So 55 people have answered and still 30 seconds odd are remaining. Please think about it The image of an image 1 by x 1 by x is x. So that's the hint Which I have to give Almost 10 second prior to the completion of time. I don't know now. I might see sir Did you check the new rules for travel? I have seen mungara I'll move What is this guys? Lane mirrors are at right angle surely they will make three images, okay? sure Now the problem is beta in how many of the images will he see using his right hand. He's actually Using it right hand. He should see the actual image. So the image of an image will make it correct, right? so So only one that is B Yeah, I got it Explain I did not understand very good. Aditya very good. Very good. Very good. Very good. Very good. Very good. Very good Very good. Very good. Relax. See by There are plane mirrors, right? Where is the cursor down the cursor also was not visible in minutes, right There is an object by this object will see one image here This objects will see one image here if he's using right hand it will appear left hand here left hand here y or n Okay Now the third image was being which is being formed is the image by this Left will become right here left will become right here So here in this image only he will be able to witness that he is using right here got it Aditya every year very very Relax, no Very good. Very good. Relax. Chuck Leaderboard first 16 people have answered it correct. So yes, there is a shuffle and time to be checked Yeah, actually the black appears better, right? But I was not getting like I what I like is like the PPT screen should be Marged into the right. So I'll just try to create a PNG come and welcome to the top ranks. Mahabal is also here Aditya is also here the hustler. Please change your name there else. I will just cut it off. Okay so One two and here we go to the next question Relax and respond it won't take more than five seconds. But yes in order to just think So odd again 30 seconds remaining and almost everyone has responded So just telling you that normal means 90 degree and The angle is measured with respect to normal coming normal and with respect to normal will give it a zero degree. I Have told you the answer on this. I Guess I'll never discuss Good 42 people 17 people four people and one person dear friend a Ray of light is inclined normally on a plane mirror. What do you mean by this word? This word is this is a plane mirror. You are incidenting like this Normal is also here. So you are your angle of incidence is equal to zero so angle of reflection will also be Okay so only person in the world to have a Super computer that mall functions so bad ignore Look at the leaderboard because 42 people have answered this correct So there's gonna be a good shuffle probability and yes here it is Sharon coming to the top ranks very good Sharon dear friend. Mahabal is also there and Purva Nandini Naomi is also here ishani smriti alisha Naina Am I? Having a problem or they are all girls poor up Mahabal good. Oh That's what you call a beautiful stuff on screen. Yo Let's see whether it gets more beautiful or or solar sucho Makes an angle of 30 degree with the horizontal droid properly. You should get the answer Now I guess here people shouldn't have taken some time Also, they might be confused. So there is a good probability of getting a flip of answers Flip I don't think so that all options will be having a good majority selections two options will be having majority of the selections That's what is a beauty You belong to our enough That's beautiful to look at that almost everyone has voted very good. Oh Beautifully, yeah, my perception was wrong. You guys are beautiful. See our clarification required quickly over the chart Very good are in very good. Very good. Very good. Very good. Very good. Very good. Very good Chalo surface mirror 30 degree why aren't yeah Now incident okay, if a vertical ray strikes the mirror Find the angle between the mirror and reflected ray if a vertical ray strikes them Okay Show this is 30. This is going to be 60s. That means angle of incident Is that okay? Got it. No doubt Again again again. Okay. Okay. Okay. Okay. Okay. Okay. Relax. I'll repeat repeat repeat repeat repeat repeat repeat relax Why am I doing this? 30 degree. Okay, 90 degree 30 degree. So this is 60 good this whole is 90 right This is 60. This is 30 angle of incidence is equals to angle of reflection. This is 30 Yeah, yeah, yeah, so the reflected ray will make an angle of 60 degree with the mirror Got it Disha Disha Disha everyone everyone everyone especially those who don't get it just Very good. You guys are beautiful Look into the leaderboard again a good shuffle probability Sharon leading the show again. Very good. Aditi Isha ni Mahabal poorav alisha Ateera Naina Aniket Nungara walking in very good and someone also Someone is my new friend from Indra Nagar. Hi there all good. I'm expecting some response Like Yeah, okay, we are very one two and here we go with the next question and Sharon very good You are consistently responding the process. That's very very beautiful to look at some people are like boom Now the speed of response is the decrease rather speed of responses Yes Motivation clear kuch toh achha chalrela gawa good good good good good good The cheating facilities are available at your end also, so you might use them But it's better if you have to be time efficient Apply your brain and times up not full strength, right full strength has not Responded who 22 people got it correct 26 people mark the other way Let's see because clarification might be required Bacha It's 325 So the hands will be our hand And minute yes or no When seen the reflected way the minute hand will come here the our hand will come here Below 9 but above 8 yes or no and 25 35 is the right time again Okay, I'm a very good very good very good very good No, I don't want I am totally not in a mood because I am not talking the NTSUL and stuff. I am talking around reflection. That's why okay So sure sure sure sure hmm Okay Explanation required er for other like if you need the explanation again very good very good very good look Let us see This is the clock for us So 325 looks like this 325 the mirror of the image of H will come here The image of M will come here shop Five minutes before and five minutes after 35 25 here and here Eight eight thirty five is the answer. Okay No problem, Surya No problem because it is midway Na na na na na na na So but you got the real story now, Vishal I am not at all understanding what is the case happening, but I guess with what I explain You got it GI got it those who are in doubt only not everyone still in doubt So the question again, okay, Nanya here, okay Very very good. You guys are doing good Shalom, let's see the lead about fun responding to this fastest marble Taman Sharon is Good competing very good Meghna Aditi Neha Anirotsai hideous Neha Ganesh and Aditi Bajaj very good very good very good. And here we go to the next question Read the options you will get Easier you will feel it easier Think it's about a plane mirror if there would have been any such facility available We might not have required the other variants of mirrors I have given the answer 65 people have answered and still not all wow What was option Bravo if the rays incinerated on the mirror at our converging beta it's plane mirror plane mirror No such scope available Okay, so So can you draw diagram for converging rays, why will I draw diagram for converging rays? Think think think think think not required Exactly the word which is the crack is plane mirror no such case possible Plane mirror in inverted comma Shardini very good try try try why we learn objects and converging ways Why will they be sent? simple got it Good Sneha Anirots who was the fastest enemy mungara was the fastest one very good mungara very good very good very good Next I'd never wanted to give that much time to this, but yes, there is a scope to read it Which is actually available While you are You have given that reading time of five seconds.  So virtual is there erect is not there Smaller is not there only virtual was going to be the one very good very good very good 11 6 1 I don't think so er explanation required and we are no explanation requires Very good very good very good very good very good very good six question is done Let's see the leaderboard and this is the last simple quiz out of this chapter Okay, someone was the fastest one to respond and he gave gupta is also the fastest one to this point very good Very good. Very good. Very good. Let's proceed to the next question So might need a total of a time Why are eight nine people 11 ten people have already responded very good Total of a pillow, but I will help please While calculating I had made a mistake. Don't make that mistake Manabee first time japa time. I got like I freshly do all these questions I'm not key. I'm gonna talk to whenever it is a mistake. It's a mistake of my own again it will not be a mistake of book or something 58 people responded yeah 60 people responded by now last five four three two and one good that's surprising so for sure explanation required relax relax relax for sure explanation is required relax relax look at the beauty of the thingy concave mirror experiment and object is placed at a distance x1 from the focus the total u is f plus x1 total v is f plus x2 yes or no no doubt no doubt no doubt by simple reciprocal arrangement by simple a racey profile arrangement you know that f is equal to u v by u plus v will you please substitute the value and calculate relax I am not solving now will you please substitute the value and calculate injustice Gupta ingested we need time I hear here I am not I'm not I'm not I was just wanting to read the chat so I flip the page here it is because I read RN singles line keep can't it be like yes or no can't it be like that it will be that side like the minus side and all that beta the signs are included in here if you remember I told you a line you will never add like put sign for variables you will always put sign for numbers okay chalo should I should I solve one second but sir if the but sir if the image is formed on the other side of mirror won't it be won't no beta because see again it can form for whatever arrangement it can form okay understand this I'll explain it don't worry relax see this is a concave mirror this is the focal point beta only two possible cases and if the object is beyond f the image is also beyond f only but if the object is this side of f the image is also this side of f only so this sign of x1 and x2 will remain same okay got it good good good good good so what is the answer did you guys got square root x1 x2 or should I solution required SR solution not required SNR only those who require should send only those who require should send Marvel is sending I will solve it there sorry boy so next question I get a you f plus x1 into v f plus x2 upon v plus you to f plus x1 plus x2 equal to f very clear it is showing that f square will cancel out of 2f square which will remain x1 into x2 is equal to f square y orn y orn y orn y orn y orn sir some one second some ninth grader did something in the mentee platform and got all answers at least with me you can't do that I have a issue with it with someone you might be with me you can't okay I have to first check it a mentee hacking and let's do one might be I he told me as a relax but of my great principle is I cannot expect it like it is totally unexpected and I'll not even be surprised I'll I'll not take it as a surprise I know you guys will not do it I know it I even I disbelieved that case no this is impossible any student to which we know who we know cannot do it I really don't know any of people like you who can fall into all those believe it and I really don't want to breach into my belief okay yep here's the slide again okay good again a shuffle good Sneha leading the show Mahabal jumping a bit up good Ducks Luxe Aniket Anirudh Naomi very good Ganesh was the fastest one to respond shares and Sharduli next question so it's another 20 minutes and we are with five more questions after this like 13 questions are there so please respond to keep them carefully read them you will get the answer is used to form the image of an object okay then which of the following statement is wrong it's right it's like no brain thingy but just yeah you should know photo about about the convex mirror and photo both is there about convex mirror right there is nothing big about convex 65 people 66 people is everyone has voted okay and yes everyone is almost everyone is correct beta explanation required convex mirror cannot be related with real right or not convex mirror and real don't go hand-in-hand okay what is full full is the no not at all center of mirror beta all is the point of intersection of principal axis and mirror and principal axis does not mandatory is being at the center okay yeah good good good good good good good good leaderboard good Gupta being the fastest one Mohammeda being the fastest one Sneha maintaining her position over the show very good very good very good let's move on to the next question the very first line is the answer the very first line is the answer but reading at the second line I can think that the first line is not enough second line is required if that changes not happen there is a possible next answer as well and now expect the second case in your next item are okay I'm gonna put that like that it when he moves the mirror away from his space the image remain virtual what type of mirror he's using not everyone has responded huh okay two selections only guys as turned inverted it should be a concave if it will remain virtual and red it should be a convex okay gee I got it good leaderboard who was the fastest one and the kid Gupta was the fastest one very good very good very good very good very good Sneha still maintaining her good position huh good good good good good good a virtual image larger than the object can be obtained only by one case you the only reason why I haven't kept one upon F is equal to one upon V plus one upon U type numericals is our CHK batch okay which I was not able to complete nicely with them about one upon F is equal to one upon V plus one upon U so by next week I'll be able to and then I hit up okay 30 second remaining 60 people already responded 66 to go that means six more people to respond they are please read if you still exist over here okay because I don't think so it will need for us to be extra knowledge beyond knowing the chapter reflection and reflection by life oh that's surprising how come no please guys a person sees his virtual image by holding a mirror a virtual image larger than the object can be obtained by better convex lens for that then to have been a issue okay concave yeah anyway before moving on explanation required anyone Nandini is like lit up we are not even discussing about lenses high how and why will I look at lenses good Nandini so here is the show Sneha still leading the game with a minor oh wow Sneha Gupta Laksh was the fastest one Momita is consecutively the fastest spotter Naomi is holding a good position at the central part very good Naomi and here we go to the next question again read it you will be like Boop I wanted to change and shuffle the options because quite early to reach there right that's the biggest hint I should have kept it somewhere so that whole are tracking the option should have been difficult but no problem no problem no problem 41 people are saying okay what happened to 15 people so the first thing but a 40 20 double center of curvature right concave mirrors it will be real inverted and of same size explanation required ER only those who want to send ER please no I don't want any R explanation required Meghana very good very good but a same size an object is placed at 40 centimeter from a focal length of 20 a focal length is 20 distance 40 will be center of curvature when an object is placed at C it will make an image at C real and inverted and in same size okay no problem let's look at the leaderboard Sneha maintaining her beautiful position I need a Gupta Laksh Krithi was the fastest one to respond and here we go to the next question read it relax and respond everyone has voted very good very good very good very good very good so 60 people remaining and it's like 899 34 why will it happen all of the following statement are correct except one convex mirror real and inverted unreliable okay first statement the magnification produced by a convex mirror is always less than one the images produced by a convex mirror are always smaller than the object now very very very good leaderboard was they have excellent Sneha Gupta and Laksh are having a tight tussle yeah they are still maintaining a bandwidth of 500 marks moment are consecutively responding fastest and you know the also is elevating and better this is the last question okay so I should have kept two more I guess because we will be finishing a bit earlier for this but it's okay to compensate because at times you have finished quite late as well right good good good good good good good good good good good good good again 48 people beautiful people okay let's see the question first if an object 10 centimeter in front of a concave mirror or focal length 20 my focal length is 20 object is 10 so surely the image is going to be virtual erect but enlarged so enlarge upright virtual okay GI little okay Surya I will not be able to surely do it but please better now I'll have to recreate a PPT and all that so we will I'll just do it once in my next episode a riddle riddle Surya was going to ask me a riddle Surya you can unmute and ask as well the last to last year was like that last to last time for what our episode yeah the conclusion for electricity right what do you think is the most failed experiment of all time like this is a puzzle or can you give me options and all that like like no give me a domain to answer nah it's a riddle okay most failed experiment of all time making roads in India Nandini beautiful but at least the roads I travel are beautiful beautiful beautiful roads now now the situations have changed better local roads are like still struggling in India but highways national highways international highways are beautiful okay Surya please answer please answer please answer before people log in I have to ask yeah that's what like if you'll tell me the the first fail experiment is is is is it quickly da Surya please answer da yaar bhai please go jaan hai bus ho gaya randho aise main mob lynching ho jaati pata Surya ok ok ok tight ok ok ok ok ok ok ok ok so much of competition but I guess Nihar won the show wow clap for this beautiful bacha very good very good very good very good very good very good excellent excellent excellent excellent excellent before you guys go I have to ask some degree learning experience one to five please learning experience one to five I know it will be a downgraded thingy quickly ten very good thank you thank you thank you learning very good very good very good very good very good very good you know for easy calculations you can use square root ten as pie just enlightening for easy calculations at times square root ten is pi or pi square is ten yep okay guys bye bye bye bye nice time take care bye


The mission of our ship is that we embark and land marine elements whatever way possible. This is well-deck control. This is pretty much where they control all amphibious operations. We could weigh our ship down in the aft end and flood out this area that we call the well-deck. And we can actually launch and recover LCACs and LCUs and several different amphibious types of vehicles. You can also manipulate how they turn on. You can launch it this way and you can also launch it backwards. For when LCACs and all the AAVs when they come on the ship or when they launch out from the ship. Then you can also switch to from 100% of power voltage going through the lights. You can switch to 25%, 50%, 75%, 100%. A big difference between this mod and the original was originally they had these big incandescent bulbs out there. So you have all these lights that are required for the mission that are super hot. You have the LCACs coming in and all of a sudden the water sprays up and hits the bulbs, instantly shatter. You just lost one, ten, however many lights decide to shatter at that point. Back in the day we actually used to have to man up down here and run out there and hurry up and cover the thing. Because we don't water getting inside of the actual fixture at that point. And then we'd have to hurry up and change out the bulb. I guess this is a clear example of how LEDs make things easier for us is that we don't have to do that anymore. And this part is, how do we use this?


So the main thing I want to talk about is why do we need inherited retina disease specialists? Okay, and why so why am I why was I when I was recruited here 24 years ago that that was one of the main things So that was brought on so why do we need it Chris you're in the service now, so why? well one reason is because there's you know Implications for future generations Definitely planning another reason so why doesn't an academic center where we're supposed to be a top-10 center Why why would you every top-10 center have? Someone should have someone They're relatively rare or many of them are quite rare. So it's general ophthalmologist Practitioner didn't necessarily know much about them. We know how diagnosed them So it's helpful to have a referral center where you're for everything. That's odd Yes, you have to have someone who is somewhat knowledgeable any more reasons. There's actually quite a few another reason is that One you know a lot of people going into say comprehensive ophthalmologist Ophthalmology, I mean they're doing that to see patients to do surgery generate all that and these patients Don't generate that so you need you know They want to have a referral center that they can send someone there and so to talk about to talk with the patients these patients Take as Chris will tell you sit on the service take a lot of time They have a lot of social issues. They have a lot. They need counseling. They'll bring in the whole family They've been bounced around from specialists to special or from ophthalmologists ophthalmologists through all this process and so they They need someone who will actually talk to me and that Can mean and it's really it's a little bit more counseling. It's a little bit more oncology Psychiatry a lot of different things now There's a lot of science and ophthalmology going on too, but you have to have someone who's willing to do that and to kind of And to and to work with these patients and so there's for retina does for inherited retina disease specialist There's several different models. There's some if you go to some centers, and we don't have this that's all they do You know, they see they see patient after patient with this they run the ERG service They run the genetic service. They run everything you have to have a that's pretty specialized There are some centers that do that but not but you have to have a lot of patients coming through and it's also Kind of hard for the retina specialist for an inherited retina disease specialist because you're gonna see how many you're gonna see six eight patients in a half day, maybe six, you know, they they don't see a lot of patients and These are you're you're giving a lot of bad news in general. So you don't want to do that all too much You can also have models like mine where I do retina I know a fair amount about red inherited retina disease, but it's not my only practice. And so And I've learned through the years That you have to control your practice with that And so when you come on to the retina service, you'll see I have if if they actually followed my schedule I have one in one new inherited retina disease spot per half clinic Basically and because unlike, you know a quick new retina patient you can see in five or ten minutes I really need a half hour or so of my it'll end up eating up a half hour of my time They're here for a huge number of testing which we'll talk about a huge amount of testing coming through and It blocks up the clinic if you if you get three inherited retina new inherited retina disease patients in a row It's just going to destroy the flow of your clinic And it's so I try to do that now They're always sneaking in patients so that either they're misdiagnosed or there's something There's some there's always some excuse why you end up with two or three in my clinic And it's just and you just have to deal with that the And the so and then the other thing that I kind of insisted through all this We'll talk about it a little bit more is that I needed help just in seeing the patients and follow up and by having someone By having a genetic counselor, you know, it was And she's really a good resource if you have any projects that you want to do she really knows her stuff She's got a good database for all these patients But I needed someone who I can say why when I talk to the patients and say you need genetic testing We are going to do the new tests here I needed someone who can actually get proper consent can kind of go through in detail answer their questions And then even more importantly do the follow-up because you order these tests you draw the blood and they may the results may not come back Now I will they'll come back within two or three months It'll take a little you know, but they're not going to come back right away But someone has to track all these if you talk about 10 15 years ago. I'd ordered genetic testing and say well especially with hygiene Sometimes they've never ever come back the results when you know, they just or they come back three years later And you'd have to do follow-up and so that that didn't work on that. So having a genetic counselor is very important the the other things to have a for retina disease specialist is they these patients aren't very interesting in the biochemistry and the Pathology that you'll see and that we'll talk about today is very interesting and through the the last couple decades We've really learned a lot about the basic biochemistry. We can start to think about interventions We can genetic testing has changed dramatically from as I said before no genetic testing genetic testing in a couple to research-based genetic testing To genetic testing whenever it comes back Yes, we'll get something back and there's a more than 50% likelihood We'll know exactly what's going on and then you have to of course discuss why we're doing this and then finally The with clinical trials. We do have clinical trials there I'll talk a little bit about what is coming up for some of these diseases. The problem is as Is that there are too many genes too many genes? There's too many targets now for what we're doing. Okay, so does that make sense in terms of why and then of course You have to learn some of this stuff for the boards and you'll just you'll see I'll flash some pictures of course in your in your Your books you just have to learn there's some things I'll highlight a few diseases that do show up on the boards and some that never will and It doesn't always correlate with what you'll ever see I'm going to talk about diseases that I have never seen in my life You know these patients have never shown up, but they're so characteristic and they were described so many decades ago That they are that they're expected that you know them, okay? so The retinal dystrophy is that I see coming through my clinic Very you know are quite wrong quite wide through all this So you've got the classic one is going to be retinitis, which is shown here as a kind of classic slide here You're going to see syndromic patients in my clinic not not an enormous amount But you'll see some and that and these syndromic ones basically mean that there's that the mutations that are causing these problems Not only affect the eye, but cause other problems elsewhere in the body and of course with With one of the reasons why why there's so much genetics known about this is that There are syndromic cases, but I'd say the vast majority of the kid of the case through to see are isolated to the eye So these are healthy people that have lived long enough to have kids and keep passing these genes through various generations So you still see them we can study them in exquisite detail because usually They're there for there's something unique about these genetic defects that are targeting the eye And we need to understand why and we can try to figure these out and treat them and if you can if we can Get things under control in these patients, and I'd say it's still very rare Then you know they can have otherwise good lives So you have to this is something that's a good target to try to to try to improve their lives and then As I think Nico has presented in one or in a previous Grand Rounds Some of these are stationary retinopathies. And so what stationary means they look bad. They have some visual defects, but They aren't going to get worse. That's the problem with the most of the patients that we see with inherent especially inherited retinopathies These are not going to get better. They're going to get worse and you're trying to counsel them But there are some that truly will never get worse And I've caught several patients over the last last few years young kids you know teenagers that have been identified as having inherited retina diseases and thought that and misdiagnosed as retinitis pigmentosa and they're learning Braille they're doing cane training They're going through all this stuff and told them that they can't do things and then they turn out to have a stationary retinopathy That's not going to get worse. I can definitively tell them that genetically and say Just get on with your life.  They're old and burnt out inflammatory diseases or other things so But when you see in my in my clinic you're going to see patients always coming through with retinitis pigmentosa and the The estimated prevalence is really pretty good at one in one in three thousand So if you think about there's 300 million people in the United States, there's a hundred thousand people with this disease Now that makes this an orphan disease and why is it an orphan disease? Well, do you know the definition of what an orphan disease is? Think I think I'd still know it think it means that there are two hundred thousand people or less in the United States with the disease And that that's an important thing because an important designation Because for the FDA and drug companies, there's a lot of incentives for to develop diseases for orphan diseases they get fast-tracked they get all sorts of monetary incentives of their first to market and probably and I and retinitis pigmentosa was probably very Vocal community, and I think they were part of the part of getting this established in the federal government to do it this way And that's probably where the number two hundred thousand came from because if they put it a hundred thousand people would be arguing Well as RP an orphan disease or not, but if you set the number of two hundred thousand and retinitis pigmentosa is It fits into the category now With RP as we'll learn is it's it's very common It starts out patients when they're younger and classic RP have pretty good vision You know when they're in teenage years and they're young adult years, but as time goes on and the vision constricts Eventually they will go legal blindness and become you know become have big problems But that's very compatible with that time course of classic RP That you can be very successful in industry You know be a captain of industry be make a lot of money and then eventually you run into big problems And so when I deal with people at the when I talk with people at the retinitis pigmentosa foundation some of them surprising number of more billionaires you know that have had That have made it through you know done very well in business and now are going totally blind and they they have You know through the years if they're billionaires they've learned that in business money solves everything In medical research it doesn't solve everything of course, but they so they're an interesting kind of cohort to deal with They have a lot of very high expectations Often over expectations than me But they are on the other hand willing to fund a lot of research for this the there's a large variety of inheritances the clinical course and genetic causes are diverse we'll call it to cover that in the next slides and Unfortunately, there's only limited Clinical interventions, so the next slide I won't put up yet, but what is someone with RP? What are the classic symptoms that they're going to have and what are what are the chief complaints the patients are going to come in with? One night vision or night vision is almost always the first thing though if you take the history They say when I was a kid. I didn't see as well as it as anyone else. So that's correct anything. What next? It's more advanced you're going to get like decreased visual acuity as well with some peripheral field changes So you get like the ring skatoma, right? So even so the acuity is often late in classic RP That stays pretty good. They can still read, but yes They will start noticing constriction of their visual field They have like CME right so CME and that's important. We'll see that in the next slide that CME is important because that's potentially Okay, so that's that's correct and You know eventually if they have it long enough, they'll have no light perception other problems the So those are are truly those are the main things that you're going to see progressive visual field loss Exactly what we said right here. That's going to be the main things that they that they talk about and the They may have a family history so they may know about it. They may not they may be able to do You know function pretty well Some people can be and the onset I didn't hear age and that's you know, there's classic ages But there's a huge diversity in in RP. There's something you know, well There's some where the kids are debilitated in there You know when they're five years old, but I I diagnosed RP You know not infrequently in patients were 70 80 years old or who are doing Functioning pretty well. I've got gotten again high very high level jobs But are now starting the visual the visual field starting to constrict in and they're starting to have problems So one of the ones that probably the more one of the more disturbing ones that I diagnosed was someone who came in Who was a commercial airline pilot? Okay, and so he Made it through and you'll see this even at the VA here. How did these patients get in to be become soldiers? eyes and With the commercial airline pilot. What do you think his chief complaint was when he came in? Yeah, but in doing what function do you need a lot of peripheral vision to fly a plane? Right even that didn't bother him so much But yeah for when you fly a plane you're looking straight ahead. You got the gauges. They're all really bright They're all close to you and you don't even look to the right or the left You're looking straight ahead. You got all this so his hardest thing to do was walking through the airport terminal Okay, when you go through the airport terminal people are coming in darting in front of you from the right and left crossing there And he was bumping into people while trying to get to the plane That did not inspire a lot of fun And his field was bad enough that I said you can't you know There is no way that your employer will be happy about you're flying so But he made it a long time. He was in his fifties by this time I was surprising. He didn't seem to have any problems flying a plane at night either Anyway Yeah, a lot of it a lot of it's automated, but I think he learned anyway Okay, so that's those are the symptoms now. What are the signs? What are you when you look in on these patients and occasionally they have no symptoms at all, right? So what do you see that's going to tell you I think this is RP. What are the classic signs? Okay bone specules are classic. Yes, what else? Raterial attenuation and optic nerve like a waxy pallor. Those are all the classic descriptions. Yes Sometimes there's vitreous cells just debris that's floating around in the eye What about an anterior segment anything that you might that is common not gonna be diagnostic Rare where I see You see cataracts are common and we don't know why they get that but they do get cataracts anything else We already mentioned CME So I think we got most of them. We'll see bone specules peripheral retinal atrophy just in general You have waxy pallor of the optic nerve attenuated vessels vitreous cells both psc. So you got most of them there right there and then the macula is relatively preserved So that's but this is again classic and you're gonna see but not all these patients present classically and they're gonna be all sorts of exceptions and then you've got the patients so they've been referred in from the outside and What diagnostic tests are you gonna do and this is where again? I run my clinic and Chris will know all this I've got kind of a standard protocol at the patient if they come in an inherited retina disease spot They have a bunch of testing before I've even seen them and that's another reason I don't want to have too many patients because this is Almost as bad as neuro. It's a couple hours of testing They have to go through before they even see me So if they and so I don't want to have too many they got that's my my inherited retina disease New patient slot is always early. So what do you what are they gonna have done? They'll always have an OCT why are you getting the OCT well, they may have seen me we want to know that To you can actually see some of the atrophy and we'll talk and what else so OCT everyone gets an OCT ERG they'll be scheduled for that I like getting an ERG just it's diagnostic it can't it unfortunately goes bad early in the disease So it isn't always good for following them, but I like to have patients that if they're Truly coming in with RP or similar conditions You want to be you want to do at least a baseline ERG if you can get them to do it. So that's they'll be scheduled for an ERG That's correct. What else? Visual field is very important. What kind of visual field do I order? Goldmine, yeah, they because the standard Visual fields that you see in glaucoma are only going out 30 degrees We need to I need to know the whole field going out way out. So visual fields are very important Auto fluorescence, let me just step back with the visual field So the goldmine we do have automated octopus visual fields that are wide field to the octopus 900 The problem with that is it takes forever to do and the techs hate it the patients hate it It's actually probably faster to do a goldmine manually to do it. The other reason that I do a goldmine Is it's required for driving and especially when you get teenagers or even adults They have to get re-certified for their driving and if they don't have it done Then and they and they need to have it done binocularly at least with the three four e That's what I need to know for driving. And so I really am very insistent and they still Disregard me. I'd say one percent of the time and don't give me a binocular and I send it back the other thing that Just in personally the way that I do visual fields is There's so much worry about flow in my clinic to get these patients through That I don't care if they're dilated or not I know you're taught do visual fields when they're undilated but for my clinic and for following these patients I don't really care and I try to emphasize that just to get a visual field in and get it done I'm willing to to say when they say when they're backed up because otherwise they'll wait and sit there undilated for two Hours waiting for the goldmine field and I'd rather have some other tests done The the autofluorescence the color photo is all the other things so Autofluorescence yes, and that has to do somewhat a little bit more research than clinical than clinical management But it is it can't be a way to follow the disease So the autofluorescence is true I'll get a flio just because we can do that and we're following following them I'll get a macular pigment just because again. It's a research Tool, but and it can be useful for future studies that I'm doing It also gives you some idea of the of the health of the retina because Especially in classic RP the macular pigment is actually preserved pretty well Okay, so what else any other tests that you want? Like that's most of it Okay, and that's so they're gonna have all this battery of what I call non-invasive testing coming through They will and then when they by technicians should be at least getting the clinical history How long they had this what is the family history is very important? They need to have a dilated retina examination and Photography and they also are going to get color vision is very tends to get forgotten in my clinic But it's important to have the electroretnography I often save until after I've seen them just because it takes so much time to Get that arranged OCT and then in the end my my genetic counselor will meet with them Or if she's not available, we at least draw the blood and say that they will they will be coming through So that's that's enough to keep them to keep a patient busy through an entire half-day clinic that's that's plenty right there and Of all these things that we do I think the visual field testing is the most important for following patients and so this See if I can do this right Yeah, so you can see this is this graph is just showing how a Visual field can progress from 20 years to 50 years you know to just a tiny visual field But potentially this patient at least at 40 or 50 was could have been potentially 2020 still here and still able to read but not able to function with that without the visual field and then with that visual field in terms of mobility and then of course They'll get a an electroryptogram and Don Creel is much more of an expert than I than I would ever be but you know We're looking at Unfortunately with RP. They'll have just a flat flat scotopic ERG the cone flicker will be attenuated and Delayed in various other things and you can distinguish it between cone dystrophies Stationary night blindness is of course very important to distinguish because that is stationary and all that so but I get we get that and then Then we work on the genetics and the genetics of RP comes in all different flavors. That's the that's the challenge with this disease So you've got dominant or excessive excellent mitochondrial everything has been described and so I I don't have time to draw a whole genetic tree like this my genetic count Emily will and we'll give some You know and so you can figure out this one clearly is these are examples of dominant disease here and so Dominant is fairly common 20-30% of patients will come in with autosomal dominant disease and It's it's important to know that dominant is one of the more mild forms of RP and so usually They then that can make some of the the genetics a little bit challenging because occasionally You know, it's dominant someone is an obligate person should have the because they have children with the disease They have parents and siblings with the disease and they say I do just fine And that's sometimes because they truly are fine But usually they just have such mild disease that they've adapted and don't seem to have any problems so it's later onset milder variable penetrance and Commonly the and the reason why this is important is the first gene for RP was radopsin, you know found in the 1990s And so and that makes sense. It's it's a unique photoreceptor specific protein It's dominant in some way. It's not clear why it should be dominant But the reason why it's dominant is often some of these compounds are some of these mutations cause misfolding of the protein and with misfolding they then They then start accumulating abnormally in the cell and eventually the cell dies So that's that's the one that we see the most we got very excited when this first happened that we're going to figure out You know that ever that this was going to be the major gene and we can treat this the problem is It's only it's one of only many many different genes And we know that dominant can also be RDS peripheral and we see that quite a bit Which is another structural protein in the cell and the important thing about RDS peripheral is that it can look like anything It can look like classic RP. It can look like macular dystrophies. It can look like pattern dystrophies So it's a little more complicated, but it's reasonably common And then a number of them are ciliopathies that have to do with the cilium structure of the photoreceptors They can be RNA splicing factors, which doesn't is not totally obvious Why RNA splicing factors which are found in every cell in the body But if you have a defect in this only the eyes affected and basically it says that there's no backups in the eye the photoreceptor is such a specialized Specialized cell that it doesn't have backups that a norm that a regular cell would have that can take the place of the defective protein And as I mentioned, there's a lot of protein misfolding in misdirection Recessive is the next one. It's I would consider it relatively uncommon here in Utah at least And that's because we don't have a lot of despite our reputation We still are not a consanguine as population here in Utah with the Mormon population. They're diverse enough and But in cultures where where they are where first cousins are marrying a lot or when I was in South India last year Where a very desirable marriage to keep the money within the family was to have a niece marry her maternal uncle was it's just way too close and you get a lot of you know, a lot of Unusual rare autosomal recessive diseases and they are often severe early onset and The ones in the consanguine as population are going to be primarily You know are going to be homozygous mutations what I see here in Utah on these recessive diseases They're compound heterozygous, so they have mutations in the same gene, but different mutations. So the parents are not related One of the more common ones that we see is labors congenital amaurosis, but you're going to see that in the pediatric clinic They are severe early onset and many of these are going to be mutations that are Enzymatic somewhere in the visual cycle and the classic one for labors congenital amaurosis is rp65 and why is that important? Yeah, we have a treatment, you know it is the problem is and you can see if they picked a disease that's just plain too rare I Have I do genetic testing on all my patients I have exactly two patients with rp65 mutations and both of them are in their fifties Now it totally burned out. So they they would not benefit from the million dollars of gene therapy So you want to catch them when they're very young But in our population is there's just not enough here. And so even though they're charging $420,000 and I the company's never going to make its investment back Even at that price because they just picked something that's that's too rare But and it may be diagenic, but you know these patients Are severe the patient the two patients. I have saved rp65 mutations One I saw recently and he is literally the first patient I saw when I started practice here 24 years ago and He you know he was 20 years old then you know could read a little bit then Got himself into law school became a lawyer It's still practicing as a lawyer with with essentially light perception vision So he's intelligent functioning as best can the other one is an Iraqi refugee who's Consent, you know definitely from a consang with his family and had you know was just too far along But she had but had several siblings that were affected Then you're going to have x-linked rp.  This can be severe And they but it or they can be laid on set You know there's a lot of different ones the one that's shown here if you see this on the boards What's the answer for what this is? That's coroed oremia you need to the reason you see this as you can see that the court doesn't look like classic rp Does it right? You just you can see the coroidal vessels. They're severe atrophy And they'll have kind of clumped pigmentation round clumps of pigment rather than bone spicules So it's a little it looks different They can also be due to rp gr And that's more that gives you a more classic rp. These are important one because they're fairly common To because they are x-linked they often come in with a whole family history It's known and so the family knows not only do you know if you diagnose someone with this disease But they know they know that their uncle or whoever you know They know what the natural history is in the family and they're worried that they're going to get You know that at that age 50 they're going to be Severely blind too And the other thing that's important is this is the next the next frontier of gene therapy A lot of them we are part of the natural history studies for both coroed oremia and x-linked rp Where we're bringing patients in you'll see them in my clinic. They come in every six months Which is way too often for an inherited retina disease patient, but for a clinical study we bring them in every six months This is the drug companies are flying these patients in from all across the country just to see me at our site So I get patients that are flying in every six months from Hawaii from Indiana every they're all it's kind of it's kind of unusual, but that's the way that it works on this and Their goal is to have gene therapy because these are single gene mutations typically that again gene replacement may be useful for and the coroed oremia should be starting by Next summer we think for gene therapy and unlike classic gene therapy where you have to do a fairly invasive sub-retinal injection the the vector for coroed oremia is being designed to be Intravitrally Administrative and to penetrate through the retina they've genetically selected for it at least they claim and we're going to be One of two phase one sites. So we're going to be truly the first doing these These intravitural studies. So that's that's another reason why you'll see a fair number of these patients in my clinic Then there's uncommon or mitochondrial diseases those you may see in In neuro more often than in mind they they're often associated with neurologic disease They're going to have a maternal into inheritance. They're going to be rarer syndromic things like Kernsayer me loss and other diseases like that Then that leads into syndromic rp and so what's What is this disease here if you again if you see this on the boards and they just have a picture like that What's wrong with this patient first? What extra toes? Yes Extra fingers and toes. So what what is the answer? What rp syndrome gives you extra fingers and toes? Beetle. Yeah, Bardae beetle. So it's shown right there that one will show up Okay, and again, it's trigenic. We know the genes. What else in Bardae beetle? What else do they have?  I once a year or two ago I guess two years ago now. I was invited they had a Bardae beetle convention here in Utah And it's there. It's seeing a whole room full of them. It's very interesting But so they can have that other one other syndromic ones that you need to know about our usher syndrome, of course, right So what's usher syndrome? What is that by definition? Right, so rp and hearing loss it's autosomal dominant almost almost always Our I mean sorry recessive. It's recessive And there's different types, but that's another one where gene therapy is coming soon They know it's a big gene, but people are working on that senior. Locan is rarer, but Anyone know about that who's written that the definitive review on senior Logan's Niko did right Niko did his phd and senior. Logan's Know that Aperts is rare golden fava is rare I've written a paper on ref some disease. I've never seen it in a mouse in a Cell culture models. I've never ever seen ref some disease in my life yet But I got a paper out of that, but what's important about ref some and gyrate atrophy Is that they're very They were described long ago. We knew the genetics long ago And they are treatable with diet. That's the thing.   You have to avoid phytanic acid in the diet. So that that's why those those are known Then of course, there's plenty of them that are sporadic No history at all That might mean because there's a new mutation in the person might be that it's just recessive and oh, they're the only one in the family But they also might be a pseudo retinitis pigmentosa. It might be autoimmune You got to think about other things that are going on that might be treatable So it could be you'll hear probably from the uveitis people about cancer associated and uh melanoma associated retinopathy We get uh gene gene or anti antiretinal antibody testing But you also have to remember we talked about toxic etiologies So I have picked up toxic, uh retinopathies. And so The the one paper that I published long ago more than 20 years ago Patient came in with a funny-looking retinopathy The dr. Degree had done a just a kind of history and he Was just noted when he was referred to me that he had exposure to ms 222 Which you've probably never ever heard of but in my phd thesis I had worked on this compound Which is a toxic compound in animals that cause that's a fish anesthetic That causes problem that causes ERG agramalities in fish This patient happened to be a fish biologist and what he did Is when he threw the fish in the ms 222 for them to go to sleep And then he would reach in with his arm and grab the fish out And was getting it all over his arm and basically was exposing himself to this toxin and We Basically we told him wear some gloves for god's sakes and so and he did and he got better And so that's that's a possibility and then The other thing that you will see occasionally in my clinic is vitamin a deficiency so What causes vitamin a deficiency in the develop in the in the united states? number one cause probably Right bariatric surgery and those patients are out there and they may have had it 20 or 30 years ago because it takes forever to make yourself vitamin a deficient But you got to catch these patients and they are um Don krill is pretty good at picking them up by ERG and you just If you take a little bit of a history and find out you know if they've had this bariatric surgery Get a vitamin a level the patients are Eternally grateful and i've cured several patients by this by just Either giving them you know high doses of world vitamin a to get past their their Their deficient uptake or by giving them injectable forms which unfortunately are very expensive, but You can cure them again Set a rare complication that i've seen with someone who just was such a picky eater That he did not eat any fruits or vegetables at all ever And gave himself vitamin a deficiency and he He came in with classic. He couldn't see at night. He had to get He had to wear it use a flashlight to get around his house and when i took his dietary history Of fruits and vegetables. He basically says i i sometimes eat every two weeks. That was it That was done, you know in terms of what he ate his wife confirmed. Yes, he only eats meat and potatoes. That's it so And once he started taking Changing his diet. I never saw him again except we we called him up. He said he's doing fine too busy to come back in so um And then there as we talked about stationary retinopathies They don't have clinical progression. They often have very prominent night night blindness, but the visual field is good Other things you want to look at are that is are these congenital stationary night blindnesses And there are certain mutations that just don't cause a lot of problems rdh5 Can give you all of these spots written out as Fundus albipunktatus right here and that can just be a problem, you know that If you can diagnose them with this then they don't need to worry so much And then in terms of treatments basically you want to do social supports Um, so, you know, they they have problems at school. They maybe have problems with jobs That's why we have social work staff You want to do genetic counseling that and our we have that under control now nutritional interventions Rare but are important to have they'll ask about lutein and zeaxanth. I say it's not bad to take it But that's not going to really cure them. Um gene therapy is coming You know is here in for luxterna more of them will be coming, but they're going to be research based Stem cells patients read up on the internet. There's a lot of promises, but There's no good stem cell studies that have been done yet that have really cured patients that you know that are fda approved And or even fda, you know sanctioned for clinical trials So that's still coming, but I obviously tell patients that You know five or ten years is a long time, you know, there a lot of things can happen in In technology in five to ten years And then people are we're looking at various other more generalizable interventions either oral or injectable growth factors antioxidants Velproic acid we were part of the studies here where you know, there's always a lot of promise on these pre-clinic People may give antioxidants or some other intervention to a mouse. They get better and they say well, let's give it to humans They'll do it if they're if they if the drug is available. They'll give it Some patients may see a little bit better or not But and that happened with velproic acid There was a lot of buzz and people started because it was already on the market people started taking Started prescribing it to their rp patients But it wasn't until the foundation fighting blindness stepped in And invested millions of about probably eight million dollars to do a proper clinical trial that it didn't work We were part of that trial And then it's kind of faded away So you gotta be careful about false hope And all these things you'll see on the internet for electrostimulation stimulation other things that just are taking people's money away And then artificial vision with the argus-2 implant Was a great tour to force that they could make an implant chip implant that got them a little bit of vision The problem is that the intervention cost a hundred thousand dollars And the the quality of vision was still so poor That it didn't have a great patient acceptance and insurers blocked at it So the next step is going to be to do cortical implants So the company argus the argus-2 implant even as we were gearing up to start Implanting it was pulled off the market In two weeks or so Mark rmeyan who's the one who's the father of the of the argus-2 implant will be giving a talk here Tuesday afternoon at four o'clock You should go and if you can't you can get away And that's the betting he's a very good lecturer So okay And then i'm going to go through other things just so we A little bit faster now on this and so Other things that i'll see are cone dystrophies. They have a wide range of manifestations The most common cone dystrophy is color vision deficiency. That's in three to five percent Of males have that They can have macular cone dystrophies progressive cone dystrophies a chromatopsia is the most severe that's that's less common And they of course will have loss of color vision loss of central visual acuity Very Characteristically they'll have photophobia much more than a classic rp patient would And their visual field is often really pretty good But they may have bullseye maculopathies and the way that we've diagnosed cone dystrophies Almost the same as rp. So you can do clinical history Family history dilate examination all the same things that that are doing that we're doing they just have to have But they're going to come they're going to have different findings. They're going to have a preserved visual field They're going to have macular problems much more genetic testing will Distinguish that And so cone dystrophy it's the same Genetic counseling Maybe stem cells maybe gene therapy And of course remember that there could be ocular toxicity numerous Agents can mimic retinal retinal dystrophies. These include the tamoxifen This is kind of catazanthin where you get these crystals depositing in there the other things We look at plaque when L which can give you a macular dystrophy here And tobacco alcohol Thabutol all the other other things Other toxicities that we've picked up here in clinic are chromium Chromium cadmium toxicity and why would someone come in with that anyone know that one? There was a small outbreak a few years ago. I had to do with hip to bad hip implants That were that were sending That were leaking out all the ions in there and that that caused a pretty bad macular problems too And then there are other ones, you know digitalis the Viagra can cause transient color vision problems. And then there's other other ones there And then finally, uh, remember pseudo retinopathies. These can be post inflammatory After trauma idiopathic and the main thing one of the more And also think about, uh, rubella retinopathy can often get misdiagnosed. All these are stationary And you don't need to you don't need to work them up as as a normal As a regular retinal dystrophy and typically sometimes they have good electrophysiology I can talk briefly either we can stop or I'll talk briefly about macular dystrophies All right, we'll see if this comes back up.  That's going to be common Um, that's about a one in 10,000 disease. So it's not as common as rp But there's plenty coming out there best disease and then various other ones listed here And I'm just just we'll talk briefly about those. So star guard disease One in 10,000 so 25,000 to 35 30,000 people infected in the u.s It's 95 percent autosomal recessive But there are dominant forms too And there's thought that you know because it's involved in Deposits of lipofusin that there may be some increased risk of amd, but it's not a major amd gene, unfortunately Because because it would make things easier in the diagnosis The star guard disease normally they have normal completely normal vision at birth when when they're young They decline in central vision typically in their teenage years, but there's really wide variation Classically they'll have macular atrophy Described as be metal and they have these Piece of form flex going around so but not all star guard disease looks like this not everyone we've learned There's a huge diversity in this You'll see in my clinic. I've diagnosed people 60 or 70 years old with star guard disease that are still You know that are functioning still pretty well because if it doesn't knock out their central vision They may not notice much change on the other hand. They could be debilitated at age seven also The end stage typically just stops at 2400 vision and there's preserved central vision So you can see the flex right here. You can see the atrophy here Um the way that we diagnose star guard disease clinical history family history I exam They will have your classic dark chloride Shown here, but I don't get fluorescent angiograms very much anymore on these patients because auto fluorescence Works just as well on this I don't routinely get ERGs Because that's usually normal or only mildly affected and genetic testing is very useful on this The problem is it's a very large gene. So it's we still miss even though we know that Uh, essentially every patient with star guard disease will have a mutation in the abca for gene They still miss them because of large deletions. It's it's just a hard gene for them to sequence But I'd say they're missing only 20 of them now. So it's relatively they're getting better at this And we don't have time to go through the the biochemistry in this but it has to do with abnormal The abca for gene is important in moving all trans retinal after bleaching out of the out of the cell and if it doesn't if you If you have all trans retinal if the all trans retinal is there too long It starts generating a whole series of toxic compounds that are fluorescent And that's what you see when you see the increased fluorescence Um, the way that you treat it is that we have patients avoid excessive vitamin a avoid excessive sunlight We are part of many different several different clinical trials that are looking at either vitamin a or visual cycle inhibitors things that cause Vitamin a antagonists is another reason the way that they're looking at that We're also part of a trial looking at complement inhibitors and how they may be Slowing down the disease. So there's you'll see a number of clinical trials coming through and they need genetic counseling, but You know, it's it's a recessive disease. So again, if they don't if they're not marrying close relatives, the chances are One in 20 or one in 40. They'll find just a random carrier because there are lots of carriers out there Um Dominance stargarten disease is really rare, but I do have a family of about 18 Patients that I've been following here in from california. It's a completely different mutation in el ovl 4 It's a completely different mechanism, but it can look just like stargarten disease or pattern dystrophy And I'll kind of skip through that that'll be That I sometimes gives a research talk Other things that you'll see in macular dystrophies are best disease. That is dominant We don't know the exact incidence and but it's well known It's a mutation in the vmd2 or best one disease gene and it has these classic The teleform lesions that That can be associated with best orphan mutations And that you know can progress Get these scrambled egg or pseudo the teleform lesions They're loaded with lipophiesin and some patients do really well and some patients do very poorly It's just and I've even seen such variable expressivity that I've seen one patient with Full-blown best disease in one eye and the other eye is totally normal as an adult So it's just it's it's really kind of a bizarre disease And the way that you do that The way that we have assessed that is clinical history family history Autofluorescence and then the classic things that you need to know is they'll have it an abnormal electro oculogram And a normal erg classically, but there's always exceptions and we do genetic testing for that too And I don't know I don't know where gene therapy is right now. It's I don't think it's it's progressed enough to be anything important Then finally there's going to be the very rare diseases that I've never seen in my life But that are written up well Swarovski's fundus dystrophy The reason why that comes up is it is a model for amd and some of the same mutations And the temp 3 gene are also can also cause macular degeneration And typically they get these macular changes. They get carotoneobascularization, which is unusual for a lot of these other dystrophies And that's found mainly in england And then malatia levantanese also known as doin's honeycomb dystrophy Shows up on the boards. The main things you need to know is they've got these radial flecks here And it's a well-known mutation And it is Associated it some of the same genes can cause age related macular degeneration again, that's Too rare for you to ever see in my clinic And then north carolina macular dystrophy is one other one that I'll just kind of which I it took me 20 years of practice before I finally found one patient with this and the main things to know about this Is it's dominant? They have horrible looking maculas But this is compatible with 2020 vision these patients have can have really good vision surprisingly And it turns out this is actually congenital and non-progressive Even though it was only and it was the first macular dystrophy to have linkage But it was the last one to have the gene identified. So that's the that's just kind of interesting with that And there's no treatment yet So that's it Okay, so when you come to my when you rotate with me You know, I always encourage It's christ to say, you know the see the inherited red disease you go in and see them first really try to work them up See what you can learn. Okay All right


Yo what's poppin' people, welcome back to another video. Thank you guys so much for the support. And today's video is all about big worms.  But before we do that, I have a giveaway for you guys and I also have to announce the last giveaway winner. So let's hop into it. So for today's giveaway, I have a pack of prawns. These are in Bluegrass Magic. Beautiful little color right there. We got a Crush Mini 25X.  Baby bluegill. And then we got some lime. This is 65 pound braid. It's gonna be perfect for your flipping setup, your punching setup, or like frog or any other top waters is to be perfect for. And then I have a Crush 50X right here. And I believe this is in Black Magic. Yep, Black Magic. So if you guys want to enter this giveaway, all you have to do is be subscribed to the channel, hit the notification bell, and also hit the like button on this video. And if you could drop some video suggestions in the comment section down below, that'll be a little extra on to this giveaway. And I will pick a winner here shortly. As for the last giveaway winner, I'm gonna pop your name up on the screen right now. Thank you so much for the support and congrats on winning the giveaway. If you could, please DM me on my personal Instagram page at Noah Pescatelli, and I'll get all your information and ship the package out to you. We're gonna go ahead and hop into this video. This is a compilation of big worm catches you guys have been asking for this video. Noah posted a video just over big worms and a ton of cool catches.  So I hope you guys enjoy it. Let's hop right into it. Oh, I got him. Dude, big Allen. Oh my gosh, oh my gosh. Dude, this might, dude, this is a double digit, bro. Allen, Allen. Dude, dude, holy cow. Oh my gosh, Allen. Oh my gosh, Allen. This might be my PB. Oh my gosh, Allen. Please grab that thing. Please grab that thing. Please grab that. Bro, dude, dude, dude. Oh my God. Allen. Holy cow, bro. Dude, you're dirty, bro. I'm sorry. I'm sorry, man. We fish here many a times.  It's been a while since I've caught a giant, that big dog. Oh my God, that's a big fish. Guys, look at that.  Look at his little tongue. Oh my God. Guys, that is a mega. That is like, Allen, look how thick his back is, go over the top.  I've, guys, we gotta go buy a new scale. I lost mine and I just, I'm mad right now. I really wish I had my scale, but that's every bit of almost nine pounds. I promise you, I don't think he's 10. No, I don't think he's 10. No, probably not. He's over eight.  He's like, Allen, wear me out. Allen, dude, welcome back, bro. Now we gotta get you one, man. That is just so sweet. On the shaky head, just straight, just tanked it. Oh my God.   Is he a big one? Adam's hooked up with his first one. Let's go. That's a good one. Oh yeah. Easy, two and a half. Yeah. Adam on the board, throw in the old Chattadonky. There you go. Dude, I thought he was a lot bigger. Holy cow, Adam, he hammered that thing, bro. Oh gosh, that's the biggest one today. That's a four pounder. What the heck? He might be three and three quarters. I think we might need to get a weight on this guy. That was pretty good. That's the best one today on a worm. Plum worm, did you bring the pack of them? No, I don't think so. What's the thing, did you? Oh God, I'm scared. That's not good. All right, we got, he's still on the hook. We aren't gonna get a weight on this one without the scale. What do you think? I'm thinking three and three quarters, but he's heavy, bro. Might be four. He's a four. He's definitely four. He's heavy, bro. I was right, bro. How much? Three and a half. I thought it'd be three and three quarters. Three, eight. That's surprising, cause he seems pretty heavy. He's pretty skinny. He has a fourer-like body, is too skinny. Yeah, he's got a big old head. He's got that pretty much. It's the best one today though. Solid three and a half, I'll take him in. I'll take that all day, every day. All right. I think I can release him in this grass. See, you see what I'm saying? Just take. I just don't feel comfortable doing this. Just toss him out there a little bit. There we go. Yeah, there's no water there, bro. Yeah, he like hammered it, dude. And then he kept, there's a fish swimming right here. Heck yeah. Ooh. Ooh. God, dog! That's a bass. I thought it was a carp. Guys hook said it with one hand. I got him in the head. Wait, what? Wait, no? Wait, what's just happened, bro? I swore that was a carp. It looked like a bass. No, that was a bass, yeah, but yeah. Like I was reeling it. I don't know what's going on, dude. That was really weird. And then you got another one? Oh, dude, I'm, oh my gosh, Adam! Oh, he might be five. That's five. Four to five. Dang, bro. Oh, bro, there you go. That's definitely a little bit better.  Yeah, that's sweet. It's weird. That's a four and a half all day. Yo, Adam, show me what you caught, man. That's what we talking about here on Kicking Their Bass. It's a Florida fish. That is a Florida bass right there. I'd say four to four and a half. Yeah, I think it's between four and four and a half. We got the scale. You got the scale? Poppa Schwaten. Poppa Schwaten. Scale along. Yeah, he looked huge when he jumped though. I'll give him. Yeah, and they're fighting so hard. Four eight. Four six. Four six, gosh, yeah. It was almost four and a half. Yeah. Four six. Scaled on a lot, baby. There you go. Biggest fish today, Adam. What's the color on that fish? Yeah. Yeah, dude, he has like some weird. It's like gray. Yeah, that is weird, dude. It's awesome. I love it. Okay, good job, bro. Oh, this is a big girl.  Oh my gosh. Did he actually die? Oh my God. What the heck, bro? He doesn't knock that guy out. Dude, dude, that's a good one. He was in the same spot as yours. Dude, that's a good one. Oh yeah, yours is still alive. He's just a little knocked out. Oh, that's an easy two and a half pounder. Geez. Kind of doubled up. Yeah, we kind of doubled up. Dude, we just stopped here. That was quick. Do you feel how cold these fish are? Oh, there he is. Oh, he's a good one, big one. Yes, yes, yes. Yes. Yes, dude, yes, yes, yes. I hooked him in the tongue. He's bleeding a little bit. Let me handle this real quick. Gosh, he's not as big as I thought he was. He's bleeding a little bit. So guys, we're gonna weigh this really fast, okay? I didn't gut hook him, but I hooked him in the tongue and that's usually like weak spot on a bass. Let's zero it out. Weigh you so fast, buddy.  I think he's about three pounds. Oh my God, one ounce away. Two pounds, 15 ounces. Look at that beautiful fish. Finally a good one, man. Three pounder. Let's go. You have no idea how bad I've been wanting a good fish by it. There he goes. Look at him take off right there. Boom, let's go. Let's freaking go, man. Let's freaking go, guys. That's awesome. We did it, guys. We've been searching for a while, but we finally got us one. The size that we want is that three plus number. We sure made it happen. We're not getting many bites, man. We've been fishing for a long time, but you gotta stay consistent and keep doing it. And he was right on this little grass edge. And what I've noticed, guys, with this big worm today is when they eat it, they all just hammer it, okay? They either hammer it or they're pecking at it to eat it. And that one was one hard hammer, because I was a big one. What they've been doing is they hammer it, and right after they engulf the bait, they start taking off. Every single one's been like that today. Been a long day, but guess what? We didn't give up, kept it going, and it's rewarding. Jerry's coming over here now. I am, Jerry is probably the most sassy alligator that I've ever seen. Jerry, you need to just stay back.   You know that? You think I'm kidding, man.  Better back down. Come on, Gary. Yeah, that's what I thought, bro. Get out of here. Yeah, get out, bro. What was I calling him? Was it Gary? All right, Gary. I think it's Larry. Larry, get out of here. You got some little arms, man. Skipping arm day or something. Little tiny shoulders, too, man. What you gotta say? Oh, you talking back? Are you talking back? Yeah, get out of here, Gary. That's what I thought. Kids these days. Oh my gosh. Guys, this is a giant. This is a giant. He's running at me. This is like a very big fish. Very big. Come on, baby. He's running. Guys, this is a giant. I mean, a giant, giant. Oh my gosh. Oh my gosh. Oh my gosh.  That's almost a five-pounder. That is almost a five-pounder. Mm. That's cool.   Look at that. Dude. I thought he was a lot bigger. I seriously thought I might have had a trophy there for a minute. The way he was tugging, but my drag wasn't all the way set. But when I hooked him, I didn't even move him. I felt his big head shake. All right, zeroed out. This is a four and a half pounder. I don't think he's quite five the way that I'm looking at him now. Wait. Wait. Why did my settings change? We don't have it on the right mode. Well, we're weighing in kilograms. Gonna have to convert this on my phone. I was about to say I'll weight him, and he said like two something. I'm like, what? 2.21 kilograms. Whatever that is. Let's put it in a converter. Dude, that's easy four, four and a half pounder, dude. Gotta be. Guys, that is what we're talking about. I promise you that's a four and a half pounder. Oh, that's a biggin. Gosh, let's go. There he goes. Big girl was wore out, man. She was tugging. Let's go. God, on a tough day like today, man. That's why you never give up right here. It was 2.23 kilograms, right? 2.23 kilograms of pounds. Oh my God, he was almost a five pounder. 4.91. Dude, that was a... We're calling it a five pounder, bro. Let's go. Dude, we just got a five pounder. I was about to say, like, when I... I don't know how to change the settings on that scale, but when I first weighed him, I was like, what? Like, it showed two pounds. I'm like, all right, there's something wrong. It's like there is just something wrong with this scale. That thing is showing this fish to be two pounds. And then I realized that it went over 16 ounces, and I was like, oh, this isn't kilograms. There's nothing better, guys, than catching a big bass on a tough day like today. Solid five pounder on the big worm. Dude, that is so awesome.  We've caught a three. We've caught a five. We caught one that was maybe a pound and a half and then like another pounder and then one that was just tiny. So we're doing pretty good for, you know, how tough it is today and how rough the fishing's been. But let's go ahead and talk about, you know, why that fish was possibly in this pocket. That's the main lake right here.  Big drop off right there. There's a ditch that heads out of this. And if you guys are wondering how I know that, I count down my bait and I figure out how deep it is out there and I can kind of feel it as dragging it up. So I know there's a ditch running out. There's a flat right here. And he was sitting right here on the edge of the flat. Not only was he sitting on the edge of the flat, there was a slight, I don't know if you can tell there's a little brush pile. I think it's right there. If you guys can see that.  Like I said, fall pattern. The fish are starting to push the bait up shallow. We came to a pocket caught a five pounder. That's exactly what we want to do. Oh, he spit it out. Oh, he's running away. There you go.  Giant. Giant. Oh my gosh, he's huge. Oh my God. Oh my God. Oh my God. He ran right up on the bank.  Look how he's barely hooked. Oh my gosh. Dude, is this going to be in kilograms again? This fish is over four. He's about four. Oh no. I think it's right now. My heart is racing. Oh my God, he is four. Oh my God. Four pounds, one ounce.  Dude, that is a football if I know of one.  Don't call me right now. It's not a good time. Solid four pounds, one ounce. Let's get him back in. They're loving the big water, man. Look at that football. Oh, yeah. Let's go. They're out there on that flat, guys. Just what I was saying. Right here, pocket off. They're starting to push the bait back in the pockets now since the summer to fall transition. Sitting out here on the flat, baby. Let's go. Oh gosh. Dude, they're bigging. Bigging, bigging, bro. Oh my gosh.  Look at that. Oh gosh. Four pounder. Oh, that might be bigger than four, homie. Look at that, baby. That's an easy four pounder. Just think about that, Adam. I think that is a good four pounder. He knocked the heck out of it, bro. We got all this wind pushing up on this grass line out here. Hit it on top of the right. Dude, my bait landed. Right on my bait landed. I felt just the hardest knock in my line. And he was on there. Four pounder, baby. Man, it's happening quick out here. I feel like this night bite, we were talking about it. You know, as the sun's going down last hour or two of the day, it's almost the best time to fish, especially during the summertime. That's what you get right there.  You don't even know what hit him, dude. There he goes. We got him right out into the deep. Let's go, brother. Let's go. That's him. Oh my God. Please don't come off me. Oh my gosh, guys. That is a huge fish. Dude, look where Adam just caught. You're not going to believe it. Holy cow. Check it out. Dude, that's every bit of five. Let me say one thing. I usually bring my scale out with me. I cannot find it at the moment. Me and Adam actually looked in my truck and we just could not find it. But I'm telling you right now, that is well over four. That is a five pounder. I like turn around and I look at Adam. He's like, holds it up. I'm like, wow. Okay. Geez, he was not coming off. He was in there. Unless he broke your line. Look. His eye. His eye. It was messed up. Oh, wow. On this side, he's good. That's a big end dog. That is a big end dog. Give me something on that one, huh? He just took off. Oh my God. That's definitely a big one. I'm going to ski this bad boy in. That a good little fish. Got a little bit of slop with him. Dude, he knocked me so hard. That was crazy. The other one on that big worm. Right there in the grass. Geez. Giant. Giant. Oh my gosh. Oh my gosh. Oh my gosh. Oh my gosh. That you talk about a freaking football. Like that's every bit of almost four pounds. Three and three quarters. Oh yeah.  Look at that. He might be four dog. I think he's four. I got to stop guessing the weights, man. I'm going to go back to scale, but I can tell you every bit of almost four pounds right there. He felt so big when I jacked him, dog. There he goes. Oh, there he is. There he is. You guys see him running with it? There he is. Good boys. We hooked up my first big worm fish today. Dude, look at him tugging right there. Like a pound and a half. That's a fatty though. It is a fatty. God, look at that.  Or catch a fish on a worm that big. The worm is probably longer than the bass, honestly. Yeah, he probably couldn't even eat that thing. His stomach would explode. Dude, he tapped that sucker. It's only a pound and a half. If that, the fat belly might be. Yeah, for sure. A pound and a half are easy. The colors on them are awesome though. Oh yeah, they're cool down there. All right, guys, let's get them back in and see if we can catch another one. That's a beautiful fish. The markings are cool on there. Yeah. It's like clear as water. What is this? That is all pollen, maybe. Or maybe it is pollen. Are we in the winter? There it goes. Hey. Oh, there he is. Yeah. Yeah. Dude, that's a big, I think. Yeah, that's a big one. Watch, watch. Watch how big he is. Oh, gosh. Nice. Four, but he's about three. He might have been in a deep hole in the middle. Dude, that's so fun. That's so fun. That's the solid three. Adam, you got the scale? Yeah. Yeah, that's a hundred percent at least. Three. That might be three and some chains. That might be three and a half. Dude, he felt so big. I don't know why he felt so large. Whoo. That's what we're talking about, boys. Throwing a freaking mega right there. Biggest worm you can buy. You want to do it? Big worm, big bass, baby. Yeah, two and three. Two and 11? Okay, two and three quarters. I'll call them that. That's a beautiful one, though. Really is. Big worm, bro. Catching a three pounder? I don't mind, man. I don't mind. We were just talking. We were fishing around these pads. They weren't biting. We were on the grass. We were like, man, I can't believe we haven't had a bite out there. I threw it out in the middle because we were talking about maybe there's a deep hole. And sure enough, he hammered it out there. Beautiful, beautiful bass. Got a boy. Yes, sir. That's what we were talking about. That's a good one, man. I'll tell you what, thank you. For some reason, he felt so large when I was reeling him in. I didn't think he was probably over four, but he felt just big. Gosh, look at that. Let's go, baby. All right, Adub. Keep beaming some casts out there, bro. They might be stacked up. Gosh, he hammered it. He hammered the big worm, dude. Let's go. That's a fatty, dude. He ain't big, but that is a fatty. Look at how freaking hunchback that thing is. Let's go, dude. Dude, he hammered that thing and just took off. Look at this. It's like a little hunchback. He's so fat. I don't mind that. He ain't a giant, but look at that. That is awesome. Thank you, buddy. Second fish today, beautiful guy. We're upgrading every single time. Now, the next one better be big. Oh my God. Why are they all small on the big worm? Oh, I got him. Gosh, on the big worm, bro. It's a good one, too. Not bad. On the big worm. Dude, let's go. Easy two-pounder. On the big worm. Oh, hammered it, man. That feels so good. It's been so long.  He might not even be two pounds. That's pretty impressive, man, to eat a worm like that.  I started dragging it. It was right when I started dragging it, and he went, tic, tic, tic, tic, tic. Fun of that, bro. The thing is about, he's a little over a pound and a half of this fat. Tell me. I don't think he's two pounds, though. Probably a pound and a three. Don't weigh him, dude. Not yet. A pound and a half. A pound and a three-quarters. Not two pounds. I don't even know why I'm weighing a fish this small, but... Let's see what you got. Almost two pounds. A pound and three quarters. Over a pound and three-quarters. One pound, 13 ounces. Beautiful little fish. Thank you. A big worm. Can I beat that right there? Fat tummy. Almost a two-pounder. Let's go. Good job, brother. Yes, sir. Me and Al and Bob are both on board. That's so fun, dude.  Something about a big worm. I want you guys to leave your comments in the comment section below. What's your favorite big worm?  I'm curious about that. Like, I was thinking in my head, I was like, I'm going to start dragging it. And like, right when it hit my head, just start dragging it, he hammered it right then and there. Like, my first swipe. Hey, baby. Sorry about the noise, guys. We got some supporters out here. Ha-ha-ha. The Lamo team, man. They were cheering you on, Al and Bob. Dude, that's a good one. I know. That's awesome, bro. Oh, no. He might be two and three quarters. Let's get an official weight on him. Like I said, guys, sorry about the noise, man. There's people cutting grass. But that's a solid two and a half to three pounder right there. If I could take a guess, I'm going to say two and three quarters. Close. Two pounds, 11. Let me see. Pretty good. 2.1. Or 2.10. 2.10. Well, you say 2.1 and Bob? He's trying to kill me over here. 2.10. 2.10. All right. There we go. That's a good one.  That's a good one. That's a good fish. Two pounds, 10 ounces. Thank you, buddy. There he goes. Awesome, bro. That's good. Best fish today. Don't leave me hanging. There you go.