Exam Recall Series (INI-CET May '26) - Paediatrics

Hinzugefügt: 2026-06-01

[00:00:00]Hello everyone, this is Dr. Singaram. So today I'll be taking up the discussion of pediatrics question asked in this INACT May 2026. As expected there were around around 12 questions in pediatric section and most of the questions were answerable and of course there were few challenging questions which I'll be discussing also but it was a standard paper containing uh the questions from the expected areas in pediatrics. So let us start the discussion. The question number one uh it's a very straightforward question.

[00:00:30]You can see a 12-year-old boy is bought with respiratory symptoms. You suspect an upper respiratory infection or URI.

[00:00:39]There are no other complications present. Which radiological investigations is required? So options are plain chest X-ray, CT scan of the neck and chest. Third is HRCT probably HRCT of the chest and D no radological investigation is required. It's a very simple and a straightforward question where upper respiratory infections you all know is caused by viral infections only and majority of the viruses include the rhino virus and the adino virus.

[00:01:10]Occasionally it can be due to influenza virus also. Right? So these are the usual viral infection which are causing upper respiratory infections and around 6 to eight times per year children usually get URI and this settles on its own in a period of few days. So treatment is mainly symptomatic treatment where we give paracetamol saline nasal drops and as required antistinics or decongestion nothing more than that is required so tell me in this setting would you require any radologic investigation like CT or X-ray nothing is required it's a very straightforward question and the answer is option B because it's a viral URI mainly no radologic investigations are required moving on to the next Question. A term neonate is found to have blood glucose levels of 38 mg per diliter at 3 hours of life. The baby is asymptomatic. What should be the next appropriate step in management? Is it giving IV dextrose bololis or IV dextrose infusion or breastfeeding and reassess the baby or observation alone is required without any intervention? See when we talk about hypoglycemia in neonates the blood glucose levels of less than 45 mg per diliter defines hypoglycemia as we all know about your management basically depends on whether the baby is symptomatic or asymptomatic. If the baby is symptomatic and the symptoms can be anything like lethargynous poor feeding or seizures I'll write one example seizures. Suppose the baby is having any symptoms like seizures then we have to act fast. What should be your immediate management? You have to give a IV bolus of 2 ml per kg of 10% dextrose should be given.

[00:03:03]After that you have to go for IV glucose or dextrose infusion. So this is the standard management.

[00:03:11]If the baby is symptomatic, suppose the baby is asymptomatic, our management depends on the blood glucose levels again whether it is less than 20 mg per diliter or it is more than 20 mg per diliter.

[00:03:29]If it is a second case more than 20 mg per diliter what we do we just ask the mother to breastfeed the baby and after 30 to 40 minutes we can reassess breastfeeding and reassessment is all that is required if the blood glucose is more than 20 mg per diliter.

[00:03:49]On the other hand if the blood glucose is less than 20 you have to start IV glucose infusion.

[00:03:56]IV glucose infusion should be started.

[00:04:00]So can you see it is the uh symptomatic or asymptomatic status along with blood glucose level determine the management.

[00:04:07]So if I go back to the question it is clearly written the baby is asytomatic and the value is 38 mig per diliter which is more than our cutff of 20 mig per diliter. Okay. Right. So in this baby what will you do? Will you give IV or breastfeeding? It is only breastfeeding and reassessment.

[00:04:26]So option C is a clear answer because a baby is asymptomatic and the value of glucose is more than 20 mg per diliter.

[00:04:33]Okay, that is our second question.

[00:04:35]Moving on to the next question. It's a question based on developmental milestones assessment in a child. We have a 20-month-old child walking with support, scribbling and obeys one-step commands but speaks only one meaningful word. What is the most appropriate next step in the management? Is it reassurance and followup or detail speech and hearing evaluation diagnoses autism immediately and start anti-epileptics? Which one should be the further management? See this is a 20-month old child and let us take all the milestones given in the question.

[00:05:12]Child is able to walk with support. When is the child able to walk with support?

[00:05:17]Walk without support. Walk without support is very well attained by the age of 15 months. Walking independently by 15 months. So that is normally attained for a 20-month old child. Then scribbling child is able to scribble well by 18 months of age. So for a 20-month old child also it is normal.

[00:05:36]That is the second one. Third is obeys onestep command. Child starts obeying onestep command from the age of 10 months itself. So again that is a normal milestone attained by the child and it is clearly written in the last part of the question the child speaks only one meaningful word. Okay. Please remember child start speaking one to two meaningful words by the age of 12 months. That means one year itself. And by the time the child is 18 months of age, how many words child can speak?

[00:06:12]Child can speak 8 to 10 words. Now you can see the child is 20 months of age but can speak only one meaningful word.

[00:06:22]Is it normal or a delay for the child?

[00:06:24]This is language developmental delay for the child. Okay. Right. Definitely there is a language delay in this child.

[00:06:33]But if you see the other areas of development like fine motor, gross motor, social, everything seems to be okay for this child or I can conclude this 20-month-old child is having isolated language developmental delay whereas all the other domains are normal in this particular child. So now tell me if it is only isolated language delay what should I do? Definitely I have to do some sort of evaluation and what is that evaluation? It is nothing but hearing valuation should be done. Okay?

[00:07:05]Because one of the common reasons for language delay is hearing impairment.

[00:07:10]Okay. Right? Think about it. If the child cannot hear properly, child cannot produce the words also properly. Right?

[00:07:15]Once that is done, then then the child can be referred for speech therapy as well. So that is why the clear answer for this question is option B only where you have to do detailed speech and hearing evaluation. Moving on to the next question. Which of the following auto antibodies is most commonly associated with fetal heart block? Is it anti-DsDNA antibbody or anti-ro antibody or anti-smith antibody or anti-JO antibbody? Please see that this is an important question related to something called neonatal lupus. Okay, it is something related to systemic lupus arithmettosis but very very important to note it is not an autoimmune disease of the fetus because generally we know is an autoimmune disease but when we talk about neonatal lupus it is not an autoimmune disorder of fetus then what it is it is nothing but mother is having and during the time of pregnancy there is a transplantal transfer of maternal antibodies maternal al antibodies.

[00:08:20]So basically it's a passively transferred metal antibodies belonging to IGG group. Okay. Right. So these antibodies after entering the fetal circulation can some can have some problems. That is what we are talking about and we should know what are the implicated antibodies in this condition.

[00:08:42]If you have a look at this picture, this demonstrate the maternal transfer of metal antibodies through the placenta into the fetal circulation. And can you see which area is affected? The fetal heart is affected. And that to an important site of involvement is AV node. And when AV node is getting affected, it is going to result in heart blocks. Okay, it is going to result in heart blocks. Now we have to know what are the important antibodies implicated in the causation of this condition.

[00:09:08]There are three main important antibodies. First is the most commonly implicated antibbody which is anti antibbody also called SSA antibbody.

[00:09:19]Number two is anti- LA antibbody which is also called SSB antibbody. Number three is anti- R NP antibbody. So these are three antibodies implicated in the causation of fetal heart blocks and this fetal heart blocks can have range of manifestation from just prolongation of PR interval to complete hard block. What is complete heart blocks? Atrio ventricular dissociation can also happen. Atrial ventricular dissociation can happen. Right? So any sort of heart block related problems can occur due to all these antibodies.

[00:10:01]Based on all these discussion, the clear answer is option B only which is anti- RO antibbody. Moving on to our next question, an interesting and an important one also. A 20-month old female child had normal developmental milestone until 6 months of age after which she had regression of milestones.

[00:10:20]Key word here is regression. Regression means what? Loss of previously acquired milestones in the child. She also has repetitive hand ringing movements and rhythmical stereotypal stereotypical hand clapping moments. So these are two important clues hand bringing along with that there is also hand clapping movements which are stereotypical repetitive movements in that particular child. Along with that there is also failure of normal head growth. What are we trying to say? Child's head size is not increasing means child is developing microphille.

[00:10:55]So based on all these combination of features which is the most likely diagnosis is it red syndrome, asperger syndrome, fragile syndrome or childhood disintegrative disorder or disease. See this is very very fitting into the condition of red syndrome only. It's a very famous condition and the classical features of red syndrome have actually been given in the question. Okay. Right.

[00:11:20]So let us go uh go through uh quickly about the important manifestation of red syndrome and apply that in the question.

[00:11:27]Okay. The approach to this question is first regression of the milestone was given. Number two stereotypical hand movements. Right? That is what is the hand clapping moments and the midline hand movements. Okay. We call it as handbringing moments also. It's also called hand ringing moments.

[00:11:43]Okay. Basically these are repetitive movements of uh midline hand movements without any particular purpose. Okay. Unpurposeful stereotypical hand movements are classical for this condition. And one more is child is having microphille.

[00:11:59]Child is also having microphily. And you should understand one thing microphille was not at the time of birth. Few months after birth only child's head growth started to decline. That means it is one of the causes of acquired microphille.

[00:12:12]one of the cause of acquired microphily.

[00:12:15]All this fits into the classical description of red syndrome. Okay.

[00:12:19]Right. So this is what I was talking about. This is the picture explaining the midline stereotypical hand movements noted in this particular child. All the other classical features are given in the question itself like initially child develops normally after few months to one year after birth they start developing acquired microphille. Along with that there is a regression of uh milestones also. In addition to this child also can have speech defects and attacksia. Okay. Now coming to the genetic part of it which is also your previously asked question. Just quickly telling you the gene defect is mech P2 gene. Me P2 gene and that gene is located on X chromosome. That is why the mode of inheritance of this condition is X linked dominant. This is also an important previously asked question. X- linked dominant mode of inheritance. All these are salient points about red syndrome that should always be kept in mind. So the clear answer is option A.

[00:13:19]Red syndrome fits into the clinical description given in the question.

[00:13:23]Moving on to our next question. A 6 week old infant presents with features of menitis. Which of the following combination of organisms are common cause of menitis in this age group?

[00:13:36]Fourth uh bacteria is given namely lististeria, monocytogenous, hemophilus inflence at type B, staff orius and streptococcus. You should know which is a combination of organisms resulting in menitis in this age group. Okay, this is purely based on our knowledge of the organisms as ethiology for menitis in different different age groups. For that we'll do a quick recap. If you look at the organisms in the first two months of age, chiefly implicated organisms are gram negative bacteria which includes E.coli and Klepsilla commonly.

[00:14:18]After that we have stafylocus orius.

[00:14:24]Next would be group B streptococky.

[00:14:28]Group B streptococky, ruby streptoco and one more would be lististeria monoccytogenous and out of the different organisms the first two group then is the gram negative bacteria like eoline lepsilla are the most common the first two months of life please don't forget that then when we move on to after 2 month that is 2 to 24 months here the most common is hib what is hib hemophilus influence type B that is most common in this age group. Followed by that we have streptococky pneumon stecocky pneumonia and one more is nigeria menagitis or meningococky that would be the common organisms after 2 months till 2 years of age then once it is beyond 2 years of age it's going to be strep pneumonia which is the common cause strep pneumonia after 2 years the most common strep pneumonia Following that it is menoy and then comes hemophilus influencer type B or HIP. Okay. Right. So this is the list of organisms which are implicated in the ethology of baton managetis. So if I go back to the question this is 6 week old child that means first two months only. Lististeria monocytogenous is implicated. H influence at type B is not implicated. Staff definitely implicated. step pneumonia is not implicated. So one and three or option A is a clear answer for this particular question which deals with organism response for menitis in a young child.

[00:16:12]Okay, moving on to our next question.

[00:16:15]Consider the following hormonal abnormalities and then uh you have to tell which is seen in 17 alpha hydroxy deficiency which is a type of congenital adal hyperlasia or Cah in short form.

[00:16:28]Four things are given. Menoccorticoid hormones are increased. Adrenal androgens are decreased. Pregnant is decreased and cortisol is increased.

[00:16:37]Okay. Right. We have to make a decision and then we say 1 2 2 3 like that.

[00:16:41]Right? All those things we have to take a look at. But before we go to the final answer, we should know the basic pathway of adrenal steroids in because based on this pathway only we can derive what happens to the different um levels of the metabolites and hormones in this condition. Okay, which is the block we are we are dealing with it is 17 alpha hydroxy right the 17 alpha hydroxy deficiency. So if you see because of this deficiency there will be a block here and the cortisol level will be decreased. Then this also will get blocked and testosterone level also will be decreased but there is no block in this pathway meaning the levels are going to be increased for all the metabolites and hormone in this group.

[00:17:25]Okay. So if you see pregnanone will be increased the aldoststerone also will be increased. So all of these will be increased. Cortisol and testosterone will be decreased. Okay. So again have a look at it. Increase pregnanulone increase aldoststerone decrease cortisol and decrease testosterone. Let me go back to that question now.

[00:17:46]Minerallocorticoid that is aldoststerone is increased. That is true. Okay.

[00:17:51]Adrenal androgens are decreased.

[00:17:53]Testosterone was decreased. That is also true. Pregnone which is a precursor metabolite that was actually increased.

[00:18:00]So this is wrong because it is actually increased. Cortisol increased is wrong because cortisol has actually decreased.

[00:18:07]So which is true regarding the hormonal abnormalities one and two only. So the clear answer for this question is 1 and two are the correct set of hormonal abnormalities expected in 17 alpha hydroxilase deficiency. Option B is a correct answer for this question. Moving on to our next question. A 20-day old baby present with prolonged jaundice, amlal hernia and macro glossium. Baby was feeding well and there is no fever.

[00:18:36]What is the likely diagnosis? Neonatal sepsis, down syndrome, congenal hypothyroidism and galattocemia.

[00:18:45]See sepsis I will take the option discussion one by one. Neonatal sepsis nobody can diagnose based on clinical features. It is impossible because all clinical features of neonatital sepsis are very non-specific. Please understand that point. It is non-specific clinical features. So we cannot diagnose a condition based on any clinical presentation. Right? It is basically a sick baby sick neon. We say baby has sepsis until proven otherwise. So we depend on blood culture for a diagnosal sepsis. So in the question we cannot diagnose that down syndrome all of you know will have a different set of abnormalities like the mongaloid faces okay simeon crease sandal gap and all those things would be noted you don't get this combination of umbilical hernia and macro glossia in down syndrome so that is also ruled out congenal hypothyroidism is a likely possibility and the answer for this question also which I'll be explaining with a picture galtosmia we all know is characterized by liver involvement okay right liver involvement ment okay can be associated with the hypoglycemia along with that there is also catact as a manifestation what is the name of the catact it is oil drop catact nothing of that is given in the question so that also can be ruled out so the clear answer is congenal hypothyroidism only this has been previously asked in your exams also so I'll do a quick review of that see congenal hypothyroidism some of the notorious features is what is given in the question can you see that this is very very clear the baby's having an out pouching the amlus What is an umbilical hernia which is also given in the right-sided picture as well.

[00:20:21]Then a big tongue coming out from the mouth that is macro glossia.

[00:20:27]Macro glossia. These are some notorious findings of congenital hypothyroidism that should always always be in your mind. Okay. Then tell me what is the most common ideology for congenal hypothyroidism. Okay. It is a condition where thyroid gland is not developed properly as an anomaly. What do you call that? Thyroid disenesis. Thyroid disenesis is the overall most common ethiology for conjun hypotheism. Then one more you can quickly tell me screening required for babies definitely all babies whether they are symptomatic or asymptomatic we should do screening for hypothyroidism. And what is the name of the screening test? at the TSH levels which would be elevated in the setting of hypotharism. An important question is when should you do the TSH estimation?

[00:21:17]Is it immediately after birth or few days after birth? It is few days after birth. Usually 2 to 4 days after birth only you have to do the testing for TSH.

[00:21:28]Why first 48 hours or 2 days we are waiting. Very simple. In the first 48 hours what happens is due to the delivery itself there is a TSH surge which is happening. Okay. Right. So all babies in the first 40 48 hours normally itself TSH will be elevated. So that is why we wait once the TSH surges over only we have to do the testing typically 2 to 40 2 to 4 days after birth only this TSH testing should be done. Anyway, the clear answer for the question which is fitting into the clinical picture is congenital hypothyroidism. Moving on to the next question. Which of the following is not considered in the clinical criteria for diagnosis of Kawasaki disease? We all know Kawasaki disease is the most common vasculitis of childhood in Indian children and that has got a propensity to affect the heart because coronary arteries are involved in this condition of Kawasaki disease.

[00:22:24]But this question is asking about the clinical features. Polymorphis rash, puroline conental discharge, cervical lymphnopathy and perangual peeling. We just have to analyze each option one by one. Is polymorphic rash a feature of Kawasaki disease? Definitely yes. Okay, that is one of the main features polymorphic rash. But an important point to be noted is the rash is generally like macular papar like that. But it is never vicular or bullis. Very important point. It is never vesicular or bulus.

[00:22:58]So polymorphic rash is a feature only cannot be the answer for the question.

[00:23:01]Purland conjunctable discharge conjunctal discharge is definite feature of Kawasaki disease. But purolent tells you it is something like an infection but Kawasaki disease is a non-infection.

[00:23:12]So it is actually non-purolin conjunctal discharge. So that would be the answer because it is not a feature of Kawasaki disease. Cervical lymphnopathy again is an important feature in Kawasaki disease. Remember usually it is unilateral and the size of the lymph node is usually more than or equal to 1.5 cm.

[00:23:33]So that is a definite feature of Kawasaki disease. Perangual peeling I'm talking about surrounding the finger nails there can be skin peeling which can be noted that is also a feature of Kawasaki disease. Okay. Right. So that is also considered under the clinical criteria. So anyway, option B is a clear answer for this question. Now I want you to remember these facts about Kawasaki disease. See in a child with fever and other manifestation we can think about Kawasaki disease. But this slide tells you when not to suspect Kawasaki disease. One of that has already been given in the question. Exudative that means purulent conjunctivitis. Never think about Kawasaki disease because purine connectivitis tells you it's an infection and not Kawasaki disease.

[00:24:18]Okay. So this should be kept in mind.

[00:24:20]Then what is the second one? I told you polymorphic rash is there but never bull or vicular. So big rash not kawasaki disease. Right? That's what you need to remember. Third is oral leion. We all know kawasaki disease can have redness of the oral cavity including the mouth, tongue as well as the lips also. Right?

[00:24:39]In fact the famous finding of the tongue is called strawberry tongue right all of us know about it but very important is discrete lesions are never characteristic of kawasaki that means what can you see from the picture one or two lesions are never characteristic of kawasaki disease right it should be like uh full diffuse iththemma should be noted not like one or two lesions inside the mouth area that is what is meaning of discrete that mean isolated or few lesions are not characteristic of oral mucosite involvement in Kawasaki disease. That should be remembered very clearly. Then what is the next picture showing? Generalized lymphnopathy. What did I tell you? It is only localized lymph node enlargement and that to cervical lymph node enlargement only is noted in Kawasaki disease. So if you see multiple groups of lymph nodes affected like cervical, axillary, inguinal and like multiple areas are affected then Kawasaki disease should never be thought about as a possibility. Right? So this picture tells you Ben when not to suspect Kawasaki disease. One of that was already asked in the question that is purely connectal discharge is not a clinical feature of Kawasaki disease. So option B is the answer for this question. Then moving on to our next question. This was a tougher one but if you think little bit you can arrive at the answer easily for this question.

[00:25:58]What is that? All of the following disorders are associated with donia and basal ganglia involvement. Which among the following needs to be diagnosed or excluded as it requires a distinctly different treatment approach compared to others? Option A pantoinate kynise associated neurodeeneration. Option B TA2G6 associated neurodeeneration.

[00:26:23]Option C Wilson disease. Option D kufurak syndrome. Okay, the question says that all these conditions are associated with donia and basal ganglia involvement but which needs to be excluded because it has a different treatment approach. Okay, see all of us know this PKN, PLN, Koferup syndrome, we have not even heard about this, right?

[00:26:46]Why? Because these are all very very rare condition and also you can take the clue like this neuro degenerative condition. Do you think neurodeenerative conditions have a good treatment option?

[00:26:56]No. Usually we give them some sort of supportive or symptomatic treatment only. But if you see Wilson disease, we all know that Wilson disease has some very good treatment option and if detected early in the disease itself, this can have a very good prognosis as well. Right? So that is why Wilson disease is a best possible answer for this question. Let me just give you a few details and make it even more clearer. See here panaththenate kynise associated neurodeeneration is nothing but brain ion accumulation and neurodeeneration. Here the treatment approach is purely purely supportive treatment.

[00:27:33]For example uh spasticity is one of the important features of this condition. We can give back to decrease the spasticity but that is not going to cure the disease only supportive treatment. Then the PLAN that is also another neurodeeneration with brain ion accumulation. Here again it is supportive treatment only. Supportive treatment only. Then kofarakup syndrome.

[00:27:58]Can you see that it is something like a condition characterized by Parkinson's dis Parkinson syndrome type of features along with donia. So here also we'll give only supported treatment. For example, if there are Parkinson features what we can do is we can give leodopa to decrease the intensity of the symptoms.

[00:28:15]Right? So all these are only supportive treatment. Then what is the only option that was left? It was Wilson disease.

[00:28:21]Why Wilson disease is a must must exclude. Number one, it has got a distinctive pathology. It is not a neurodeeneration. You all know that it is due to copper accumulation inside the different parts of the body like brain and liver causing all the problem. So it has got allgether different pathology.

[00:28:39]Number one. Number two, potential to halt disease progression. What is the meaning of that? If you detect this condition early and treat with drugs like chilus, you can greatly improve the prognosis in patients with Wilson disease. Number three, fatal if untreated. Suppose you don't even think about the possibility okay right of Wilson disease and you delay your diagnosis like the child is becoming very old. What is going to happen? It can result in irreversible damage to the liver and brain and it is going to be fatal only. Right? So for that reason only always remember if you have a young patient or even an adult also who is having donia and basal ganglia involvement one of your higher possibilities or likely possibility to be kept as bilson disease because that is a treatable condition. That is what the question was typically testing about and we all know the quick points about bills and disease treatment. Number one is dietary copper restriction obviously very important. Number two, copper chilators like pensamin is a standard treatment approach in the management of this condition. Then next is zinc which decreases the uh copper absorption from the intestine also helps in the maintenance treatment of Wilson disease.

[00:29:52]And of course in late stages and child presence late you have to consider liver transplantation also right. So you can see Wilson disease if you think about that condition early and exclude it or diagnose it you can have good treatment option that's it. So based on that idea only the clear answer for this question is option C which is Wilson disease. Now moving on to next question. Sinosis is most likely to be seen in which of the following condition? It's a very straightforward question and you can see all are related to some sort of cardiovascular disorders. Atrial septile defect is a asyanotic heart defect. So sinosis is never going to be seen. Okay.

[00:30:31]Right. So that is out unless atrial septile defect can have a very longterm complication in the form of isel mango syndrome which is given separately as an option. I'll come to that discussion little later. Okay. So as such ASD initially is not associated with sinosis. So that is out. Then partial anomalous pulmonary venus connection in short form PAVC that is also a communication like left to right where there's a mixing of oxinated blood with a deoxxinated blood.

[00:31:00]So that is also asyotic condition only.

[00:31:03]So that is ruled out. Okay. Right. Where what happens basically the pulmonary veins have got connection not to the left atrium but to the superior vina and then drain into the right side of the heart. Right? That is what it's called left to right here and that is also asyotic condition only. Advanced ioticsenosis again is not going to be associated with cyanosis. It is associated features of decreased cardiac output.

[00:31:30]Decreased cardiac output.

[00:31:32]Okay. Right. It is not going to be associated with the features of um sinosis to begin with. So that is also out. So the clear answer is syndrome only. We all know syndrome is a condition of reversal of shunt in case of left to right shunt. We all know left to right shunts conditions.

[00:31:54]What are they? BSD, ASD and PDA. We all know about it. In this condition, if the shunt becomes reversed, that is instead of left to right, it becomes right to left. What is going to happen? Right means deoxxinated blood is going to mix with oxinated blood. Um, and that is going to ultimately result in sinosis.

[00:32:15]So, syndrome is a reversal of shunt causing sinosis in patients with left to right shunts. Right? That is what you need to make a note of. So clear answer is just an analytical question only.

[00:32:27]Option D. Eisenmega syndrome is associated with sinosis among the conditions given the options. Moving on to our last question. A patient has sinosis in lower extremities lower limbs but examination reveals that his upper extremities are pink and well oxygenated. Which of the following is the most likely underlying condition? It is is it severe peripheral vascular disease, large patents arteriosis, atrio ventricular septile defect, oscular webbor rendo syndrome. Okay, let me just take it with the wordings in the question. Sinosis in the lower limbs but upper limbs are pink. Do you know what is the name for this? This is called differential sinosis.

[00:33:12]Okay, few limbs are sinos, few limbs are not sinos. It's called differential sinosis.

[00:33:17]Now the question becomes more easier which of those four condition is associated with differential sinosis. It is only possible with large patent ductus arteriosis and I'm going to explain it to you very shortly. See here it's a condition of not just PDA PDA with Eisenus syndrome. What is the meaning of ising I told you reversal of shunt. Okay shunt reversal. Okay, let us see quickly.

[00:33:47]Let's imagine that this is the outline of the iota that I'm drawing. Outline of the iota and this is the outline of PA. What is that? Pulmonary artery. Let's imagine.

[00:34:01]And this connection is what we call it as patent ductus arteriosis.

[00:34:07]Generally in patents arteriosis, it is left to right. That means from iota to pulmonary artery only the blood should flow. But here I'm saying patent rectus addresses with isener syndrome. What is going to happen? The blood flow will now be reversed from where to where it is going to be. It is from pulmonary artery. The blood will enter into the iota like this. Okay. Pulmonary artery carries what blood? Deoxxygenated blood.

[00:34:28]So what I'm trying to say the de oxygenated blood is entering into the iota. Once it goes into the iota it will go downwards only right into the descending iota.

[00:34:40]And ultimately it is going to supply the lower limbs only. So what are we trying to understand? The lower limbs are getting the deoxxated blood which is getting mixed in the iota. So due to this deoxxinated blood entering into the iota there will be development of sinosis. There will be development of sinosis.

[00:35:00]But if you see the upper limbs, if you see the upper limbs, the arteries which are supplying blood to the upper limbs are derived from this area of the arch of iota where there is no mixing of blood happening. Right? Only beyond this there is mixing of blood or what I'm trying to say is there is no mixing of blood here or only what type of blood is coming into the upper limbs? Fully oxygenated blood is coming into the upper limb. Fully oxygenated blood is coming into the upper limbs. So that means will the upper limbs look normal or sinos definitely they will look normal only. So can you see upper limbs are normal but the lower limbs are sinos in this condition. This is what we call differential sinosis. This is what we call differential sinosis.

[00:35:49]All right. Okay. So that is why the clear answer for our question among the option provided is large PDA is likely to be associated with differential sinosis when E is syndrome develops. So this is yet another analytical question.

[00:36:02]If you know the simple pathophysiology of patus arteriosis then if you put it in terms of syndrome you will derive the answer for this question. Okay. Right.

[00:36:11]So that was our last question in the discussion of pediatrics section of this INAC May exam. So I hope all of you have done well and thank you for patient listening and very best wishes for your exams.