Welcome to Spotlight Advanced. I'm Colin Lover. And I'm Liz Wade. Spotlight uses a special English method of broadcasting. It is easier for people to understand, no matter where in the world they live. Imagine you work at a hotel. You answer phones and show people to their rooms. You meet a lot of interesting people at your job. And you have seen some strange things. One day someone comes into the hotel. They walk up to your desk and tell you they found a wallet outside. It was lying on the sidewalk. They ask if you would return the wallet to its owner. Then they leave. You look through the wallet. You are hoping to find something to identify its owner. Instead you find a key, a list for shopping and money. The money is worth US$100. There is a telephone number on the list. You stop for a moment and think. Only one person knows you have the wallet. It would be very easy to take the money. No one is watching. What would you do? Would you take the money? Would you return the wallet? Would you be honest? Today's Spotlight is on. Honesty and why people lie. This example was part of a real experiment. All over the world researchers entered hotels. They went to police stations and banks. They turned in wallets. Some wallets had more money and some had less. The goal was to see when people returned the wallets and why. Researchers dropped over 17,000 wallets in 40 different countries. Then they waited for the results. Before the study, most researchers believed that people would take the wallets with more money. More money would give people more reason to steal. But this did not happen. Instead, people were more likely to turn in the wallets with more money. This was true in almost every country. More people also returned the wallet if there was a key in it. Researchers believe that there are two reasons for their results. First, people do not want to believe that they are bad. Stealing is illegal in almost every country. When there was more money in the wallet, it felt more like they were stealing. They returned the wallets because they did not want to seem like bad people. Dan Ariely is an economist who studies dishonesty. He talked to NPR News. He said that the study showed that people choose to be honest because it is more socially acceptable. He says, This study shows in a very natural way that our choices about dishonesty are not rational. We do not think in terms of costs and benefits. We think about what we feel comfortable with socially. The second reason researchers believe people returned wallets with more money and items is because they felt bad for the owner of the wallet.  You become panicked or distressed. You search and do not stop. This is especially true if you lose something important to you. Empathy is the ability to understand another person's experiences. We think about how we might feel if we lost a wallet full of money. This also affects situations where we lie. It is easier to tell a lie when the lie is small or if we think what we do will not change anything. But if we think about how we feel when someone lies, we may not do it. In this way, honesty depends on empathy. How honest we are also depends on our own needs. A person may be more willing to lie if they need something very badly. How honest we are also changes when dealing with different people. Stereotypes are beliefs we have about people without really knowing them. These beliefs about groups of people shape our behavior. They make it more difficult to feel empathy. Imagine that you believe that all people from a particular country lie. You may dislike them even though you do not know much about them. You may be honest toward everyone else, but you may not believe that people from this country deserve honesty. You may not be honest because you do not believe those people will be honest. But how honest you are can also depend on where you are from. David Hugh Jones is a researcher at the University of East Anglia. In 2015, he decided to study what honesty looked like in different countries. He created an experiment. He asked people from many different countries to report the results of a coin flip. The person in the experiment would throw the coin in the air. If the coin landed on heads, the person would get money. If it landed on tails, they got nothing. Hugh Jones also had people answer questions about music. Correct answers would also get a reward. People in the study could easily cheat, but the questions were very difficult. Almost no one would know them. So Hugh Jones would know when they were honest or not. Hugh Jones found that the UK was the most honest in the coin flip. But Japan was the most honest in the music quiz. And other countries had different levels of honesty. The two different tests showed that people were honest about some things, but not honest about other things. This could have to do with cultural differences about honesty. Almost every culture values honesty, but it is not always easy to be honest. Telling the truth can be difficult. Most of the time we lie to stay safe. Judy Kettler is a journalist who reports on honesty. She wrote for Scientific American In relationships, we lie to make people feel better or to avoid awkward situations. But we also do not like it when our romantic partner lies to us. We lie to ourselves as well, believing that we are smarter than we are. Children will lie more often if other people have lied to them.  And of course, we also lie on social media. These lies can keep us happy. They help us avoid difficult situations. But lying also causes negative emotions, like worry. It can make you think everyone else is lying too. And most of the time, lying is not even necessary. Kettler says We often think being honest will be more difficult than it is. In fact, people find that being honest makes relationships better. It improves social connections more than they expect. So how can you be more honest? Kettler offers this advice. A good start is to watch when you lie. Why are you not being honest? What will happen if you speak the truth? Try to stop the small lies first. You may find the bigger lies will also stop soon after. How honest do you think you are? Have you ever tried to be more truthful? What was it like? You can leave a comment on our website or email us at contact at spotlightenglish.com You can also find us on YouTube, Facebook, Instagram and Twitter. The writer of this program was Dan Christman. The producer was Michio Ozaki. The voices you heard were from the United Kingdom and the United States. All quotes were adapted for this program and voiced by Spotlight. You can listen to this program again on our website at www.spotlightenglish.com This program is called Why Do People Lie? Visit our website to download our free official app for Android and Apple devices. We hope you can join us again for the next Spotlight program. Goodbye!


Good day everybody, this is Dr. Sanjay Sanyal, Professor Department Chair. So this is going to be a demonstration of various structures in the neck, mostly in the anterior cervical region, the neurovascular structures. So just to give you a quick overview, this is a supine cadaver. This is the right side. I'm standing on the right side, camera person is on the right side and my assistants are on both sides. So what are the structures which are initially visible in front of us? We have completely opened up the thorax and the right side of the neck. This muscle that you see here, that we have retracted up and pinned up here, this is the right side sternocleidomastoid. We have removed the clavicle on the right side. So the clavicle, the other portion is here. This is the internal jugular vein on the right side. And we can see the internal jugular vein is receiving the common facial vein as well as the retromandibular vein. There is no retromandibular vein forming the external jugular vein in this particular cadaver. We can see this is the retromandibular vein which divides into an anterior and posterior division. Anterior division means with the facial vein, the posterior division is opening into the internal jugular vein. This is the internal jugular vein which we have lifted up with our instrument here. This is highly macerated because in the embalming process, they had perforated it and therefore there is extravisation of blood here. This is the remnant of the subclavian vein on the right side. We have mentioned all these things in a previous video. The next structure that we see here is this one here. This is the common carotid. This also, as you can see, it has been perforated during the embalming process and therefore there's a lot of extravisation of blood. Both these were encircled in the carotid sheath and behind that we can see this is the vagus nerve on the right side. I'm going to show more of it as I go along. All these were enclosed in the carotid sheath. The next structure that we see here is this muscle here. This is the omohiod. This is the inferior failure of omohiod. This is the facial sling which we have lifted up with our instrument here. This was created by the pre-tracheal layer of deep cervical fissure and this was attached to the clavicle and therefore this is the superior belly of omohiod and which is attached to the hyoid bone. The next structure that we can see here, I'm going to retract this is this muscle here. This is the sternohyoid and we can see it is going from the sternum which has been removed to the hyoid bone up here and I'm going to lift it up here and we are going to, my assistant is retracting it. Under that we can see this muscle here. This is the sternohyroid. It is going to the thyroid cartilage and above that this piece that we see here this is the thyroid hyoid. This is the thyroid gland. This is the thyroid gland. And this muscle that we see here this is the cricothyroid muscle. So therefore this is the thyroid cartilage. This is the laryngeal prominence. This is the superior thyroid notch. Below that this is the cricoid cartilage. So therefore this muscle is the cricothyroid and up here we can feel it but we cannot see it as the hyoid bone. This is the other side. We have retracted the muscles without separating them and we can see the great vessels coming out from the arch of aorta. This is the arch of aorta. This is the bricocephalic trunk. This is the common carotid as I mentioned earlier. This is the right subclavian on the right side. This is the left common carotid and this is the left subclavian. And we can see there's a gap between approximately one centimeter between the bricocephalic trunk and the left common carotid. Down below this is the trachea and we can see it is bifurcating at the level of the sternal angle of Louis and further posteriorly we can see this is the isophagus. With this background, let's go a little deeper and we shall bring back the structures in the normal position. We shall retract this sternothyroid also and we shall pin it up stairs and I'm going to pin it now. So having retracted that out of the way, let's start with the common carotid here. As I told you, the common carotid is highly macerated because of the embalming process but we have salvaged quite a bit of it. The right common carotid as it goes up approximately at the level of the upper border of the thyroid cartilage, we can see it is dividing into two branches. This branch, the smaller one, this is the external carotid and this one is the internal carotid. Internal carotid has got a bulb here. This is the carotid sinus and in between the two, in this connective tissue, there is a fibro structure which is called the carotid body which acts as a chemoreceptor, a peripheral chemoreceptor. The carotid sinus acts as a paroreceptor. I will draw your attention to this nerve which is running in front of the bifurcation which I have lifted up with my instrument. What is this nerve? This is the hypoglossal nerve. Hypoglossal nerve causes in front of the bifurcation and it enters and I've shared more about this as I go along. This pink structure that we see here, this is the submandibular salivary gland and this is a little bit of the carotid gland that we can see here and this muscle that we see here, a little bit is visible, this is the mesetermosal. We have not descended out any further than that. Having shown the common carotid and its bifurcation into internal and external carotid, now let's take a look at the subclavian artery on the right side. So this is the subclavian artery on the right side and we can see this is the first part of the subclavian artery. How do we determine the subclavian artery, the parts? We can determine it by this muscle here. I will draw your attention to this muscle which starts from here and goes down and further down it becomes pinkish in color, this brown and pink muscle. It is attached to the first rib. So you have guessed it already, this is the scariness anterior muscle. So therefore the portion of the subclavian artery from the origin to the medial border of the subclavian, scariness anterior, this is the first part of the subclavian artery. The second part is behind the sub-scaliness anterior and the third part is from the lateral border of the scariness anterior to the outer border of the first rib. So this much is the third part and after that it becomes known as the axillary artery. So therefore this piece that we see here this triangular space between this brown muscle and this brown muscle and the pink muscle. This is the scalyne triangle bounded by the scalyness anterior, the scalyness medius, both of which are inserted on the first rib and emerging through the scalyne triangle are this neurovascular bundle. What are they? The upper trunk of the brachial plexus, the middle trunk of the brachial plexus and the lower trunk of the brachial plexus. And apart from that, definitely not the least is this third part of the subclavian artery. So therefore all these structures together are the contents of the scalyne triangle. And therefore any one or more of these can be entrapped in what is known as the scalyne syndrome. Having mentioned that, now let's come back to the branches of the first part of the subclavian artery and the second part that we can see in this dissection. As I told you earlier, the first part of the subclavian artery is from its origin to the lateral medial border of the scalyne's anterior. What are the branches that we can see here? This is the first branch. This is the internal thoracic artery and you can see this is a cut portion here. It was entering into the thorax, it's going down. It was running on the inner surface of the chest wall. And I will draw your attention to where my finger is tracing right now. This is the internal thoracic artery on the left side and similarly on the right side that you see. I'm going to shine the light here. You can see this is the internal thoracic artery on the right side. So therefore this internal thoracic artery is this internal thoracic artery. This is the first one. The next branch that we can see in the first part is this big artery here which I have lifted up. This big artery. What is this? This is the vertebral artery and take a very good look. We will see the vertebral artery is starting from here and it is disappearing in this place here. So therefore there is a pyramidal-shaped space here which I'm going to trace just now with my instrument. This is one boundary of the pyramidal space. This is another boundary of the pyramidal space. This is the scalenus anterior, as I mentioned earlier, and this is the longus coeli muscle. It goes through this pyramidal space. So this is the first part of the vertebral artery or the V1, the so-called cervical part. After that it will go into the transverse pyramid of C6 up and that will be known as the vertebral part. Then it will go become the suboccipital part and then it will become the intra-cranial part. So this is the first part of the vertebral artery. So that's the next branch of the first part of the subclavian artery. Then we have the next branch. The next branch of the subclavian artery is this one here, which I have lifted up. This is the thyroservical trunk which I have lifted up here. Please take a good look at this. This is the thyroservical trunk. Now, thyroservical trunk is supposed to give four branches, but in this case, again, we have a small anatomical variation. The first branch is the inferior thyroid artery, but in this case, it is not coming from the thyroservical trunk. It is coming separately and I have lifted it up here. This is the inferior thyroid artery. We can see it is coming separately and the inferior thyroid artery, if you note carefully, it goes up like this and it makes a loop like this. This is the classical course of the inferior thyroid artery. And this inferior thyroid artery is going towards the thyroid gland and you can see this is the thyroid gland. So it is going towards the thyroid gland. And this inferior thyroid artery is accompanied by this nerve. Can you see here? This is the recurrent laryngeal nerve. I will show more of the recurrent laryngeal nerve just a little while later. So therefore, when we are ligating the inferior thyroid artery during thyroidectomy, we have to be very careful not to injure the recurrent laryngeal nerve. This is a point to be remembered and noted. Let's continue with the branches. This, as I told you, was a thyroservical trunk. We can see the other branches. This is the ascending cervical artery. This is the transverse cervical artery and this is the suprascapular artery. So ideally, the thyroservical trunk is supposed to give four branches. The inferior thyroid, transverse cervical, suprascapular ascending cervical. The ascending cervical and inferior thyroid are supposed to be the terminal branches. But in this case, we had a slight anatomical variation. That brings me to a few quick words about the transverse cervical itself. The transverse cervical is also called the cervical dorsal in some books. And the cervical dorsal or the transverse cervical, as it goes, it becomes divided into two branches, a superficial and a deep. Now in this case, we can see it is dividing. It is dividing into a superficial and a deep. The superficial one runs with the spinal accessory nerve on the levator scapulae. This is the spinal accessory which I have lifted up. And it runs on the levator scapulae where my instrument is tracing right now. But this deep branch, as you can see, the deep branch is going inside. The deep branch is known as the dorsal scapular artery. And this is the one which runs deep, medial to the scapula and it participates in the scapula and nostromosis. And it's the one which is responsible for the dancing scapula which is seen in coactation of aorta. So that's about the cervical dorsal or the transverse cervical artery. The suprascapular artery, which I mentioned just now, is accompanied by this nerve here. This is coming from the upper trunk of the brachial plexus. This is the suprascapular nerve which goes and supplies the supraspinitis and infraspinitis muscle. So we have seen the four, three branches of the first part to recap vertebral artery, internal thoracic artery, thyro-survival trunk. Thyro-survival trunk giving four subbranches, in this case, a little variation. Now let's come to the second part of the subclavian artery. The second part is behind the scallionis anterior. And we can see it is rather difficult, but we shall pull it out and we can see that this is the second branch from the second part. This is the costoservical trunk. Why is it called costoservical? Because it gives two branches. One is the supreme intercostal, to the first and second intercostal spaces. And the other is the deep cervical, which supplies the muscles of the neck. That's why this trunk is called the costoservical trunk. The third part of the subclavian artery does not usually have any branches, but sometimes the suprascapular artery, which I showed you here, or the torsoscapular artery may arise from the third part of the subclavian artery. So we have seen the full course of the subclavian artery and we have also seen how it can be entrapped in the scallionis anterior syndrome, and we have seen the branches of the subclavian artery. Now let me show you another structure. This was the internal jugular vein, as I told you earlier. This is the common carotid artery, which divided up. This nerve that we see running, it was running in the carotid sheath. This is the vagus nerve. And if you trace the vagus nerve, we can see it is coming, arising from way high up, and I'm retracting these structures here. You can see the vagus is arising from here. You can see my instrument has gone way, way, way up. It comes out through the jugular foramen, and it runs straight down. Where does it run? It runs in the carotid sheath. Behind the internal jugular, and the common carotid and internal carotid. So this is the vagus nerve. So let's see what happens to this vagus nerve. The vagus nerve on the right side, we can see it's coming down. It runs in front of the subclavian artery, and we can see it is running in front of the subclavian artery. And then it goes behind the trachea and it divides into aplexus. And after that it will do many further things. But I will draw your attention to this branch of the vagus. We can see this branch. This is the vagus accessory complex. In this particular case, it is known as the right recurrent laryngeal nerve. Let me show you the same thing from the other side. This is the right recurrent laryngeal nerve. Again, let me show you. This is the vagus. This is the right recurrent laryngeal, and this is the right recurrent laryngeal. This right recurrent laryngeal nerve, it runs in the tracheoesophageal groove. This is the trachea, and behind that is the esophagus. And it runs up like this, and it is in accompaniment with the inferior thyroid artery, which I mentioned earlier. And we can see both of them. I'm going to hold both of them together. This is the one I said has to be safeguarded while we are doing the thyroidectomy. This is a very important relationship which I wanted to draw your attention to. The next important relationship that I will draw your attention to is this branch of the external carotid artery. This branch, this is the superior thyroid artery. How do we know? Because this was a thyroid gland. So therefore this is the superior thyroid artery. And we can see the superior thyroid artery is accompanied by this small nerve here, which I have lifted up. And we can see the two of them are running together and I've held both of them close together. So you have guessed it. What is this nerve here? This is the externalaryngeal nerve which supplies the cricothyroid muscle. So again, when we're doing a thyroidectomy, we have to be very careful while ligating the superior thyroid artery so as to not to injure and to safeguard the externalaryngeal nerve. If you injure the externalaryngeal nerve then we will produce a parallel of the cricothyroid muscle and that will lead to a weakness, the voice. In contrast, if you injure the recurrent laryngeal nerve while ligating the inferior thyroid artery, we will produce hoarseness of the voice. Now let's take a quick look at the opposite side. This is the left common carotid. On this side, we can see this is the remnant of the internal jugular vein. This is the left subclavian. The running behind is this the left phrenic nerve. This is the vagus on the left side and it is giving a separate branch to the trachea here. What about the recurrent laryngeal nerve on the left side? The recurrent laryngeal nerve on the left side, it comes under the arch of aorta here. And we have cut it here but we can see the rest of the recurrent laryngeal nerve here and I've lifted it up here. This also follows the same course as the right side and it runs in accompaniment with the inferior thyroid artery but we have not dissected the nerve and so therefore we have to follow the same precaution on the left side as we did on the right side. So these are the structures which I wanted to show you and before we conclude, just to draw your attention, this is the media stynum that we have removed. This is the arch of aorta. We can see the three main branches. This is the descending aorta. This is the bifurcation of the trachea and this is the isophagus and we can see the trachea, the thyroid and the descending aorta is giving rise to the posterior intercostal arteries. So these are the structures which I wanted to show you in the dissection of the neck and the media stynum. Thank you very much for watching. Dr. Sanjay Sanyal signing out. My MD1 students are my assistants as well as the camera persons. Please like and subscribe. Have a nice day.


This is, I think, a better format for the morning. If you guys are ready, I'm going to give you a light stand-up. So let's start with number one. I'm going to give you guys a routine. I'm going to get you to go home already. So, anybody? Because I haven't done that yet. So that makes it a little challenging. Because some of this stuff, I will tell you, you're going to see pretty much almost every time you go home, we'll describe a book on that rotation. We'll include this here at Primaries. There are a lot of weird syndromeic stuff. And a lot of the actual problems are on patients as well. So, let's do number one. We're going to split it up. What do you guys want to name your team? We're playing for Pride here. What's your team? Team one. Team one. Okay. What's your team? Pride. Pride. Okay. Going out strong. So, a number between one and ten. Chris. Seven. Seven. Three. Three. They get to go first. Okay. So, you guys get to... I'm going to start off the question. And then you guys get to the answer. There's a decent amount of time if you can. Then we'll switch over to the other team. Okay. Which of the following is not a classic feature of congenital glaucoma? D. D is in dog-conjunctival injection. That is correct. So, in March 20th, you guys remember that. Now, this goes into another question that we're going to talk about later, I believe. Maybe not. How long... How much time is there? Or what age is... What age range do you see corn and larchin? Like, when is corn and larchin stopped? You've got high pressure in the eye. And, you know, you're probably thinking, is every single case of congenital glaucoma going to present whether they're in March 20th? What's kind of your age now? As you remember. When the corn stops stretching. So, usually around... Okay. So, between zero and three, corn is still very... There's a lot of plasticity in the corn here. So, you can see a lot of stretching if the congenital glaucoma occurs at any time. Okay. Now, if it occurs after that, how do we distinguish? Like, there are different types. Congenital would imply that it happens around what age range? Depending on that range. Or probably more likely in the first year. Okay. But you're going to see that in March. It can happen even, let's say, in 2015 months. That would still be kind of considered congenital glaucoma glaucoma. And then after that, we start calling things infantile. Okay. So, infantile is probably... You know, I think if I were... Let me back up on that definition. It's quite better to say that if something presents after a year, it would be considered infantile. But the ICD-10 code is actually the same. It's very similar. So, what do you call a congenital or infantile? I think it just suggests when the patient presented to you. But in that zero to three range, you're going to see those plastic symptoms. And so, let's go through the other symptoms. Topstria. Do you guys remember topstria? What is that? Obstria. Ornate. Obstria or breaks and decimates membrane. Can I do the usual? Are they vertical or horizontal? They're usually horizontal. Sometimes they can be circumferential. Yeah. So, we've had a few cases on service recently that have this very significant slope. Normal circumferential. It's just going to spiral out. Concentrate surface around. That's not a good point. So, if you guys see that test question, it happens almost every other year. You can see a test question about topstria. Or they'll tell you about stria on the cornea and these breaks on the cornea. And they'll describe to you that they're either vertical or horizontal. And they're trying to get you to see if they need to go home or not. And the direction is important because usually it's a force that's injury. It's vertical. So, remember that for your O-caps exams. Vertical stria are usually implied for such injury. Okay. Hip for up. Water in the eyes, photophobia and blood for spasm. Those are probably, but that's the classic triad. Okay. Hip for up, photophobia and blood for spasm. Okay. Now, this one is open up for anybody. So, we're raising a hand first. Which of the following age ranges portends a better prognosis for patients with PCG? Sorry. So, again. B. B. Correct. So, this is very important when you're counseling patients. There are minority cases. I think if your book says 25 or less than 25% of cases will present as newborns immediately when you're near the birth. As soon as the baby comes out, obviously the cornea is cloudy. They have massive blue felmas. But most of the cases are going to present in that window between birth and the year. So, you can tell parents that the prognosis is usually better if they're between 3 and 12 months. Okay. All right. Next question. Which of the following are not disdain machine features in the accident of all three years? Chris. You said B and C. B and C. So, that is partially correct. Sorry. Sorry. You are correct. There's one more. Sorry. All right. And we want to go for it. Okay. So, the answers are which of the following are not disdain machine features? Chris, you got two out of the three. Autosomal recessive. That is true. That's most cases. I'm sorry. That's false. That's right. Mostly are autosomal. And actually, Chris, I'm sorry. You threw me off there. C is not the correct answer because there are some cases that are sporadic. Okay. So, and then the last one would be D. Okay. Those are all not disdain machine features. It is autosomal. It can occasionally be sporadic. So, the answers are actually B and D. I'm sorry. I'm throwing myself off. These not questions are meant to kind of probe you to make sure you guys know the information. So, let me go over this again. Accent-filled regress. It is bilateral. It's usually autosomal dominant. Occasionally, it is sporadic. And the rule of thumb for most of these syndromic problems for the general public is about a 50% risk. So, if you almost always, it's going to be around 50% risk. If it's associated with some sort of syndrome. So, posterior vertebrate toxin. Do you guys remember what posterior vertebrate toxin is? Anybody? That's the name. So, everybody. Interdisplacement of the Schwalbe's line. Interdisplacement of the Schwalbe's line. So, you have to look for it at the peripheral point. Can you see it in normal patients? You can. Yeah. Can you see it in normal patients? Okay. And then the last three, F, G and H. That's a part of what syndrome? It's all lumped together now. Accent-filled recurs. But these last three, magistrate, epiplasia, epispidias, and the posterior teratrial abnormalities have to do with the recurs. Okay. But now it's just all lumped together. But I know that a reverse anomaly could be associated with pituitary abnormalities. Yeah. I mean, it's not something you think about a lot because we're kind of focused on more of the classic ones, the magistrate, epiplasia, things that are obvious in your book. All right. Moving on. Number four. Which of the following are not distinction features of Peter's anomaly? Chris, you said E. E, that's correct. So, Lecoma. Do you guys remember what Lecoma is? I don't know if you guys have seen Peter's. There's a lot of Peter's floating around. Have you seen a lot on service, Renee? Yeah. Yeah. Peter's on Pete's. Yeah. There's a large population of Peter's population here. So, Lecoma. Does everyone mention what Lecoma looks like? Oh, is it like kind of like a corneal? Yeah. Remember, Lecoma is white. It's just basically a white spot on the cornea. And what does that white spot do, too? Come on, guys. The first years. Come on. You know this. Chris. It's a malformation of the cornea. Almost. No, it is. It is. It's a malformation. But the answers are given in the question here. What happens? You're seeing what processes. What's attached to what? Not just the white spot on the cornea. It's usually a white spot on the cornea. It's just the tip of the iceberg, so to speak. What's underneath it. You'll see variations. You'll see some that are very mild. And some that are extremely severe. So it's here at a corneal adhesions, or even at the particular corneal adhesions. And what the white spot you're seeing is the loss of the endothelium that's made since some of the posterior stroma.  Remember, that's the tip of the iceberg. You have to look further. In often cases, we have to put these kids to sleep because we have to look and see exactly if they have a viscous significant cataract. These are complete abnormalities in the anterior cycle. If you have a virus that's just attacked up to the cornea, and even worse is if you've got a lens that basically is drawn up and it's attached to the cornea. So those are very complex cases. You probably want to know that before going into the cataract circle. So, good idea to put these kids to sleep, examine. Might need ultrasound. UPM may be helpful to be able to look at the entire anterior segment and see exactly where the attachments occur. So now, remember what I told you that for most of these anomalies and syndromes, what's the risk for polygoma? 50%. 50%. So F is not the right answer. The answer to this question is E, but F would be 50%. So the answers are actually E and F, right? I think, Terry, you just said E, right? So the answer to this is actually E and F, because it's about 50% risk for polygoma. Okay, number five. A parent with a one-year-old, an aerated child presents to your office asking about the long term risk of polygoma. Which statements are not true in really a polygoma? Nobody wants to go for it. So we're just going to do these one by one. So less than 50% risk of polygoma. Is that true? It's about 50%. So 50 to 75%. It's about 50%. So I'm trying to basically create some generalizations for polygoma, because you're going to see these patients clinic and the patients are going to ask you before they ask you for polygoma. So it's okay for you guys to head to say approximately 50% and the polygoma kind of takes away the better, okay? Most of these problems are about 50% risk of polygoma. D, if polygoma is not present at birth, there's no long-term risk of polygoma. Is that true? No. That's false. There is always a long-term risk of polygoma in the patients that are in the baby, and even in other types of polygoma. The most common mechanism of polygoma is maldevelopment of the ankle. Is that true? No. So what you should have is basically... Well, the iris stump rotates forward to block the ankle. Block the ankle, okay? That's one of the common things that you see. Now, I will tell you that we still consider doing ankle surgery for some of these patients. I think it just depends on what they present. And sometimes you can get away with ankle surgery, because ankle surgery is thought to be helpful if what is maldevelopment. What are you doing in ankle surgery? As an example, what we're typically doing, either in a goniotomy or trapeziolobium situation, what is it that we're cleaning? Are we cleaning the trapeziolobium canal? Are we cleaning the collector channels? In a goniotomy? Yeah. Yeah, you're going through... Yeah, you're going through... Well, I know that trapeziolobium you're cutting this lung canal, right? Aren't you going through the trapeziolobium canal and then stripping it? So, let me be a little more precise here. So, think about the normal pathway in the Achle South Pole. And we typically think of what site as the area of highest resistance for the lung. TM, Schlumpz canal, collector channels, or downstream. Where is the site of... where we think there is a motion resistance? It's the juxtapotent molecular. Which is part of the... TM. TM. So, when we're doing ankle surgery, our thought process is, there's something wrong with the mesh one. Because we're not actually cutting through Schlumpz canal. We're cutting into Schlumpz canal. But if you cut the back wall of Schlumpz canal, you're now into what structure? It's also light. It's lighter. Yeah. Okay? So, we don't make the cut so deep that we're going into splatter, creaking, spiral legs. All we're doing is we're cutting the mesh work. And that basically starts to break down the area of highest resistance in the world. Go through the mesh work, through that cut that we create, and now accesses to the Schlumpz canal into the collector channels. Does that make sense? So, in aniridase, we do do ankle surgery. And that's because there is some thought process that in some cases, depending on when you present, that the mesh work may actually be dysfunctional. So, cutting the mesh work early on may be helpful in a patient with aniridic glaucoma. But later, the stump may rotate into the mesh work. And unless you remove the stump, you'll apply an acronym to effectively treat glaucoma. Does that make sense? So, just think, PDF for glaucoma is, you've got all these weird syndromes and things to tuck away. But the surgery is quite simple in terms of what we're talking about. In terms of angles. All right. The most common mechanism of glaucoma is senitial angle closure. That's true. Based on what Chris you said, the iris stump is causing senitia rotating into the mesh work. So, that means, for that question, question five, the ones that are not true would be A and B. So, I've got a question about that. When you use that term, just for semantics, senitia, I always think of a senitia being like PAS, like from long-term closure, you have PAS kind of forming. Sure. But all PAS comes from what? What eventually is pulled into the mesh work? To the iris. Okay. Whether it's uvidic glaucoma, whether it's aniridia, and the stump is just pulling in. It's rudimentary for mature iris tissue. The inflammation causes some contractile issues and pulls the iris up into the mesh work. I keep thinking of different mechanisms here. I keep thinking that the iris stump actually closing it off versus PAS actually forming. And I thought that this meant PAS forming. So, let me back up. I will, in this question, in general, when I use the term PAS, whether the mechanism be aniridia or inflammation or neobascular glaucoma, I'm saying that the iris is the clogged mesh work. It's either being pushed in or pulled in. So, like the neobascular glaucoma, you have that abnormal membrane that's laid down early on. And that membrane has to contract off forces and it will actually pull the iris up into the mesh work. Does that make sense? So, you know, when we think about neobascular glaucoma, we have these abnormal, low blood vessels that clog the traumatic glaucoma mesh work. That's not ultimately what causes the damage, right? Because if you give them anti-bed jet, you get rid of all those growth vessels. Long term, one of these patients have terrible glaucoma. It's because of this abnormal membrane that pulls things in and then they just zip up their angle of iris. The iris just gets pulled up into the angle and zips up the entire angle and you can't see the mesh work at all. Okay? So, that's like a severe form of neobascular glaucoma. But I'm using the term as a reference to synepia, PS, those terms to be are some anomalies. So, whatever the underlying mechanism is, the iris is being drawn into it. And we're saying that C is also correct, like, not a right answer, but actually it's about the angle of iris. Yes, I'm sorry. So, A, B and C. The answer is reply or A, B and C. Now, by sitting, knowing that we talked about C, don't remember that there is some thought process early on. There can be some non-revelment in the angle and primarily, we think of synepia closure as the main mechanism. Okay? All right. Question number six. An infant with Sturge presents with congenital glaucoma. Which of the following is not correct? It is not correct. And we said C. C is not correct. So, let me, let's read the question one more time because I put some clues in there. Patient with Sturge wedge presents with congenital glaucoma. So, let's go through these. Elevated at the scolovidus pressure is the likely mechanism of glaucoma as Sturge patient presents with congenital glaucoma. Is that true? So, remember that the clue is congenital. Yeah. So, that's not true. It's not true. It's not true. Okay? So, we classically think of Sturge wedge as the elevated at the scolovidus pressure at the helpline stage, etc. But the key here is that this patient presents with congenital glaucoma. So, another generalization, very broad generalization, if you guys see a patient with congenital glaucoma no matter what the cause is, let's say it's primary congenital glaucoma, it's aniridia, it's Sturge Weber, it's Axanfel Regers, it's an anterior segment, it's Genesis. What is the underlying mechanism practically all of these congenital glaucomas? Maldevelopment in the angle. So, just Genesis. So, just tuck that away as a generalization, because I want you to be able to simplify congenital glaucoma. There's a lot of syndromes out there. If they present early on, that's why we're doing angle surgery, because we think there's just Genesis in the angle. Okay? It's a very simple generalization, but it applies just about to every case. So, A is not true. Glaucoma is more common in the nevus when this involves the upper eyelid. Is that true? That is true. Irodo trapezoidal disgenesis is the lightning mechanism in glaucoma? Yes. That is true. Glaucoma drainage device is preferred over an angle surgery. Is that true? No. Why? Because of E. There's a high risk of corral fusions and corral hemorrhage strain surgery. Okay? So, the answers, again, are A, that is not true, and D, is not true. We would still prefer to do angle surgery in the Sturge-Weberation presented with general glaucoma. Now, this question is different. Let's say I said the patient with Sturge-Weber, an eight-year-old presented with glaucoma and high pressure. This would be different. Our mechanism would be elevated episcoviness pressure. Probably, angle surgery is not likely to be helpful. Okay? It's because of elevated episcoviness pressure. So, do we currently have a way to bypass episcoviness pressure, or... I mean, if you do a goniotomy, the patient with Sturge-Weber with glaucoma six years old or eight years old, if you cut the trabecular mesh work, does that really get to the root of the problem? No. It's further downstream. Does that make sense? So, when you cut the trabecular mesh work, that's something that's more proximal to not a downstream mechanism. So, in order to get around this, you can do a bypass. So, you can do a trabeculectomy, or you can do a glaucoma drainage device. I will tell you just by personal preference, to do a glaucoma drainage in kids is very difficult. Those of you who manage one of our post-ops at the Veterans know that's a challenge already. Okay? Is managing patients, adult patients with a fist showing. Now, let alone a kid, you can imagine how difficult that is. You can't put somebody to sleep every week to manage a trap. Okay? It's just not practical. And just, their exposure to general seizure will just be horrific. Every week, having to go through E-ways, we can manipulate the web. It's just, now, well, does this happen around the world? Yes. Do they manipulate the web? No. What they're hoping to do is tie the sutures just a little bit loose. This is where kind of the arc of glaucoma comes in. But it's a risky, it's a very, it's something that has not a lot of control to it. So, you're either going to get patients that do well, or you're going to have patients with flat chambers the next day, you have to go back in and refill them. So, for me personally, I don't do trabeculectomy to these kids. It's just too difficult to manage. So, most of these kids aren't going to get a true shot of what I can do with my hospital. Okay? But this does happen around the world. Why? Primarily, it has to do with economics, and it also has to do with supply chain. Okay? Most parts of the world don't have access to oral immigration devices. They're expensive. Although, Aravind has made this a lot cheaper. They've created a mock-up of the Aravind tube. It's mainly just for adults who don't know how to use it in kids. It's essentially a device that they've gotten down just below $100 maybe. $50 or $75 for a knockoff at the very least. Okay, seven. Which of the following is true regarding a fakia after congenital cataract surgery? Okay, let's start with A. 15 to 50 percent of more development of glaucoma. Is that true? I'm going to go with true. True. Okay? Again, that 50 percent that's thrown in there. Again, this is why it's okay. I think if you just kind of tuck that away, if you see patients that are presenting glaucoma, infants, general patients, you can kind of hedge and say roughly 50 percent, but for certain cases there's a range. Okay? But this is where the 50 percent will come in. B, the patient is only at risk for developing glaucoma within the first three years after surgery. Now let me back up and say this is a fakia after congenital cataract surgery. Okay? So the patient presents the congenital cataract, you operate, you're not being faking. Is there a certain risk window? Or are they always at risk of developing glaucoma? Always at risk. Always. Okay? So this is false. It is false. Okay? This is a lifetime risk after they graduate from health and address practice. They come in with the adult practice and we follow these patients for the rest of their life. Okay? So this is false. C, the mechanism of glaucoma is related to irregular dysgenesis. Now think about this. This is a patient that had a normal presenting eye otherwise and normal pressures have just taken general cataract and removed the cataract. No. That's not true. That's not true. Okay? So usually what can happen after a fakia there's thought to be this roll between the lens, the zonules and the cellular processes. When you don't have the lens inside of the eye anymore you don't have as much stretch on the zonules and then likewise you may not have enough stretch on the spur of the spur and that may affect the overall treatment of the patient. So remember you've got two sets of muscles that are attached to the spur of the spur. You have your circumferential muscles. I'm talking about the cellular body muscles okay? And then you've got your tangential fibers, right? There is that relationship. There's an interplay of the tangential muscles. So you remember an angle recession, right? An angle recession you get a splitting of those fibers between the circular fibers and the tangential fibers. Okay? And by splitting that muscle you basically open up the cellular body. Okay? And so it's almost related in that same way but not quite. If you have a patient with traumatic glaucoma an angle recession, right? You get that splitting of the muscle fibers and there's thought to be contraction of the tracheal muscle because those cellular muscles can't maximally pull the cells, right? Okay? So it's almost although we're not splitting muscle fibers in a patient with congenital cataract there is this interplay between the lens on those cellular processes and how we work together. Okay? So next part. So C is true. D removal of all residual cortex and they produce the occurrence of glaucoma. That's true. Yes. That is true. Small portal diameter is a risk factor for development of glaucoma. That would go with true. Yes. Cataract surgery in the first year of life is a risk factor for development of glaucoma. I'm going to say yes. Yes. That's true as well. Okay. Eight. Which of the following surgical techniques is the preferred method of treatment in a one-year-old with PCG parloratogenal glaucoma and cloudy corneas? B. B. Trabeculatomy. Okay. So, Tara, do you remember the difference? Can you explain for the group what the difference between goniotomy versus a trabeculatomy? They essentially do the same thing. The approach is what you need to remember. So, with goniotomy it requires clear cornea because you're like directly viewing the ankle structure and then I think trabeculatomy it's like inter I guess you don't don't doesn't require direct viewing because it's an indirect approach. So, not quite I think both of them you're talking about a view versus a direct view or I guess a direct view versus like trabeculatomy it's like There's a special word is it at internal or at external traditional idea? At external at external okay so the way to remember this very easily so what instrument do you need that's critical to performing goniotomy during surgery it's in the name gonioscope okay so those of you that have seen using a gonioscope or goniotomy prism and surgery you're using a microscope you're tilting the patient's head away from you putting the prism on the eye and directly viewing through the microscope looking directly at the patient okay so thus if you're using something that is allowing you direct view it requires a relatively clear goni if you don't have a clear goni doing a goniotomy is very difficult now this comes this is these are things just for you to tuck away in terms of generalizations if you need a clear goniotomy or trabeculatomy you don't and that's because you're doing the surgery from the outside in you take down the conjunctiva you do your sclerodisection into Schlegz canal and then you pass either a suture or a catheter or a harms trabeculatomis another device that is really no longer used it looks like a pitchfork and basically you slide the device into the angle and then you pull it through the meshfork and clean the meshfork but you're doing that from the outside in approach so it doesn't matter if you're goniotomy they're not any from the outside remember the water as it's coming through trabeculatomis Schlegz canal the back wall of Schlegz canal if you cut that you now enter the scleron so now you can do that full dissection from the outside in take down the conch cut the scleron get into Schlegz canal pass your suture or your catheter around and then do your cleavage now this has changed because now we have newer techniques some of you guys have seen the gap procedure which allows me to do the surgery I can do a full trabeculatomy now usually for the goniotomy you're treating just the nasal area but now with the trabeculatomy at internal I can do essentially the same surgery that was previously at external and I can do it from the inside as long as I have a reasonably clear point it doesn't have to be exquisitely clear but as long as it's recently clear for me to be able to make the cut in the meshfork and then pass the suture or catheter around the whole 260 degree trabeculatomy now at internal but for your boards for your questions just remember that you need to have a clear point here for goniotomy so you're using gonioprism or gonioscope on your trabeculatomy that's done at external okay nine the parents of a six month old child with PCG wants to know how successful anal surgery will be in their child what is the 70 to 80 percent and what do you guys remember that we already talked about in the previous question what's that magic window where anal surgery seems to be a better prognosis three to twelve three to twelve one okay so if they were sent really really early one month old with congenital prognosis that's not as good of a prognosis versus someone who presents in that three to twelve month window that's kind of a magic window for prognosis success with surgery okay ten which of the following positive medications should be avoided in infants with glaucoma this was discovered by norms of risky here reported case series C C alpha adrenergy that is correct do we use myotics so maybe you guys have rotated their beads not really every well you can but you can but we don't usually so I'll tell you for myotics make the biggest difference it's a wonder drug for a fake glaucoma okay what do myotics do they constrict the pupil what are they doing they're pulling on trapezoid mesh work so it actually increases aqueous outflow right that's the idea so that's why it works so well in a fake glaucoma because remember we took out the lens in a fake glaucoma we don't have that stretch that we normally do okay and so by pharmacologically that stretch in a fake glaucoma myotics may be helpful so you'll see it in a few of our patients but be looking at now when you're in the bead service look for the a fake glaucoma patients that may be on phosphine iodide rarely use it but it is available on hybalcarpene but typically if we're going to put somebody on long term myotics we're using a phosphine iodide in case you ever have to write the prescription it's very rare but it's 0.125% I think the idea alright how about CAIs how about dimox do we use dimox for infants is that safe yes yes I mean if someone's going to be on for a while it's probably a reasonable thing to check electrolytes and their normal things that can be checkable for patients that are on long term CAIs but we use them temporarily now a common thing that you guys may get called on is that they're going to call you from Wyoming or Montana and we'll tell you this classic story of kids tearing without less than 20 years and one thing that you guys can do in conjunction with consulting myself or talking to other trees is place in the patient on dialogues before they get here to our facility or in the UAE why is that helpful so we can see we might have a chance to do angle surfing if you can clear the colony ahead of time okay so the dosage for this is 10 to 15 milligrams per kilogram per day okay so Dr. Hoffman likes to just say 12 he just says those are 12 milligrams per kilogram but the range is 10 to 15 okay so 10 to 15 milligrams per kilogram per day and then divide that tier if you have to start a pediatric child on CAI dialogues 11 you've decided to use a beta blocker in an 8 month old PCG patient cells for the colony times 2 which are the following important considerations you know start from the beginning beta blockers are contraindicated to the children younger than one year old is that true that is not true that is false we still use them B nasal lacrimal duct conclusion can be helpful is that true yes yes it's a good idea to tell your parents to do nasal lacrimal duct destruction when they're using all blocker drops particularly beta blockers because they're going to be a lot of systemic absorption 0.5 percent is a preferred concentration is that true do you guys know what the normal concentration is that we use the adults like the COSOFT or the Timalol straight 0.5 that's the normal dosage so for kids you might want to back off 0.25 percent okay so that's that comment you guys are just used to writing Timalol BID COSOFT BID you forget about percentages you're working with kids if you're going to prescribe straight Timalol in a 0.25 percent concentration so be aware of that that when we typically prescribe COSOFT let's say you want to do combined therapy it is 0.5 percent that's a COSOFT or a generic COSOFT so if you're going to be prescribing straight Timalol try to use it 0.25 percent okay D should be avoided in patients with asthma or significant chronic disease that's true okay 12 which of the following is not true regarding Joad Juvenile which of the following is not true C and E C and E that is correct so let's go through each one presents between the ages of 4 and 35 that's correct most are inherited as an autosomal dominant correct that's why family history is important and if you notice in our client next time you guys see patients with Juvenile parents too in many cases you'll see that a parent has Juvenile in the name of local women as well C the angle can appear dysgenic like in PCG is that true that's not true okay remember these kids present later in life right so their angle has been working fine and then after the age of 4 between 4 and 35 they suddenly get glaucoma you should think of that as being just a miniature version of adult local women the mesh work is becoming dysfunctional it's not dysgenic it's dysfunctional so the angle anatomy looks normal when we're operating on kids with PCG the angle looks very, very mouth-developed it looks very mature you can't see landmarks you can't see the mesh work you can't see this girl square very well all you see is a high iris root insertion and then it almost looks like it's just corn that's it so remember for Juvenile they've had time to develop their angle now their angles are going to look normal progressive myopia can continue to develop until 10 years of age it's a little tricky this is true it's not true because throughout their life they actually get myopia they can progress right because the so the answer so you're saying that it is true that they can develop progressive myopia past the age of 10 yes so D is not one of the answers for this question but that statement is true okay book balance and hops are common you see that in Joe Agnes you know these kids look normal there's really nothing wrong with them except if you can notice that they're becoming more myopic then you obviously you check the pressure look at the nerve and it really looks comfortably classic violence true or false the wall of CCT as well established should be at the bulk and it should be routine measured in all children at the bulk home it's false false there's no criteria it's not that's your clue okay not just because it's hard but even when we come into EUAs we don't check the chemistry inside the award last question the normal corneal diameter of a full term full term newborn is switching the following it's a question say the range B B 10 is normal so what about the age of 1 what should you expect the normal corneal diameter between 11 and 12 11 and 12 okay alright some things about EUAs just look quickly and then we run out of time in general when we're doing EUAs we try to check the IOP as soon as we can because general anesthesia can do what to do to the IOP it can lower it so we try to not always I mean the book tells you to try to do it immediately after activation or after reduction try to get the pressure but that doesn't always happen okay what's the normal pressure for a newborn you guys are going to be called to a service and someone's going to tell you this patient has an eye problem you'll be checking the pressure assuming you've gotten a good examination without any squeezing what should be kind of the normal pressure range for a newborn low teens low teens okay and then over their time usually about middle childhood the pressure will kind of go into that normal range that we talked about 10 to 22 newborns should have teens in the low pressure one question I forgot to ask neurofibromatosis you guys remember there's two types of neurofibromatosis there's only one of them that's associated with glaucoma do you know which one an F1 an F1 and an F1 is on which chromosome 17 17 do you know how do you remember that that's why 17 letters 17 letters in the bottom right of the house thanks one more thing about anoremia because this always comes up you guys remember most of the cases are autosomal dominant one third are sporadic this is where you can make a life or death diagnosis what is associated with sporadic with two realms tumor okay it's important to get those patients screened and the sporadic a sporadic form of anoremia they need to get my I don't know what the protocol that usually is like renalgia sounds in the end checking for a room tumor okay alright any question can you run out of time is that helpful that's great thank you Justin hopefully some broad generalizations as you're rotating on service I'll tuck away don't forget the 50% rule don't forget that when kids percent young it's because of irregular disgenesis of any cause at your second disgenesis surge webber PCG the mesh work is dysfunctional and forget the anoremia that you need for goniatomy because you've used the gonioprism you've got to look directly through can't do a gonioprism here thank you