Dr. Sharma masterfully distills dense pathological data into high-yield diagnostic "pearls" for rapid exam mastery. It is a textbook example of how to streamline specialized knowledge for maximum efficiency in high-stakes medical education.
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Day 4/10 | TEN ON TEN 4.0 | #inicet #fmge #neetpgAdded:
Hi everyone, welcome to day four of the 10 on 10 series. Today we have 10 tumors that we are going to discuss. So more of a pathology related questions that we'll have today. Let's get going with question number one where we have which of the following environmental factors is most strongly associated with the induction of a specific mutation in P53 leading to HCC. So I can say a path micro correlation happening here and the answer is aflatoxin B1 exposure. While the reason for that is that aflatoxin is considered as a peanut or a groundnut contaminant why you shouldn't be storing your nuts, peanuts, groundnuts in moist containers because fungus can grow and that fungus is Aspergillus flavus. That aflatoxin can then cause mutation in P53 that is the policeman resulting in hepatocellular carcinoma and to be very precise the mutation occurs at codon 249. I think we have learned it in a very fun way that if you write P53 the codon has to be fill in the blank so the two number is missing three is written four is missing five is written and with P well I can only think of a nine so the codon out here is 249 and that's the answer leading to HCC. Can all these also result in HCC? Of course yes but they are not associated alcohol, hepatitis B and C. They cause HCC but not related to P53 mutation. Lastly we have something mentioned as vinyl chloride exposure. If you remember three chemicals called VAT chemicals can cause a problem in the liver but that's not HCC that is the angiosarcoma of the liver and the VAT chemicals are vinyl chloride, arsenic and thorotrast. Moving on to question number two is a 22-year-old female with a history of no history of cirrhosis, no history of hepatitis, a very young female. There is a large mass in the liver and the serum alpha-fetoprotein levels are normal.
Firstly the age is not indicative of a cancer. Alpha-fetoproteins are usually increased in a liver cancer but that is also not increased but when I saw the biopsy I could see some very large oncocytic cells, a lot of collagen and they've asked me about a molecular alteration because I know that usually what I study is the conventional HCC which was the previous question also over here and that tends to show me an increase in alpha-fetoprotein that occurs in 30, 40, 50 years of age but at same time there is a variant called fibrolamellar HCC which occurs at a very very young age of 19, 20 years like in this case in which the alpha-fetoprotein levels are normal. So my question is then why is it occurring? That is because of a chromosome 19 alteration and that is the answer over here option B chromosome 19 deletion PRK gene mutation and the tumor marker over there is not alpha-fetoprotein in fibrolamellar HCC alpha-fetoprotein is normal. It is actually neurotensin that is increased. So how we've learned fibrolamellar HCC occurs around 19 years of age. It is chromosome 19 problem and teenage ending that's when you would be most tensed so neurotensin is the tumor marker increasing. Moving on to question number three is a 60-year-old male coming with a classical triad of hematuria, flank pain so RCC triad right? And of course there will be a mass. They are saying there are prominent perinuclear halo cells present which is characteristic of chromophobe RCC. Chromophobe RCC is the one which is going to have the best prognosis when it comes to renal cell cancers and it tends to show you the plant cells. What are plant cells? They are cells which have a raisinoid nucleus which is not very visible but around the nucleus I'm sure you can see there is a perinuclear halo which is mentioned over here. That is why I marked chromophobe RCC. Why didn't I mark clear cells? Because for clear cell RCC they should have shown me or mentioned completely whitewashed clear cells which they did not and that's why I didn't mark this. Moving on to question four which is on the same line that which of the following patient is most likely to develop a medullary RCC.
That is going to be associated with sickle cell trait. A point to be noted medullary RCC is not associated with sickle cell anemia. It is not associated with people having all of sickle cell hemoglobin. It is associated rather with sickle cell trait which is a heterozygous situation having adult and sickle hemoglobin. That's the correct answer. One more question over here whenever they mention smoking or anything to do with tobacco that is stand alone a risk factor for renal cell cancer that you should know and next if they would have said VHL syndrome VHL three alphabets it is a deletion of three P and the renal cell cancer with which it is associated is clear cell RCC.
Moving on to question five 30-year-old male with a painless testicular mass.
With that age and painless testicular mass seminoma anyway starts coming to my mind. Then they say there is a clear cytoplasm maybe they are trying to tell me about the classical fried egg appearance and if they would have given me a gross seminoma shows you the cut potato appearance but the giveaway over here is going to be immunohistochemistry showing you positive for PLAP. LDH and PLAP are the two tumor markers that they will always write for seminoma. If this would have been the ovary they would have replicated it as dysgerminoma and other tumor markers can also be OCT3/4 so giving all these answers seminoma is the best one that I mark. A quick recap the tumor marker for yolk sac tumor is alpha-fetoprotein the tumor marker for choriocarcinoma beta hCG ultra easy questions but a revision never harms anyone. Coming on to question six in the histological diagnosis of prostate distinguishes cancer glands from benign glands? And the answer to this is the absence of the basal cell layer. In one word or one sentence I'll explain this to you. Whenever they give you anything to do with glands that are from the prostate in the prostate gland till the time you are seeing only a single row of cells that will tell you that it is something cancerous. As soon as they mention that there is a basal layer means an additional base, a support is there you are you're everyone's happy to get support right? So whenever we see support either that will indicate oh everything's happy and normal this means it is normal prostate or at the max whatever has happened is a benign condition like a BPH in the prostate.
But as soon as this basal layer goes missing the support goes missing is when I get very tensed because that is when cancer has occurred. So cancerous will not have any support will be absence of basal cell layer. Moving on to the next question well this is a question which is more of a formality because it's tumors and how can I not talk about papillary thyroid cancer. They're asking you that in the absence of actual papillae what is the most important histological feature? It has to be the orphan Annie eye nucleus. Is it a real finding? No it is said to be a formal and artifact it's an artifactual finding and the most common mutation of PTC is BRAF V600E mutation. Well asking you about its survival it's 100% survival so it is said to have an excellent prognosis. Moving on to question number eight is a grade four astrocytoma like a glioblastoma. How is that distinguished from a grade three kind of a brain tumor? So what is the classification or the grading that you do? I hope you remember the AMEN. What does that stand for? A stands for atypia M for mitosis how much is the cell dividing? E for endothelial cells increasing that's nothing but the blood vessels increasing and N for necrosis. What are these four parameters? Now I'll tell you in grade one brain tumor nothing is present AMEN everything is absent. In grade two brain tumors only atypia is present. In grade three brain tumors like we have over here it is atypia and mitosis. So in grade three what is going to be there?
Atypia and mitosis. Whereas in grade four most of these features are present.
So in grade four if I ask you what is additional you will say number one endothelial cell proliferation which is nothing but the blood vessels and or necrosis can be there. So what is the additional component of grade four? It is E and N. Repeating when you will write AMEN in grade one nothing is going to be present. In grade two A is present. In grade three A and M is present and in grade four either all four of these or any three out of these four findings would be present. I'll call it a grade four tumor. All blastoma tumors in the brain are grade four like a bomb blast very very bad like glioblastoma, medulloblastoma. These are all grade four tumors. Moving on to the last two these are just spotters. A quick recap a radiology of this tumor you can see the classical dural tail sign which makes it a meningioma the only tumor which is dependent on hormones in the brain progesterone receptor positive. The last one that we have is a kidney and you can see a kidney mass extracted. You can see the classical color which is said to be the mahogany brown color and in the center you can see a central stellate scar that makes it an oncocytoma. It's a benign tumor and the word oncocyte tells me that it's going to be very very rich in mitochondria. That wraps up all the 10 tumor related questions and now I'll be meeting you tomorrow in another set of questions where we have everyone's favorite lot of genes, chromosomes, numbers which we will be talking about.
So see you soon.
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