's never going to be a N. C. Because it's not compensated And the reason why it's B and C is because both of them are actually involved and quite to a high level Sorry, 7.1 and 17 there as well, which normally gives a mixed picture. It's quite rare to see a mixed picture, but the reason you see it is because that both both of them involved at high levels and, clinically the patients very unwell. So it's hard to just say it's one or the other, you know, solid solidly there. Okay, that's the end of it. Any questions? That's great. Thank you very much. So I'll just leave a minute. If anyone's got any questions, please do put them into the chat. Um, and we have put in the feedback forms as well. If you'd like the certificates at the end, Um, that would be great. So I will wait and see if everyone's got any questions or anything, which I doubt they will. That was really great. Thank you. It's very interesting. And I certainly learned a lot, so I make myself thank you very much to Doctor happy. You're here for an excellent lecture. Um, thank you for everyone for joining us today. Um So we've got a couple of thank you for coming through a great set of questions, and I completely agree. So if anyone does have any questions, it just seems to be many. Thank you for coming in, so I can't. Can't agree more. Yeah. More so you can go up from there and learn as well. So the good general questions. That's great. Thank you. So just just to remind everyone we do have two or three sessions coming up next week, so keep an eye out on the instagram page. Um, and we'll keep you all up to date with it. Um, And again, I keep reminding you all, but please do fill in the forms, the feedback forms, and you will receive a certificate. Um, and there are links to our social media. Just been put into the chat there. Uh, if you've got any questions, please do you send us any messages? So that's great. So thank you very much. Uh huh. Deep again. And thank you to the team in the background for putting everything there. We'll see you all next week.