okay got it okay done welcome back guys now we are doing endocrine pathology right in yesterday's class we done the thyroid pathologies okay initially this class we're done with the path thyroid pathologies and I said that today we'll be continuing with the parathyroid disorders okay of course it was scheduled to do in last class the parathyroid disorders but unfortunately it's yesterday we took almost two hours class so let's continue with the parathyroid disorders in this today's class Okay so without any further late let's begin the topic the parathyroid glands now look here I am going from the basics let me go do it from the basics okay first let me tell you what is the normal functions of the parathyroid and parathyroid disorders so how many parathyroid glands do we have see this is the thyroid gland okay so how many parathyroid glands do we have there are four parathyroid glands out of which two are superior parathyroid glands oh my God yeah 2R Superior parathyroid glands and two are inferior parathyroid glands now McQ which uh can be asked in exam is so the superior parathyroid glands they go okay the superior parathyroid glands they are derived from where they are derived from the fourth pharyngeal pouch okay it is there from the fourth pharyngeal pouch and the inferior parathyroid gland is derived from the third pharyngeal pouch okay you know the pharyngeal pouches right you know these things OK these things called as the pharyngeal Arches differential arches they consist of a pharyngeal pouch as well as a pharyngeal cleft okay you know these things right for example now I'm making a cross section over here now for example look here I am just making a cross section over here and I'm showing you this is the first pharyngeal art second foreign these are called as pharyngeal pouches they are called as a pouches on this side there is pharyngeal cleft okay pharyngeal cleft now what I have discussed with you fourth pharyngeal pouch from this area from this fourth pharyngeal pouch who is going to develop Superior parathyroid gland and from the third pharyngeal pouch who is going to be developed it's a inferior parathyroid gland it's an inferior parathyroidism I am telling you don't forget from the third pouch even thymus getting developed okay thymus is getting developed from the third pharyngeal pouch so tell me the parathyroid glands are derived from pharyngeal pouches which pharyngeal pouches total for pharyngeal pouches okay I used to remember something like see four is bigger number right the four is a bigger number so Superior okay so Superior parathyroid glands are derived from the fourth pharyngeal pouch and inferior inferior means less less number your pharyngeal pouch so three and four Superior and inferior simple okay now done after this let me discuss about the histology so what's there inside is parathyroid gland so what's like what exactly is there inside this parathyroid glands so the parathyroid glands are made up of Chief cells also called as C cells okay so what this parathyroid glands are going to secrete the secrets the hormone called as parathyroid hormone what is the function of the parathyroid hormone the parathyroid hormones increases the blood levels of calcium McQ parathyroid hormone increases the blood level of calcium and decreases the blood levels of phosphate so parathyroid hormone is having two functions function number one is it increases the blood calcium levels how it increase the blood calcium levels that I will discuss it will decrease the it will decrease the phosphate levels okay phosphate levels so that's why I used to remember like parathyroid hormone as phosphate phosphate trashing hormone phosphate trash keeping the phosphate in the trash okay decreasing the phosphate levels in the body excrete the phosphates out of the body so that's why phosphate trashing hormone just like anybody kind of thing parathyroid hormone phosphate thrashing hormone for the two functions one is increasing the blood calcium levels and other is decreasing the blood phosphate levels are now next question is how how how this parathyroid hormone how parathyroid hormone increase the blood calcium levels okay let me write here the functions functions of parathyroid hormone see the number one function is parathyroid hormone it activates okay the parathyroid hormone it activates an enzyme okay it activates an enzyme called as Alpha One hydroxylase where this Alpha and hydroxylase is present it is present in the proximal convoluted tubule parathyroid hormone it activates an enzyme called as alpha 1 hydroxylase and the alpha 1 hydroxyl is activated do you know what it will do it helps in activation or will do it helps in the activation of vitamin T it helps in the activation of vitamin D vitamin D is going to be activated what is active form of vitamin D the active form of vitamin D is called as calcitriol all are same all are same active form of vitamin D calcitriol 1 comma two Phi dihydroxy colic calciferol okay one comma two five dihydroxy two hydroxylations one common to find a hydroxical calciferol all RC now what's the function of vitamin D they're a function of vitamin D Vitamin D it will go to the intestines okay it will go to the intestines initiating there it increases the calcium absorption so what parathyroid hormone is doing I have said you parathyroid hormones increases the blood calcium levels increases the blood calcium levels by how by indirectly activating vitamin D so you should know better there are hormone activates vitamin D vitamin D of calcium okay this is first function the next function of vitamin D is parathyroid hormone it acts on it acts on the kidneys it acts on the kidneys especially the digital convoluted tubule increases the calcium reabsorption okay increase the calcium reabsorption say you need to understand here it is absorption so number one function okay number one function is the absorption the new calcium is being absorbed from the JT the other function of the parathyroid harmonies by acting on the digital convoluted tubular McQ parathyroid hormone action digital tubule increases the calcium reabsorption OK reabsorption means the calcium is not getting lost in the urine so more and more calcium will try to get reabsorbed this is the second function so in severe conditions in like you know High values okay hyper parathyroids I mean lots and lots of quantities so the parathyroid hormone so now do you know what it will do it activates Osteo class it will give the signal to the osteoclasts causing bone resorption directly first it will activate the osteoblast osteoblasts later they will produce a chemical called as rank like and there is a complex mechanism that I will explain you but for now just remember parathyroid hormone in super high quantities okay so it's going to activate the osteoclast when osteoclasts happen bone resorption means the resorption means breakage okay bone breakdown is going to happen so what happened to the blood calcium levels increases the calcium is now mobilized from the bones into the blood the calcium is being mobilized from the bones into the blood so what are the three functions of the parathyroid hormone see pth parathyroid hormone three functions I used to remember something like this one is absorption second one is reabsorption and third one is the resorption simple question is absorption second one is reabsorption third function is bone resorption resorption not reabsorption resorption bone resorption means bone breakage okay so these are the three functions by which it is increasing the blood calcium level see calcium levels are increasing calcium levels are increasing here also calcium levels are increasing in the blood so these are the functions of parathyroid hormones now here I want you to know one important Point here itself okay guys this is your bone okay this is your bone sir okay nice and beautiful bone now inside the bone so there are two fellows present okay two types of cells present one is looking like a good guy okay simply just looking like a good guy but later you will understand he is the real villain okay so there is this one fellow present and there is other fellow present okay who looks like a villain but he's actually innocent okay so in the bone there are two types of cells present which are called as Osteo lasts and Osteo last okay osteoblast and osteoblast what osteoblast will do everyone knows they have been born formation okay they help in the bone formation board build up okay bone build up ask your class what they will do they will cause bone resorption the point is the parathyroid hormone it will come and activate the parathyroid hormone receptors the parathyroid hormone receptors are present on the osteoblast parathyroid hormone activate the osteoblasts now this osteoblast will produce certain chemicals okay now they will release some chemicals these chemicals are called as rank okay rank okay receptor activated nuclear Factor Kappa not near just simply remember the osteoblasts are going to produce a chemical called as a rank so now this rank it will come and act on its rank receptor this is the rank receptor sir what exactly is it this is rank receptor so where is rank receptor present rank receptors present on the osteoclasts osteoclast so this parathyroid hormone it will come and activate this rank receptor now this osteoclasts are activated now the activated osteoclast will do the bone resorption so it's the osteoclastic activity every time I say it's osteoclastic activity regulated by the osteoblast it's the osteoblasts regulate the activity of osteoclasts then osteoblasts are activated by which hormone parathyroid hormone parathyroid hormone in high quantities okay now after this you know it like say the parathyroid glands parathyroid hormone so by breaking the bone by bone is option the increase is the calcium levels in the blood parathyroid hormones reduce the calcium clearance which means it decreases the calcium excretion means increases the calcium reabsorption of the digital convolution I have explained you that and in the intestines the parathyroid hormone activates vitamin D so vitamin D what it will do helps in the absorption of calcium you know it so functions carbonated all the functions I have explained you okay all the functions I have explained you say regarding what happens in the kidneys I have explained you and what is happening in the bones what is the osteoblast activates asked your class by rank ligand okay you know it right so functions done sir after the functions now let me directly go into the disorders okay let me directly jump into the topic of the disorder cell there is a hyper parathyroidism in the name itself is there hyper parathyroidism which means what more amount of parathyroid hormone simple high levels of parathyroid hormone so what happens if there is high levels of hyperparate hormone Simply Basic right more amount of pdh more calcium is there in the body that lots and lot of lots and lots of calcium will cause unnecessary problems okay so what's the most common cause why is there why hyper parathyroidism why more parathyroid hormone most common cause is parathyroid adenoma look here this is a parathyroid gland sorry this is a thyroid gland okay this is the thyroid gland now in the thyroid gland are you able to appreciate the there is a tumor okay there is a tumor to this parathyroid gland parathyroid gland got a tumor so it's called as a parathyroid adenoma is the most common cause of primary hyper parathyroidism primary hyper parathyroidism right now I'm talking about the primary hyperparathyroidism primary means there is some problem at the level of gland okay there is some problems are happening at the level of gland what is the problem parathyroidenorma are there can be parathyroid hyperplasia okay parathyroid gland have autocon hyperplasia OK not a tumor just the parathyroid glands become bigger parathyroid hyperplasia which are seen in syndromes like multiple endocrine nucleations men's syndrome there will be parathyroid hyperplasia so what are the two causes what are the two causes where the parathyroid hormone levels are going to be elevated one is parathyroid second one is parathyroid hyperplaces done now what is the most common site which gland can get this adenoma it's a right inferior gland here also they go okay it's the inferior glands it's the inferior gland the two right inferior gland is the most commonly going to develop this endomas okay so what are the genetics what are the genetics involved so why this parathyroid adenoma why maybe because of some gene mutation cyclin D1 over activity so cyclic given over activities associated with the parathyroid endomas leading to hyper parathyroidism I have explained you that is parathyroid hyperplasia parathyroid hyperplasia it is associated with what so the parathyroid hyperplasias they are associated with men's syndromes okay I will discuss about this also in today's class sir in men one syndrome multiple endocrine neoplasia type 1 in men type 1 say imagine there is this one fellow okay there is this one fellow sir who is having men one okay man one so this patient is going to have three p tumors what are these three p tumors pituitary edinomas means one p for pituitary adenomous literary gland tumors second p is parathyroid parathyroid adenomous parathyroid related tumors and third p is pancreatic pancreatic tumors pancreatic tumors insulinoma glucagonoma gastronoma kind of tumors so in men one syndrome guys in men one syndrome the patient can have parathyroid adenomous simple what we have seen in this slide sir in primary hyperparathyroidism why second one over activity secondary one over activity or it can be seen in men's syndromes okay it can be associated with men's syndromes regarding men's syndrome what are the genes mutated that we will discuss later in men one syndrome men one gene is mutated that we will discuss later okay which gland is going to be most commonly going to develop this parathyroid edomas right inferior gland done now after this what are the clinical features if there is a person who is having hyperparathyroidism hyperparathyroidism more amount of parathyroid hormone so what this parasyroid hormone is going to do sir it's going to increase the blood calcium level so much going to increase the blood calcium levels so much so much so first of all in the labs in the labs what you will see is parathyroid hormone levels are more calcium levels are more calcium levels are more I have said you parathyroid hormones phosphate trashing hormone phosphate trashing hormone so what happened to the phosphate levels in the body so the phosphate levels in the body goes down and because more excretion parathyroid hormone excretes more phosphate out of the body so in primary hyperparathyroidism the patient is going to have elevated parathyroid hormone levels elevated calcium levels but less phosphate levels okay so what are the clinical symptoms sir see the clinical symptoms here are represented as bones stones groans and bones okay the famous demonic bone Stones grounds and moons what is this bone suffering to Sir in high quantities I have explained you in high quantities parathyroid hormone causes osteoclastic activation leading to Bone resorption so painful bones okay painful Bones the bones are undergoing destruction okay asked like the there is bone is option so this is all problem is because of bone resorption by osteoclast osteoclasts are doing bone resorption so what is happening sir the bones are getting brittle so there will be micro fractures that will happen in the bone there will be micro fractures so the bones are getting destroyed the bones are getting damaged so there will be inflammation in the bone so osteitis okay as there is damage that's happening in the bone there will be hemorrhoids that's going to happen okay I will show you the images also first bones are getting damaged because of the excessive parathyroid hormones as the bones are being damaged so it will be little little fractures and little little hemorrhages also that is going to happen in the bone so these hemorrhages are going to appear like a cyst so system okay osteitis there will be cysts and after that the bones are also going to heal right bones are also tissues the bone is being damaged so after the bone destruction the more scarring will be occurring so fibrosis are the bones okay fibrosis so osteitis inflammation of the bones cysts are going to be seen hemorrhagic cysts are going to be seen and there will be fibrosis so this condition is called as osteitis fibrosa cystica so osteoid is fibrosystica also called as brown tumor Brown sugar it's not actually tumor it's nothing but the cysts there is hemorrhage that's going to happen in the bone I will show you the images later on I will show you the images okay so there will be Hemorrhage that's going to happen in the bone this is the bone tissue normal healthy bone tissue okay and see there is hemorrhage here it's happened represented with hemocity Hemorrhage Hemorrhage is going to happen okay so anyway I will come to this area in a minute but let me tell you sir excessive amount of parathyroid hormone is going to cause more destruction of the bones destruction of the bones is going to cause osteitis fibrosis done next bones completed after the bones next Stones the excessive calcium what this calcium will do so there is more calcium in the blood the calcium will try to precipitate in the kidneys the calcium is trying to precipitate in the kidneys and forming what kidney stones so kidney stones are okay so bones Stones completed so this calcium will also deposit okay in the like you know in the central nervous system but here I right now first let me discuss about the abdomen sir what are the abdominal related problems here so the calcium is excessive amount of calcium okay the excessive amount of calcium can lead to constipation sir this is the important Point okay the excessive amount of calcium will cause muscle spasms okay and constipation no groans okay so that because of this constipation the patient can have grown sir so excessive calcium can cause prones okay this is one thing nausea vomiting that's not that important next psychiatric wounds what is this monster okay mons means you know right the person unnecessarily making sounds okay psychiatric problems okay moons they're making the sounds because the calcium is going to deposit in the central nervous system okay the calcium is going to deposit in the central nervous system leading to psychosis because of this calcium deposition in the basal ganglia this regions there can be psychosis memory loss can occur depression okay so these are the central nervous system features so what are the clinical features in a patient who is having hypercalcemia inflation is suffering with a hypercalcemia that is primary hyper parathyroidism in primary in primary hyperparathyroidism the patient can have hypercalcemia remember the mnemonic which you need to know for your exams is in primary hyperparathyroidism the patient is going to have bones bones groans and moles okay bones bones Crohn's moans and Stones okay these things you can interchange like change them anyway so bone related problem is the kidney stones abdominal related problem main problem is the constipation and psychiatric problems are going to be seen because of the calcium deposition in the central nervous system so that's the moans psychiatric moons psychiatric bones depression can be there okay there can be psychosis like you know memory loss can be seen in this hypercalcemic conditions now all these things you already know just a recapping thing just a recapping thing so usually in the initial phases okay initial phases if there is little hyper calcium whether it's okay asymptomatic little hypercalcemia that's tolerable asymptomatic but in kidneys in too much quantities there will be nephrologists kidney stones you know it in git in git I have explained you constipation constipation I have explained you about the constipation okay now apart from calcium constipation see here I have written pancreatitis also so why pancreatitis you know right calcium is enzyme activator it's an enzyme activator okay calcium is the enzyme activator normally the pancreas okay if you look at the pancreas the pancreatic enzymes can you tell me some important pancreatic enzymes which are produced in inactive form inactive pancreatic enzymes what are they um trypsinogen trypsinogen Imo sleep see noogen chemotrypsinogen trypsinogen and chemotrypsinogen see they are in inactive States they are in an inactive State once they came into that urinum okay once they come into the diode their adryption will be converted into trypsin okay once they come into the diode trypsinogen will be converted into lipsyn with the help of enzymes like intro kinase with the help of enzyme like a enzyme called as enterokinase or intro Pepto days will be converted into trypsin so the important point is and chemotrypsinogen they are produced inactive form in the bank glass but in the conditions where you are having hypercalcemia when you are having hypercalcemia that hypercalcemia this calcium excessive calcium can activate this enzymes in the pancreas itself calcium is an enzyme activator So within the pancreas itself the trypsinogen is converted into trypsin chemotrypsinogen is converted into chemotrypsin now what they will do now they will start to the activated enzymes will start to Foster digest the pancreas will cause the damage to the pancreas so this is called as Auto digestion of the pancreas leading to pancrea Titus okay so there is hyper calcium yeah kidney stones in the same way in the JT constipation is there okay sir but can be also pancreatitis okay there can be also pancreatitis so typical certices okay in a patient who is having hypercalcemia lots and lots of calcium there is a chance that he can develop the ulcers because of more acid production because of the more acid production there is a chance that can have more ulcers so in the central nervous system I have discussed central nervous system which is a psychiatric moons depression can be seen okay memory loss can be seen the same same features okay here also confusion anxiety memory loss depression same things okay eyes importance you don't know this so ice problem is the calcium will start to deposit in the ice especially in the limbus region so calcium deposition in the eyes can lead to banned keratopathy image based question which was asked image based question so what is this look here there is a calcium deposition within the ice is going to cause this banded appearance this is called as a band caratopathy like primary hyperparathyroidism okay so reposition of calcium in the limbus region next bones you know the bones what is the bone problem sir the bone problem is going to be osteitis fibrosa cystica it is also called as brown tumor Brown tumor okay Brown tumor the bones are getting damaged the bone mineral inside the bones are getting damaged bone resorption excessive bone resorption Whenever there is option osteoporosis osteoporosis is going to occur Whenever there is osteoporosis there is a chance that fractures can occur yes so it is a vertebral compression fractures are the most common okay so vertebral compression fractures are most common in osteoporosis okay vertebral for compression fractures the especially the lumbar vertebra okay so the vertebral compression fractures that can be seen in primary hyperparathyroidism hypercalcemia okay so all the clinical features are completed bone problems psychiatric problems git problems and what else JD problems kidney problems bone problems and central nervous system problems bones grown stones and bones okay sensor so never forget about the pancreatitis and image based questions are also important this is the band keratopathy after this look here in this patient who is having primary hyperparathyroidism this is also very important look here because of this excessive parathyroid hormone what I have said you want results is going to occur more and more the bones are getting destroyed so you can see this right the bones are getting damaged okay you can see this areas in the skull also that the bone is getting damaged so this is called as salt and pepper skull okay salt and pepper skull so salt and pepper skull is seen in primary hyperparathyroidism because of the bone absorption actually bone absorption and in the hands also when you take the ETC of the hands what you can say is there is a concavity because of the excessive bone resorption there is a concavity in the radial side okay so there is a concavity on the radial side of the phalanges on the radial side towards the radial side okay so this is the side of the radius right this is the side of the radius towards the radial side of the phalanges there will be active board resorption that can be seen as concavity okay so that's the one thing which I want to do then after this so in x-rays what you are seeing here this is not a tumor sir actually it's looking like a tumor right in the bone this is not actually a tumor these are the hemorrhagic cysts is going to happen in the bones forming the sister so these are brown tumors these are called as brown tumors are osteitis fibros are cystica okay osteitis fibrosisca this is actually the bleeding that's happening in the bone okay hemorrhage so done so what is the laboratory diagnosis how we can input the diagnosis the diagnosis serum parathyroid hormone levels are elevated serum calcium levels are all salivated but look at the serum phosphate levels the serum phosphate levels are damn low serum phosphate levels are less why because it is primary hyperparathyroidism pth phosphate trashing hormone phosphate is going out of the body phosphate levels are less answer now here as a just integration I'm just putting this what are the other conditions in which the serum calcium levels are going to be elevated the primary hyperparathyroidism because of that parathyroid idenoma are because of parathyroid hyperplasia you can have Phile amount of parathyroid hormone high amount of calcium levels okay done but what are the other conditions in which the calcium levels can be related so that certain drugs can increase the blood calcium levels as a direct increase of red calcium levels sarcoidosis which I want you to know is this sarcoidosis are very important okay sarcoidosis and certain cancers especially multiple myeloma it's a cancer cell so Mr cell carcinoma of the lung rest carcinoma renal carcinoma so these are the cancers which are I want you to know very much in multiple myeloma conditions and SEC squamous cell carcinoma best carcinoma and real real cell carcinoma these conditions are associated with the elevated calcium levels in the body okay just for this one thing is also the calcium levels are elevated in the blood okay so after this let me discuss about our primary is done sir primary is done primary hyperparathyroidism is completed which means so there is some problem in the parathyroid glands adenoma hyperplasia that's causing excessive amount of parathyroid hormone secretion denser see what is the secondary hyperparathyroidism secondary hyperparathyroidism means there is some secondary cause some other causes there in the body some other cause is there the t is a leading to elevated parathyroid hormone levels okay there is some secondary cause let me write here there is secondary cause this secondary cause is leading to increased parathyroid hormone secretion ok so what is the secondary Coster if you ask me the secondary cause is renal failure okay real failures that so kidney problem renal failure chronic kidney disease renal failure now tell me sir function of the kidneys normal function of the kidney cell the function of kidney disease calcium reabsorption okay calcium reabsorption normally calcium will be reabsorbed in the kidneys and activation of vitamin D What vitamin D will do sir vitamin D in the kidneys vitamin D is activated What vitamin D will do vitamin D increases the blood calcium levels increase the blood calcium level increase of red calcium levels now tell me kidney if it is gone the answer now do you think calcium reabsorption is going to occur no calcium reabsorption is not going to occur the calcium loss in the urine set the calcium is going to be lost in the urine calcium loss and do you think vitamin D is going to be activated no this is the very very important McQ vitamin D activation not there red calcium levels are not going to be maintained so this now hypocalcemia now there is hypocalcemia in the body this hypocalcemia is activating the parathyroid glands it is activating the parathyroid glands okay parathyroid glands okay so then here the parathyroid glands are absolutely normal kidney failure no vitamin D so blood levels of calcium is going down as the blood levels of calcium is going down now parathyroid glands are going to produce excessive amount of parathyroid hormone y excessive amount of parathyroid hormone why because see whatever this parathyroid hormone is going to do till at the end of the day kidney is not there calcium is lost out of the urine okay calcium is not going to stay in the blood okay so simply remember like that see in primary in primary hyperparathyroidism how to differentiate between primary and secondary say both in primary and secondary okay let me just show you here oh yeah yeah both in primary and secondary the parathyroid hormone levels are elevated no doubt but in primary the calcium levels are elevated but in secondary the calcium levels are less kidney problem all the calcium is going out of the body thyroid hormone will try to increase the calcium but the calcium will go out of the body calcium is not staying okay so remember like that so in my secondary let me tell you the problem here is the vitamin D activation not there vitamin D is not getting activated okay remember that thing and there will be renal Osteo dystrophy renal Osteo dystrophy why the word realitystrophy because it's very clear there is some renal problem some renal problem so because of this real problem the calcium levels are decreasing in the body parathyroid glands are getting activated the parathyroid glands produces more parathyroid hormone but parathyroid hormone will do parathyroid hormone what it will do causes the bone destruction Whenever there is bone destruction what happens there is Osteo is trophy Osteo dystrophy bone damage Osteo dystrophy so it's the real problem which is leading to the Bone problem so usually in your future you'll understand that patient who is having anal failure the patient who is having the renal failure he will have a secondary hyperparathyroidism which will cause the bone destruction so if you look at this is the image based question which was asked many times in like board exams as well as Indian exams these are the vertebra right these are the vertebra now what you will see here is sir this is called as a regular Jersey spine see in the body of the vertebra you can see this lucency okay so it's looking like White Band and black band white black white black white black so this is called as rugger Jersey spine so rugger Jersey spine it is seen in hyperparathyroidism ok but especially seen in the secondary hyperparathyroidism secondary to renal disease or kidney failure okay so this is called as regular C spine now what about the parathyroid hormone levels elevated sir whatever the blood calcium levels calcium levels are still decreased X ratiosity spine regurgitate spine okay so these are some important points which I want you to know how to differentiate between primary and secondary hyper parathyroidism okay now so you want us to write primary and secondary hypo hyperparathyroidism how to differentiate say primary hyper secondary hyper what is the difference in clinical setup you can understand your patient developing the problems it is secondary hyperparathyroidism okay but labs parathyroid hormone is elevated in both the conditions red calcium levels and phosphate levels so what about the calcium levels so the calcium levels in primary hyperthyroidism is more okay primary hyper parathyroidism is more and in secondary hyperparathyroidism it is less phosphate levels in both the conditions parathyroid hormone is more so what happens phosphates will be accelerated sir okay so in both the conditions phosphate levels are going to be less done now after this hyper completed hyperparathyroidism is completed now let's discuss about the hypoparathyroidism hypo hypo means what less amount of parathyroid hormone why there is less parathyroid hormone why why the most common cause is surgical removal okay during surgery to the thyroid gland okay during surgery to the thyroid gland by mistake by mistake the parathyroid gland is removed but these days this is not happening I was like you know these days surgeons are going to be so much precise that they know what they're removing okay what actually happens to be really Frank what actually happens is while they are doing surgery to the thyroid gland they will disrupt the blood supply to the parathyroid gland they will cause the disruption of the blood supply as there is disruption in the blood supply that can lead to hypoparathyroidism it's not just the surgical removal of the gland exactly to be very precise it's the disruption of the blood supply to the parathyroid glands will lead to hypoparathyroidism okay so don't forget about that but generally most of the books it mentions most of the most common cause is surgical removal but you know it's not just the surgical removal surgical disruption of the blood supply okay so surgical removal in developing countries developing countries and most common cause in Western countries already developed countries okay most common cause is autoimmune destruction okay autoimmune destruction Means Auto antibodies are destroying the parathyroid glands other antibodies are destroying the parathyroid glands right so what are the two causes of hypoparathyroidism the two causes ok the two causes can be surgical during surgery damaged okay our autoimmune destruction of the parathyroid glands hypothyroidism can also be seen in Niger syndrome hyperparathyroidism can be also be seen in Niger symptoms so what is this digital syndrome and desire syndrome there is a deletion of certain genes deletion of 22q 11.2 22q 11.2 that's a genes that's a gene Locus okay so there is a deletion of these genes so because of the deletion of these genes from birth itself from birth itself these genes are not there so there is absence of third and fourth pharyngeal pouches so there is a options OK there is not the option hypoplasia not developed so the hypoplasia of third and fourth pharyngeal pouches third and fourth pharyngeal pouches are not developed okay so desert syndrome it's a deletion of okay it's a deletion of 22 Q 11.2 third and fourth pharyngeal purchase are not developed now I have explained you it's the third and fourth pharyngeal pouch from the fourth pharyngeal pouch Superior parathyroid glands third pharyngeal pouch gives rise to inferior parathyroid glands we have discussed so as the third and fourth pharyngeal poses are not developed there is hypoplasia of so you can write options simple not developed absence of para thyroid glands parathyroid glands are not developed and even thymus even thymus is not developed why I am telling you because I have explained you third pharyngeal pouch don't forget Okay so look here it is the third pharyngeal pouch third pouch will give us thymus also so now in this condition fourth is not there third is not there so inferior parathyroid gland Superior parathyroid gland and thymus are not going to form okay so these basions with the daijar syndrome what kind of symptoms they are going to suffer with so these patients with the Niger syndrome they are going to suffer with aplacia thymus is not there okay thymic aplacia as a thymus is not there thymus is the site where T lymphocytes are going to mature proper maturation is not going to occur so when the teal lymphocyte proper maturation is not there this patient can have recurrent infections okay these patients can have recurrent infections the parathyroid glands are not there when the parathyroid glands are not there what happened to the blood calcium levels the blood calcium levels will decrease because the blood calcium levels will decrease hypocalcemia a patient is now having hypocalcemia with the recurrent infections treasure syndrome deletion of 22 Cube 11.2 absence of third and fourth pharyngeal pouch as well as thymic aplacia and hypomagnesemia what are the other causes what are the other causes of hypoparathyroidism one cause surgical damage second cause autoimmune destruction third cause desert syndrome fourth cause hypomagnesemia so magnesium is very much important just I used to remember something like this so magnesium it is very much important for the production of parathyroid hormone if magnesium is not there parathyroid hormone is not that simple as simple as that so magnesium is very much important for the production of parathyroid hormone hypomagnesemia hypoparathyroidism that's it okay four causes I have explained you okay four causes I have explained you okay so what are the clinical features sir the clinical features if you are having hypocalcemia let me write here typo thalassemia what are the clinical features that are going to be seen so you should know take a note normally our neurons normally our neurons the excitability of the neurons excitability of the neurons is most of the students will think the calcium is responsible for excitability no okay is the sodium which is responsible for the excitability calcium decreases the excitement of the neurons remember calcium decreases remember very important decreases the excitement of neurons okay enough physiology I hope you have said this calcium will inhibit the overactivity of the neurons whenever the calcium is going down okay whenever the calcium is not there so what happens sir okay hypocalcemia whenever there is hypocalcemia neurons what they will do they will hyperexide okay over excitation so there is whenever the neurons whenever they are over exciting whenever the neurons are over exciting this Alpha water neurons whenever they're over exiting what happened to the muscles there is excessive contractions excessive contractions that's called as detaining okay that's going to be called as titanism so hypocalcemia will lead to Titanic okay hypocalcemia will lead to Titanic hypocalcemia more excitation of the neurons more muscle contraction leading to tetanine okay leading to Titanic okay now how can we know that the patient is having hypocalcemia how can we know that the patient is having hypocalcemia by doing certain physical test by doing certain physical examination we can say this fellow is having hypocalcemia how just take this person and just tap on his face okay don't slap just tap on the parotid periodic line you know the parody gland right so the inferior border of the parotid gland just make a tap so whenever you are tapping if the patient say if the patient is having hypocalcemia then there will be urilateral contractions there will be unilateral contractions that is called as Chavo stick sign okay that's called as choostick sign tapping will cause unilateral contractions facial contractions this is called as chavoistic sign so what do you find on physical examination physical examination findings one is stable stick sign and the next thing is so when you try to measure the BP of this patient okay he came to you generally usually we doctors what we'll do we'll just go for the normal checkup right the nurse is going to take the BP so when the nurse is increasing the pressure in this PP cuff increasing the pressure in the pp cuff so what actually happens is if if the patient is having hypocalcemia immediately the muscles will contract immediately the muscles will contract okay immediately the muscles will contract so this is called as carpopidal spasm okay pedal spasm so that is called as trouser assign so what are the two signs which are seen one is the chavoistic sign it's a sign of hypocalcemia and other is a trouser sign trousers is a car popular spasm on increasing the pressure in the BP cuff when you are increasing the pressure in the baby cough it will cause spasm okay so javastic sign and trousers now how can we put the diagnosis simple it's a hypoparathyroidism right High EPO hypo so parathyroid hormone levels are less calcium levels are also less calcium levels are also less phosphate levels what happened to the phosphate levels phosphate levels will be more okay hypoparathyroidism is completed okay hypoparathyroidism is completed now after this hypoparathyroidism actually there are other types of hypopiathyroidism also like a secondary hypoparathyroidism okay like pseudo hypoparathyroidism okay so that's called as a pseudo hypoparathyroidism I do yeah they're important important okay let me tell you why why to leave it so let me itself okay this will be very much important for the exam going batches okay as you guys are not going for any direct exam but anyway let me tell you what is pseudo hypoparathyroidism in the name itself it's there pseudo means false falsely it is looking like there is hypoparathyroidism what is the problem it's the end argon resistance It's The End organ resistance means parathyroid hormone is there parathyroid hormone is there but the tissues like bones and kidneys okay so it's the kidneys and bones they are not receptive they are not receptive they are not welcoming a parathyroid hormone the parathyroid hormone is there such no problem but the kidneys and bones are not responding to the parathyroid hormone as they are not responding to the parathyroid hormone what happened to the blood calcium levels will be less the parallel hormone is there but still the blood calcium levels are going to be less way because kidneys are not responding bones are not responding simple as simple as that okay so know between the activation no calcium reabsorption okay no calcium absorption nothing is going to happen okay so there is end are gone resistance this is important end are gone resistance why see it's observed that this in these patients who are having pseudo hypoparathyroidism genus okay so genus gene mutations are seen okay genus in relations are seen Universe class thyroid also we have discussed genasis okay genus in mutations are seen with okay next what are the clinical features same clinical feature sir same clinical features similar to hypoparathyroidism but this problem is there from the birth itself this problem is there from the birth itself okay end Argon receptor mutation as a as the problem is there from the birth itself the bone formation is not properly happening in this baby so as the problem persists since the birth baby will have rickets maybe we'll have rickets maybe because the red calcium levels are less vitamin D is not there parathyroid hormone is not there sorry I should say parathyroid hormone is there but it is not functional it is not able to activate the kidneys as well as the bones so there is rickets from the birth so this is called as this is called as Albert Osteo dystrophy McQ this is McQ what is all but Osteo dystrophy Albert's oste aristophy is it's it's a bone problem see Osteo dystrophy seen in pseudo hypoparathyroidism parathyroid hormone is there but it is not able to activate the kidneys and bones and as simple as that okay so what are the clinical features same clinical features sir all same clinical features okay so um hypocalcemia means Titanic is going to be there okay hypocalcemia means tetany is going to be the chavoistic sign prosely a sign these things are going to be there bone formation is like you know bone formation is not going to happen properly but here one important thing sir in this Albert Osteo dystrophy which is there from the birth in this Albert archery look at this hands these are the knuckles right we say these are the knuckles okay Knuckles so the fourth and fifth metacarpals are not developed okay the fourth and meta these are the metacar first metacarpal second third fourth fifth see the fourth and fifth metacarpals they are going to be short not properly developed okay as they are not properly developed if you are if you ask this patient to have his fish like this you can see my Knuckles right these Knuckles are because of what these are the metacarpals okay metacarbons so first this is the first metacarpal second third is fourth and fifth metacarpals are not going to be like you know properly developed short beta carpals so you cannot see these Knuckles so this is called as this is called as knuckle knuckle so here you can see the knuckle here also you can see the knuckle but here you cannot see any knuckles so that's a temple there is no knuckle so there is a knuckle knuckle dimple dimple sign so knuckle knuckle sinus hypoparathyroidism are Alberts simple okay so short stature in these are all the clinical features of Alberts Osteo dystrophy which is there from the birth in which condition to the hypoparathyroidism pseudo hypoparathyroidism so calcium is not there parathyroid hormone is there remember parathyroid hormone is there but calcium is not there so short stature as a calcium is not there over excitation of the neurons can lead to tetany so look here the muscles are getting contracted so much contracted okay this is serial hypocalcemia not just in Albert's dystrophy it's seen in everyone who is having like you know severe hypocalcemia so the see how the it's not previously the people used to thought that the person is possessed with some devil this is not some like you know the patient is not possessed with any Devils it's actually the muscle contraction extreme muscle contraction is causing this position which is called as opposed onus position okay ophist position Okay so tetan is going to be their short stature the deposition of the uh like you know there can be mental retardation okay even these patients there can be mental retardation there can be archival sign or knuckle knuckle dimple Tipple sign okay archival signple dimple sign okay so these are the things which I want you to know so what are the labs how the labs are going to be in pseudo see in pseudo hypoparathyroidism very much important the parathyroid hormone is there so if you look at the parathyroid hormone levels actually there are more parathyroid hormones are paragraph hormone is there but it is not able to activate Okay so calcium levels are calcium levels are less forget about this alkaline phosphorase it will be normal in pseudo hypoparathyroidism parathyroid hormones are there parathyroid hormone is even elevated McQ because it's unable to activate so more and more parathyroid hormone is producing okay but falsely it is looking like hypoparathyroidism non-functional pdh so done sir okay so regarding parathyroid I have discussed importance okay image based question just as a recap operation serine hypocalcemia hypocalcemia severe hypocalcemia tetany dystrophy okay next sign trous a sign okay next spine seen in Spanish okay you can see our state is brown tumors okay our state is fiber of the cystica this is salt and pepper appearance of the skull serial primary hyper parathyroidism here you can see the concavity in the radial side of the bones and keratopathy okay all these are the image based questions which are needed for your exams thumbs up now after this okay let's discuss about the other disorders from here the topics will be like you know very easy simple now what is this so this is your adrenal gland TK now you know adrenal gland is made of profitable cortex as well as adenal medulla now what is the problem here tell me what is the problem here there is a tumor in the adrenal gland cortex gland cortex this is called as adrenal adenoma this is called as what adrenal adenoma sir where is it present it's present in the cortex not in the middle now this you know what it will do the stupid tumor is going to produce excessive amount of Aldo tiron okay steroid it's going to produce excessive amount of aldosterone okay so now tell me what is the name of the syndrome so this adrenal adenoma producing excessive amount of aldosterone it is called as which syndrome do you have any idea the name of the syndrome is called as corn syndrome okay the name of the syndrome is called as corn syndrome now tell me what is the normal function of aldosterone normally you know it right now whenever there is excessive amount of aldosterone what happened to the sodium reabsorption normal aldosterone helps in see let me write here uh let me write here the normal functions okay normal function of aldosterone what are the normal functions of Carlos Johnson three functions are there one is increases the sodium reabsorption increases the potassium and proton excretion excretion in urine okay so normal functions of aldosterone the three functions of aldosterone is aldostron increases the sodium reabsorption increases the potassium and proton excretion okay excretions but imagine now we are having corn syndrome where the aldosterone levels are going to be super high there is so much amount of aldosterone what happens so much sodium is going to be absorbed right so what are the clinical features the clinical features are going to be hypernatremia more sodium is getting reabsorbed so that causes hypertension more sodium means more sodium means hypertension the patient is now having clinical features like hypertension okay hypertension second so the potassium and proton are going out of the body more potassium excretion more proton excretion so as the more and more potassium is going out of the body that will cause hypo themia and alkalos protons are going out more protons are excreted so alkalosis more potassium is going out so hypokalemia okay so this hypertension is because of more sodium the more sodium the absorption hypertension less potassium is there in the body more potassium is going out so hypokalemia and metabolic alkalosis so these are the clinical features which are seen in corn syndrome corn syndrome so consonant completed now after constant Rome the next syndrome that I want to discuss here is called is a few chromosytoma purechromocytoma so what exactly is this your promo cytoma quickly quickly what exactly spherochromocytoma and what you should know for your exam especially this is important for the board exam sir I will show you some histological pictures also sir look here this is your cute little adrenal gland this is your adrenal gland now in the adrenal gland what is the central region called as this is called as Adrenal medulla at renal medulla okay arterial medulla so this Adderall Middle Light is made up of which cells do you know do you have any idea the saturnal medulla is made up of which cells so it's made up of chromafin cells it's made up of promethane cells now if you are having a tumor here previously I have discussed there is a tumor in the Eternal cortex if there is a tumor in the general cortex it is called as corn syndrome if there is a tumor here okay there is a tumor here then it is called as this tumor oh my God it's tumor it is called as pheochromocytoma cytoma so now tell me so this few chromosytomas what they will produce what they will release aldostron cortisol testosterone no Adrenal medulla produces epinephrine nor epinephrine adrenal gland produces adrenaline cortex and medulla medulla so this chromaphene cells normally produces adrenaline now there is a tumor now as there is a tumor what they will do they will produce excessive amount of okay now they will produce excessive amount of epinephrine and our epinephrine okay they will produce excessive amount of epinephrine and not epinephrine so what are the clinical features that are going to be seen the clinical features are going to be so they are sympathetic hormones right epinephrine norepinephrine they are the sympathetic hormones hormones what are the clinical features sympathetic features are going to be seen more sympathetic features are there in the body what are they hypertension hypertension so sympathetic hormones will cause increase in the baby hypertension Whenever there is hypertension there is headache nausea vomiting so let me see here what are the clinical features the clinical features are going to be excessive levels of catecholamine going to cause hypertension that hypertension can lead to headache empathic features more sweating sympathetic feature okay nervous system sympathetic hormones increases the heart rate so that's why here also in few chromocytoma this palpitations and tachycardia nervous system activates your central nervous system excites the neurons so anxiety okay anxiety okay so these are the important clinical features I want you to know yes of course weight loss is going to be there it's a long term thing okay but important point is hypertension tachycardia more bp okay headaches headaches are going to be seen okay so these are sweating sweating palpitations all these are the features of your chromosytoma okay now let's answer one by one okay these are the questions which were previously asked now look at here few chromosytoma it's the tuber of itself so it's a tumor of chromaphin cells sorry in the Adrenal medulla in the lateral medulla see not only an adult say look you should understand sir this chromatin cells are there no they are present in other places also the chromafent cells they are present in other places in the body also like in sympathic ganglia in some places in certain places they are presents up so if you have humor of chromafin cells outside the adrenal gland Hey look it's a tumor of Promethean cells outside the underground that is extra adrenal pure chromosytoma cytomas are called as paraganglioma see they go extraordinary few chromosytomas are called as era gangliomass McQ McQ so paraganglers are nothing but the tumor of chromaphin cells but not in the kidney outside extra adrenal pure chromosomes are called asparagangliomass so this paraganglia Mass they will produce okay they'll produce nor epinephrine only they will produce not epinephrine only okay no epinephrine not epinephrine only so predominantly okay so after this uh what I should teach you some other extra points I should teach you look here they go one by one it's a tumor of chromaphin cells in the medulla okay what is the most common side yes Adderall middle is the most common side what they will secrete not epinephrine not a preferent also epinephrine also epinephrine true okay so this extraordinary chromosytomas are called as paragangliomas just now I have discussed they're associated with now question mcqromocytomas they are associated with which syndrome men syndrome last at the end of this class I will explain you about the main syndromes sir fewochromocytomas are seen in bin type two okay just wait I will show you now itself if you want so look here in Main main type 2 when 2A and to be what you are seeing sir a kofio chromocytoma okay feochromocytoma so few chromos items are associated with when type 2. okay associated with when type 2 sir pure chromosytomas okay main type 2. okay not only mean type 2 1 hippolindo syndrome okay one hip cylinder syndrome so these are the points which I want you to know so few chromosytomas they follow the rule of 10 okay they follow they are like you know little discipline they follow some rules what is this rule of tensor I used to remember something like this you know uh just uh like you know funny mnemonic which I made for myself 10 percent okay ten percent of the time 10 percent are extra adrenal that is ten percent of the time foreign glands bilateral ten percent of the time they are familiar okay these are the like you know familial conditions that familial passing in the family's Valor genes and ten percent of the time they will turn into cancer malignant 10 percent will be multiple multiple okay multiple RC not just one tumor multiple tumors are same children okay so I used to remember like extra PF we have means like you know boyfriends kind of thing right extra boyfriends are malignant you know why because as multiple children multiple children okay more boyfriends more children something like that okay so what exactly I mean by here okay what exactly I mean by here is the is Rio chromosytomas who follows the rule of ten ten percent of the time they are extraordinary bilateral seen in children turn into cancer okay you know it anyway okay violated you know it right so with the follow rule of ten so how to put the diagnosis sir how to put the diagnosis thing this is the adrenal gland this is the adenal cortex adult cortex now where is the tumor presence here is the tumor fiochromocytoma okay here is a tumor sir now what this tumor is going to produce so this tumor is going to produce nor epinephrine epinephrine they will do that due to epinephrine norepinephrine they will cause all the unnecessary symptoms in the body tachycardia palpitation sweating all the things it increase BB hypertension okay but at the end of the day once a normal is there do you think the narrative is going to be there throughout the day no it's an orbital frame it's going to be metabolized where in the liver and epinephrine is going to be metabolized in the liver so into what into the degradation products metabolites so they are vinyl mandelic acid IC acid that is VMA okay I used to remember like VMA VMA so when are metallic acid levels and second one the degradation for the second degradation product of this catecholamine second degradation product in the liver it is called as meta reference so these are the degradation products [Music] now where they will come out sir so where they are there they will come out in the urine they will come out in the urine so in the urine the vinyl metallic acid levels especially especially important the most sensitive is the methanephrine levels they'll be very very high so just collect a urine sample and if you look in the urine sample the vinyl metallic acid levels and The Meta reference especially meta different levels are going to be super high So based on the urine examination you can put that Agnes this fellow is having so that's the important point which I want you to know so what are the diagnostic tests the diagnostic tests correct the urine correct the urine and check for methanephrine levels okay total meta different levels that's a very important thing okay also vinyl mandelic acid levels will be elevated okay so these are the some important points which I want you to know chromosytoma completed sir uh like you know if your homocytominations the general points are completed chromosyama what else you should know is so there are multiple Genesis PCC fiochromocytoma foreign can be asked okay this few chromosytomas are paragangular mass are U2 which is in mutations what are the gene mutations which can lead to the sphere of chromosytoma you know syndromes which are associated see what are the symptoms which are associated with a few chromosytomas when type two one hypolito syndrome neurofibromosis type one struggable syndrome you know it right but what are the gene mutations which can lead to few chromosytomas here are the gene mutations red gene mutation one hip field indigene mutation neurofibrom versus type 1 generation x-ray dehydrogenase gene mutations okay so here I have given a list don't go through this table unnecessarily they go gene mutations causing few chromosytomas red Gene one hyperinogen neurofibromatosis type 1 gene mutation and succinate dehydrogenase in mutation these are the gene mutations which can lead to few homocytomas if your chromosomas gene mutations will lead to a tumors after this same under the microscopy okay take a few homocytoma take a biopsy and put it under the microscope and you look at the histology if you look at the histology what you will see is Del balance pattern is same okay cell balance pattern so what the hell is this pattern okay what is this zeld balance pattern this is zelbalen means in German it means a ball of cells like in a ball which is made up of cells ball which is made up of cells so this Del balance pattern it is seen inferior chromocytoma okay he's a scientist okay we have first like you know coined the okay the term the cell balance pattern okay so what is the cell balance it's a Arrangement the arrangement of the chromaphin cells in the form of nests in the form of a balls what is called as a cell balance pattern okay now this tumor cells this tumor cells they are also surrounded by this is they are surrounded by sustentacular cells okay sustained tacular cells I will show you in the histology the tumor cells is they are arranged in the balls okay they are arranged in the form of balls the balls these are made up of this chromophene cells okay but these pure cells they are also surrounded by cells called as sustained tacular cells okay now you look at the histology okay you can look at the histology now look here this is the few chromosytoma sir here in the few chromocytoma are you able to appreciate this tubular cells they are arranging in the form of balls so they are arranging the form of bugs and here you can see the sustentacular cells okay here also these are the tumor cells here they go this is a sustained angular sensor these are the ball of cells where you can see the sustained angular cells okay you're also like the tumor cells are arranging in the form of balls surrounded by sustained ackler cells okay now McQ which was asked so when you stay in these cells when you stay in this cells immunohistochemistry when you go for the immunohistochemistry not just hemotoxicillin Oreos and this is a hn hemodox but when you go for the immunohistochemistry what you will see what will be coming positive sir in few chromocytoma synaptophysin positivity will be same promogranin positivity will be seen non-specific stress positivity S100 positivity is going to be C why because see the synaptophy is in synaptogranin sir these are going to be positive in cells with neural crystalline origin our new endocrine in origin okay usually the synaptophysin uh synaptophysicromagranin where they are presents are where they are present so these are the proteins which are present in the cells which are derived which are new Endocrine cells okay which are neuroendocrine cells so here our few chromosytoma cells are also neural Endocrine cells they are also neuroendocrine cells so that's why as the cells are a new endocrine cell see the chromafin cells are neuroendocrine cells that's why in this neuroendocrine cells you can see the synaptophysin synaptog positivity they are going to be sensor okay so you can look here this is the histology so you can still look here the cell balance pattern okay cell balance pattern now what is this a b c and d representing see the histology modern histology of the few chromocytoma first a is strain this is normal HD strain pink and blues okay hnd next B to D the b2d so B chemistry okay using chromogranin synaptophysin and S100 positivity okay here you can see the sustain tacular cells they're having this s standard positivity okay they are taking this okay so synapto synaptofacin chromogram and non-specific stress positive and ascended positive decent simply in your exam only only what the velocity is histology gel balance pattern okay gel balance pattern the tumor cells are surrounded by sustained angular cells immunohistochemistry will come positive for synaptophy promo Granite non-specific stress and a standard possibility after this what else you should know is third this is lateral gland this is the tumor this is a few chromosytoma okay this is a few chromos item this is a tumor these are tumor in the adrenal gland this is a few chromos item now see how it is like a pink color pink Okay pink to radiation color that's okay but when you put potassium dichromate here when you put a potassium dichromate here okay now you are applying you have taken the tumor you have made a cross section you have chopped it into two parts now you have taken potassium dichromate and you are applying the potassium dichromate here now immediately do you know what happens the tumor is going to turn into brown color okay so your chromos item is going to turn into berm cursor do you know why so this reaction is called as promethane reaction where this reaction is called as OK this is that you must see how it is turning into this brown to almost blackish in color this reaction is called as chromophene reaction by chromophene reaction here the explanation is given look guys look here same the freshly that tumor surface turns brown turns brown the freshly cut tumor surface turns brown when potassium dichromate solution why because it's a few chromosytoma inside the few chromosyama what do we have epinephrine norepinephrine is there so this potassium dichromate reacts with this epinephrine or epinephrine so this is due to oxidation of stored catecholamines already catecholamines is there when you put potassium dichromate the stored catecholamines will be oxidized okay so oxidation of the stored catecholamines okay synthesizer by the tumor this is known as chromatin reaction okay so just that's enough simple here image from Acid reaction chemistry shows positivity for synaptophism okay gene mutations red oncogen mutation one hip and erosion mutation neurofibromatosis type 1 generation as well as HGH succinated hydrogen mutation okay associated with associated with when type two one syndrome neural fibromosis type 1 and shows Weber syndromes okay extraordal fear chromosomes are called as paraganglios that's it okay next so what is a neuroblastoma one minute neuroblastoma see humor of Adrenal medulla tumor of Adrenal medulla is okay that is seen in adults normally but they go what is this neuroblastoma neuroblastoma means it's the most common most common tuber of again Adrenal medulla only same cell tumor same comma in cell tuber but in children okay tumor of adult metal is the most common children this is not a serious condition sir why because in few chromosome more amount of epinephrine benefits is getting produced here humor is there but not much not much yes of course not even if everything is getting produced but not much not much okay so why why this neuroblastoma the neuroblastoma is because of this nmic okay nmic so this nmic it's a transcription Factor okay amplification of this nmic oncogene okay so Gene the gene is going to be Amplified okay nmic Gene amplification will be seen in neuroblastoma in mutation zero fourth gene mutations I gave you okay sir nmic Gene amplification is associated with neuroblastoma okay dancer it's seen in children most most common presentation is going to be just a distinction of the abdomen abdominal distension is going to be seen okay less likely these patients not have much symptoms okay hypertension is going to be not not usually present so not usually present but important point which I want you to know is see here I have just kept the rosettes the rosettes the flower kind of arrangement even here this neuroblastoma that tumors will see how they are looking like there is a Rosetti appearance there is rosettes so these rosettes are called as on histology Okay so here they are Homer of right process Homer right roses are seen in neuroblastoma neuroblastoma Homer right project see how that tumor cells are arranged is not a cell balance pattern it's not the cell balance pattern now it's almost looking like a flower appearance the petals okay the flower petal appearance this is called as Homer right projects or Homer right pseudor rosettes okay so look here in pathology there are different different types of rosettes now I am discussing about see they go in neuroblastoma in euroblastoma what kind of projects are seen Homer right rosettes Homer right rosettes are seen if you ask me tumor cells they are arranged like this like a flowers ok but in the center there is pinkish appearance there is pinkish appearance you have pinkish appearance then it is called as okay it's called as Homer right pseudo rosettes okay Homer right roses Homer right roses okay over right roses see in that Center there is pale neurophyll OK this pink color material but there are something called as they call flexor okay winter stainer roses okay flexor winter steel roses they are seen in retinol blastoma where there is a clear Central clearing will be seen and there is something called as perivascular pseudor rosettes okay perivascular pseudorosides in the center blood vessels can be seen okay blood vessels can be seen so this hoverboard roses okay over right was itself the homeroid results are the tumor cells present in the center there is pink color appearance pale European is going to be seen sir okay look here see the center there is pink color appearances these are pseudorite sorry Homer right Homer right processor so what are the important points which you need to know regarding the neuroblastoma in the children the most common tumor of Adderall Middle Line children not as like you know as serious as a few chromosytomaster because more complications more clinical features are going to be seen there are not many clinical features are not going to be seen hypertension is also not usually seen because of energy amplification okay histology student like Homer right process Homer right roses are going to be seen with a central pink color appearance okay dancer after this what else you should know the last one hyper aldosteronism ah this one I have already discussed with you hyperlustrialism but what are the example sir hyper alterationism what is the example I have given you corn syndrome what's the con syndrome there is adrenal adenoma okay adrenal adenoma there is a tuber in the adrenal gland cortex that's the cause okay one thing one cause for hyper aldosteronism over amount of followers but that's not the most common cause the corn syndrome or adrenal adenoma is not the most common cause of hyperadostronism most common cause if you ask me most common cause is particle hyperplasia adrenal gland cortex is there right this cortex the adrenal gland cortex have undergone hyperplasia hyperplasia particular gland cortex poor cortex means more aldosterone okay so most common cause of hyperaldostronism is adrenal gland cortical hyperplasia cortical hyper pressure the other cause you can say adrenal adenoma leading to Corn syndrome okay adrenal adenoma causing hyper aldosteronism is called as corn syndrome you know the features hypertension because of hypernatremia hypokalemia can be seen metabolic alkalosis can be seen I have discussed with you constant room cleared now what happens if the adult gland is damaged total damage leading to adrenal insufficiency okay so the next topic one last topic is adrenal insufficiency what exactly is the saturnal insufficiency okay see the sudden insufficiency is also called as AKA okay AKA see in normally it's insufficiencies or insufficiency means less right less subtraction but in the name it will be like addition Edison's a disease Edison's is not actually addition but subtraction means adult gland is gone adult gland is getting damaged cortisol are going down so let me write here one by one so adrenal insufficiency also called as Edison's disease there is nothing addition okay but subtraction gone okay so also called as Edison's disease why why the adrenal gland is getting damaged why it is getting damaged the most common cause for the damage of the saturnal gland is tuberculosis tuberculosis of it affects the lungs but not just the lungs but also adrenal glands adrenal TB okay so most common cause the tuber clauses what's the most common cause in the world autoimmune disease autoimmune destruction of the internal gland Auto antibodies came and destroyed the ordinary gland okay autoimmune destruction or adrenal TB simple so there is this one condition okay which is called as water house friedrichsen syndrome okay Waterhouse Federation syndrome what is this gland is undergoing necrosis the adrenal gland is undergoing ecosystem this is called as adrenal hemorrhagic necrosis in which infection say it's seen in meningococcus infections okay if you get this infection meningocoxemia meningococca infection infection is going to cause hemorrhagic necrosis of the adrenal gland adrenal gland is gone and lateral gland is gone adrenal insufficiency so can you tell me some causes of other insufficiency TB autoimmune damage are atrial hemorrhagic necrosis which is called as Waterhouse friedrichion syndrome because of its organism meaning of okay so whenever the adrenal gland is gone whenever the adrenal gland is gone what happens sir aldosterone is not there so hypotension aldosterone is not there so no sodium reabsorption sodium levels will go down in the body hyponatremia hypotension aldosterone is not there and cortisol remember cortisol is also very much important cortisol will also come from Material gland only party soil very much important for the maintenance of the tone in the blood vessels particle is very much important for the maintenance of the BP Alderson is not there cortisol is not there so hypotension aldosterone is not there as art ocean is not there potassium is not going out potassium is not going out so leading to hyperkalemia aldosterone is not there so protons h plus they are not going out protons are accumulating in the body leading to metabolic acidosis okay metabolic acidosis there's going to be metabolic acidosis okay and in these patients who are having like you know other insufficiency usually patients will also have hyperpigmentation the exact reason for the hyperpigmentation is not clearly known there are some theories but not exactly no not nodes so radisson's disease is usually present with hyper pigmentation hyperpigmentation so with this hypoaldostronism is also completed sir okay hypoallergenism is also completed okay so the disorders are completed now let me ask you one thing so imagine there is a person there is a person who is having a tumor in his pituitary gland he is having tumor in his parathyroid gland he's having tumor in pancreas also so there are multiple endocrine tumors are there multiple endocrine tumors are there so what is this condition called as multiple endocrine neoplasias okay multiple endocrine nucleations what are they what are they sir type 1 and type 2 okay multiple endocrine places one slide okay every time in your exam 100 without this there can be no exams 100 of the question is going to be there multiple endocrine neoplasias are of two types Min one and Main two okay men one and Men two men one is also called as Verma syndrome not Verner Verma okay warmer okay multiple endocrine neoplases is also called as warmer syndrome I have explained you so this type 1 men type 1 okay multiple endocrine new pressure type one it's a three p tumors will be there three p tumors what are these three tumors I have explained you pituitary tumors parathyroid tumors and pancreatic tumors pituitary parathyroid and pancreatic tumor okay why why sir why why because of a gene mutation mutation men one gene mutation men one gene which is present on the chromosome number 11 men one gene which is present of the chromosome number 11 when it is mutated going to cause multiple endocrine neoplasias pituitary parathyroid pancreatic tumors out of these three pituitary parathyroid pancreatic pituitary parathyroid pancreatic the most common tumors are parathyroid okay most common tumors are parathyroid tumors inheritance pattern is autosomal dominant inheritance pattern so you will get this disease autosomal dominant inheritance pattern okay familiar so tell me multiple endocrine your place at F1 foreign actually what happens is parathyroid hyperplasia will be same not actually tumor parathyroid hyperplaces are seen in one but anyway what is the gene mutation when one gene mutation when one gene is present on which chromosome chromosome number 11 what is the inheritance pattern horizontal dominant next meant two so men two is divided into two a and two B cell when two it is divided into two a and two B okay it is divided into two n to be both into see here also 2 is there here also two is there between some common features are there some common features do you know what are they m c d m c t means medullary carcinoma of thyroid in yesterday's class go and revise the thyroid disorder thyroid cancers medullary carcinoma of thyroid medullary carcino thyroid cancer off para follicular C cells parapholical cells producing calcitonin tumor cells in amyloid background okay apple green birefringence under the polarized light we have discussed in the last class so in men 2A which is called as a simple syndrome they call okay when two a is also called resistible syndrome where the patient is going to have patient is going to have MCT medullary cosmop thyroid gland and feochromocytoma just now we have discussed fewochromocytomas so if your chromos items are here also so both in 2A and 2B both in 2A and 2B these are common medullary constant of thyroid remember it's like MCT MCT and PCT MCD and PCT are commercial here also MCD PCT here also MCT PCT then what is the difference between main two a and to B the differences are that in main two a the patients are going to have parathyroid endomas means parathyroid involvement is going to be seen in meant to be the mucosal neuromas in the mucosa okay in the mucosa small small tumors will be same OK small small tumors will be same which are called as a mucosal neuromas mucosal neuromas okay and marfanoid habitus if you look at this fellow he's going to have morphinoid habitus Marfan syndrome like blender thin tall with large like you know limbs okay so morphinoid habitus vectors excavatum can be seen okay and mucosal neuromus so not tell me when two is divided into two n 2B 2A is also called a civil syndrome what is common between two and two B common things are medullary calcium or ferrite as well as few chromosytoma this is common between both two and to be what is the difference sir 2A is going to have parathyroid enormous parathyroid gland tumors can be seen and 2B the patient is going to have mucosal neuromas and morpheroid habitus okay the same here also they go when men one okay men one which is also called as per our syndrome warmer okay warmer warmer syndrome three p tumors parathyroid pancreatic pituitary parathyroid pancreatic filtered parathyroid pancreatic pituitary mainly it's a parathyroid hyperplasia they also have explained parathyroid not to tumor parathyroid hyperplasia is most common mint 2A also called a simple syndrome what are the common things see few chromocytoma middle recover thyroid here also fewochromocytoma medullary carcinoma thyroid common the morphinoid habitus mucosal neuromas can be sensor because the neuromus can be same so with this the important topics which you need to know for your exam okay Paradise parathyroid disorder Central disorders okay so hope the class is helpful from tomorrow we can start with the new pathology uh most probably we'll be doing with the lung pathology okay we'll be starting with the lung pathology so the respiratory system we'll be doing with the respiratory system okay so of the class is helpful okay guys bye bye for today see you tomorrow