Marrow GT 15 review Part 4 | Dr. Prince Ghai

[00:00:05]Today we'll be starting part four of grand test 15 from Maro.

[00:00:11]Starting with question number 151. It says a patient who is posted for renal transplant in 5 hours is started on an interlucan 2 receptor antagonist to prevent acute transplant rejection.

[00:00:23]Which of the following drugs would have likely been given?

[00:00:28]So they are basically asking us about the drug which inhibits interlucan 2 receptor and that drug is baseliximab.

[00:00:38]So basiliximab inhibits interlucan 2 receptor and also it is known as anti CD 25 antibbody and another important point is it is a murine human chimeic monoconal antibbody.

[00:01:07]looking at other options. So first option say cerolyimus. So cerolyus we know is mtor inhibitor and cycllosporin as we know it is calcinurine inhibitor and lmtozummab is humanized immunoglobiline G1 that binds to CD52. 2 or we can say it is NTCD 52.

[00:01:46]Coming to the next question, it says a 35year-old factory worker presents to the OPD with severe back pain following a workplace injury involving heavy lifting. So there's back injury. He's diagnosed with a lumbar disc herniation at level L4 L51 MRI. The patient is employed in an industry covered under ESIC and has worked there for 3 years.

[00:02:09]what is covered under the extended sickness benefit for this employee under ESIC.

[00:02:16]So if we talk about extended sickness benefit, we know that it covers 80% of the daily wages for a duration of 2 years for a set of 34 diseases.

[00:02:41]And these diseases include tuberculosis, leprosy, diabetes, malignancies, Parkinson's, mcnia, gravis etc. And the difference between extended and enhanced sickness benefit is that in extended sickness benefit the employee is going to get 80% of the daily wages. Whereas in case of enhanced sickness benefit, full wages will be provided.

[00:03:11]But that's only for sterilization procedures.

[00:03:21]For example, in case of vasectomy, if a male under goes vasectomy, so he will get enhanced sickness benefit for how many days? 7 days.

[00:03:34]And if a female under goes tubectomy, so she will get enhanced sickness benefit for 14 days.

[00:03:45]So let's look at the options one by one.

[00:03:48]Option A says 70% of daily wages per day for a period of 91 days. No, we know that the person or the patient will get 80% of daily wages and that to beyond a period of 91 days. Permanent life pension decided by a medical board. No.

[00:04:08]And the third option says extended cash benefits for a period of 2 years. This is correct. And also we have to note that in the question they are saying that the person has worked there for 3 years. So a minimum of 2 years should be served by the person in that at his workplace. Only then he will be qualified to avail extended sickness benefit. And option D says vocational rehabilitation services for up to 3 years. This is also incorrect.

[00:04:38]Coming to question number 153. A 25year-old female presents with weakness and fatigue. On examination, her blood pressure is low.

[00:04:47]Lab investigations reveal metabolic alkalossis. There is hypomagnesmia, hypocalemia, hypocalceura and high urine chloride. Based on these findings, which of the following renal ion channels are affected in this condition?

[00:05:03]So we will look at the option one by one. So epithelial sodium channels they are affected in little syndrome and the characteristic feature of little syndrome is that the patient will have hypertension and in this case the the blood pressure is low which is why this option can be ruled out very easily.

[00:05:28]Then coming to the option number C that says sodium potassium 2 chloride coransporter and this channel is present in the thick ascending limbo of loop of Henley and this is associated with Barter syndrome and we know that Barter syndrome presents with polyurea polyypipssia and there's high eldoststerone because of RAS activation.

[00:05:58]And also the patient has hypocalemia, metabolic calculosis, hypomagnesmia, hypocalcemia and hyper calcurura. So the characteristic feature will be hypercalceura which distinguishes it from gleman syndrome which has been asked in this question. Here we can see there's hypoglyceura. So this can also be ruled out. And sodium bicarbonate coransporter it is affected in type two renal tubular acidosis.

[00:06:34]Coming to the option number B which says sodium chloride coransporter. So this is the channel which is present in distal convoluted tubule and this is affected in gleman syndrome and we know that gelman syndrome mimics thioide diuretics.

[00:06:54]So what happens there is defect in this channel called sodium chloride coransporter.

[00:07:01]When this channel is affected which is present in DCT so there is going to be renal wasting of sodium chloride.

[00:07:11]So sodium chloride there will be renal wasting and then what will happen? The ras will get activated. When ras gets activated there will be increased reabsorption of sodium and there will be increased excretion of potassium.

[00:07:30]And this increased excretion of potassium is followed by increased excretion of hydrogen ions which causes hypocalemia and which causes metabolic alkyossis.

[00:07:44]And the blood pressure in these patients is normal to low. And also there's one channel which is responsible for magnesium.

[00:07:57]The magnesium is also not able to re get reabsorbed and it is excreted in urine and it causes severe hypomagnesmia.

[00:08:06]That's why the patient presents with seizures.

[00:08:10]So hypommagnesmia is also a characteristic feature of gleman syndrome. So the answer will be option B that is sodium chloride coransporter.

[00:08:20]Coming to the next question. A 52-year-old farmer presents with migratory polyarthritis.

[00:08:27]Chronic diarrhea, generalized lymphodinopathy and hyperpigmentation. A dodal biopsy reveals characteristic pass positive diastasis resistant macrofasages. So these are the key words in the lamina propria to prevent neurological relapse. Which antimicrobial regimen is the most appropriate? Long-term management. So the given clinical scenario is suggestive of whipple's disease.

[00:08:54]So it the diagnosis is whipple's disease and it is caused by a bacterium known as trophy vipplei and then and also this bacterium has a propensity to affect central nervous system.

[00:09:23]If you look at the option, option A says oral tetracycline, then intravenous vancomyin followed by oral rifampin.

[00:09:30]Option C says intravenous sept trione followed by oral TMS and then option D says oral penicellin and streptoycin.

[00:09:42]So the management is initially we are giving the induction treatment with sept trione for 2 weeks that is option C. So initially we will give sept trione for 2 weeks and later on in the maintenance phase we will give trimethopram sulfthoxazole for 12 months and we are choosing this drug because it can cross a blood blood brain barrier and it can treat the CNS manifestations of the whipple's disease and also we should remember in the previous question or in the previous question discussed in the previous parts we have seen that coxella bernetti coxella bernetti also causes culture negative endocarditis and trophy vap is another organism which causes culture negative endoarditis and also it causes oculomestigatory myythmia that means there will be rhythmic jaw and eye contractions or movements coming to the next Question 155. A 16-year-old boy presents 3 days after sustaining a nasal injury during a football match. So there's the nasal injury. He complains of progressive nasal obstruction and mild pain. So there's progressive nasal obstruction following a football injury. On examination, there is soft fluctuant swelling. As we can see in the image on both sides of the nasal septum, the patient did not seek treatment immediately after trauma. If this condition is left untreated, which of the following is the most likely complications of the given condition?

[00:11:23]First, we have to make the diagnosis and the diagnosis in this case will be septal hematoma.

[00:11:39]We know that if this is the septum.

[00:11:43]Okay, if this is the septum, so the septum is receiving if this is the nasal cartilage which is present in the nasal septum and we know that this is avascular and it is receiving its blood supply from the paricchondrium.

[00:12:04]In septal hematoma what happens?

[00:12:09]There's a hematoma. Suppose this is the hematoma which is formed between the nasal septum and the paricchondrium. So the blood supply in this case will be cut down. When the blood supply is cut down the cartilage will undergo avascular necrosis.

[00:12:24]Now the reason being the hematoma is obstructing the vascular supply to the septum.

[00:12:33]So eventually it will cause fibrous thickening of the septum and if there is secondary infection in the septum it can lead to septalapses and there will be necrosis of the cartilage and the patient can have depression of nasal dorsom that means there will be saddle nose deformity. So option B is the correct answer. In case of deviated nasal septum, the patient will only present with nasal obstruction and nasal polyp they are painless and there's going to be a mass present in the nasal cavity.

[00:13:09]and juvenile nasal fangial angio fibram.

[00:13:12]The key feature or the diagnosis clincher will be the patient will have recurrent epistaxis because we know that juvenile nasoparangial angop fibram is a very vascular tumor which will cause progressive nasal obstruction and the patient will present with epis recurrent epistaxis and it does not occur following a trauma.

[00:13:39]Coming to question number 156 it says draconulasis is transmitted through. So draenulasis is also known as guinea worm and it's a very direct question.

[00:13:54]So it is transmitted through consumption of water containing cyclopes.

[00:14:00]So we will quickly have a look at this important life cycle.

[00:14:06]I am zooming in as you can see human drinks unfiltered water containing pop ports with L3 Larae. So the infective stage of Larae is L3. And when Larae are released into the gastrointestinal tract they will penetrate the host stomach and intestinal wall and they will mature and reproduce in the human gastrointestinal system. So in the third step we can see the fertilized female worm migrates to surface of skin. So after the female worm has been fertilized she's going to move to the surface of skin and there will be a blister and that blister will contain a lot of larae.

[00:14:50]So whenever the person or the infected person rather comes in contact with water the L1 larae they are released into water from the emerging female worm that blister it bursts open to release a lot of larae and then L1 larvae they're consumed by a cop port and Larae under goes two molds in the cop port and becomes L3 Larae. So the development will takes place inside the cop port. So this was the life cycle of guineaorm.

[00:15:28]Coming to the next question which is also a very direct question. It says feroptosis and pyroptosis they are mediated by. So we know that ferroptosis is a new mechanism of cell death.

[00:15:40]So feroptosis it is induced by membrane lipid peroxidation and there will be increased level of iron intracellularly and also there will be increased level of reactive oxygen species and The most important feature is loss of mitochondrial crist and the outer mitochondrial membrane will be disrupted.

[00:16:26]So these are the key features of feroptosis and we know that feroptosis is linked to various human pathologies such as cancer, neurodeenerative diseases and stroke.

[00:16:38]And coming to pyroptosis.

[00:16:47]So in case of pyroptosis the first step is activation of inflammosome.

[00:16:57]So inflammosome gets activated in the first step and in the second step there is involvement and activation of gasphase one and in the third step there is generation of interlucan one and we know that interlucan one causes fever and inflammation and there's is also luccoside recruitment.

[00:17:31]So looking at the question they say feroptosis and pyroptosis are mediated respectively by caspay activation and lipid peroxidation. This statement is wrong. Caspace activation is present in pyroptosis and lipid peroxidation is present in feroptosis.

[00:17:46]Option B says lipid peroxidation and caspace activation. This statement is true. We have just seen that lipid peroxidation induces feroptosis and caspace activation induces pyroptosis.

[00:17:59]Option C says lipid peroxidation and RIP K1 and RIP K3 this statement is also wrong. RIP K1 and RIP K3 complexes they are involved in the process of necroptosis not in pyroptosis.

[00:18:16]And option D says both are caspace dependent. No only pyroptosis is caspace dependent. Ferroptosis is independent of caspasis. And if they ask us what are the caspases or what type of caspacases are involved in pyroptosis caspace 1 4 and 5. So caspace 1 4 and five are associated with pyroptosis.

[00:18:44]Coming to the next question. A woman with a family history of breast cancer underos genetic screening as and is found to be positive for BRCA1 mutation.

[00:18:54]Which of the following procedures should be suggested to this patient?

[00:19:00]So we know that patients who are positive for BRCA1 they are at an increased risk of ovarian cancer and breast cancer.

[00:19:16]So ideally what we do is salpingo ofctomy is done between the age of 35 to 40 years in those patients who are positive for BRCA1 mutation and it can be delayed in patients with BRCA2 with up to 45 years. So what we have to remember is in BRCA1 mutation salpingoorctomy is done profilactically when the patient reaches the age group of 35 to 40 years.

[00:19:57]So the answer will be salpingo ofctomy and also we will we have to know that BRCA1 BRCA 1 and BRCA2 they both are tumor suppressor genes.

[00:20:10]They are tumor suppressor genes and BRCA1 is present on long arm of chromosome 17 and BRCA2 is present on long arm of chromosome number 13. And also there's one important question BRCA 2 is more strongly is more strongly associated with male breast cancer. Even though both the genes that is BRCA 1 and BRCA2 are associated with male breast cancer but if they ask us which one is most strongly associated in that case it will be BRCA 2.

[00:20:53]Coming to next question a public health researcher compares two regions and finds that one region has a lower crude death rate but poorer health indicators overall.

[00:21:05]The discrepancy is attributed to population structure differences. Which of the best explains this observation?

[00:21:14]So first of all, we should know what is crude death rate. We know that crude death rate is total number of deaths divided by midear population multiplied by 1,000.

[00:21:29]And it does not take into account the population structure of a particular area.

[00:21:36]So here they are saying in an area which has a lower crude death rate but poorer health indicators overall. Generally if we look at this phrase it says poorer health indicator. So the poorer health indicators indicate that the mortality or the death rate in that particular area should be high. But in this case the crude death rate is low. It is contrary to what we expect.

[00:22:02]But it could also be possible that in that particular area more of younger population is present which is why the crude death rate is low despite the presence of poor health indicators. So this is the probable explanation for this that despite having poor health indicators the crude death rate is low because in that area more of younger population is present compared to older population.

[00:22:36]So it says crude death rate is independent of age distribution.

[00:22:41]This is wrong. It is highly dependent on age structure.

[00:22:45]Option B says crude death rate is influenced by age sex composition of the population. This is true. And option C says crude death rate is a direct indicator of disease burden. It is not a direct indicator. It is a non-specific measure and it does not tell us the direct burden or true burden of a disease in a population.

[00:23:09]It says crude death rate reflects only communicable disease.

[00:23:14]It does not only reflects communicable disease rather it includes all the causes of death be it communicable diseases or non-communicable diseases. That's why this statement is incorrect.

[00:23:29]Coming to a question number 160. A 3-year-old child presented with the abdominal distension and was found to have leftsided belotable flank mass. So in a three-year-old child a leftsided bellotable abdominal mass is present and later on it was found that there was mutation in WT1 gene and this line mutation in WT1 gene clinches the diagnosis of the patient. Which of the following syndrome is associated with this malignancy? Option A turn syndrome, B neurop fibromyitosis 1, option C obsoclonus myoconus syndrome and option Dennis rash syndrome. So, WT1 gene mutation.

[00:24:14]So, in WT1 gene mutation, there's going to be Wilm's tumor.

[00:24:23]And we know that there is misssense mutation.

[00:24:30]There is misssense mutation of WT1 gene in Denanish Draash syndrome. and Denanish drast syndrome is associated with Wilm's tumor. So we will quickly look at the various syndromes which are associated with Wilm's tumor. So the first one is Wagger syndrome and Wagger syndrome W stands for Wilms tumor, N stands for ania and G stands for genital abnormalities and R stands for retardation that is mental retardation and this is due to WT1 and PAX 6 gene deletion.

[00:25:14]This is deletion of these two genes.

[00:25:17]Coming to the second syndrome which has been asked in this question that is Dennis Dashrash syndrome. So there is misssense mutation of WT1G.

[00:25:31]So the features in this condition will be gonadal disgenesis that is male pseudo hermaphrotitism and the patient will present with early onset nephropathy and also gonadoblastto.

[00:25:47]So these are the three key words which will clinches the diagnosis of den syndrome. Coming to option. Coming to syndrome number three that is beck with vidman syndrome.

[00:26:06]In this syndrome there's overexpression there's overexpression of IGF2 that is insulin like growth factor on WT2 region and in this case the patient will present with organomegali macroia hemihypertrophy hippatoblastoma etc. So this was about Wilm's tumor. Coming to next question.

[00:26:38]So next question says a physiologist studies saliva at rest and during maximum stimulation primary salivory secretion by asina cells is isotonic but final saliva is usually hypotonic.

[00:26:55]During high salivory flow the composition of saliv saliva approaches that of plasma. So the condition that is given here is high salivory flow.

[00:27:08]What is the most likely mechanism for this change?

[00:27:14]So if you look at the basic physiology, we know that there are two steps.

[00:27:20]So the first step normally is production of primary saliva.

[00:27:28]We know that primary saliva is produced by asinina cells and it is isotonic in nature. So primary saliva is produced by asina cells and it is isotonic in nature which resembles plasma.

[00:27:45]And step number two says the function of or it explains about the function of salivory ducts.

[00:27:53]So when the saliva passes through salivory ducts there is reabsorption of two ions that is sodium ion and chloride ion and there is secretion of two ions that is potassium and bicarbonate ions and water cannot flow efficiently which is why the saliva becomes hypotonic.

[00:28:24]So now we will see what happens when the flow of saliva through these ducts is rapid. There is high salivory flow.

[00:28:35]In this case what will happen? The saliva will rush through the ducts.

[00:28:42]So the saliva will rush through the ducts and the ducts will get less time to modify the saliva. What modifications will happen? There will be less reabsorption of sodium and chloride.

[00:29:00]When there will be less reabsorption of sodium and chloride, that means more amount of sodium and chloride will remain in the saliva. Which is why the saliva will become less hypotonic and it approaches plasma concentration.

[00:29:22]So in nutshell we say that when the flow rate of saliva increases through duct the duct is not able to modify the composition of saliva and saliva becomes more isotonic or we can say less hypotonic tonic that means it resembles plasma.

[00:29:42]So they say increased sodium and chloride secretion by asina cells. No reduced ductal modification due to rapid flow. This is true. Duct is not getting enough time to modify the composition of saliva. Option C, saturation of ductal transport mechanism. No. Option D, increased sympathetic stimulation altering electrolyte transport. This is also incorrect.

[00:30:06]Coming to next question. It says, a 32 year old male sustains thoracco abdominal trauma and subsequently develops progressive disna.

[00:30:22]There is history of thoracco abdominal trauma and this dysnia. Imaging reveals plural eusion and thoracicis yields milky white fluid with elevated triglycerides.

[00:30:34]Based on the clinical findings which is the most likely site of injury. First we have to make the diagnosis. We know that from plural eusion findings that the plural eusion fluid is milky white in color with elevated levels of triglyceride. This is nothing but kyoththorax.

[00:30:58]Kylothorax happens when there is injury to the lymphatic duct or thoracic duct.

[00:31:04]So we have to find out which opening allows the passage of thoracic duct. For that we need to know the basic anatomy of the various openings which are present in the diaphragm. If we look on the anterior side or the most anterior side, we can see that there's venina cable opening present.

[00:31:30]So the venina cable opening is present in the central tendon of the diaphragm and it is present at the level of T8.

[00:31:38]And then if we go a little below or a little posteriorly we can see that there is one esophasial opening which is present and esophasial opening is present in the muscular part of the diaphragm at the level T10.

[00:31:53]And if we go more posteriorly we can see that there's one opening which is present for the aota at the level of T12 vertebra. So this opening for a also allows the passage of thoracic duct as vein and hemizygus vein. So the most posterior opening should be the answer to this question.

[00:32:22]So this is present at the level of T8.

[00:32:25]The second opening at level T10 and the third opening is present at the level of T12.

[00:32:33]So the answer will be the opening which is present at the level of T12 that is aotic opening and aotic opening allows the passage of ata. Ata means aota and then we have thoracic duct and then we have vein.

[00:32:55]So option three will be the correct answer.

[00:33:04]Coming to the major openings through diaphragm. So at T8 we know this opening is present in the central tendon. It allows the passage of inferior venneava and right frenic nerve. This is right frenic nerve. And at T10 which is present in the muscular part there's opening for esophagus and vagus nerve both right and left. And at T12 art structures are present aota, thoracic duct and isus vein. And this is present in the crust of the diaphragm. And also it allows the presence passage of hemizygus vein.

[00:33:39]Next question which is a direct question in genomic imprinting DNA is modified by so in DNA imprinting or in genomic imprinting DNA is modified by the methilation of CPG island.

[00:33:54]So there's methilation of CPG island.

[00:34:06]We know that epigenetic modifications they take place or they include, acetilation, deacetilation, methilation of core histone proteins.

[00:34:34]These three processes are involved.

[00:34:37]Looking at the option acetilation, phosphorilation, deamination and methilation.

[00:34:42]So genomic imprinting the DNA is modified by methilation.

[00:34:51]Coming to the next question. A 60 a 75 year old male is being operated on for carcinoma of the head of the pancreas under general anesthesia and using volatile anesthesia for maintenance. Which of the following volatile anesthetics is least likely to produce carbon monoxide despite degradation in the presence of soda lime?

[00:35:11]So in the presence of strong bases such as soda lime we know that soda lime is a mixture of 2% 2.5% of potassium hydroxide plus 1.3% of sodium hydroxide.

[00:35:27]So in the presence of soda line various inhaled anesthetics undergo degradation and they liberate carbon monoxide and we know that carbon monoxide has high affinity for hemoglobin and it binds to hemoglobin and it causes hypoxia.

[00:35:52]So what happens when inhaled anesthetics such as n florine, desurine or isofllorine are given they in the presence of strong bases liberate carbon monoxide and carbon monoxide can cause occult hypoxia because it has much higher affinity for binding with hemoglobin and there will be tissue hypoxia as well because less amount of oxygen will reach the different tissues in the body. But there's one compound which which does not form carbon monoxide and that is seoffllorine. Seoflurine we know the byproduct of seafllorine is compound A and Soflorine it does not form carbon monoxide. So answer D will be the correct option.

[00:36:43]Question number 165. A 28-year-old woman presented with a history of chronic abdominal pain, diarrhea, low-grade fever, weight loss and fatigue. She underwent a colonoscopy which revealed the following finding. Which of the following hisytological findings is characteristically seen in the underlying condition? First of all, we have to make the diagnosis and the diagnosis is very clear-cut if you understand the image. The image is showing us the cobblestone appearance.

[00:37:07]So, we can see this bumpy appearance which is present. This is cobblestone appearance.

[00:37:14]And this cobblestone appearance is present in Cronhn's disease.

[00:37:21]So the Crohn's disease is the diagnosis.

[00:37:24]So what is the characteristically seen in underlying condition that is in Crohn's disease? First option says cryptopapsis. No, cryptosis is non-specific finding. Cryptopsis is seen in both ulcerative colitis as well as Crohn's disease. Then it says diffuse inflammatory infiltrate that is also a non-specific finding. So this cannot be the answer. Non-catiating granulomaas yes nonciating granulomaas they are only present in crohn's disease and not in ulcerative colitis.

[00:38:02]And also we know that there's transmural inflammation.

[00:38:09]There is transmural inflammation which is present in Crohn's disease. And Cronhn's disease has another characteristic feature that is skip lesions.

[00:38:17]There is non-ontinuous involvement.

[00:38:23]So option C will be the correct answer.

[00:38:28]Next question. A 72 year old woman was diagnosed with burket lymphoma.

[00:38:32]Cytogenetic studies demonstrated transllocation 814 chromos chromosomal transllocation. Which of the following best explains the role of this transllocation in the pathogenesis of burket lymphoma in this patient?

[00:38:43]Expansion of a trucleotide repeat. No.

[00:38:46]Protooncogen activation. Loss of heterrozygosity. Alter DNA methilation status.

[00:38:54]So if we look at the pathogenesis of burket lymphoma briefly we know that mic gene or protonco gene is present on chromosome number eight right. So what happens there is transllocation of this segment.

[00:39:19]So there is going to be transllocation of this segment to chromosome number 14.

[00:39:27]And this is how the chromosomes are going to look like in burket lymphoma.

[00:39:31]We can see that the mic region on chromosome number 14 is is present very close to imunoglobiline heavy chain. So it is present very close to immunoglobiline heavy chain or heavy gene.

[00:39:52]And when my mic gene was present on chromosome number eight, it had its own regulatory sequences which could control the mic gene. But when the gene is transferred to chromosome number 14, the regulatory sequences are lost. When the regulatory sequences of mic gene are lost, there is overexpression of the there is overexpression of the mic gene and myc gene is a protoonco gene. And this overexpression is happening because of loss of regulatory sequences which were present with MYC gene when it was present on chromosome number eight.

[00:40:37]So in this case the option B will be the correct answer.

[00:40:43]Looking at other option option A says that expansion of a trucleotide repeat.

[00:40:47]This is incorrect. Trylotide repeat is present in disorders such as fragile leg syndrome and loss of heterrozygosity and altered DNA methylation status are not present in burkit lymphoma. Coming on to next question which is very commonly asked. A 50 yearear-old female presents to the outpatient department with complaints of fatigue for the past 2 months. So 50year-old female fatigue for 2 months. She's a known case of rheumatoid arthritis. So she is having a autoimmune disease known as rheumatoid arthritis and she's currently under treatment. CBC shows hemoglobin of 9 g per deciliter. Mean corpuscular volume is 78 phentol.

[00:41:29]Peripheral smear is showing microitic hypocchromic red blood cells. Which of the following iron profiles is seen in the patient? Looking at the question, it looks like the patient is having iron deficiency anemia.

[00:41:42]But iron deficiency anemia is incorrect diagnosis here because this anemia is present in the background of a autoimmune chronic disease. So this anemia is present in the background of chronic inflammation. That's why this is anemia of chronic disease.

[00:42:06]And if we look at the findings of anemia of chronic disease, we know that in anemia of chronic disease, all the parameters will decrease.

[00:42:19]All the parameters will decrease except for serum feritin which is increased.

[00:42:27]So if we know this much we will be able to answer this question very easily. So we will have to look for an option where the levels of serum feritin is increased and rest all the parameters are decreased. Option A all the parameters are decreased except for TIBC. This suggests iron deficiency anemia. So this cannot be the answer. Option B says iron is decreased, TIBC is decreased, feritin is increased and transferent saturation is also decreased. So this is the correct option representing anemia of chronic disease. And option C says serum ion is increased, TIBC is decreased, feritin and transfer in saturation is increased. So everything is increased except for TIBC. This is exactly the opposite of iron deficion deficiency anemia. And this is present in cyeroblastic anemia.

[00:43:21]So cyeroplastic anemia the profile is going to be exactly the opposite of iron deficiency anemia. If you look at the option D it says normal serum normal TIBC everything seems to be normal and this is seen in thalismia.

[00:43:37]So option B is the correct option.

[00:43:41]Question number 168. During a microbiology practical class, your tutor demonstrates neglar reaction to the class in the microbiology lab for the identification of claustrdium perringence in clinical specimens. Which of the following is incorrect regarding this test? It is used for the quantification of toxin. No, we are just using this test negler reaction which is a neutralization reaction for the identification of toxin.

[00:44:09]We are just identifying the toxin. We are not quantifying the toxin. Option B says alpha toxin produced by lostium forms the basis of this reaction. This is true. This toxin has less activity. Yes, this is also true.

[00:44:28]Opacity is absent around colonies on the side with antitoxin present. This is also true. So they are saying choose the incorrect statement. So the incorrect statement would be it is used for quantification of toxin.

[00:44:41]So we will quickly look at the neglerar reaction. We know that neglar reaction is shown by the clusterium for fringingens and it is a neutralization reaction.

[00:44:52]We can see that on one side anti-alpha toxin is present on one half of the plate and there's no antitoxin present on the other half of the plate.

[00:45:04]So where the alpha anti-alpha toxin is present there is going to be neutralization reaction which is why we are seeing no pacification here but on the right half of the plate we can see that there is no antitoxin which is present. If there is no antitoxin there will be no neutralization reaction that means opacification will be present and this opacification is attributed to the alpha toxin of clustrdium perringens and this alpha toxin has leith like activity.

[00:45:42]Coming to the next question, it says a patient with osteocaroma develops oliguric renal failure following highdose methotrix therapy. Despite urinary alkalization, plasma drug level remain toxic. A recombinant agent is administered to rapidly cleave the drug.

[00:46:00]So there's a recombinant agent that they have used to cleave the drug into glutamate and inactive metabolites.

[00:46:07]Which agent was given?

[00:46:10]We know that luccoorin or folinic acid is used in the toxicity of methtoresate but it is not a recombinant agent and also it does not cleave the methotraate into glutamate and other inactive metabolite. So this cannot be the answer. Looking at option two it says raspberry case. Raspberry case is a recombinant urate oxidase and this is used in the treatment of hyper urismia in tumor lysis syndrome.

[00:46:43]So what it does is this will convert uric acid into lentoine and it has no use in the treatment of methtoraxate toxicity.

[00:46:55]Option C says glucarase and option D says mena. Mesna cannot be the answer. We know that Messina is used to prevent hemorrhagic cyitis which is seen with cycllohosphomide and iphosphomide.

[00:47:16]Even if we rule out all the options we we are left with the option C which is glucarpidase. So glucarpidase is a newer recombinant agent which is used in the toxicity of methtoresate and it rapidly cleaves the drug into glutamate and other inactive metabolite and the name of that metabolite is damp.

[00:47:40]Dampa stands for two for diamino and methile teroic acid.

[00:47:46]And the unique feature is that glutamate and dampa these are metabolites which are less toxic and they will be excreted by liver. There will not be any pressure on kidneys to excrete out these metabolites. So they are excreted by liver and they will cause a fall of 99% of methtoate in the plasma back to within 5 to 15 minutes.

[00:48:17]So the correct answer will be option C that is glucarase.

[00:48:22]Coming to next question. An adolescent boy was given iron supplements for microitic hypocchromic anemia. However, he did not show clinical improvement.

[00:48:30]Investigations revealed hemoglobin of 9 g per deciliter and menor index is 13.

[00:48:35]This is very important.

[00:48:38]And elevated levels of HPA2 and HPF.

[00:48:42]Which of the following is the curative treatment for this patient? We know that menor index of less than 13 suggests thalismia and menor index of more than 13 is present in iron deficiency anemia. So essentially we say that menor index is used to distinguish between thalismia and iron deficiency anemia and menor index is calculated by mean corpuscular volume divided by RBC count. So one clue which goes in the favor of thalismia is menor index. The another clue is elevated levels of hba2 and hbf.

[00:49:24]So now we have made the diagnosis that the patient is having thalismia.

[00:49:29]So in thalismia the curative treatment is hematopoitic stem cell transplant.

[00:49:38]Iron killation therapy is given to prevent the organ damage from the iron overload because in patients withmia they very frequently receive blood transfusions which is why they can have iron toxicity. So we give them des feroxamine defracerox and defer prone to treat the iron toxicity. So this cannot be the answer. This is not a curative treatment. Regular scheduled transfusions they are only for symptotomatic relief. They are not going to cure the condition permanently.

[00:50:10]And splinctomy is performed in patients who are having hyperplenism.

[00:50:16]And also patients who undergo spleentomy they are at an increased risk of infection from the capsulated organism.

[00:50:24]And splinctomy is less preferred because these side effects are quite severe which is why the definitive curative treatment will be hematopoetic stem cell transplant. Coming to the next question which of the following is not a content of the aduct canal.

[00:50:41]Option A is profound femorous artery.

[00:50:44]Option B femoral artery. Option C, sephanus nerve. Option D, nerve to vastus mediialis. We will quickly look at the anatomy of adductor canal.

[00:50:53]So the anterolateral wall is formed by the vasus mediialis muscle.

[00:51:00]Antolateral wall is formed by vasus mediialis muscle. The floor of the posterior medial wall is formed by the the floor of the posterior middle wall is formed by the adductor longus and adductor magnus. And if you look at the medial wall, the medial wall it is formed by a fibrous membrane. And this fibrous membrane is joining the anterolateral wall and the floor.

[00:51:27]And this membrane is covered again by on the outside by sartorius muscle. So if we look at the contents of the canal, so it contains femoral artery and femoral vein.

[00:51:44]and also it has sephinus nerve and nerve to vasus mediialis. So these are the contents of adductor canal.

[00:51:52]So nerve to vasus mediialis is present.

[00:51:54]Sephinus nerve is present. Fmormoral artery and vein are present. Profunda femorous artery is not a content of the adductor canal. Profunda femorous artery as we can see it is present on the outside of the adductor canal not inside the adductor canal. Coming to the next question. A 60-year-old male presented with fever, easy fatigability and weight loss. The bone marrow aspirate of the patient is shown below. Which of the following genetic abrasion is most likely present? So this is a very classical image of acute promyocitic leukemia. As in the image we can see that this cell is having various rod-like structures which are pink in color. So these rod-like structure which are pink in color they are known as over rods and a cluster of and a cell having a cluster of over rods is known as cell. So these are essentially cells which are containing various clusters of or rods.

[00:53:01]And this classical cell that is cell is seen in APML that is acute proyioitic leukemia also known as AML M3 according to WHO classification and we know that the most characteristic transllocation which is present or the most common genetic abrasion here which is present is PML RA fusion gene. So there is going to be PML RA alpha fusion gene. Option A says BCR ABL which is incorrect. BCL ABR BCR ABL is present in chronic myoid leukemia.

[00:53:38]Option B says PML ra and option C says CBFBY. This is present in AML M4 and runs one ETO is seen in AML with transllocation of A21.

[00:53:58]So option B is the correct answer.

[00:54:04]And also there's another point which is associated with this condition is AML M3 is associated with DIC that is disseminated intravascular coagulation.

[00:54:14]So coming to the next question it says a child presents with short stature frontal bossing and trunkal obesity.

[00:54:20]He's diagnosed with lens syndrome. Which of the following lab findings is most likely?

[00:54:26]So in lam syndrome if if you look at the pathogenesis so the growth hormone receptor is insensitive to growth hormone.

[00:54:44]So what happen normally? What happens? Growth hormone it binds to growth hormone receptor and then it will stimulate liver to produce IGF-1 and IGF-1 is responsible for all the action of it is responsible for all the action of growth hormone.

[00:55:14]But in this condition the defect is at the level of growth hormone receptor. So what will happen?

[00:55:20]There will be increased level of growth hormone. Growth hormone will keep on accumulating.

[00:55:27]And since the receptor is defective the message is not going to be transmitted from growth hormone receptor to liver which is why the level of IGF-1 that is insulin like growth factor will decrease. So this is going to be the profile in a patient who is having lens syndrome. So it says low growth hormone, low IGF, no. Low growth hormone, I high IGF, no. High growth hormone, low IGF-1.

[00:55:56]Yes, this is the correct option.

[00:56:00]Coming to the next question. You are posted in the department as an intern.

[00:56:04]The resident doctor shows you the MRI of a patient with persistent nasal discharge and stuffy nose. So there's nasal discharge and stuffy nose. The patient also complained of hard of hearing and frequent headaches particularly over the occipital region.

[00:56:21]So there is persistent nasal discharge, stuffy nose, occipital headache. The resident doctor asks you the diagnosis and discusses the salient features of the condition seen in the MRI. All of the following are true regarding this condition except.

[00:56:37]So we can see that in the posterior wall of the nasoperings. So this is the posterior wall of the nasoperings. There is a cyst which is present in the midline and this cyst is known as thornwald cyst.

[00:56:59]So when the patient has thornwald cyst it can cause persistent nasal discharge as described in the question.

[00:57:07]And also there can be obstruction to the ustaceian tube. So the patient can also present with serrus otitis media which can be seen in some of the cases. And there is dull type of oxipital headache and recurrent sore throat episodes which are present.

[00:57:25]So the diagnosis is thorn cyst. We have to select the incorrect statement. They are saying all the all of the following are true regarding this condition except so the first option says it arises from the midline recess representing attachment of notocore to endoderm.

[00:57:44]True.

[00:57:46]Option B says there's spontaneous regression occurs by adulthood. This statement is incorrect.

[00:57:54]Option C says patient presents with persistent nasal discharge. This is true. located in the midline of the posterior wall of the nasop ferings.

[00:58:01]This just we have just seen this is also true. So there is no spontaneous regression.

[00:58:08]So what is the management? The management is massupialization.

[00:58:13]So surgery is going to be the management massupialization of swelling.

[00:58:26]That's why option B is the incorrect and is the answer to the question option question 175 which among the following instruments is a bone liver.

[00:58:39]So if you look at option one so opt So if you look at the labeling number one it is nothing but osteotome. Osteotome is a chisel-like instrument. So this is not a bone liver.

[00:58:53]And uh labeling number two is bone curate.

[00:58:59]If you look at the distal end of this instrument, this is the key finding to look at and it suggests that it is a bone curate. And then the instrument number three is instrument number three is bone liver which they have asked and instrument number four is langen back retractor.

[00:59:24]It is langen back retractor.

[00:59:30]So the correct answer is option number three.

[00:59:38]We will quickly have a look at the most important instruments which are asked in orthopedics. So this instrument is a perostial elevator and curate is identified by the presence of a spoon-l like structure on the distal end. a tiny spool- like structure which is used to cure it and osteo has a chisel-like shape and bone gouge has this depression which is present on the distal end of the instrument.

[01:00:15]It is like a semic-ircular depression which is present on the distal end of the instrument.

[01:00:21]Question number 16 176.

[01:00:24]A 70-year-old man who has prostate cancer is being treated with long acting G&R agonist. After prolonged injection of G&R so there is prolonged injection.

[01:00:35]Which of the following will most likely be seen in this patient? We know that G&R can be given in two ways.

[01:00:46]one is the pulsatile dose and the other one is continuous.

[01:00:53]So if we are giving G&R in the pulsatile dose there will be increased level of LS there will be increased level of luteinizing hormone and follicle stimulating hormone and if you are giving it in a continuous manner there will be down reggulation of the G&R receptors and this down regulation of G&R receptors will cause decrease in the levels of FSH decrease in the level of luteinizing hormone and also testosterone will also decrease.

[01:01:31]So we have to find out the option where all the levels are decreased.

[01:01:38]Option A has increased level of testosterone incorrect. Option two has decreased in all the three. So answer will be option number B.

[01:01:50]Question number 177.

[01:01:53]A 62 year old patient has a history of cataract surgery.

[01:01:57]On slit lamp examination, the anterior chamber is deep. Iris shows tremulousness. That means there's trembling of the iris also known as irido iridono iridois.

[01:02:12]Fundus is clearly visible and the pupil is jet black in color.

[01:02:17]So all these findings that is iridois jet black pupil deep anterior chamber they are characteristic of aphacia and there is history of cataract surgery as well.

[01:02:34]So the answer will be aacia.

[01:02:39]Coming to the next question. A 28-year-old woman presents with painless burn injury over her hand.

[01:02:48]Okay. There was injury on her hand which was painless. That means she's not having any painful sensation.

[01:02:53]Examination reveals bilateral loss of pain and temperature sensation over the neck and upper limbs with preserved touch and vibration.

[01:03:02]They are saying that pain and temperature is gone but touch and vibration are preserved.

[01:03:11]There is wasting of intrinsic hand muscles and absent biceps reflexes. MRI of the cervical spine is shown below. So cervical spine is highlighted below.

[01:03:21]What is the most likely diagnosis?

[01:03:23]So from the question we have key words there's involvement of lateral spinoalamic tract that means pain and temperature are gone and there is posterior column tract which is preserved that means touch and vibration they are preserved and also the loss of sensation of pain and temperature is present over the neck and upper limbs that means there is scape like distribution which is present and also if you look at the T2 weighted image or this MRI image we can see that there's a serrin which is present in the spinal cord. So this hyper intense lesion which we can see on the MRI it is nothing but a serrx. Sarrin is a fluid fil cavity.

[01:04:13]It is a fluid fil cavity and it is seen in siren media.

[01:04:23]So we know that the diagnosis is sirenia.

[01:04:27]Looking at the option multiple sclerosis, no.

[01:04:32]ALS, no. Sirenia is the correct option.

[01:04:37]We will quickly have a look at the important features of saranglia before we discuss other options.

[01:04:43]So we know that sirenia is a central chord syndrome. In this case the patient will present with painless burn as indicated in the question. So there will be loss of spinothalamic tract that means pain and temperature and dorsal column will be spared that means touch and vibration will be spared.

[01:05:05]Here we can see that serrings is present in the central of the spinal canard.

[01:05:10]There selective loss of pain and temperature. So there is dissociative anesthesia.

[01:05:18]Most common site for serrings will be lower cervical part of the spinal cord that is C5 to C8 and it is associated with Arnold Kar type one.

[01:05:31]This is very important. Sirenia is associated with Arnold Kar type one.

[01:05:36]In Arnold Kar type one there is tonsular herniation. The tonsil part of the cerebellum herniates into the foram and magnum. That is what we call Arnold Kari malf foration and there's cape-like distribution as we discussed that is there's loss of sensation which is present around the neck and both the arms.

[01:05:57]If we quickly look at the other options which go against the given history and findings. Multiple sclerosis is a disorder of demination which is scattered in time and space and there is patchy loss of sensation and motor deficits and there is no cape like distribution in multiple sclerosis which is why this cannot be the correct answer. ALS is characterized by both upper upper motor neuron lesion and lower motor neuron lesion and also there's going to be progressive weakness in faciciculations and uh if we talk about option D subacute combined degeneration it is seen in vitamin B12 deficiency there is no mention of megaloblast or any features of vitamin B12 deficiency here and it involves the dorsal column that means vibration and touch will be affected but vibration and touch are affect uh unaffected in this question. So this cannot be the answer.

[01:06:58]Coming to the next question. A 35year-old woman experiences an increased frequency of mixturation with pain relieved by mixuration and aggravated by over distension of the bladder.

[01:07:10]Urine protein test shows no pus cells.

[01:07:12]So there are no pus cells. Urine culture is negative. Cystoscopy revealed.

[01:07:17]fissures and punctate hemorrhages in the bladder mucosa. So by saying that there are no puscles and urine culture is negative we are ruling out UTI and on cystoscopy we are seeing very characteristic findings such as fissures and punctate hemorrhage in the mucosa of the bladder and there are characteristic ulcers which are present as we can see here this is known as hers ulcer what is the most probable clinical diagnosis so the diagnosis and all the key findings are pointing towards interial cyitis.

[01:07:56]Interest cyitis that means there's inflammation in the bladder and this is characterized by hunners ulcer.

[01:08:07]So interial cyitis is a type of chronic cyitis and it is most commonly seen in females.

[01:08:15]So the patient here presents with supra pubic pain. There's urinary frequency, urgency, disura and there is no evidence of bacterial infection as we have seen in this question. The culture is negative and the mucosa of the fundus of bladder will show a characteristic ulcer that is hana's ulcer and also on doing the cystoscopic examination there are fissures and punctate hemorrhages.

[01:08:39]So the diagnosis will be intertestial keratit cyitis and melacoplacia is characterized by mccois gutman bodies. So my gutman bodies are present in melacoplacia and tuberculosis. We know that there are no hers. There's thimble bladder which is present in TB of the bladder. This is thimble bladder and polyoid cyitis is seen in patients who are having prolonged indwelling catheterss.

[01:09:13]So there's no history of indwelling catheter in this question. So this cannot be the answer. Coming to the next question. A 48-year-old multiparis woman presents with complaints of a mass descending per vaginum. This is probably a case of prolapse. For examination, pelvic organ prolapse is assessed using the pop Q system.

[01:09:32]So pop Q system stands for pelvic organ prolapse quantification system.

[01:09:39]The most dependent point of the prolapse is noted to be 2 cm above the highal ring. So in this classification system the reference point is high min and the most dependent point of prolapse is 2 cm above the high.

[01:09:56]How will this point be recorded in the popq system.

[01:10:02]So if we look at the popq system we know that in total we are having six references point. So two references points are present on the anterior vaginal wall. They are AA and BA.

[01:10:19]So they are present on the anterior vaginal wall and two are present on the apex of vagina or epical part of vagina that is C and D and two reference points they are present on the posterior vaginal wall that is A and BP. So in total we have six references points. So a reference point suppose this is highman. So a reference point which is present above the highman will be denoted by the sign minus and a reference point which is present below the highman will be denoted by the sign plus. So in this case it is present 2 cm above the highman. That means it is minus2 cm. So option C will be the correct option.

[01:11:05]Coming to next question. All of the following statements about fetal circulation are true except inferior when a cava carries the oxygenated blood. This statement is true in fetus inferior when a cava is carrying the deoxxygenated blood. Option B. Ductus vinosis connects umbilical artery to inferior venneava. This is wrong. Ductus vinosis connects umbilical vein to inferior venneava not umbilical artery.

[01:11:32]Pulmonary arterial resistance is very high. This statement is also very true.

[01:11:36]Ductus arteriosis churns blood from the pulmonary artery to a specifically to descending aota.

[01:11:44]This statement is also true. So option B is the correct answer. If you look at the schematic diagram of circulation which has been shown here is see there are certain important concepts or key points that we have to remember in the fetal circulation.

[01:12:07]So if you see in the image there are three colored arrows. Red arrow represents oxygen content is high.

[01:12:12]Purple represents medium content oxygen and blue represents low oxygen content.

[01:12:18]So coming back to concepts. So first concept says that the oxygenated blood from the placenta will be carried through the left umbilical vein. So placenta is involved in the oxygenation of blood and it is further delivered to left umbilical vein.

[01:12:41]Now what will happen? around 50% of the blood from left umbilical vein will go into liver and the remaining blood will go into inferior venneava through ductus vinosis. So here we can see that ductus vinosis is connecting the left umbilical vein to inferior venneava.

[01:12:58]Then what will happen?

[01:13:01]The blood which is reaching the inferior venneava it will reach the right atrium through foram and oale. So it will reach the right atrium and from there it will cross the left atrium through forammen ovale. And then from left atrium the blood will go into left ventricle.

[01:13:23]And then what will happen from left ventricle? The blood is ejected into the ascending aota. As we can see where it supplies the upper part of the fetal body that is coron coronary circulation, brain and upper limbs.

[01:13:42]And then what will happen? A major portion of the blood will enter the right ventricle and from right ventricle it will go into pulmonary trunk. We know that the resistance in pulmonary trunk is very high which is why only about 5% of the blood is reaching the lungs and then the pulmonary veins and rest of the blood goes into ductus arteriosis and this ductus arteriosis is connecting pulmonary trunk and descending aota. So blood from pulmonary trunk goes to ductus arteriosis and from ductus arteriosis it goes to descending a iota and then the blood merges in the systemic circulation. From there it goes to umbilical arteries and umbilical arteries will take the relatively deoxxygenated blood or less oxygenated blood to placenta where it will be oxygenated. So there are two shunts which are important. Ductus vinosis connecting the left umbilical vein to inferior venneava and ductus arteriosis which is connecting the pulmonary trunk to descending a which is why option B is incorrect because ductus vinosis connects umbilical vein to inferior venneaba.

[01:14:49]Question number 182 milk sample collected from a dairy plant after heat treatment is tested to verify whether pasteurization was adequate or not. So which of the following test is used to assess the adequacy of pasteurization?

[01:15:05]So this is a direct question.

[01:15:06]Phosphotase test is used to look for the adequacy of pasteurization.

[01:15:14]And also we have to remember that if there is negative phosphatase test that means it is adequate pasteurization.

[01:15:32]So the key point here to remember is if there's negative phosphotase test it means it is adequate pasteurization. If the test is positive that is there is inadequate heating or there may be postpeurization contamination of the milk. Looking at the other option methylene blue reduction test.

[01:15:52]No it is used to detect microbial load and the quality of milk and catalyst test will detect the catalyst producing organism. So this will not be the answer.

[01:16:03]Turbidity test is used to look for the adequacy of sterilization.

[01:16:10]not pasteurization. Therefore, this is also the incorrect option. Coming to the question number 183. A national health policy of a certain country includes the two given interventions. How should these interventions be classified? So the first statement is saying identifying carriers of genetic disorders and discouraging their reproduction to lower the disease transmission.

[01:16:34]So statement one is saying or talking about eugenics that means we are identifying people who are having genetic disorders from the population and we are discouraging their reproduction to lower the disease burden in the progeny. This defines eugenics and option B says implementing programs to improve nutrition, housing and education to optimize human potential.

[01:17:03]This defines euthanics.

[01:17:06]So option or statement one is eugenics and statement two is eugenics. Both represent euthanics. Both represent eugenics. Incorrect. Statement one is eugenics.

[01:17:22]and statement two is uh 10x. So option C is the correct answer. Coming to the next question, a 1.5 year old girl is brought for a routine checkup. Her weight for height is plotted for the first time and shown in the given chart.

[01:17:36]She has no bipedal edema. She's alert and playful. Very important finding and has a good appetite.

[01:17:43]As for the government of India's national protocol for management of malnutrition, which of the following is the most appropriate next step? So first of all we will look at the graph. We know that the weight or height is less than minus3 standard deviation and this qualifies for severe acute malnutrition.

[01:18:10]But also in the same question we can see that the child is not having bilateral pedal edema. She's alert and playful and also she's having good appetite.

[01:18:21]So we have to select the most appropriate next step. Option one says immediate referral to NRC for inpatient care. No because the child is having good appetite and she is alert so she should not be sent to NRC.

[01:18:38]Option B says conduct appetite test if passed enroll in a supplementary nutritional program at Anganari. So option B seems to be the correct answer.

[01:18:47]And option C says start THR at 80 kilo calories per kilogram per day without appetite test.

[01:18:53]This statement is also wrong.

[01:18:56]Option D start empirical antibiotics and advise high calorie diet at no the patient is having no infection. So we should not start any of the antibiotics empirically.

[01:19:09]So we are we usually send the child to NRC if the SAM child or child with severe acute malnutrition is having medical complications such as the child has failed appetite test or maybe the child is having bilateral pedal edema or there are some dangerous signs which are present and looking at the option C.

[01:19:34]Option C says without appetite test you are starting the THR that is take-home ration. So national protocol it recommends or mandates that appetite test should be done before starting any supplementary nutrition.

[01:19:50]That's why it is incorrect statement and empirical antibiotics are not indicated without any signs of infection.

[01:19:58]Coming to next question a post-operative patient presented with complaints of abdominal distension following leprotomy. So following an abdominal surgery there is distension of the abdomen. He had not yet passed flatus after surgery.

[01:20:11]This is important point. On examination bowel sounds are absent.

[01:20:16]So till now the history is pointing towards obstruction.

[01:20:21]X-ray shows gas field loops of the intestine with multiple air fluid levels.

[01:20:26]Which of the following electrolyte abnormalities most commonly associated with this condition? So they are talking about paralytic following an abdominal surgery and paralytic alas is a a dynamic obstruction and we know that most common electrolyte abnormality which is responsible for paralytic alas is hypocalemia.

[01:20:53]So option B is going to be the correct answer.

[01:21:00]Coming to the next question.

[01:21:04]A woman from rural South America presents with shortness of breath and palpitations. Examination of the eye is shown in the image given below. Echo cardiography reveals bio vventricular dilotation with massive cardiac enlargement. That means there is dilated cardiomyopathy. Which factor is most likely responsible for transmitting this patient's disease? So the sign which has been shown in the image is Romana sign.

[01:21:32]The sign which has been shown here is Romana sign and we know that Romana sign is seen in Shaga's disease and Shaga's disease is caused by trapanosoma cruzi and trypanosoma cruzi is also responsible for causing dilated cardiammyopathy.

[01:21:53]And the vector for trapanosoma cruisy is redoit bug. As you can see in the picture this is redid bug.

[01:22:05]So in this question the answer will be rede bug.

[01:22:12]If you look at the other options quickly first option says derma center tick.

[01:22:17]Derma center ticene is a vector for rocky mountain spotted fever and soft tick is a vector for relapsing fever and CC fly is for trapanoo that means African sleeping sickness coming to next question. A 35-year-old multiparis woman presents on the 14th day postpartum with complaints of irregular vaginal delivery. She reports to that the loia has remained red and has not decreased in amount since delivery.

[01:22:59]There is no history of fever or foul smelling discharge on examination.

[01:23:03]Uterus is palpable abdominally and corresponds to approximately 16 week size.

[01:23:10]The uterus is soft and non- tender.

[01:23:12]Ultrasound reveals no ecogenic material.

[01:23:15]Which of the following is the most likely diagnosis?

[01:23:19]So ultrasound findings are normal.

[01:23:21]Uterus is enlarged and palpable even after 16 weeks postpartum.

[01:23:30]So this suggests that there is sub involution of the uterus and it occurs due to insufficient eradication of spiral arteries.

[01:23:53]The other differential diagnosis that we can see in this question could be retained products of conception. But this is ruled out by this statement.

[01:24:01]Ultrasound reveals no ecoenic material.

[01:24:03]That means there are no products of conception which are present in the uterus.

[01:24:11]So we can distinguish the subinvolution from retained placenta by doing a ultrasound. If there are no retained products, treatment is usually with utrotonic medications like oxytocin and prostaglandin analoges. And if there are products of con conception which are present in the uterus we will do suction and curage.

[01:24:33]So the answer will be option B that is sub involution of uterus. And we know that uterine a tony it presents very early and it is a it is an important cause of primary postpartum hemorrhage and it will occur immediately after delivery.

[01:24:49]But here in the question they are talking about 14 days postpartum.

[01:24:57]Coming to the next question. A forest guard presents to the casualty with fever, headache, myalgia and rashes as shown in the image below. So the rashes are present on the palms as well.

[01:25:10]And there are other symptoms such as fever, headache and myalgia. He gives a history of insect bite. So there's a history of insect bite. Most likely causitive agent rkettia orientia. Susugamushi, Rkettzia, probasaki, Rkettzia ty. We know that out of these four there's only one organism which causes rash on palms as well and that is ricketettsia ricketetti. So option A is the correct answer.

[01:25:43]Rettsia rketts causes rocky mountain spotted fever.

[01:25:56]And the vector for this condition is derma center and derma center and we know that ricketettia they are obligate intracellular gram negative cocobacilli and they are non-mile and non-capsulated and these organisms one another important point they contain both DNA as well as RNA and the diagnosis is made by indirect imunofllororesence essay and also wheel philix reaction is positive in Rocky Mountain spotted fever and the drug of choice is doxycyc.

[01:26:45]So doxycycline is the drug of choice for almost all the ricketettsial infections. So we should know that there are three conditions which present with rash on palms and soles. So rash on palms and soles is present in three condition. First condition is hand, foot and mouth disease which is caused by cooxaki virus A16. Second condition we have just seen rocky mountain spotted fever and it is also seen in secondary syphilis.

[01:27:23]So this is an important point.

[01:27:27]Coming to the next question. A child who was trying to lift a heavy object suddenly drops it due to muscle relaxation. Which of the following is true about this reflex? So heavy weight when kept on the hand it falls down due to muscle relaxation. This is inverse stretch reflex and the receptor in this reflex is golgi tendon organ.

[01:27:56]It is a dyinaptic reflex.

[01:28:05]So we have to look at the we have to find out the true statement. Monocyinic reflex having golgate and an organ. No, it is a dyinaptic reflex. Diinaptic reflex having golgate tendon organ as receptor. This statement is true and this is the answer. It is not monossinaptic reflex.

[01:28:22]And it says diocyinaptic reflex having muscle spindle as receptor. No. Muscle spindle as receptor is present in stretch reflex not in golvi tendon reflex or inverse stretch reflex.

[01:28:37]Here we can see that it is a dicinaptic reflex and the aphrant fiber is constituted by type 1B fibers and also there is one inter neuron which is present in between which is why it is a dyinaptic reflex and the response in this reflex will be muscle relaxation and hence the object is going to fall down.

[01:29:04]Next question is very direct question.

[01:29:06]Identify the instrument. So this is a umbilical cord scissor.

[01:29:15]It has a very peculiar appearance as we can see. So option A will be the answer.

[01:29:24]We will look at few other important instruments as well. So episottomy scissors they are angled as we can see and they are used for making the perennial incisions and the second instrument is medinen bomb scissor. So medin bomb scissor they are used to cut and dissect tissues such as paronium and adhessions embryo scissor these are used to perform the destructive procedures such as cleotomy E and decapitation and destructive procedures are not followed in modern obstetrics. We are avoiding these procedures.

[01:30:26]191. A child was brought with recurrent seizures and on evaluation was found to have hypocalcemia.

[01:30:31]So there's a history of recurrent seizure and hypocalcemia. He has certain characteristic facial features as shown in the image. Cardiac evaluation reveals truncus arteriosis most likely genetic abnormality.

[01:30:44]So in this condition if you look at the facial features there are low set ears which are present.

[01:30:52]There are low set ears which are present and there is micro geneathia small jaw.

[01:31:00]So microgathia, low set ears, hypocalcemia, cardiac abnormalities and recurrent seizures they all point towards digode syndrome. And we know that digode syndrome is due to the deletion of chromosome 22q 11.2.

[01:31:24]It says expansion of CG repeats on X chromosome. This statement is wrong.

[01:31:28]This is seen in fragile leg syndrome.

[01:31:30]Deletion of short term of chromosome number five. This is also wrong. This is seen in cryohat syndrome. Mutation in CFTR gene on chromosome number seven.

[01:31:38]This is seen in cystic fibrosis. And deletion of chromosome 22q 11.2. This is the correct answer. It is seen in kryto syndrome. And the pneumonic for kryhat syndrome is catch 22 where C stands for cardiac defects. A stands for abnormal faces. T stands for thymic hypoplasia which is why the child has recurrent infections because of a decrease in the number of T- cells or mature T- cells and C stands for cleft pallet. H stands for hypocalcemia and hypocalcemia is due to the presence of parathyroid hypoplasia and 22 stands for there's deletion of the chromosome number 22 Q11.2.

[01:32:24]Coming to the next question. A 52 55 year old female and chronic anthroquinone laxative presents for a screening colonoscopy which reveals diffused leopard skin pigmentation of the colonic mucosa.

[01:32:37]So they have taken a biopsy and the hystopath finding is shown in the image.

[01:32:41]The most likely pathological diagnosis.

[01:32:43]There's history of laxative chronic laxative use.

[01:32:49]And we can see there's brownish pigmentation which is present here. So there's brownish pigmentation which is present here. This is known as melanosis coli.

[01:32:58]This is known as melanosis coli and it is seen with certain laxatives such as senna which can cause pigmentation in the colon and this pigmentation is due to lipopusin.

[01:33:23]which gets deposited in the epithelial cells of the colon. So the answer will be melanosis coli.

[01:33:33]193 match the following eponyms eponymous features of mercury poisoning.

[01:33:38]Option one says arithism.

[01:33:41]So it it means personality changes.

[01:33:45]Option two is acrodia or pink disease.

[01:33:48]So there are pink colored rashes. So 1 C and two D. Minimata disease is mental retardation. There are psychiatric features. So three has B. Mercurial lentis anterior capsule of the lens discoloration A. So the correct sequence is C, D, B and A.

[01:34:15]C, D, B and A. Option C is the correct answer.

[01:34:20]Coming to next question. A woman with cervical cancer is posted to undergo the procedure shown in the image below.

[01:34:26]Which of the following is true about the procedure?

[01:34:31]We can see that they have taken a conical section from the cervix. The tissue which is removed is conical in shape.

[01:34:40]So this is nothing but that they have done.

[01:34:49]So coronization is a gynecological procedure which is performed under anesthesia where the entire outer margin of the cervix and the endoservical lining short of the internal loss is removed as we can see in the image. So what are the indications?

[01:35:10]The indications are when the transformation zone is not visible or not completely visualized then we are doing the conization and when there is endocervical dysplasia and also when there is discrepancy in the findings between cytology culposcopy and biopsy and also when we are suspecting micro invasion. So these are the indication for conization and also we should remember that conization is a both therapeutic as well as diagnostic procedure. So they are asking us about the true statement. First option says not useful in if the transposation transformation zone cannot be completely visualized. No, it is useful suitable only for lesions of ecto service without endocervical involvement. Incorrect. We are using it for endocervical lesions as well. Has no bearing on the future of pregnancies. This statement is also incorrect.

[01:36:10]It can cause pre-term labor.

[01:36:16]So it has a bearing on the future pregnancies as well. Can be both diagnostic and therapeutic. Yes.

[01:36:24]Coming to next question. A 64 year old woman presents with confusion, tinitus and hyperventilation.

[01:36:32]She has been on long-term highdose aspirin for rheumatoid arthritis.

[01:36:37]AG is most likely to show which of the following. So the patient is on aspirin.

[01:36:43]So aspirin is a selicilate.

[01:36:50]So there are toxic level of aspirin which are present in the body. So what it will do? It will stimulate the medularary respiratory center which will cause hyperventilation.

[01:37:06]When there will be hyperventilation, there will be excessive wash out of carbon dioxide and there will be respiratory alkyossis.

[01:37:17]So respiratory alphosis is present and also we should remember that as the toxicity will progress the cellicilate will do uncoupling of oxidative phosphorilation.

[01:37:35]So there is uncoupling of oxidative phosphorilation that means anorobic metabolism will increase and there will be accumulation of lactic acid.

[01:37:54]So there will be metabolic or rather high anion gap metabolic acidosis. So it is going to be a mixed acidbased disorder. That means high nine gap metabolic acidosis plus respiratory alkyossis.

[01:38:10]So the answer will be respiratory alkyossis with metabolic acidosis and metabolic acidosis to be precise high anion gap metabolic acidosis.

[01:38:22]Coming to question number 196. A 58-year-old cerotic patient presents with the asitis. Asitis is present controlled by diuretics along with bilerubin of 3.5 albamin 2.6 six INR 2.4. So there's moderate asitis, minimal hippatic and kealopathy.

[01:38:40]Calculate the child puck score in this case.

[01:38:44]So we can remember the child puck score by remember remembering the middle value. So berubin of 2 to three is gives us two points and albamin of 2.8 to 3.5 gives us two points.

[01:38:57]Prothroin time of 4 to 6 is two points and INR of 1.72 to 2.3 is again two points. NKalopathy and asitis if it is controlled it is two. If it is uncontrolled it is three and if it is absent it is.1. So we can calculate the child puck score. So in this case we know that Billy Rubin is more than three. When belubin is more than three the score is going to be three and alumin is less than 2.8 that means the score is again going to be three INR is 2.4 4 that mean more than 10.3 which comes in the third category the score will be three asitis is controlled that means middle value score of two and minimal enkapalopathy it is also middle value that is a score of two so 3 + 3 is 6 9 11 uh 9 and 11 and 13 so the total score is going to be 13 so option C is the correct answer and it is going to be severely decompensated.

[01:40:09]The impression will be severely decompensated sorosis because the score is present in the range of 10 to 15.

[01:40:22]197 question a multiparis woman presents at 36 weeks of gestation or on examination funal height is less than the period of aminoria.

[01:40:30]So funal height is less than period of aminoria.

[01:40:36]Fundal grip the fetal pole is not palpable. So funal grip is nothing is palpable and lower pole of the uterus is also empty.

[01:40:48]That means the child is present in transverse position.

[01:40:55]On lateral grip a soft irregular breach is felt on one side of the midline.

[01:41:01]Identify the most common fetal position in the given condition. We know that the child is present in or the fetus is present in transverse lie.

[01:41:13]This is the this is what we have identified and the most common fetal position in transverse lie is dorso anterior.

[01:41:26]As we can see it is dorso anterior. when the back of the fetus faces anteriorly and it is dorso posterior when the back of the fetus faces posteriorly.

[01:41:40]Coming to next question, a patient walks with stomping gate. This is the key word. When asked to close his eyes and walk, he is unable to do so. Which of the following tracts is probably affected? So stomping gate occurs when there is a loss of this proprioceptive input and it is associated with posterior column tract. Posterior column.

[01:42:05]Option B is going to be the correct option and it is seen in conditions such as vitamin B12 deficiency and diabetic neuropathy.

[01:42:24]In spinal cerebila tract there will be atexia which will be present that's why it cannot be the option. In vestibular spinal tract it helps to maintain the posture and balance in a person. So damage to this tract will lead to postural instability and also there's going to be vertigo. In this condition we cannot say any vertigo. So this is not possible.

[01:42:53]Coming to the next question. The investigation of choice for dysphasia lucoria is esophasial manometry. No single contrast barium swallow.

[01:43:01]CTography digital check x-ray. So the answer to this condition is CT angography. We will briefly look at the condition that is dysphasia lucoria.

[01:43:12]So in this condition what happens?

[01:43:16]It is due to compression of the esophagus by a developmental vascular anomaly. That means the aberrant right subclavian artery which comes from the arch of aota.

[01:43:27]So this aberrant right subclavian that I'm marking with the yellow color. It is directly coming from the arch of aot. It is going behind the esophagus and compressing it.

[01:43:40]That's why it is known as dysphasia lucoria because it will cause dysphasia.

[01:43:44]that is difficulty in swallowing and the investigation of choice is CT NGO.

[01:43:56]So they can ask you this question by showing you CT as well. As we can see this is in this CT image this is trachea and this is esophagus and esophagus looks compressed and this red arrow represents the aberrant right subclavian artery which is compressing the esophagus and hence the lumen of the esophagus is quite narrow and also this image shows CT Ngo Gio and this is aberrant right subclavian artery which is going and compressing the esophagus from behind.

[01:44:41]Coming to the last question in the assessment of a patient with diminished hearing the function of which of the following structures is tested when the tuning fork is struck and placed on the mastoid.

[01:44:53]So we are placing the tuning fork on mastoid to assess the bone conduction.

[01:45:00]So the cia in this case the coccia will be stimulated directly through the vibrations of the sound which is passing through the bones of skulls.

[01:45:15]So we are basically checking for the cclear function.

[01:45:24]So the answer will be option A that is CIA.

[01:45:33]So here I conclude the discussion of grand test 15 with the question number 200.