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Brilliant so we're going to be doing L1. So this my stuff is a lot of anatomy and radiology, so um we'll get a we'll get a start now with our first s. P. A. So a patient presents with a shortened abducted and externally rotated leg. What is a likely fracture that has occurred so is it a fibula fracture, a hip fracture, a shot the femur fracture, a tibial tuberosity fracture, or the neck of femur fracture okay 10 more seconds to answer ok, brilliant, So a lot of you have well, actually quite split, so we have one for a. C and e. The answer is actually e, so what's happened here is um you've got a neck of femur fracture and the so, in terms of the different differentials, um the fibula fracture is more likely to present with a different kind of history, patient's are commonly rolling their ankle immediately and this is what happens when you get a fibula fracture. A hip fracture is too vague. Um This won't be the single best answer because there's lots of bones that makes up the hip. You've got the iliac um so the ileum you've got the acetabulum you've got lots of different things in the hips, so that wouldn't be the single best answer in terms of shafter femur fracture. Um You won't really present you I mean you will present with the external um so you will present with a shortened leg, but the external rotation is more likely to be the neck of femur fracture. Um tibial tuberosity generally occurs as an avulsion fracture from the patella or quadriceps tendon and that will have a different mechanism of injury um So you have a different presentation as well and yeah so the neck of femur fracture does give you the classic shortened abducted and externally rotated leg okay. Next question so what muscle is primarily involved responsible for extension of the knee. I'll give you 15 seconds sounds to this one okay, so we've gone through b and e um I would say the answer is actually a so the quadriceps, so um the quadriceps is actually is actually involved in the extension of the knee as the tendon will connect to your tibial tuberosity at the front of the tibia, so when the muscle contracts, it will extend that knee and straighten it um and just to note that the quadriceps is made out of four groups as a group of four muscles, so you've got rectus femoris vastus lateralis, vastus medialis, and vastus intermedius, which is actually deep to the rectus femoris. Now for the other answers, biceps for morris is involved in the flexion of the need as it forms part of the hamstrings. Um The gristle is muscle is involved is one of the medial thigh muscles so that will deduct the leg to bring it in. Um the sartorius muscle actually goes from the lateral side to the medial and from superior to inferior, so it's all goes across the thigh and what is involved in is an external rotation of that leg. Semi tendinosis um is also part of the hamstrings and that will be involved in reflection of your need. Okay next question, oh sorry not next question and this is just a diagram of the different um the muscle so salty sartorius will go across your leg um and that is gracilis so that will go from that, will add up, so bring your leg in and these are the hamstrings um well. Um So we some semimembranosus, semitendinosus, and biceps for morris is good to know that biceps for morris will have two heads, a short head and the long head. Another part of the hamstrings is actually a doctor magnus um There is another head of a doctor magnus that forms part of the hamstrings, but another part of a doctor magnus forms the medial compartment okay and this is just the compartments um This might seem quite complex. If you break it down into your anterior compartment, your medial compartment in your posture compartment, that should clarify things a lot more um so within your anterior compartment, you've got the quadriceps and the arteries and within the medial compartment, you've got the adductor longest adductor brevis, and adductor magnus, so it's good to note that all of them are adductors, so they will bring that leg in um and also the gristle is as well which I mentioned earlier and the posterior is going to be your semimembranosus, your semi tendinosis and your biceps for morris now. In terms of the innovation of each of these is quite it's quite important, but also quite simple in the sense that the anterior is going to be innovated by your femoral love and if you think about it anatomically, your femoral nerve will run across the anterior part of your leg, so it's good to note that the medial um will be um innovated by the obturator enough. So if you think about the obturator, it runs inside the inside the pelvis, so it sort of goes to the medial side of your leg and um for the posterior it will be the sciatic nerve, so the sciatic nerve will actually run um in the posterior part of your leg and it exits underneath the piriform piriformis muscle, which will then innovate the hamstrings um but just a note on a doctor magnus, which is over here. It is innovative by obturator, however, the sciatic head of it will be innovated by um certain sciatic the hamstring head of it will be innovated by the sciatic nerve right okay. Next question, so from lateral medial, what is the order of the femoral triangle contents, okay. I'll give you um 30 seconds to answer this one and if you do have any questions at all, do you pop them in the chats, okay, nice, we'll wait for one more once a nice, okay, so everyone's going to be that is perfect, okay, sorry, so right the answer is actually be so when you think about the femoral triangle and the contents you need to think of the pneumonic naval so n. A. V. E. L. So, from the lateral, you've got the femoral nerve, a for artery, V, for the femoral vein, and ease for empty space. Now, this place does have some kind of clinical relevance so the empty spaces for the femoral canal and this um this is space just for any excess abdominal pressure to um go through and ellis, for lymphatics okay and the borders of it is so you got the superior border, which is the inguinal ligament. You've got the medial border, which is going to be your doctor longest and you've got your lateral border, which is the sartorius and that forms your femoral triangle brilliant, so what muscles attach onto the pez anserina, So this is one of the few attachments you will have to know okay, I'll give you guys another 15 seconds to answer it, Let's aim for like four responses, that's possible okay, wait, nice, perfect, okay, so I'm to pull that um so a lot of you have gone for d. And that is indeed the correct answer. So um when we talk about the pets answer Ryan, we need to think about the s. G. T. Muscle, so your sergeant muscles um and those will attach onto the pens answer Ryan. So your clinical relevance of the actual attachment point is the bursa underneath. So um there's something called pets answering bursitis um and that is just inflammation of that bursa from multiple causes, so you've got trauma causes um or yet to the acrogenic causes, so there's there's lots of causes that can trigger bursitis, but I'm sure someone else will go into that When we talk about inflammation ok brilliant. So next question is a patient presents with swelling in the back of the knee. This is known as a baker's cyst, what is the space in which is swelling uh is present, called mhm, I'm pretty sure right I kind of gave it away, but um yeah never mind, I gave it away. Um So well then before the, because everyone got the right answer with this one, um but basically it is indeed the popliteal fossa, so we'll just talk about a few swellings now, some of them might be more relevant to you guys. Some of them might not be, but it's good to know anyway just from further information, so swelling in the femoral canal is likely to be a femoral hernia. Now these can become a surgical emergency when there is strangulation of that hernia, so this is when it becomes a scheme ick and the blood supply is cut off. So the swelling in the popliteal fossa is likely to be a baker cyst. Um This is going to be the outpouching of your synovial cavity um and this sort of bulges into the posterior wall of the knee. It will cause occasional kicking and locking of the joint, um but it's most likely not to need treatment because it doesn't normally cause symptoms. Now, the flexeril tenaculum um this one is more more likely to cause tingling and altered sensation and you get some muscle weaknesses as well, um and just to clarify this. What I meant by this is the flexeril retinaculum of the hand um and this is likely to cause carpal tunnel syndrome, so tibialis longest is actually a made up name. The real muscle is called fibula is longest. Um Now, I think is one of the most interesting ones really so it's going to be the swelling in the inguinal canal, so this is called an inguinal hernia. Now these, this one has two causes, so you've got the failure to obliterate processes vaginal these, and there's going to be an indirect hernia and you've got the weakness in the abdominal wall um that causes the outpouching and that's going to be a direct um inguinal hernia, so nonetheless though these are both going to be caused by a part of the intestine, that bulges out when the pressure is exerted in the abdomen, so the indirect haniya well so basically because you've got that failure to obliterate um processes vaginal list. Um There is a pathway down to the scrotum because embryologically, this is that pathway that it goes down, but when you don't close that pathway, um the contents of your abdomen can go through that, so what happens is your intestine will enter the deep rink um and it will go through the superficial ring. Now, the deep ring is going to be lateral to your inferior epigastric vessel and it will go immediately towards your super superficial ring and this will then enter the scrotum. Now indirect hernias are going to be more likely more likely to happen in children um and this is because it's an embryo logical thing where it doesn't close um The direct hernia is actually a bulging through the super, so it's a bulging through the superficial ring, but it doesn't enter the superficial ring so what what tends to happen is you will get a bulging in the abdomen wall, but it won't enter the scrotum right. So this is just a bit about the popliteal region, which is obviously where you've got your uh tibial nerve that splits off into your common peroneal nerve. You've got the popliteal vessels in it and you've got some lymphatics in there as well, okay and the baker cyst of looks like this. Um in the diagram, it doesn't actually look like that in a patient, but what you will probably see is a little bulge in the back of the knee and this is just the borders of your popular to a fossil which is going to be your biceps for morris um um The gastrocnemius heads and your semimembranosus iss and plant aureus also runs through it as well, which is a muscle involved, okay, and just a bit about the inguinal hernia um So as I said before the deep ring is going to be lateral to your inferior epigastric vessels, so these are your inferior epigastric vessels, they should run through here and the deep, so the superficial ring is actually um medial to it right. So next question you are studying the anatomy of the lower limp and you recall it a muscle has a superior gluteal nerve above it and the inferior gluteal nerve below it. What muscle is this okay. We'll wait for two more responses and we'll end at that brilliant, so um the majority of you have gone for option D. So that's your piriformis and that is correct, yeah so that is the landmark for nerves basically so um these are some of the gluteal muscles basically and the performers is one to remember because this is where the sciatic nerve will come through alongside the inferior gluteal nerve now there is um there is clinical, the clinical relevance is when this muscle becomes inflamed. You get symptoms of sciatic nerve compression um which is something like sciatica. Um You get a bit of motor dysfunction and sensation alterations in and that is because you're compressing the sciatic nerve and this is just a diagram of what it looks like so the piriformis is here and that sciatic nerve will run through there and when this becomes inflamed, you're going to compress that site technology, which gives you all those symptoms right. Ok next question, um so a patient presents with the inability to plantar flex after an injury that sustained during the training for an upcoming competition, so there are competitive sprinter, but they've recently taken a course of cipro ciprofloxacin for a recent infection now. They have a past medical history of ankylosing spondylitis what is the most likely injury sustained. I'll give you a bit longer to answer this one because it's it's a bit of a mouthful, we'll wait for two more responses because I think this. This question is definitely one to consider and um give it a shot basically so, I'll give you about 10 15 more seconds down to this and don't worry about getting it wrong, is anonymous and mistake making is lesson learning and it's a safe space to make mistakes right brilliant, so I'm going to end the poll there, so the majority of you have gone for option A um does anyone want to actually put their so if anyone type into the chat, why you think is option A you can say it's a guess if you want, but just show us some ideas you know give, uh do tell me why you think it might be the damage to the thing because you can't plan to flex okay fine um That is a very good suggestion and that is um that is definitely a cause of failure to plant plantar flex, however, a thing in medicine you've really got to consider is the history, so the actual answer is see, so you've got ruptured achilles tendonitis, so when you read the patient history you've got a few things to consider here um so ciprofloxacin is a quinolone and this will have a tendency to cause some kind of tendonitis um More specifically at least tendonitis achilles tendonitis. Um Now you won't really notice at this stage, but ankylosing spondylitis is a genetic disorder um that typically affects the bones of the spine, but it will also affect the achilles tendon as well so the gene responsible is going to be a hLA b 27. Um This is a group of seronegative spondylitis, spend spondyloarthropathy ease, but don't worry about it too much. You will come across this in year two. Another thing is he is a sprinter um and that will cause major force onto your gastrocnemius um and that muscle is attached onto your achilles tendon, so sudden trauma alongside your ciprofloxacin history is likely to cause this achilles tendon rupture. Um Now, tibial nerve damage, is you are correct in the sense that it will cause the loss of plantar flexion, but it will also come alongside the the loss of that sensation in the, in the sole of your feet to the plantar aspect um So common peroneal damage that is more likely to manifest as some kind of foot drop and the loss of association to the door some of your foot um and a. C. L. Injury. Um You will have a different mechanism of injury um and it's sort of more knee related um so this patient sort of got a history of no history. It's got some kind of symptoms of plantar flexion, so has more towards the foot area. Um No injury to the popliteal fossa is just gonna it's more like to present with some kind of baker cyst um and you're more likely to get a global loss of sensation because the tibial nerve and the common peroneal nerve are there and this is sort sort of where they branch off in that region. Okay. Next question, so patient has become acutely confused and decided to kick a brick with it inner soul. He now complains of numbness and um to the plantar aspect of his foot what nerve is damaged. Spoiler a lot said it before all right should I plan my questions more carefully, never worry, um but yeah give it a shot, yeah, okay, so I'll give you guys about 15 10 more seconds on to this ok done right, so uh all of you have gone to see and that is the correct answer because not because I said it earlier, but basically the tibial nerve does run through that location, so when you talk about the inner soul. Um You want to think about the flexeril retinaculum of the, of the foot. This is not very clear diagram but the pneumonic to go by is tom Dick and nervous harry. So within this flex of retinaculum, you've got the tibialis posterior, your flexor digitorum longest, um and these are the tendons, sorry that run through it your tibial artery, you've got your tibial nerve and the tendon of flexor high list as longest, so, this is the pneumonic to go by, so tom Dick and Nervous harry to remember the contents of your medium malleolus flexibility inoculum right so moving on to the next L0. Um let's crack on straight away, so um you are a medical student preparing for your neurology block on placement, and as part of this, you want to elicit the ankle reflex, which nerves are responsible for this. Thanks, okay, I'll give you guys five more seconds brilliant, so the majority I have um there is no majority actually it's just quite split answer. Um so we've gone for a c. N. D. The answer is actually a so, when it comes to reflexes, there is a very nice um pneumonic to go by um so that's going to be so working from the bottom to the top right. You want to think about your ankle, your knee, your biceps and triceps, so you got s one s two for your achilles tendon. You've got L3 L4 for your knee, you got c five c six for your biceps and you got c seven c eight for your triceps, so you can see the number go up in order if you want to go, buy some rhyme as well, you can so, s one s two buckle my shoe L3 L4, kick the door, c five c six pick up sticks, c seven c eight, let them straight. Um In terms of the cream cremasteric reflex and the anal wink um just for just for completeness, we'll say L1 n two L1 L2 testicle move uh s three s four wings galore Father was reading a story there, but we'll move so anyways, so a patient has come into a and E with a posterior hip dislocation what is the most likely nerve damaged now. I urge you guys to think more anatomically about this question, so you've got to think which nerves is more likely to become damaged, so think about the mechanism of injury and think about where this um what this dislocation will affect okay 15 more seconds. Don't worry if you get it wrong, just put an answer Even if you don't know any answer, will do okay, but we'll end it there brilliant, so actually most of you have got a right um we've gone for option A so that is the sciatic nerve and that is correct, so when you get a posture to hit this location. This is sort of sort of what it looks like, so you get that neck of femur moving back and potentially compressing your sciatic nerve because you know the femoral nerve will lie at the anterior aspect. Obturator will run on the inside, so obturator sort of runs along the medial aspect and your scientist will run behind and that is a looks likely no damage starting to end up skipping questions, so a patient has presented with damage to their superficial peroneal nerve what is the most likely clinical presentation of this okay any answer we'll do just put something down and I'll give you guys 20 more seconds to answer this. One give you some time to read it and think about it, let's get you more answers in ok, brilliant, I'll just enter there, so we've got quite a wide split. We've got some people answering d. C. And e. So the answer is actually going to be so you've got weakness implant a flexion and weakness in the version. So this is the role of the superficial peroneal nerve. Um If you talk about a so numbness at the first webspace of the dorsum of the foot, This is going to be more likely a deep peroneal damage um so as you can see here. That is what it innovates the deep peroneal that little spot over there and that's the only place that the deep perennial will actually innovate. You can go back to our questions, sorry, so inability to dorsiflex weakness in version. This one is going to be more like the, the D perennial because that is involved in your inversion, Actually sorry they'll be involved in the version. This is made up sorry there is no weakness in inversion for this one, inability to plant the flex, inability to avert the foot, um so the inability is actually university the plantar flex that's gonna be tibial, sorry, inability to plantar flex and go with me. This question is outdated. I got it wrong, sorry, it's actually inability to to dorsiflex um the peroni, a, while the deep peroneal is actually involved in all right, let me come back to this one sorry, and give me a second. I will come back to this question, give me some time to think about it. I think I might have made a mistake so that's all my parts my bad. We'll move on to this window so um what nerve root is responsible for the knee jerk reflex, So if you go back to the pneumonic I was talking about okay. I'll give you guys um 20 seconds answer as well, big ass, all right, we'll end it there, so the uh there is a split between a. N. C. Um Now If you remember from the pneumonic earlier. Um s one, s two um back on my shoe L3 L4 kicked the door, so the knee jerk is actually going to be L3 L4 um s three s four. Um I don't think there is a reflex for that, so it will be L3 L4 but good thinking though um he got the right numbers, but it's just L3 L4 Also just regarding his question, avoid the question, I think it's wrong. Um Apologies that's in my half this slide might have been made in a rush, but yeah. So next question, a patient presents with the inability to adopt a duck the hip and it's complained of needle thin ominous what nerve is most likely damaged and we spoke about this earlier nice ok, lot of responses then so everyone has actually gone for see brilliant, So glad some people remembered what I spoke about at least so optiray terrorism involved in the medial side of things, so your medial um your medium uh thigh compartment muscles, so that's your adduction of your hip and that numbness is actually this region here, so or is it in this little tiny region. The medial aspect of the fi, um now the femoral uh the femoral tends to innovate the and serious side of your your thigh and the posterior is innovated by the sacral plexuses. Yeah we'll leave, we'll leave that there so um when when I send out the slides just feel free to look at these in your own time and get to grips of what's innovative what's basically all right, so the next L0. We're going to fly through it, so this one is a bit of revision from pCS one or PCS to or pcs three. I think they switched it around now, but it's gonna be histology so um what are you likely to find in the histological samples of the vastus directors muscle, and I do hope they actually put this in because the last time I did a talk on histology. They it was completely wrong because they switched around PCS. So hopefully this is more relevant, okay, we'll try and get one more answer in from someone, and we'll end it there brilliant, so everyone's gone for see, so that is the correct answer. Actually so we're thinking about highly striated, uniform pattern, multi nucleated, so this is going to be your typical striated muscle cells interrelated discs, multis, righted mononucleated, that's going to be your cardiac cells. No striations, mononucleated, could be pretty much any other cell um any squamous epithelium um So it's quite vague that wouldn't be it interrelated discs um Highly stride, it doesn't exist that I know of um and no striations interconnected discs. Also none that I know of it could be smooth muscle, but the most likely you're going to find. In fact the vast vast rectus is going to be your muscle cells, so your skeletal muscle cells sorry to be precise, okay. Um What does this sample represent um hold on. I'll trade the picture hold on therapy ok, sorry, um what sample does it represent, giving you some time to look at it, so is it a tendon bone cartilage, skeletal muscle, or a dermish okay 10 more seconds. Actually probably better if I switch back to this yeah, just have a look at it right, we'll end it there, so um most of us have gone for dean um So the answer is actually going to be hey, so attendant now um in attendant, there's going to be lots of collagen lots, lots and lots of collagen, so you see uniforms patterns of these collagen fibers, and here I believe you've got dense irregular collagen now just to clarify. Um When everyone went for skeletal muscle in skeletal muscle, you should be able to see striations, so those are going to be like lines in between those um each fiber so that's what separates it really. Um Now, I see there's lots of new nuclei in here, those are more likely to be your college and secreting cells so that would not be it um In terms of cartilage, it's do non specific because there's lots of types of cartilage, so that wouldn't be the right answer. If it's highland cartilage, it should be more hydrated and acquis, um There should be more chondrocytes, which are your cartilage cells and connective tissue to uh is too vague of the definition anything could be connective tissue, so blood is connective tissue, adipose tissue, is connective tissue right um I haven't touched much on histology just because you can review it um in PCS, but we move on to the final L0 c o l 09 so it might be a big jump, but this is a bit of radiology now um sorry not this part, so this is where everyone should get engaged in the chat function because it's not sbs, but this is more quick fire um pattern recognition questions, so um on question number one, what is the pathology. So if you have a look at this um x ray film right in the chat, what do you think what do you think it is you can private message it you can in case you don't want to embarrasses off which is completely fine, we're here to learn no weights for, I'll wait for 15 seconds and someone anyone is there anything that you can see okay right, so um a lot of the times in medicine, we tend to try and look for pathologies, but in this, in this case, this is actually a normal pelvic x ray, so there is nothing wrong with this. One is a normal x ray um and you just trace along the bones. There is no evidence of any fractures and bone density is quite normal, so I wouldn't consider osteoporosis um and you look at the spine is all which is also normal and yeah it's just there is nothing wrong with this patient that's why it's it's all right next one um what is the pathology. Hopefully, this um should get more engagement, sir, all right any other takes, we're about a fracture, nice, okay, well yeah. That is indeed a weber a fracture. I was going to ask for a bonus question um what would you classify it I was just I was just expecting um lateral lateral malleolus fracture um So this is actually the fibula fracture here um and with weather A um I'll go through the um systems now, but Weber A is actually going to be below the syndesmosis, so the syndesmosis is this the joint line here, so because the fracture is here which is an avulsion fracture uh Most likely anyway um that is going to be Weber A because it's below this joint line. If it's going to be on parallel with the joint line, will be Weber be and if it's above the joint line will be weber see and the classification of it will alter your treatment, so it depends on what you do for the patient um the higher the fracture, so the high above the joint line, the more serious it is because it ends up becoming non weight bearing and there could be serious um consequences of not treating it, but this is what I mean by Weber a, b, and c um also well done to whoever said well. Webber a. I. Was above and beyond knife, so Webber A is going to be likely A below the joint line. Weatherby is going to be on par with the joint line and whether C is above the joint line brilliant next one, so what is the pathology. I'll give you 15 seconds to try and answer this one and he takes on it anything abnormal that you can see with this joint or the bones. Patel up, nice okay right so as you can see that would be a different view, so it is indeed a patella fracture as you can see from here, um Most likely, it's gonna be caused from some kind of like trauma to the need that's probably going to be a patella fracture there brilliant Now. This is a hip x ray healthy x ray, sorry, um what is the pathology and just to let you know this is a four year old male patient as a bit of background, any ticks, okay, 10 more seconds, this extra brownie points where forgets his right all right, I guess no takes fine so this is actually a normal pediatric x ray, so um I was expecting some of you guys to try and like capitalize on this little thing here, but this is just growth plates, so a lot of pediatric patient's will present with growth plates and um on an x ray because these aren't actually um the part of the bone there isn't actually solidified, is still highland cartilage highland, they're still they're still cartilaginous so those parts of the bone will still be growing, so it wouldn't be dense, it won't be dense, um cancels bone, so you would see like a little line over there and same with these things as well, so you wouldn't they wouldn't have fused at that point, but yeah that's that's just a thing to look out for, especially when you move up to us to other years. Right next question so what is the pathology here, nice yep so perfect got femoral neck fracture um as you can see on this side, that will be the left femoral neck fracture. Um Extra points can you tell me if that is ok, brilliant. I was going to say what fracture that is yeah you got it right so that is indeed a intracapsular fracture of the neck of neck. A fema. Um Extra points how would you treat this. If I told you this was a, this was a 70 year old patient um This is a 70 old patient who normally mobile, mobilizes quite well plays tennis on the weekend, um What would you do for the patient. This is really testing everyone here especially for case one any text, so so for this patient, if they were a 70 year old hip screw um hip screw him, screw, so if this was a 70 year old, if you mobilize is quite well, um I would say um a total hip replacement now this patient's quiet 70 year old is quite old um and because they mobilized quite well, you would consider a total hip replacement because the joint is lubricated and you want to replace that joint. Otherwise, a hemiarthroplasty will wear out your acetabulum and because they mobilized quite well, you want to replace the whole joint. If this is a, if this was a 70 old patient who was bedbound um, doesn't move a lot, then you would consider a hemiarthroplasty that's well. I think anyway, Hopefully, I got that right hopefully um next one, what is the pathology, this is the last one from me, anyway, I should start that was a lie um what is the pathology here any takes you don't have to give me a specific name you, just you can tell me what's going on. What looks wrong him yep nice pretty much, it is an alia crest fracture um as you can see there's a clear fracture line down there and I would say you've got a bit of um pubic cubicle fracture down there as well. Um yeah, brilliant next one, what is the pathology here. Give you 10 seconds on to this one, so actually before we do that anatomically, do we know what this is for the lower lynn plot. Twist This, this is this is a foot by the way so there's any calcaneus so yeah and if you can see here, that would be a little fracture, so it's just a calcaneal fracture. Um yeah that that's literally it and this one will be quite hard to spots. I might, I think in the interest of time, I'll skip this one, but you could consider it that might be a little line. There is very hard to spot, but some x, some um some fractures are really difficult to spot and there might be a very tiny line, but that would be a medial cuneiform fracture, so these are the cuneiform bones and media um and lateral uniforms, but the middle one is fractured and this is a yeah gone someone someone tell me what this fracture is radius yep for this kind of fracture here would you say there's a specific name for it. I'm not sure they taught you guys in year one, so I would probably say this might be a colleagues fracture, so you've got a dorsal angulations of this um on the hand and you've got fracture of a complete a complete fracture here of the radius um and the cause of the dorsal ambulation could you could consider it to be a colleagues fracture okay, so the first aloe is the physiology of pain mechanisms so put in a simple way. The four phases of nociception in is one trans duck shin, so exposure to a noxious stimulus that produces an axion potential, phase two is transmission so the traveling of that stimulus along nerve fibers um phase three is perception, so your own experience of the pain and phase four is modulation, so what our brain does in response to the pain. Um It's also important to know different types of sensory fibers that carry pain um and the ones responsible for pain in particular are a delta, which are myelin ated and see which are non myelin ated, so see fibers will, the the stimulus will travel much slower and with a delta, it will travel faster due to the myelin nation. So the first L0. Is a 19 year old woman gets a paper cut while organizing some paperwork, she experiences sudden sharp pain at the site of the cut, but which type of nerve fiber is responsible for transmitting this sensation um Is there a pole um basically If you go to the bottom versus share screen, there should be a little poll button. Um you can relaunch the poll from there um okay, can you see it nicely and they're perfect, okay and then the answer being a delta so well done as we said before, sharp pain is transmitted with a delta fibers, how's it showed yeah okay, so this one is a bit more of a vision so which nerve endings are sensitive to thermal pain, so heat oh well a real long uh okay give you a few more seconds, so the correct answer was free nerve endings yeah okay, so it's just important to learn the sensation detected by these different um nerve endings as you can be tested on them, and as you can see here, um Therm pain in particular is transmitted through free nerve endings or any type of pain, whereas the others are more for touch and vibration and that kind of thing so have a little look at those and we'll move on, so a 40 year old gentleman has stubbed his toe on a doorstep. As a result, nociceptive stimuli travel from his left foot to his right postcentral garris along his spinal cord, but where do these fibers decussate, so, I will give you a bit of time to think about this one okay, so so this one um the correct answer was d and you just needed to know which tracked was carrying them, so the spinothalamic tract is responsible for conveying pain, temperature, and crude touch, and we know about the spinothalamic tract is that the deck ization occurs one or two levels above whether um where the nerve's enter the spinal cord, So the next question which of these is not an example of how pain modulation can reduce the perception of pain. Give you a few more seconds and we'll end it there, so it's a little bit of a split this time, so the question was asking how can it um what is not an example of how pain modulation modulation reduces your perception. So everything all of the other examples are of how we can reduce our perception of pain, such as um using tens machines or stimulating the other sensory pathways, which kind of um compete with the pain pathways, So you feel less of it. Also opioids, which increased gaba activity are also involved in reducing our perception of pain, whereas anger and feeling fatigued exacerbate your perception of pain, so we're gonna move on now to the molecular and cellular basis of inflammation, so the five cardinal signs that you need to be aware of are shown here and some of the reasons behind why you see these signs also show so um so with acute inflammation, you need to know about the vascular changes that occur, so you get transient vasoconstriction followed by visa dilation. You also get an increase in permeability of the vessels, meaning that fluid and plasma pro, proteins can come out into the tissues, which can cause the swelling and you also get a concentration amount of red blood cells in that area and then the cellular changes that you should be aware of is that a lot of neutrophils migrate to the site um to try and fight any infections present um and then also there's a release of inflammatory mediators such as histamine, serotonin, prostate landings and so on so the stages of healing by first in tension are shown on this slide. The four phases are one him a stasis um which is formation of the fibrin clot, second the inflammatory phase, third the proliferative flays, and then finally the remodeling phase just shown by this diagram, so stages of healing by second in tension, the difference here being the proliferative stage, which is where granulations tissue needs to build up from the bottom of the wound upwards rather than just be able to close across, um and here we get myofiber blasts need to contract in order to bring the wounds edges closer together because it's such a wide wound um the next L0 that we need to discuss was the skin structure and function, so the skin is formed of the epidermis, dermis, and hypodermic knees, and again we just have a little reminder here of the sensory receptors, most of which are found in the dermis, but merkel cells and free nerve endings being found in the dermis in the epidermis. Sorry, so just going a bit deeper into the epidermis. We can see that the main type of cell is a crack keratinocyte, but we also have a few other cell types and the important thing to know here is the different layers of the epidermis, so you have the stratum basil, spinous, um granulosus, um lucid um and corny um And we can remember this with the pneumonic come, let's get some beer so corny um being on the top and then bizarrely being at the bottom and then it's kind of it's less important to know the details of the dermis, but should know that there are two layers the papillary dermis on the top and then the particular layer and that fiber blasts are the most abundant sell in the dermis um and these function to generate connective tissue and then also that collagen, especially one and three are found in abundance and elastic fibers which play a role in um in the structure of the skin and it is the actually the degeneration of a lasting over time that leads the sagging that we see with age so like wrinkles. We have a question here and relaunch the pole so hair lloyd scars keloid scars are generated due to a prolonged inflammatory phase of wound healing, which leads to excessive fibroblast activity and the deposition of collagen beyond that of the original wound margins, but which of the following is not a risk factor for this give you a little bit of time and then we'll end uh so only um only thing here which is not a risk factor is actually being male because males and females can develop kilos scars equally and I think yeah, so the risk factors are shown here and yeah interestingly the highest incidents actually between the ages of 20 and 30 okay, so another question about nerve endings during a power cut alex, attempts to find a box of matches in the drawer to light a candle, but which one which is the most highly abundant in the fingertips helps her to find the correct object. Relaunch the pole again give you a little bit more time okay. We'll end it there so well done to whoever said, d. Because these are the ones that are responsible for discriminative touch, so being able to tell the difference between objects okay, so a little bit more of a molecular biology question, but how long does it take for a correct curtin, a sight to travel from the stratum base allah, to the stratum corneum of the epidermis, so how long do you think okay a few more seconds and the correct answer is 30 to 40 days, so it takes 30 to 40 days for it to make the journey from bizarrely to corneum and then so after the formation of the waterproofing layer, the granulosus um the claritin insights die because they become cut off from oxygen and nutrition and then once they reach the surface, the dead cells flake off in tiny specks. We call danda so dandruff is actually the accumulation of danda held together by some some oil or see them, and it actually takes a healthy adult between 4 to 6 weeks to make a completely to um completely renew the cells of their skin like shedding my skin. Yeah another question um why do some individuals at birth have a lighter shade of skin than others okay, A few more questions and a few more seconds, and then we'll go to the answer so well done to whoever said, e, so everyone has the same amount of melanocytes. It's just that some milan sites produce less melanin, which leads to a lighter shade of skin oops, yeah, so um different seasons can color depend on how much melon is it being produced uh So the final ello we're going to cover is common analgesics, so the first one that's worth mentioning is paracetamol. Um Interestingly, the mechanism isn't fully understood, um but it's thought to have effects on the central nervous system by inducing effects on the prostate landing, serotonin, endogenous opioids, nitrous oxide, and kind of a um cannabinoids. Another important thing to know about paracetamol is the mechanism of paracetamol toxicity uh being that um well as you can see here, So if you take paracetamol, it's usually converted to paracetamol chondritis, but if this pathway gets overrun, then it also goes through another metabolic pathway with c i p for 50 and then you get this toxic intermediate um that can lead to happen to toxicity so um yeah and that's important to know another another type of analgesics that commonly use and they also are anti inflammatories are insets, and these work by inhibiting cox enzymes, as you can see in this diagram here and common examples are also shown here, so another type of anti inflammatory that often use our steroids and there are two main types used medicinally mineralocorticoid magnetics, which help to maintain fluid and electrolyte balance. If a patient has hypoalr, aldosteronism, such as in addison's disease, so another type of steroid are gluca, cortical man, medic, emetics, and these are for um anti inflammatory and immunosuppressive purposes. You can further divide these into the short acting ones such as hydrocortisone, intermediate acting such as fred, missed alone, and also long acting such as decks, mm, okay, yeah okay, and then also it's worth knowing about opioids, so these are given for more severe case of pain and only once you've tried all of the other options on the pain ladder so such as paracetamol, nsaids, um only then will you prescribe an opioid just because they can have quite high levels of dependence, So these work by binding to opioid receptors in the brain, spinal cord and GI tract, they stop inhibitory neurons from releasing gaba, so this promotes the release then of dopamine nor adrenaline and serotonin um yeah, so these can reduce sensitivity to pain and also give you the feeling of being calm and you for it. Um Here's a. S. P. A. A young child did not receive their recommended course of vaccinations and consequently has contracted measles. Her g. P. Prescribes kalpoe, which is a liquid paracetamol for the child as she's spiking a fever, but which protein is responsible for an elevated body temperature, give me a little bit more time ok kind of end it there, so the correct answer is prostaglandin E, too so a common effect of increased prostaglandin E to production is a fever. That's one of the ones you just kind of need to learn JohN is an intravenous drug user who wants to give up using heroin. He presents to the e. D. With terrible symptoms of withdrawal from opioids. What is the first line medical treatment in this case okay a few more seconds and we'll end it there, so the correct answer was methadone. It is also an opioid, but um it doesn't give you the same feeling of euphoria that most opioids generate, so actually um can help reduce withdrawal symptoms without adding to the craving for opioids, which is why it's so one of the first line choice is to help with detoxification of um opioid addicts. Next question, a 50 year old presents the gp with lower back pain, which the g. P believes is from muscle strain. The patient has a past medical history of depression, gastric ulceration, and hypertension, which of the following medications are contra indicated. In this case give a little bit more time and through the answer now, so and naproxen is an nsaid um which up regulates the production of leukotrienes as a result of shunting in the academic acid cascade, so this results in more luca, trains being made and these act on bridal cells to increase um acid production, which can lead to an exacerbation of peptic ulcer disease. However, I have just realized that one of the other answers. Aspirin probably also be contra indicated in that case because it also works like an inset, so apologies for that, ok fludrocortisone mimics the actions of aldosterone for but from where in the adrenal gland is aldosterone is aldosterone released front and a couple more seconds and the answer is sona glomerulosa, so the adrenal gland makes a lot of the steroid hormones um androgynous steroid hormones that we try and mimic when we give steroids, and it's important to know that aldosterone as well as other mineralocorticoid Czar, released from the top layer the glomeruli, losa um the layer down from this is the zona fasciculus to which is responsible for producing glucocorticoids and finally the zona reticularis produces the androgens which go on to become eastern testosterone, for example okay, so mrs hughes has started on a short term course of prednisolone, but um to help with the flare up of rheumatoid arthritis, which of the following is she most likely to be advised about before starting the treatment. So this question's about knowing the side effects. Common side effects. Have taken steroids a little bit more time quite tricky, okay, well under the so the correct answer here is that she may need to have her BP monitored because steroids can induce hypertension, so um we've got three L s to cover the first one is the physiology of bone health, so we'll start off with the celio components, so there's three types of cells in bone. Um These are the osteoclasts, the osteoblasts, and the osteo sites, So the way I remember the osteo class and blasts because they sound. Very similar is that blasts build bone and clasts collapse bone, so the blasts are the ones that form bone and the osteo class on that resort bone or destroy bone in order to make new, and then the osteo sites are the ones that maintain bone that so if you think about the way that this happens, it's the osteo clasts basically like tunnel ear's, they tunnel into the bone and the osteoblasts come behind them, sort of forming the bone behind them until eventually the osteoblasts get trapped in this tunnel and they differentiate into these osteo sites that just sort of sit there and make sure everything's fine. So this happens all the time throughout your life, your bone is alive uh Contrary to popular belief, it's always changing especially when you're jumping on it. When it's put under stress, it's always remodeling so it's very important to like keep exercising especially when you're older because that helps maintain your bone um so it went unhealthy bone. You'd have in sort of equal balance of osteoclasts must be a blast, so that's continually reforming healthily, but in people with osteoporosis, you've got more osteoclasts working than you do osteoblasts so that means that you end up this week woven bone because you've not got enough osteoblasts reforming the bone, it's just getting destroyed so onto the structure of bone um So just this is just a quick recap, so the units of bone are called austrians and they are made out of osteo sites, The cells that we were talking about earlier um in the middle of the austrian, You've got a diversity and canal which contains the vessel and the vessels and nerves as you can see here um and then the osteo sites have these projections that look like really long fingers. I don't know if any of you are old enough to remember solid fingers on youtube, but it always reminds me of that and they're called canaliculus I uh or the uh the canals that the osteo osteo side projections travel through a call canalicular that's what it's called canal particular um and then the other thing to remember is just the uh overseeing canals are connected with fruit canals are called Volkmann canals. It's quite a lot to remember, but hopefully this diagram should help so onto um fracture healing, so um the fracture healing process is quite similar to the wound healing process. If you think about bone, it always just as an alive tissue um just like any tissue. When you break it, it bleeds, so initially it will form a hematoma just like any time that you and yourself it will bleed and form a human toba, um and this happens pretty much immediately after you into yourself. So then um after information after the hematoma forms you have information, this is when say, for example you've broken your leg, your leg will get all red and swollen. This is because you've got um the all the immune cells coming in um to cause this information process after that you've got granulations. This is when you start to get vessels forming throughout the wound um it's called angiogenesis then um that happens in the first few days of your fracture. Then um you have the callous formation, so initially this is a soft callus and then eventually over the next few weeks it will become a hardened callus because you'll have calcium infiltrate the callous um So that's important to remember is that you've got soft callus and then once you've got calcium infiltrated infiltrating called calcification that's when it becomes hard callus. Um Because then you got consolidation, which is basically just the first start of remodeling you've got the osteoblasts coming in to reform the bone and then remodeling takes place over many many years so um just like any old bone, you've got the remodeling going on continuously, so our first fba let me try and um uh sorry for the the poll. Sorry, so the first SBA is a medical student fractures the humerus in a skating accident after the injury. She tries to remember the stages of bone healing. She knows the bone will have formed a hematoma, but cannot remember what the next stage is what is the second stage of bone healing, sorry, I'll get the poles and let's see if I can restart this um lovely, we go that should be up for you now. I'll give you 20 seconds. Should I remember what the second stage of bone healing is just give it a go just a couple more seconds, give it a guess if you don't know that's okay, okay, great. I'm gonna end the poll now so um that was quite good yeah a lot of you said the right answer, which was, inflammation, so if you remember the hematoma forms and then just like any wounds and immediately it goes red, hot, swollen, and it's got the inflammation so that is the second stage of bone healing followed by the granulations, callus formation, and remodeling okay, So next up, we have a similar question, I'm sorry yeah similar question. A five year old boy presents with his mother in a trauma and orthopaedics clinic for a checkup two weeks after fracturing his tibia and fibula. The doctor emphasizes the importance of calcium intake, promote bone healing, during which stage of bone healing does calcification of immature bone occur. That's going to relaunch that poll, there you go okay well done for answering, give it a go, if you haven't I'll give you two more seconds okay, let's send the pole so well done. About half of you got that right and the answer was hey, it's a callous formation, so if you remember the callous formation is when it goes from a soft callus when it's non calcified and then it goes to a hard callus when it is calcified. If that helps you remember okay, so next up, we have another sba, we've got five of these, so. An 80 year old woman experiences a pathological fracture of her humerus from a dexa scan, she's found to have low bone density and was diagnosed with osteoporosis overactivity of which cell causes osteoporosis. Okay here, we go lots of quick answers there well done lovely, fantastic, maybe that's an easy one okay, I'm gonna end it there well done so everyone got that right fantastic, so the over activity of osteo clasts uh causes osteo process, If you remember osteoclasts collapse the bone so that also causes this week woven bone wonderful, well done, everybody okay, another one, um so a 7 65 year old patient presents in her gP practice with concerns about her risk of developing osteoporosis. She asks how she might be able to reduce her risk, and the Gp tells her that weight bearing exercises such as jumping, running, and walking would help as they increase the activity of a certain cellular component of bone, which sell at the g. P. R. Phone, too, so which cell uh increased with weight bearing exercises, give it a go okay a couple of seconds all right well done, everyone, so the majority of you got that right and the correct answer was osteoblasts, so if you remember osteoblasts build and when you do rates very exercises that the activity of osteoblasts has increased, um so well done everybody okay. My final question on this L0. A. Medical student is discussing the microanatomy of bone with the histology gist. She cannot recall the structure that's osteocyte projections pass through and what is this structure called so a bit of histology for you. They're a bit of the microanatomy, okay well quick, answers well done, guys were going quick on the draw. When we thank you, so and that they're so well done you all got that right and the correct answer is the canaliculus. I hopefully um salad fingers helped you remember that all right, so that's that's L0 well done, everybody else some really good answers there. So um now we have um the physiology of bruising. This is quite small L0. So, I'll just do a couple slides, and we'll have a couple of questions on this. It's not too important but just so you understand the basics, so bruises also known as a contusion, essentially a hematoma under the skin. When you have a blunt force trauma, the capillaries under the skin get damaged and the blood leaks into the interstitial tissues and then you see this red or as you can see different colored uh bruise emerge so um if well let's talk a bit about the colors of bruises. So immediately after an injury might it might be more bright red and this is oxygen rich blood and then eventually all this is pretty helpful infographic here, so eventually it will darken um as it loses oxygen. Then I might go into more of a purplish color as iron is released. Then, uh If you see any green that's because hemoglobin is being breakdown broken down into billy verdin, so I'll go on set up a little bit later as well um so then a green to yellow yellow is because billy verdin is break down into billy ruben um and then eventually it should fade away um So it's very difficult to time give a timeline to an injury based on the color of a bruise um. This might help you give an idea of at what stage in uh what stage bruises at based on much color um. The way I remember because that's a lot of different chemicals there, so the way I remember billy verdin, uh hemoglobin gets broken down into billy verdin. If you know french or do french at school, there is french for green, so you might remember billy verdin is green and then you should all know, hopefully I'm not sure actually maybe at this point, but you will come to know that billy ruben causes jaundice. If you have excess billy ruben, you have jaundice and you turn yellow, your skin turns yellow, so if you think billy ruben is yellow and then um if you really want to know, billy ruben turns into hemosiderin in at right at the end there, but that's not highly essential Just a couple of questions for you on these, so, a seven year old boy sustained an injury to his knee after falling from his bike. The skin is not broken, but quickly has a large bruise forming his knee. After 10 days, he notices the bruise has changed color and now has yellow edges, which process is responsible for the bruise changing to this yellow color. Give a go, the cancer is there well done guys through a couple more seconds just to read the answers. If you haven't okay well done fantastic, so most of you got that right uh the answer was the breakdown of billy verdin into billy ruben. If you remember, yellow, think billy ruben because your skin turns yellow when your jaundiced, um and billy verdin is green because of their okay um well done, everybody, so just one more question on this. L0. As I said, it's quite small L0. Um so, a 30 year old man sustained an injury while playing cricket when a cricket ball strikes him with force in his right arm which type of injury is he most likely to have sustained Yeah, okay, okay, well done a lot of answers there, so I'm going to end the poll there so a bit of a mix on this one, so um I'll try and explain all the different meanings of these injury types. Um Doctor led beat, It does a good optional lecture on this. I believe um so some of you said abrasion and I'll tell you what the actual answer is. It is contusion, so contusion is the same as a bruise and that's because he's had a blunt force trauma. You can just imagine him having a big bruise on his armor um so abrasion is close. It is also caused by a blunt force trauma, so I wouldn't actually blame me if you picked that sorry, to the people who did it, it's kind of mean of me so abrasion is caused by blunt force trauma as well, that basically just means a tear or a graze of the skin um caused by a bump force trauma. So for example if you graze on me, that's an abrasion, an incision is a sharp force trauma that's caused by for example a knife and it's just like a long or it's any incision by sharp force trauma that breaks the skin contusion as I said as a bruise um lacerations. A lot of people think it's the same as an incision, but it's actually more of a a blunt force trauma where you've got tearing, type of things that would be a weird with a ragged edge caused by blunt force trauma and an avulsion is a complete uh separation, For example if you got a finger torn off or like you uh had earlier, we had the avulsion fracture of the fibula so well done, that's all the s. B. A. S for that one, so the final L0, so we're getting through this fairly quickly, so should all be done before eight o'clock, so this is probably the most important L0. That i'm going to share with you guys, So this is identifying different types of blood disorder that may alter normal hemo, stasis and bruising, so I absolutely hated homeostasis when I was in first year, but I've got a few things that I should help you remember the regulation cascade and that kind of thing so um when we think about caligula, ation disorders, um sorry, if you can see my little pole thing there. Um When you think about calculation disorders, we're thinking about the symptoms for all of these coagulation disorders are fairly similar, they're pretty much the same and it's basically any surface or any way you can bleed from, will bleed more excessively so um nosebleeds come more easily, that's called epis taxus um your bruise more easily your gums will bleed more easily. This is called it's like I don't know if it's a proper name for gum bleeding, but it's like gingivitis is gum information just like a ginge um men are, I'm sorry mirage area, so you've got more heavy menstrual breeding. There's like the typical ones that people come in with, so like I've been brushing my teeth and I've just been bleeding everywhere this kind of thing and then more seriously you have can have complications such as joint bleeding, bleeding in the urine, and rectal bleeding, so um the five differentials we're going to go through today. Uh hemophilia a. B and c, von willebrand disease, and vitamin K deficiency and these are the ones that you need to know so if we go first just onto a little thing to help you with the coagulation cascade, so it looks so overwhelming when you look at it like this. This is a really helpful guide from osmosis here. Um So the way um If you remember you got the intrinsic pathway here and the extrinsic pathway here, they combine at factor 10 from the common pathway. Um This is uh and then it becomes this fibrin clot um and then secondary to this, you've also got the primary coagulation, which is just involving platelets and then you've got the secondary calculation, which is all this so um as you can see if you see by the letters here. This kind of shows you which factors are affected by which disorder but we'll go through this in more detail, but this is uh it's a little a pneumonic, I always used to help me remember the intrinsic pathway, so there's a christopher Nolan film called Tennant that came around came out when I was in first year um and the first letter of letters of 10 it uh the same as the first letters of the numbers in the intrinsic pathway, so 12, 11, 98, and 10 that might help you remember the order there and then the extrinsic pathway is just uh seven uh and then they join at 10 here interesting pathway, so hopefully that helps to remember remember 10 it's 10, 12 11, 98 10, oops subscribed, so first of all hemophilia, so there are three types of hemophilia. Abc um a fairly easy way to remember is just 89 11, so trying to be like 89 10, but 89 11. It goes up a. B. C. 89 11 um hemophilia A is by far the most common uh followed by hemophilia, be followed by haemophilus, see, so it's quite fairly easy to remember if you remember in that order abc most common to the least common like 8928 11, so it goes up as well. Um uh hemophilia A and hemophilia B are both excellent, so it's much more common in males and it isn't females, although females can be carriers and passed on to their sons. Him Ophelia see uh equally inherited by both, I believe um and hemophilia. Be uh you might have noticed the christmas hat, is also called Christmas disease um. Because it was discovered by a man called mr christmas, I can't remember his first name steven, I think maybe uh so that's hemophilia. Uh Then we have vitamin K deficiency, so vitamin K is found in the green leafy vegetables such as kale, spinach, cabbage, broccoli, and sprouts um. So if you're not getting enough of these green leafy vegetables, then you might end up with vitamin K deficiency, which causes coagulation, uh coagulopathy with what we call it, so it causes more easy bleeding. Um So there are four vitamin K dependent factors that are affected by vitamin K deficiency, so these are 279, and 10 um So the way I would remember this is two plus seven is nine, not 10. Hopefully that makes sense to you um so as you can see it affects quite a few different factors uh in the intrinsic pathway specifically as well. Um Finally, we have one Willebrand's disease. This is by far the most common coreg you're ation disorder um Some studies have said it could be up to one and 100 people have all Willebrand's disease. This is caused by a defect in one von willebrand factor, which as you can see here is bound to factor eight in the intrinsic pathway, so um one Willebrand says it actually affects bleeding on in two different ways, so it affects the primary coagulation with platelets because one willebrand factor is, is responsible for platelet aggregation, so it will stop the platelets from aggregating, stop them from forming that platelet clot and secondary in secondary calculation. One willebrand factor is bound as I said two factor uh eight, and if they're not bound, if the separated, then then the factor eight will disintegrate, so this intrinsic pathway is like destabilized intrinsic pathway, doesn't work a lot of information night, b. I, they're still keeping with me, so this is a little table that might look like a lot. I don't expect you to remember at all what I would um focus on is the fact that von Willebrand's disease increases the bleeding time. If you remember, von Willebrand's disease is the only one that affects platelets, so if you think about that it's inhibiting platelet aggregation, so you're going to bleed for longer, and then vitamin K deficiency is the only one that increases the prothrombin time because that's the, the time between the extrinsic pathway and the fiber information so um because vitamin K deficiency stops uh fiber in from being formed um So that's basically all I take from that is just remember when will a one C is bleeding time. Vitamin K deficiency. Presumption time okay. Hopefully, that's all retained we'll have a check with the sba s, so, try and try and do this. Final s. B. A. S, if you can uh just get a second okay. Oh yeah Actually, this is just a funny video, If I can play, I don't know if I can now, I can't anyway look up uh what's the bleeding time. It's very funny, but if I can play it um oh no yeah actually it was funny clip fuel, Hopefully you can hear it, uh who is known scientifically as the bleeding time. What's the bleeding diet 10%. You hear that I'm not sure anyway. Hopefully you could it's very funny if you didn't ha ha, ha ha, um So this is the first s. P. A. Uh the five final s. B. A. S, well done everyone for staying this long get through these five and then we'll be done so a patient presents in the g. P. For review of their warfarin, is found to have a concerning lee, reduced iron are leaving that at high risk of blood clots. From further conversation, the patient reveals that they have altered their diet to try and lead a healthier lifestyle. They indicate they now have three spinach kale and up to museums per day to try and try and have sprouts or broccoli with as many meals as possible. What is it about these foods that could have recall caused a reduced i and our uh let me just show that poll give me a second, so there we go um just have a real read this question that can be quite difficult, just have a proper read before you answer. Give you a few more seconds just have a read and I have to think about your answers okay. I'll stop the poll now, So this is a bit of a mixed mixed answer question um So the actual answer was there hi investment Case, I think everyone knew that they were high in vitamin K so well done, um but the reason is because they increased proce, on bring production um So if you think about a, a person who's taking warfarin, that you want them to not have blood clots. If they're having lots and lots of vitamin K, they're going to be increased risk of blood clots because this proce, on front is being produced at a higher rate. Um So this is a bit mean a is quite reasonable answer. It is not a competitive inhibitor of warfarin. Um That's just uh I mean yeah I mean you won't correct me if I'm wrong that might be a bit mean, but the beer is like the proper answer. Yeah I think I think is more is more like a clinical um thing yeah anyway, sorry guys um so well done let's move on to second question, so a mother brings her toddler into the g. P. As he has sustained a graze on his leg, which didn't stop bleeding. The doctor ordered blood and genetic tests and confirmed that the toddler has one Willebrand's disease. She explains that there are different pathways involved in the clotting cascade and one of them is the intrinsic pathway, which are the four clotting factors involved in the pathway and mentioned uh let me just re launch the pole for you, so which are the four factors in the intrinsic pathway. Go, try to remember that Pneumonic I mentioned okay. Uh I've got a lot of responses. So end the poll there well done, so the majority of you got that right and the answer was d uh remember my pneumonic is the christopher nolan film tenet, so t. E. N. E. T. Uh 12 11, 98, 10, and 10 is the one that combines the intrinsic and extrinsic pathways. Try and remember that if you got that wrong, hopefully that'll stick all right, it's great, so the next one is a patient in their g. P. A. Patient presents in their gP with a history of uncontrolled bleeding and easy bruising or start bruising wrong foods. Uh The g. P. Doesn't test and find the patient is deficient in coagulation factor nine. What is this condition called, give it a go let me read on the poles all right, there you go so deficient in coagulation factor nine. Uh Here we go lots of answers well done guys, okay, well done, so um let's see so. The actual answer was hemophilia be lovely, well done most of you got that right if you remember 89 11, um So a. B. C. 89 11 and so nine is hemophilia, be well done good, job, okay, okay, another one, so another one along the same line. So a patient mentions frequent nose, these, and heavy menstrual periods of their gp. Upon investigation, they are found to have an increased bleeding time, but a normal prothrombin time in a and um aptt, uh so which condition do these results indicate, let me re launch the pole hoops, let go, give it a go, so I'm sorry, if it sounds quite hard, it's from that table I showed you at the end, so it increased bleeding time okay all right, so I'm going to close the poll well done for your quick answers so that was quite mixed um but well done to the majority of you who got to the correct answer which was von Willebrand's disease. If you remember von Willebrand's disease that the only clotting disorder that affects platelets and platelets is what determines the bleeding time um so yeah okay, so vitamin K is the one that increases the prothrombin time, so this one has a normal perform in time that's well done. Um ok our final question of the night world and everyone's saying this long I won't keep you much longer after this. Um So on a trip to the dentist, a patient is found to have poor dental hygiene. When asking about their brushing habits, the patient reveals that they rarely brush their teeth as they're nervous about causing a bleed in their gums and as they have christmas disease, what is this condition also known as okay, okay, okay a couple more seconds, okay, well done for answering everybody, so this is another mixed one um so the correct answer is um hemophilia B is christmas, diseases that was discovered by mr christmas um I don't know how often that's going to come up, but it's quite good to remember. I guess um remember little santa hat on hemophilia be okay, thank you very much everyone that's me um brilliant um Also just on the vitamin. K, note, I just found something that might be quite useful to share. Um It won't take any more than like two minutes um Everyone's happy to stay if you would like to leave uh I know I would if I were you guys not just been the feedback form and go, but in terms of vitamin K, so essentially what warfarin does so with vitamin K, you actually need it too you need that as part of a catalytic uh reaction and what vitamin what warfarin does it stops this um It stops vitamin K from the cycled as reduced and oxidized, so um when you reduce, sorry when you oxidized vitamin K you end up with active pro, thrombin, but when you check in warfarin that stops the whole process, so when you give a patient vitamin K um due to light so vitamin K is a warfarin antidote, um but what you do is when you check loads of vitamin K at them. Um You just hope that there is enough vitamin K in the system um to counteract the effects of warfarin, but that's what you basically do in a nutshell, so you're just hoping that the system carries on by producing or prothrombin um yeah that's vitamin K brilliant.