Day 2/10 | TEN ON TEN 4.0 | #inicet #fmge #neetpg

Added: 2026-05-09

[00:00:01]Hi everyone, welcome to day two of the 10 on 10 series. Today we have five mixed bag of MCQs and most importantly five life cycles which all of you are going to identify. Let's get going with question number one which is a previous year question giving you a histopathological examination of the heart of a patient who died due to heart failure and this is hoping that you are not you know zooming in in the exam you don't have an option to so you should be able to identify it at this magnification. Still I will zoom in for you to show you the classical ninja star nucleus which is seen in dilated cardiomyopathy. When asked you about the different kind of mutations or the causes of DCM, the most common causes I don't know and that happens to be idiopathic but when the cause is known to be most commonly alcoholism and if the most common genetic cause is asked that is titin mutation and in fact most of the ninja star nuclei appearance is seen associated with titin gene mutation. Let's move on to other ones.

[00:00:53]The arrhythmogenic right ventricular cardiomyopathy where there is a right ventricle showing you fatty infiltration and I hope you also have revised that this can be associated further with a syndrome that is known as the Naxos syndrome. Next we have restrictive cardiomyopathy the most common cause of which is amyloidosis and the next is hypertrophic cardiomyopathy. If I rearrange the terms I get the name of the gene that is the myosin heavy chain gene mutation. This shows you the classical banana shaped heart and the cardiac fibers are all randomly arranged known as helter skelter appearance a very quick recap of all cardiomyopathies. Moving on to question two is a young female with a 4 cm mass in the right breast. I can see densely packed cells very bland looking nuclei and there is mucin infiltrating the stroma. Out of all of these it goes more in favor of mucinous or colloid cancer.

[00:01:42]Colloid is a misnomer it's nothing to do with the thyroid but yes it is also said as mucinous because I can see that these are the very bland looking tumor cells and mostly in the background I can see pools of mucin. In fact before a biopsy for every breast mass an FNAC should be done and because there was so much of mucin all the blood vessels got entangled as if they are like you know those headphone wires that tend get entangled similar to that and that is known as the chicken wire blood vessels.

[00:02:07]Another brain tumor where chicken wire blood vessel can be seen is oligodendroglioma.

[00:02:12]Moving on to the next question out here where a young 34 year old man comes to the clinic with diarrhea, poor appetite and there is non-bloody four to five episodes of stools per day over the last three months. A duodenal biopsy has been done and the histopathology is given here and let's be pretty honest about it that you're not seeing too many findings because at such a low power it's very difficult to discern such things.

[00:02:34]They've asked you what is the most common cancer. Even going by the fact that there is diarrhea this not this is could not be most commonly infective because it's been quite a long time plus they've not mentioned anything to do with other systemic complaints of an infection like a fever etc. Further a duodenal biopsy will always guide me more towards diarrhea in the duodenum. I will start thinking of celiac disease.

[00:02:55]Maybe it is associated with barley, rye, oat and wheat which is gluten sensitivity and then over here instead of seeing the proper finger like villi I can see many places the villi are getting flattened. Villous atrophy seen in the duodenum goes more in favor of celiac disease and the tumor associated with this so I had learned it is a disease happening with eating of gluten and it is going to result in a tumor that is EATL that is enteropathy associated T cell lymphomas.

[00:03:23]Now over here also to note celiac disease is seen in people who have HLA DQ2 DQ8 polymorphisms and if they would have shown me a proper picture where I would have seen that the villi are completely flattened that is villous atrophy or the crypts are increased that is crypt hyperplasia then the name of the criteria that we follow is referred to as the Marsh criteria. Moving on to the next question that I have over here is a 45 year old male patient inflammatory or chronic inflammatory condition leading to fatigue, weakness and pallor and lab investigations have shown a microcytic hypochromic. In yesterday's session I showed you some images today I'm giving you an image based continuation of theory. This is what we think of in microcytic hypochromic either it is sideroblastic anemia or iron deficiency or thalassemia or lead poisoning or anemia of chronic disease and considering the history given to me over here I would want to go more in favor of anemia of chronic disease. They said that there is an effect on the iron metabolism and which cytokine is responsible for it and that is interleukin-6. Whenever there is a chronic disease like let's assume rheumatoid arthritis which is most commonly asked in the exam there is an increase in interleukin-6. That interleukin-6 asked over here is now going to go and act on the liver and what is released that is hepcidin which is pretty obvious that hepcidin comes from hepatic from the liver and the work that it does is inhibiting everything.

[00:04:47]If you're eating a lot of iron it will not let you absorb it. If you will say I'm going to use the iron from the stores basically ferritin it will not let you use it. So basically it is a negative regulator it is not allowing any kind of iron to form any kind of iron to get absorbed any kind of iron to be used. So indirectly I can say that it is a negative regulator of iron.

[00:05:08]Now all of this was under the control of interleukin-6. Reminding you about the others interleukin-1 is responsible for fever or pyrexia. Interleukin-6 as I've told you is for anemia of chronic disease and since you're going for INI-CET exam this is also the one that is going to be the interleukin responsible in the pathogenesis of multiple myeloma the cancer of the plasma cells. This is also the one that is going to regulate acute phase reactants. You know some molecules increase in the blood when we have fever some molecules decrease in the blood when we have fever. So for example positive acute phase reactants like C-reactive protein they increase in the blood when we have fever. Similarly we have negative acute phase reactants which decrease in the blood when we have fever. So if I ask you which are the negative acute phase reactants everything that is reminding you of trans so if they say transthyretin or they say transferrin or they say transcortin anything with trans will decrease and also the most important albumin is going to be a negative acute phase reactant. Coming to the last TNF alpha TNF alpha is going to A for A it is responsible for decreasing the appetite and interferon gamma G for G. This is responsible for granuloma formation like you see in tuberculosis cases. Moving on to the last MCQ followed by five life cycles. The image shown over here is a classical cell in cell phenomenon known as emperipolesis a very famous AIIMS INI-CET question. So in emperipolesis I can notice a big cell which has engulfed a smaller cell and that is what I'll mark over here. The conditions in which you see it are all three letter things known as mark that is myelodysplastic syndrome and myeloproliferative neoplasm then in the liver it is seen in autoimmune hepatitis. In lymph node disorders it is Rosai-Dorfman disease and in leukemias it is CLL. Moving on to the five life cycles that I have to know so I would want all of you to take a pause identify it on your own before you hear out the answer from my side. This out here is a classical case of Leptospira which I've always learned as Leptospira with all the Rs which causes leptospirosis or Weil's disease and the one buzzword in the exam which helps me identify leptospirosis is that there will be a lot of conjunctival redness called as conjunctival suffusion, conjunctival injection just conjunctival redness that Weil's disease results in.

[00:07:27]Now why did we call it Leptospira because everything with Rs will come here. We will see rat urine which will be contaminating this rainy water as you can notice and rainy water is used by all our rice field workers, farmers and that is how they come in contact with this Leptospira and they end up having the Weil's disease. So rat urine contaminating rainy water going to rice field workers and on culture media we see the Dinga's ring which is seen on the EMJH media. For knowing antibodies we do a test which is known as the microscopic agglutination test. Moving on to the next life cycle again take a pause try to identify. This is the easiest one because over here I can see a human being and then I can see a snail mentioned over here and most importantly if you couldn't identify anything you should have identified the spinous eggs because spinous eggs will always point me towards Schistosoma. We know three types of Schistosoma. Let's try and identify from the eggs itself. If there is a lateral spine as we see over here lata hua sota hua man so lateral spine is in Schistosoma mansoni. Then if there is a terminal spine that is seen as Schistosoma haematobium. And if a spine is kind of visible kind of not which is rudimentary spine that is Schistosoma japonicum. Repeating lata lata hua sota hua man so lateral spine. Haematobium shows you terminal spine and rudimentary spine is seen by japonicum. If you see man and snail that is indicative of Schistosoma. Further apart from S for Schistosoma S for spine S for also skin.

[00:08:54]Schistosoma does not come through eating not through ingestion it comes through skin penetration and the larva that will penetrate is going to be another S sounding thing that is the cercaria larva comes through the skin. Also when you ask me about the adult worms I can see they are not hermaphrodites. The sexes are separate male separate female separate which adds on to the S story that I'm talking about here.

[00:09:15]Let's move on to the next life cycle.

[00:09:17]Here we have something coming through ingestion then I can see there is some involvement of the GIT some involvement of the liver but if I zoom into what am I eating or ingesting this is a quadrinucleated cyst that goes highly in favor of Entamoeba histolytica and that is why when the intestine was mentioned Entamoeba causes flask shaped ulcer in the liver it causes anchovy sauce appearance but the buzzword is that when you are ingesting these quadrinucleated cyst you will always think of Entamoeba histolytica. A question on theory I taught you yesterday as the first question of the 10 on 10 series so that was theory and this is a life cycle. You know the treatment I've mentioned it yesterday it is metronidazole followed by paromomycin. Let's move on to the next one out here. Again, for you to take a pause, the best way of identifying life cycles which only have one host which is only human beings, so you don't have any other animal going ahead with it. You are supposed to look at the egg. This is a case of Ascaris, which is roundworm, because I can see two types of eggs. One is the fertilized egg, and other is the non-fertilized egg, which is seen with Ascaris. It happens due to the ingestion of these embryonated eggs. Then I can see those roundworm adults which are forming inside us, and we know that that is Ascaris or roundworm. So, best way to identify is you will look at the egg. If you further see, everything that the fertilized egg will say yes, yes, yes, and non-fertilized egg will say no, no, no. So, if you ask me which of them has a thick albumin coat, the fertilized will have it. If you ask me which of them has a space on both sides of the egg, the fertilized will have it. If you ask me which of them is going to float on saturated salt solution, again, fertilized will be floating. So, everything for fertilized egg of Ascaris is yes, and for non-fertilized egg, it is going to be no.

[00:10:59]Coming to the last life cycle, which was pretty an easy one. I gave it purposely.

[00:11:03]You have a mosquito, then you have a human being over here, and in the human being, classically, the red blood cells have been targeted, which points towards Plasmodium or malaria. The mosquito has to be the female Anopheles mosquito, which is a definitive host. Definitive means the sexual cycle of the malaria is happening in this, and then this is going to go and infect the humans. In the humans, the main house of a malaria is RBCs, but before going to the RBCs, the malaria goes into the liver.

[00:11:30]Ideally, as it goes to the liver, and from the liver cells, the malaria then goes into the red blood cells, which is the usual cycle. Sometimes, the malaria tends to sleep off or become dormant in the liver. I can say it gets hypnotized and sleeps off in the liver, and that is called as hypnozoite. And that is what can then, later on, get reactivated, which is known to cause relapses in malaria, which is very commonly seen with two particular types of malaria, that is Plasmodium vivax and Plasmodium ovale. I have another question for you, that one way the mosquito has basically gone and bitten the human being, and that is why the human being had malaria.

[00:12:06]On the other hand, once the entire life cycle of this is done, then some form has to come back to the mosquito. So, when the mosquito bites, it's not always that it is giving malaria. Maybe it is taking malaria from us. So, now note that when it comes and bites us, what is it giving us? It is giving us the saliva. So, which is the form of malaria that we get? It is the sporozoites which are going to come from the mosquito.

[00:12:27]When the female Anopheles mosquito comes and bites us, it's the sporozoites come in the saliva. The entire life cycle happens. Male, female gametocytes are going to form. So, the next time when the mosquito bites us, which are the form which is going to go away from us?

[00:12:41]So, the gametocytes are going to go away, and they are going to enter the mosquito, because finally, the male, female sexual cycle will happen in the female Anopheles mosquito.

[00:12:51]That wraps up all of your life cycles, all of your five MCQs that you had to do today, and now I'll be meeting you tomorrow at the same time where we've got no images, but 10 clinical questions, and how to approach them and integrate them with path and micro. So, see you tomorrow, and I'll be waiting for all of your comments and your feedback, and I hope you've been following this 10-minute, 10-question series. So, see you tomorrow, guys.