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Haematology & Oncology SBAs for Medical Finals

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Summary

This on-demand teaching session, known as Crash Course Finals, is designed for medical students preparing for their final exams. The hosts are clinical specialists and doctors from Aberdeen University who provide insightful, special topic discussions every week. This week's focus is hematology and oncology, and the forthcoming one will dive into psychiatry and palliative care. Each session presents 18 SV questions with a variety of difficulty levels to ensure comprehensive learning. This teaching course provides students an interactive environment to discuss, ask questions, and delve deeper into each topic. Conveniently keep up with the program schedule via their social media. The program also offers an ambassadorship role for students interested in promoting Crash Course Finals in their respective universities.

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Description

High yield SBA style questions for UKMLA delivered by a haematology/oncology registrar

Learning objectives

  1. Understand the implications and management of tumor lysis syndrome in patients undergoing chemotherapy.
  2. Identify the signs and symptoms of metastatic brain deposits in cancer patients and be able to initiate appropriate initial management.
  3. Recognize the characteristics of different types of anemia including macrocytic anemia associated with vitamin B12 deficiency.
  4. Understand the diagnosis and management of hemochromatosis, a disorder of iron metabolism.
  5. Distinguish between different transfusion related complications, including transfusion associated circulatory overload and transfusion related acute lung injury.
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Computer generated transcript

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

We'll just give it a few more minutes for people to come in. So, hello everyone and thank you so much for coming tonight. So we're just gonna have a quick introduction before we start if that's ok. So I'll just move on to the next slide. So just first quickly who we are. So we're just 3/5 year medical students from Aberdeen University who came up with crash course finals in order to try and help provide content that's tailored and relevant towards passing your upcoming final exams. So we run sessions usually roughly about every week covering a different special, each week. Sometimes we run them, but they're mainly run by doctors with clinical experience in the field who are there to go through SB cell questions and also to answer any questions that you guys might have as well. So this week's on hematology and oncology and our next one will be on psychiatry and palliative care. So I'll just move on to the next slide. So this is just a quick overview of some of the specialties we'll cover and this is also just a really good chance to get involved and become an ambassador for crash course finals. It's very easy rule. So if you're interested in it, it's mainly about advertising for the crash course finals and the university you're in. So if you're interested, please send us an email along. And this is also just a really good way to keep it up to date with our social media. So we are on Instagram, Facebook and we have a link tree. So it's just the best way to keep up to date with which events coming up next. And the session today will be split into easy, medium, hard. So there'll be 18 SV questions overall, six in each section. So first of all, we'll start off with the easy section and then we'll keep increasing the level of difficulty and these are just somehow shows just before we start. So we just ask everyone's on mute. And if you pop your questions on the chat, we'll be monitoring the chat and we'll pass them over to the doctor running the session tonight to answer them and just moving on to the next slide. So I'll just pass over now and thank you again for coming and again, pop your questions in the chat if you have any. OK. So I'm the doctor gonna be leading this session. So my name is Killian Turbot. I'm one of the doctors currently working in the Glasgow Royal Infirmary. I'm an I MT one. And so today we're gonna be doing session on hematology. And oncology. Um So as Emma said, we'll go through some questions and any questions, please do pop them on the chat and we'll try to answer them at the end of each round. So we'll go on to the first question. So number 155 year old male is undergoing chemotherapy for Burkitt lymphoma. Investigations reveal hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia. His creatinine levels are also raised. So, what is the most appropriate management of his hyperuricemia? So, a urgent flu restrict uh resuscitation and repeat blood in 24 hours. B prescribe colchicine for acute attacks. C oral phosphate binders or D respirate case. So we'll just give uh people about th uh 30 seconds to answer. Um and we'll get and then we'll see what the pool say at the end. OK. So everyone should have had time to um answer the question. So the answer is D so rasp, OK. So what we're looking at here um based on the kind of bio biochemical picture is tumor lysis syndrome. And this is a syndrome which which can occur um in chemotherapy and, and some oncological settings, most, some commonly hematological malignancies such as burs lymphoma, but also a LA LL um and um some other kind of B cell lymphomas. Um And that's when the cells of the cancer because there's so many of them and they're so chemosensitive um are destroyed and release all their insides basically. And so we get high potassium because there's lots of potassium in cells. We get breakdown of DNA products. So DNA breaks down into uric acid um as well as um phosphorus. And because of the high phosphorus, calcium is is lowered in the, in the blood stream because the calcium tries to mop up that um that phosphorus. So the correct answer for this for the treatment of the hyperuricemia is the rasburicase um which is a recombinant enzyme to try to um break down the uric acid into allantol, which can be filtered out by the kidneys. Ok. So number two, a 58 year old female patient with a history of metastatic breast cancer presents to the oncology clinic with a new onset of headaches, nausea and confusion over the past few days. She's currently receiving chemotherapy for her metastatic disease. On examination. She is disorientated has PPI edema on fundoscopic examination. A brain MRI reveals evidence of cerebral edema. So what is the most appropriate initial step in this in the management? A IV Mannitol B, refer to neurosurgery C IV dexamethasone or D perform a lumbar puncture. OK. So hopefully that's given everyone time to answer the question. Um So the answer is IV dexamethasone. OK. So this is in keeping with a metastatic deposit in the brain. So this is uh having signs and symptoms of raised intracranial pressure. So that can be seen by the headaches and the papilledema and the PPI edema on the fundoscopy? Ok. So usually in in on oncological setting. Um And in nontrauma race, ICP, then can be given dexamethasone um race ICP due to trauma that can be treated with IV monitor. Um It would be important to say that sure. Uh uh The answer D to perform a lumbar puncture would be contraindicated because of that um risk of, of coning um with a high pressure system within the brain referral to neurosurgery may come later um in discussion and they can think about neurosurgical interventions, but the initial management would be with dexamethasone. Ok. So, next question. So uh a 45 year old woman presents to the GP due to fatigue, weakness and shortness of breath on exertion for the past few months. She has a past medical history of heavy menstrual periods and Addison's disease on examination. She appears pale and her uh conti are pale as well. Blood test revealed the following hemoglobin 9.2 which is a bit reduced from the normal range mean corpuscular volume. Uh 100 and 20 which is increased and from the normal range serum ferritin eight total iron binding capacity, 400 a reticulocyte of 2%. So, what is the most likely diagnosis? Iron deficiency, anemia, anemia of chronic disease, vitamin B12 deficiency anemia or sideroblastic anemia? No, no. Ok. So that should hopefully give enough time to answer. So, the answer um for this question is C vitamin b12 um deficiency. So, the most important thing is to try and break it down into the parameters of the blood test and identify that, that this is a macrocytic um anemia so that the MCV um is high over 100. So that means that the, the, the red blood cells are quite large. This can be due to vitamin b12. Um And then that's when you have defective DNA um synthesis in the red blood cells. So they're unable to um fully divide as they normally do. And you get these immature red blood cells which tend to be quite a lot larger. Ok. Um There was a uh it should we know that the B12 deficient anemia, um particularly pernicious anemia where you have a antibodies against intrinsic factor can be associated with other autoimmune disorders. Like it was in this case, there was a history of iron deficiency of um heavy periods but typically iron deficiency anemia would be associated with a microcytic anemia. So, MCV under a. Ok. Yeah. So number four, a 40 year old man was referred to a Hepatology clinic by his GP due to concerns that he was developing chronic liver disease patient. Um comments, he has been feeling progressively more tired over the past couple of years. He attributes this to not sleeping well as low libido is causing him his relationship difficulties with his wife on examination. He has gyneco amastia and palmar erythema. The hepatology hepatologist also notes that his skin pigmentation appears gray blood test showed the following. OK. So considering the most likely diagnosis, what is an appropriate initial management. So a there, furoxam, um Furoxam um pise for BC genetic testing or D refer for a fibroscan. OK. We'll just go to the answer. Now, um the answer for this is the venous section. So the picture of pain here is hemochromatosis, which is an autosomal recessive disorder of iron absorption and metabolism usually due to uh HF E gene mutations. OK. So you can have different wide range of um presentations, usually related to iron deposition in different tissues. So that can be fatigue, erectile dysfunction, arthralgia, bronze, skin pigmentation, which can look a little bit bronze, which can look a bit grayish at times, diabetes, myelitis, which due to iron deposition um within the pancreas liver disease, um particularly it causes cirrhosis cardiac failure, hypogonadism um related to erectile dysfunction and arthritis. So usually we would need a diagnosis with transferrin saturation, but ferritin is normally quite high in these patients. Um And then um so usually you'd get a race transferrin saturation, a raise ferritin, but a low total iron binding capacity because it's all used up um to try to um to sub up all that. Uh all all the iron. So first line man for that is the section to try to reduce the iron within the blood. And then second line is. So, genetic testing does have a, a role in in hemochromatosis. Um but it wouldn't give you any management and you usually would be referred for a fibro scan to look for um cirrhosis. But again, it wouldn't be in part of the overall management, but would give you a bit more information about ongoing um management if there was a cirrhosis there. But initially venous section would be the first choice. Let's go on to the next question. So five, a 68 year old female patient with a history of chronic kidney disease, uh stage three and coronary artery disease is admitted to hospital for elective coronary artery bypass graft surgery. During the procedure, she receives a transfusion of plaque, red blood cells due to intraoperative blood loss. Within hours. Post surgery, she develops dyspnea, tachypnea and bilateral pulmonary crackles. Her oxygen saturation has dropped to 88% and her BP rises to 160/90 milligrams of mercury. The patient denies chest pain but complains of uh feeling heavy in her chest. On examination, her venous pressure is elevated. What is the most likely diagnosis? Is it transfusion related acute lung injury or trailing transfusion associated circulator overload or tackle acute Coronary syndrome acs or an anaphylactic reaction to blood products. Ok. So the answer for this one is um is B transfusion associate circular overload. So we know that she's developing some signs, some signs of respiratory distress um with the low oxygen levels um um as well as um and dyspnea. Um and but there's no signs of chest pain, which would lead us away from acute coronary syndrome. This um has presented within a few hours and usually anaphylaxic reaction, blood products would usually present quite quickly. That least us with A and B and we know that they both can cause um hypoxia. Um but typically, um tackle, which is transfusion associated circular overload would be associated with um symptoms of fluid overload, which would be seen with the race JVP. Um and hypertension seen in this case. And we would treat this usually with IV fluamine um usually with trail or transfusion related acute lung injury. Um you would get low BP. Ok. Go on to the um I think the last question in this um section. So that's number 6, 58 year old woman presents with fatigue, bone pain, current infections. Further investigation reveals a monoclonal spike in gamma globulin region on serum protein electrophoresis confirmed by immunofixation demonstrating a monoclonal IgG kappa protein. She also has anemia hypercalcemia or renal sic insufficiency. So, what is the most appropriate imaging study for further evaluation? Is it a skeletal survey with x-rays CT scan, MRI scan or a pet scan with FD gene? Ok. So we'll go on to the answer. And um so this is see MRI scan. So these symptoms all kind of correlate to multiple myeloma or this is quite, quite sus suspicious of multiple myeloma. A good pneumonic to think about some of the signs and symptoms of multiple myeloma is Krab, which stands for calcium, which is usually raised renal dysfunction, anemia and bone pain. Ok. So usually in these, in these patients, you want to identify any kind of um deposits of myelomatous disease within the body. And the best imaging modality for this is MRI um imaging. This can be quite hard to get. So can think about low body CT. Um if MRI is unsuitable um and this might be also the case for people with metallic implants, say pacemakers which can't be taken out um If that's not suitable, then we can think about um skeletal surveys which can uh miss some um deposits and aren't as sensitive as MRI. Ok, cool. Sorry to interrupt. Um Just like to ask if anyone had any questions, please put it in the chat and we can deal with them accordingly. We'll give you guys 30 seconds or so and then we'll move on if there are no questions. Alright. Seems like there a question even. Um ok, so first question round two. So a 72 year old male with a history of atrial fibrillation presents A&E with epistaxis and ecchymosis. So his current medications include warfarin for anticoagulation. Uh laboratory investigations reveal an inr of 6.5. He denies any recent changes in his medication regimen or mitosis. There's no evidence of active bleeding which of the following is the most appropriate initial management for this patient to what was uh management so a stop warfarin and restart ₹1 under five B, stop warfarin and give prothrombin complex. Concentrate C and stop Warfarin. Give IV Vitamin K 3 mg and restart what? Under five or D with all two doses of warfarin and reduce subsequent maintenance dose. OK. So for this one, the answer is C so that's stop Warfarin and give IV Vitamin K So in this gentleman, as you can see this uh diagram, um we need to classify if this patient is having any bleeding and we know that he is having some bleeding, he is having epistaxis and he is having ecchymosis or OK, lots of bruising. Um We would give um so for this, we need to give some treatment. So this would not be appropriate to do ad um usually we would only manage major bleeding, say um upper gi bleeds or catastrophic bleeds and that we would give um prothrombin complex as well because that works a bit quicker than um IV Vitamin K So because his inr is um between five and eight, we can give IV Vitamin K 3 mg. OK. So we'll go on to the next question. A 35 year old female presents to Rheumatology Clinic with a history of recurrent pregnancy loss and thrombotic offense. She reports a previous deep vein vein thrombosis and a stroke. Laboratory investigations reveal the presence of lupus anticoagulant and anticardial lipid antibodies on two separate occasions. At least 12 weeks apart, what is the most likely diagnosis? A systemic lupus, erythematosus or sle eb antiphospholipid syndrome, C bess disease. D rheumatoid arthritis. Ok. So the answer is b antiphospholipid syndrome. Um So this basically, she's had a lot of different thrombotic events and we can see that she's had um immunological evidence of antiphospholipid syndrome with an anti lupus anticoagulants and anticardial anticoagulants. Um which at 12 weeks apart and that gives you a diagnosis of antiphospholipid syndrome. So, that's a predisposition to venous and arterial thrombosis. And you also get recurrent fetal loss and thrombocytopenia. Um usually management is with low dose aspirin. Um However, if um patients do get um VT E um on that, then we can add in other agents. So if it is with, so sorry if she does get VT um we can add in um Warfarin. Um And then aiming for inr of 2 to 3 if she does, if they do have recurrent thromboembolic events and can think about life, lifelong warfarin um usually to a higher inr 3 to 4. Um if if she's already having, having M BT while on that lower um inr range of 2 to 3. But, and, but arterial thrombosis should also be treated with Warfarin inr 2 to 3 as well. Ok. On to the next question. So three, a 25 year old male Mediterranean descent uh presents the emergency department with complaints of dark urine and jaundice on a recent meal of fava beans. He reports a similar episode in uh in childhood after consuming certain medications. So, laboratory investigations reveal hemoglobinuria and the presence of Heinz bodies on peripheral blood smear. What is the most likely diagnosis? A G six PD deficiency B, autoimmune hemolytic anemia, c hereditary severe cytosis, RD pyruvate kinase deficiency. Ok. So the answer for this one is a G six PD deficiency. Um It's ok. Clues in the question are Mediterranean descent, which is more common. So G six PD is more common in, in that kind of populace. But G six PD is an enzyme normally found in red blood cells, which helps with um repair of red blood cells. And so a deficiency means they're more vulnerable to reactive oxygen species, which means they hemolyze um and can have acute hemolytic anemia in periods of increased stress. So you can have anemia, jaundice, intravascular m gallstones due to breakdown of the heme products um which tend to then form um gallstones can have splen on megaly. Um because of all the broken down um blood red blood cells and you and you mnemonically you get hinds bodies on blood films and blight bite on blister cells can also be seen. So there's a few different triggers. One of them can be fabs but are commonly also medications. So, primaquine, uh antimalaria, ciprofloxacin um and er sulfer and sulfa drugs. So, sulfaSALAzine, sulfaurea sulfonamides. So, mainly management is to try to avoid triggers. Ok. So for a six year old child presents to the emergency department with complaints of abdominal pain, blurry, diarrhea, decreased output over the past two days. On the examination, the child appears pale and lethargic with signs of dehydration. Blood results are as follows. So, hemoglobin low uh 7.5 normal range 11 to 4.14 0.5 platelet count um low as 60,000 with normal range 100 and 5400 and 50,000 cm. Krain raised to ribbon, raised an tic over 2%. So what is the most likely diagnosis? A acute gastroenteritis? B Henoch purpura c thrombotic thrombocytopenia, purpura or D hemo uh hemolytic uremic syndrome. Ok. So the answer to this um is the hemolytic uremic syndrome. So, this is a rare condition known, affecting Children causing destruction of the red blood cells leading to hemolysis and also can have damage to the blood vessels and lead to kidney injury which we saw in this in this case. So usually it occurs following a gi tract infection. So if you see a question with diarrhea might raise your suspicion and this is usually caused by e coli particularly the 157 H seven strain and that releases a particular toxin called the sugar toxin. Um and it can also be released from SHLA and this leads the overactivation of the immune system can then lead to hemolytic uremic syndrome. So that usually presents with a hemolytic anemia, which we did see with the high bilirubin, bilirubin can be a byproduct of breakdown of red blood cells. And you particularly get the unconjugated bilirubin, which because there's so much of it, the liver can't conjugate it quickly enough to get metabolized. Um We also saw that there is thrombocytopenia with low platelets. And um AKI, we also did see that reticulocytes are raised and particularly reticulocytes are raised in and when there's low, um when low hemoglobin and that's because the bone marrow tries to produce lots of red blood cells and to counteract all that's been been lost and with in this syndrome. So management, it is medical emergency need hospital admission and supportive management, mostly with IV fluids controlling the BP, blood transfusions if it becomes very severe and if need be hemodialysis if there's very severe renal failure. So number five, a 25 year old male with a known history of sickle sickle cell disease presents to the emerging department, complaining of severe pain in his lower back and legs. He reports that the pain started suddenly yesterday and has been uh has been progressively worsening on examination. He is febrile with a temperature of 38 5 and he appears as stressed. His heart rate is 100 and 10 BPM. BP is 100 and 30/80 milligrams of mercury and expiratory rate is 24 breaths per minute. He is tender over his lumbar spine and bilateral lower extremities based on this presentation was the most appropriate initial management for this patient. So, blood transfusion to increase his oxygen carrying capacity. IV antibiotic therapy, initiation of hydroxyurea therapy or intravenous hydration and analgesia with opioids. Oh OK. So hopefully that's convenient time to answer. So, d uh intravenous hydration and analgesia with opioids is the correct answer. And this is because this patient is uh presenting with syndrome with a vasoocclusive crisis. Um And this is when sickle cells um cause small uh thrombosis um within small blood vessels and that can cause quite a lot of pain. Um if it does occur in the chest, um that can lead to acute chest syndrome as well and when it occurs in the small pulmonary vessels. Um first line management for this is mostly supportive with intravenous hydration with opioids and tends to be first line because it can, the pain can be quite severe with these patients. Um However, sometimes they can develop infections. So you might need to think about IV antibiotic therapy, but the the raised temperature doesn't necessarily mean that there is infection. It could just be the widespread um vasoocclusive crisis which can cause it as well. So we tend to start with intravenous hydration and analgesia. Ok. So number six, last um question of the round. So a 55 year old man presents to his primary care physician with complaints of persistent fatigue and unintentional weight loss over the past few months. Denies any significant medical history but reports occasional episodes of vague abdominal discomfort on examination, there are no palpable masses or lymphadenopathy. Laboratory investigations reveal elevated levels of ca 19 9 and AFP. So, what cancer is likely associated with this tumor? Most likely associated with this tumor marker? A breast cancer B hepatocellular cancer, C ovarian cancer, or D prostatic um car carcinoma. Ok. So the answer for this um is B ba cellular cancer. So, unfortunately, um list of tumor markers is something that you may have to learn. It does come up commonly um in questions. Um And, and there's a list here uh which we can go through. But ca 19 9 and A FP most commonly related to hepatocellular cancer. Um A FP, particularly with HEPA uh most common with pa um cancer. Um But there are a few breast cancer uh typically with MCA 2729 or ca 15 3 ovarian cancer typically um associated with ca 125 and prostate adenocarcinoma. Typically with PSA. There are a few other ones that you should um think about. Uh no for the test. So, C EA are um is particularly associated with colorectal cancer. Um Ca 19 9 can also be associated with pancreatic or pa of um cancer. A FP. Um as well as part of cellular cancer can be associated um with non hematoma uh germ cells. Um and the same with beta HCG S. Um And um and then as and BHD can also be um related to um troop uh gestational trophoblastic disease. Ok. So that is the end of the round. Um Or if there's any questions I'll have to answer, maybe give it a few more seconds just to see if anything pops up. Feel free to ask any questions or any topics that you guys are unsure of. We'll try our best to answer them. Ok, let's move on to the next round. Ok. So number one, a six year old male patient presents to the emergency department with sudden onset severe pain, radia radiating down his legs. He reports urinary incontinence and difficulty walking for the past few days. On examination, there is bilateral lower limb weakness, decreased sensation below the umbilicus and loss of anal sphincter tone. He is currently being treated for prostate cancer, which of the following uh is the most appropriate initial management. So, immediate surgical decompression, radiotherapy, high dose oral dexamethasone or de observed and reassess in 24 hours. Ok. So the answer um for this is see high dose oral dexamethasone. So this is in keeping with neuroplastic spinal cord compression, which is a oncological emergency. Um and this is where the tumor is pressing against um the spinal cord um and causing um compression of the nerves. Um We can see that from his loss of sphincter tone as well. Sensation changes at umbilicus. That's probably meaning that the lesion is around t 10 level, which is around the level of umbilicus or lower. Um So what we need to do is get urgent MRI spine. But if we do suspect this and given that his symptoms and his um he's been treated for prostate cancer, which typically can metastasize to bone. We need to need to treat it with high dose or dexamethasone. Um does need urgent um uh consideration for radiotherapy or surgery, but we need to start the treatment first um to help um improve the symptoms of uh see if we can help improve the symptoms. Ok. So next question. So two, a 45 year old HIV positive male presents to the emerging department with fever, nonproductive cough and increasing dyspnea over the past week. He has a history of poorly controlled HIV infection and it is not on any prophylactic medications. So sa reveals diffuse bilateral interstitial pulmonary infiltrates. Sputum samples are negative for bacterial pathogens. So, what's the most appropriate initial management for this patient? So, initiation of trimethoprim sulfamethoxazole, um RT MPS, MX administration of oral fluconazole, intravenous, um cefTRIAXone and Azithromycin or D nebulized pentamidine. Yeah. Ok. So the answer for this um is a uh initia initiation of uh trams, sulfa, uh methoxa zole um and are called trimoxazole. Um It's more commonly known and this is because this is in keeping with a pneum assistant, a new assistance, pneumonia or PCP pneumonia. And the most telling thing in this question is that he's got poorly controlled HIV. Um and this is the most common opportunistic infection in AIDS and this is an AIDS defining um infection. Um and such, all patients with act four under 200 per millime should receive a PCP prophylaxis, um which is usually low dose cotrimoxazole. Um features can have dyspnea, dry cough fever. Um but you can't mostly can't hear anything when you listen to the chest. Um chest X ray have these bilateral pulmonary infiltrates um that can be normal um and management. So, oxazole so should be offered a CD four count. It's lower for prophylaxis can give IV pentamidine. Um but the are are aerosolized but however, aerosolized is less effective but can have increased risk of pneumothorax. If patients are quite hypoxic, then can give steroids. So usually if the P two is under 9.3 KPA um because they reduce respiratory failure rates as well as death. Um ok. So next question. So number three, a 60 year old male with acute myeloid leukemia presents to emergency department with fever chills and hypotension. Recently completed a cycle of chemotherapy on examination. He appears pale tachycardic and hypotensive laboratory investigations reveal neutropenia with an absolute neutrophil count of not 0.2 and three of nine and inflammatory markers considering the most likely diagnosis. What is the most appropriate option to treat this condition? So, A IV meropenem B IV Tazocin C administration of gy colony stimulating factor or D CSF or D IV fluid resuscitation OK. So the answer for this question is B IB Taos. So given that he's been treated for a ML, it would, he would recently have chemotherapy and has a low neutrophil count. Um And this is neen and he's got signs of sepsis. So this kind of corresponds to neutropenic sepsis first line. Um And the majority of trusts would be tazocin or piperacillin andam. Usually we don't use meropenem as first line. Um IV fluids can be used um but they usually um to help with hypertension um but they will not treat the infection and usually buin is the important thing to try and get in as quickly as possible. Colony stimulating factors. Um are are not shown to help in the acute stage of um neutropenic sepsis and they, they can be used um prophylactically um after having chemotherapy to help increase um the numbers of neutrophils. Um and it's quite commonly used in chemotherapy regimens. However, um not commonly used in neutropenic sepsis. Ok. So, next question. So for a seven year old child with a history of sickle cell disease presents to the emergency department department with complaints of severe fatigue weakness and pallor children's. Um parents report a recent erythematous rash on both cheeks on examination. There's no evidence of jaundice or lymphadenopathy laboratory investigations reveal the following. So, hemoglobin 4.8 normal between 11.5 and 50 13.5 white cell count of 7.5 1000 normal between 4.5 and 13.5 1000 platelet count of 200,000. Normal range between 100 and 5400 and 50 a normal, sorry, a low reticulate reticulocyte count at naught 0.2. So what's the most likely diagnosis um, of given history of a sickle cell disease? So, is it a aplastic crisis? Is equestrian uh se sequestration, um, crisis, acute chest syndrome or vasoocclusive crisis? Ok. So the answer here um is a aplastic crisis. So these are the kind of the four main crises um that you would expect to see in a, a patient with a flare of sickle cell anemia. We did talk about acute chest syndrome and vaso occlusive crisis. Um So that's when we get a lot of pain. Um And acute chest syndrome is when it specifically happens in the chest. Um But this um patients also, ok. Um presenting with low hemoglobin and more tiredness and pain. So, um when a sickle cell person with a decreased reticulocyte, we think of aplastic crises and this is when the blood marrow is suppressed as not producing any of the um any of um the blood cells. And this is usually associated with a um a parvovirus. And this was seen with the uh this child with a slap cheek disease or Parvovirus B 19 infection. Um and that can cause a sudden fall in hemoglobin if we were to see a high um reticulate current. We can think of the bone marrow as being quite active and producing lots of immature themselves or reticulocytes. And that would be more in keeping with the sequestration crises and having problems saying it. Um but that would, that will happen with sickling within the organs with it, particularly the spleen or lung and cause pooling of blood um with worsening of anemia. Um but then the blood, the bone marrow is still working and still uh pushing it lots of immature cells which will lead to a increased tic count. Ok. So next question five, a 25 year old woman presents to her GP with fatigue and jaundice. She reports a lifelong history of intermed intermittent episodes of jaundice. On examination. She has splenomegaly and signs of hemolytic anemia. Laboratory tests reveal anemia with elevated reticulate current unconjugated hyperbilirubinemia and a negative direct anti test or Coombs test. So, what's the most likely diagnosis in this patient? A see that disease b hereditary spy cytosis c, autoimmune hemolytic anemia or d anemia of chronic disease? Ok. So the answer for this um is B hereditary spherocytosis. Um So the clues in the uh in the question um would be kind of a long history. So, from birth, so we're thinking about kind of more hereditary condition. Um So kind of not thinking maybe of anemia of chronic disease. Um and the signs of a hemolytic anemia um which is kind of the jaundice and the hyper uh un uh hyperbilirubinemia, which is un unconjugated. So, those kind of rule out to the answers B and C um she's had a direct anti da test which would be positive in autoimmune hemolytic anemia. So that kind of means that the answer would be here. Speros and this is when the red blood cell um due to genetic factors um has lost it nice biconcave shape and as said, aery are very round. Um And that will mean that there's um reduced oxygen um um binding and reduced oxygen carrying capabilities. Um So that might lead to um fatigue and can even have stillbirth. Um And, but, ok, we'll, we'll see that the patient will have power or jaundice or splenomegaly usually. OK. So, final question. So number si uh six of the third round. So a 60 year old man presents with g uh to the GP with difficulty swallowing. He is a current smoker who smokes 40 cigarettes a day for the past 40 for the past 20 years. And a gastroscopy shows a tumor like lesion in the upper esophagus. So, what is most likely cell type? A adenocarcinoma? B, small cell carcinoma, C, squamous cell carcinoma or d transitional cell carcinoma? Ok. So, the answer for this um is C squamous cell carcinoma. So, esophageal cancers, um which is what we're dealing with here. Uh Typically come in two kinds, squamous cell or adenocarcinoma, small cell carcinomas. Uh for answer B uh are typically associated with lung cancers are in your endocrine in origin, um, and can be quite aggressive. Uh, lung cancers and transitional cell carcinomas are ok, more associated with bladder cancers. Um, you have two different types of epithelium within the esophagus. In the upper portion, you've got your squamous cell which tend to be more hardened epithelium. Um, and then in the lower bit, you've got adenocarcinoma, which tend to be more secretory cells. Um So if you think about the upper esophagus, the more um higher chance of squamous cell carcinomas, which is uh which is quite linked with smoking, adenocarcinomas in the lower part of the esophagus, more uh linked to gastric reflux, particularly Barrett's esophagus. Ok. So I think that's the last question of the round. Cool. Thank you very much, Ken. No, that was a great session. Um I hope everyone enjoyed the session and, and you found it useful. Um Could I please ask that if you're in your fourth or fifth year? Could you scan the QR code and take part of the surgical survey that we're kind of running just to evaluate the difference in experience between urban placements and rural placements. So if you have time and if you can scan that QR code, uh you get a certificate for participation as well. Um But yeah, really appreciate that. Um Apart from that, you know, where to find us or on Instagram and all social media on at crash course finals. Um And if you wanna get in touch with email it, crash course finals UK at gmail.com. Um So next week the session uh we have is psychiatry and we're running on a Wednesday at 7 to 8 p.m. So do sign up, there's another cure code for you. Um Yeah, and I hope you enjoy the session, please fill up the feedback for killing for us as well. Just so we know what we can do to improve the sessions and we've hope you enjoy the session. So we'll stick around for any last questions if anyone has any. Um But yeah, thank you very much, sir. I will, the feedback form should be on the messaging on, on the messages. Sorry. Um Yeah, the survey is just for students in Scotland or in the UK, actually. Sorry. It's in the whole of the UK. So if you have time, um I really appreciate it if you guys can fill out. Um Yeah, please provide the feedback. You get a certificate for attending um the session and yeah, I hope to see you again.