 So, um, sana, um, hopefully, I'm very, very hopeful na you started to love Glen Kim in a much, much different way na minahal niyong mga Kim ninyo, okay? Kasi, you know, Glen Kim is so, so fun. It's hard, yes, but you will learn a lot of things here, okay? So, liver function test, okay? So, liver function test. So, last time we did discuss about the anatomy of the liver, the biochemical function of the liver. Now, let's go, wrong spelling. Now, let's go to the liver function alternation during diseases. So, which will lead me now to jaundice, cirrhosis, tumor, rise, syndrome, and the drug and alcohol-related disorders, okay? So, let's start. So, the first one is your jaundice. So, jaundice is actually a characteristic of your skin, your sclera, and even your nails during state of hyperbillirubinemia. John, it is also called ecterus or hyperbillirubinemia. Ecterus, we use the word ecteric or ecterus when we are describing your sample. You don't say when you saw a patient na yellowish yung discoloration, you don't say na, sir ma'am, your ecteric, that's wrong, okay? The right term to describe them is jaundice. So, again, it is a yellow discoloration of your skin, sclera, and even your mucos membranes, okay? So, jaundice becomes evident when your bilirubin levels exceed 2 mg per dl. 2 mg per dl. And this is how it looks like, okay? This is how it looks like. So, your jaundice can be of three sources, okay? It could be prehepatic, hepatic, or post-hepatic. And let me describe to you each one briefly before I go deeper into the different diseases. When we say prehepatic, ang problema ay nangyari bago pa dumating sa liver. So, meaning to say, there is really a problem when it comes to your RBC, either hemolysis or may autoimmune disease, okay? May autoimmune disease kaya nagsasabugan yung mga RBC kaya pagdating sa liver, no overwhelm sa liver sa lahat ng ikokonjugate niya na mga bilirubin, correct? So, in prehepatic, the problem started not on your liver, but with your RBC, okay? In the hepatic jaundice, ito ngayon yung talagang problema inside your liver, which we will be discussing in a short while. So, the jaundice originated because of your liver, either your liver is no longer capable of processing and conjugating your bilirubin, or rather, there is a lack of enzyme or transporter within your liver that is necessary for the conjugation of your bilirubin. Pwede rin naman siyang post-hepatic, okay? Pagkinabi natin post-hepatic, the problem arise after the bilirubin was conjugated, after the bilirubin was produced. Now, it is time for it to be disposed in the biliary tract, correct? Through your go into your intestine, barado daw. Dahil barado dun, naipon ngayon sa liver, naipon ngayon sa system, kaya nagkaroon ka din ng jaundice. It's more like the pre-renal, renal, and post-renal diseases that we are talking about in your AOBF, which I will also be talking about in your kidney function test, okay? In your kidney function test. I will not be handling clinical chemistry too next semester, but I assure you the one that will be handling it is someone that I also look up to. So, abahanin nyo kung sino ang CC2. And aside from that, okay, aside from that, aside from the CC2, hindi na kasi madidiskas dun si kidney function, okay? Hindi na madidiskas si kidney function. Nandapat-dapat madidiskas si kidney function. But ayoko napiliten yung, hindi na natin siya kaya ipagkasha ngahang bukas. Okay, hindi ko na kaya ipagkasha ngahang bukas. That's why I'll be uploading a video na lang din for the kidney function. And then if you have any questions, I'll entertain any questions ninyo about it, okay? So, let's go now to the pre-hepatic jaundice. The pre-hepatic jaundice are usually because of problems prior to your RBC reaching your liver. Usually, it is due to too much destruction of RBC. So, lahat ng bagay na may kinalaman sa mabilis na pagkasiran ng RBC would actually a potential reason or cause for your pre-hepatic jaundice, such as what? Such as hemolytic anemia, malaria, hemolytic disease of the newborn. All of those could possibly cause pre-hepatic jaundice, okay? And in this case, in the bilirubin assay, the one elevated is what? The one elevated is your indirect bilirubin or your B1, okay? Your B1. Si B1 increase. Back it, sir. Okay, babalik ko lang nang mabilis sa ating kuentuhan ng nakaraahan. Natatanda ninyo, itong part na to, some of your heme will be converted immediately to your unconjugated bilirubin on your plasma. That's why your albumin will be collecting it. Your RBC, rather your albumin will be collecting it. That's what happened in your pre-hepatic jaundice. So in your pre-hepatic jaundice, okay? In your pre-hepatic jaundice, so we have here your hemolytic anemia. We have your malaria and hemolytic disease of the newborn. It is dangerous, especially in infants, okay, to have jaundice at a very young age because that would mean that there are a lot or elevated bilirubin levels in their plasma. Why? Makikisulat na lang ako. Hindi ko lang kung nakikita nyo lang malinao because those excess bilirubin will be deposited in the brain. In that condition, we call it kernicterus, okay? Kernicterus. The deposition of bilirubin in the brain is kernicterus, okay? Kernicterus. And maybe some of you will be wondering, sir, sir, sir, is it a type of a delta bilirubin or a direct bilirubin or indirect bilirubin? To be honest, it can either be an indirect or a delta bilirubin, okay? An indirect or a delta bilirubin. Nakakukapa ako. So indirect or delta bilirubin. Makikisulat na lang din ako, ha? Himalitic anemia, malaria, and Himalitic anemia, malaria, and Himalitic disease of the newborn. So anything that has to do with rapid destruction of your RBC instead of 120 days, wala pang 120 days, nasisigiran na si RBC, it is possible na magkos na pre-hepatic jaundice, okay? Pre-hepatic jaundice. Second, we have your post-hepatic jaundice. Sa post-hepatic jaundice ang problema natin na sa dulo, okay? Ang problema natin na sa dulo. Anong mayroon sa dulo, barado yung lagusan, okay? Barado yung lagusan. That is the reason why in post-hepatic jaundice, the usual causes are the obstruction of your biliary trap. Failure of your bile to flow into your intestine. And generally, this is because of impaired bilirubin excretion. Sir, ano pung pwedeng problema? Ano pwedeng problema? Unang una, it can be your gallstone. Gallstone or in medical term, we call it your chole letiasis, okay? Chole letiasis, okay? Chole letiasis. Question, what is the other term for, ano? What is the other term for renal stones? Sige nga, renal stones. What is the other term for renal stones? I am posting it right now on your chat box. The spelling for your chole letiasis, okay? Sir, wag na pung chole letiasis. Okay, some answer, renal calculi. Okay, renal calculi. It is also known as your nephroletiasis. Okay, pag-renal. Renal stones, renal calculi, re-nephroletiasis, okay? And pag sa gallstones naman, that is your chole letiasis. Okay, so moving on. Okay, moving on. With regards to your chole letiasis, it can also be due to your pancreatic tumor, okay? Pancreatic tumor. So pancreatic tumor can also be, of course, for your post-hepatic jaundice. And in this case, the one that is elevated is your, whoops, the one elevated is your direct bilirubin. Sir, bakit hindi mo sinasama si Total Bilirubin? Obviously, elevated na din si Total Bilirubin in cases of jaundice, okay? In cases of pre-hepatic, which is increased, B1. Okay? In cases of post-hepatic, which is increased, your B2. Sir, are you going to say it as B1 and B2? No. I'm not going to say it that way in the exam. So you really have to study the table that I have given you, the differentiation between B1 and B2, because I can call it direct. Then the next day, I can call it slow reacting. I can call it water soluble. Nakukuha tayo. So I want you, I would challenge you really kasi kilangan mamaster niyong part na yun, okay? So moving on, we also have your combined, okay? Hepatocellular combined jaundice. So this is caused by hepatocyte injury, caused by viruses, alcohol, and parasites. So di ba meron kayo mga fasulopsis, buski, mga ganyan-ganyan natin. So all of those could also contribute to jaundice. So this one, both B1 and B2 are elevated. Both B1 and B2 are elevated. B1 and B2 are elevated. So now let's go to your, let's, we're starting to enter the, we're starting to enter the hepatic stage, the hepatic jaundice na. These are the different conditions that would cause hepatic jaundice. Okay? Hepatic jaundice. Tandaan sa utak ha, na ang pre-hepatic B1 si matahas. O, hepatic B2 ang matahas. But pagdating sa hepatic jaundice, pagdating sa derangement in double aerobin metabolism, it can be both or it can be either. Okay? Either. So unang-unang talistahan mga kapating ay si Gilbert. Gilbert syndrome. What is the problem will, what is the problem will Gilbert, what is the problem with Gilbert syndrome is bilirubin transport deficit. When I say bilirubin transport deficit, you have a genetic mutation in the gene UGT1A1 located in chromosome 2 that produces your UDPGT. What is UDPGT? Kahit nakamut ka sa bayan mo kung bigkasin, what is UDPGT? That is your u-redeal diphosphate glucoronyl transferase. O, di ba? So, pag naringigyan ang magulang mo at may anong galing-galing na anak po. So u-redeal diphosphate glucoronyl transferase. So it produces UDPGT. So ang problema natin sa Gilbert, wala nang nagtatransport. At dahil wala nang nagtatransport, impaired ang cellular uptake natin ng bilirubin. Meaning to say, your bilirubin being carried by your albubin, akong tin sa albubin, ito sa albubin, yung dalad-dalad niyang mga B1, hindi niya maipasok sa hepatocytes para makonjugit. Nang kukuhapu ako. So kung meron ng, kung ilalabas mo ngayon ulit yung ating pathway, nangka problem si Gilbert di ito sa bandang ito. Wala ka nang u-redeal diphosphate glucoronyl transferase dahil nga may mutation. Hindi na nakukonjugit yung B2, yung B1, ito becoming B2, kasi nga hindi na makapasok sa hepatocytes. Nakukuhap. So that is a transport deficit. Again, that is your Gilbert syndrome. Sino pa kasama ni Gilbert? Okay. And by the way, dahil dyan, B1 yung increase. Nagigets nyo naman. Later, I'll try to show you a tabular form para maintindihan niya siya. Okay. We also have your triangular nod jar. Crangular nod jar is conjugation deficit. Okay. Conjugation deficit. I think ay Gilbert transport deficit. Hindi makapasok. Dito naman ay nakapasok. Pero ang problem natin dito, hindi na nakukonjugit yung B1. I hope by just saying the definition of the disease, alam nyo na agad kung alo, anoong type ng bilirubin yung increase. So this triangular nod jar is actually a syndrome of chronic, and conjugated hyper bilirubin niya. Okay. Infants can be treated by phototherapy. I guess I was able to explain that last time since that was a question of Pamela na how does phototherapy help people na may mga bilirubin problems? Because dahil na hindi makonjugit sa loob ng kanilang liver, phototherapy would help. Okay. Phototherapy would help. Which lead me to my question. What type of bilirubin is elevated in criggler's nod jar? What type of bilirubin increase in criggler's nod jar? B1, B2. Bananas and pajamas. Okay, correct. It's your B1. Okay. These are your B1. Okay. Moving forward, we have your criggler's nod jar. So, kung mapapansin ninyo, criggler's nod jar, I want you to write this down na, kaya bisyap din to. Criggler's nod jar is the most common and the most severe. Okay. And criggler's nod jar has two types. Type one and type two. Amazing. So, we have type one and type two. So, you can see here, criggler's nod jar is a deficiency in your UDPGT or your glucoronyl transferase, which is a total or absolute deficiency. So, meaning to say, eto yung mas malala, type one is more severe than type two. Okay. So, colorless yung bile, positive kernycterus. Again, what is kernycterus? Deposition of bilirubin in your brain. Okay. In your brain. Sabi nga ni. Architectlian, Austria. So, sa ating mga big brains. So, type one criggler's nod jar and type two criggler's nod jar. Okay. Gilbert transport deficit, criggler's nod jar conjugation deficit. Both are having increased B1. Okay. Si criggler's nod jar type two pwede pang normal yung kanyang B2 na hukukapu ako. Pwede normal yung B2 pag sa type two. Pero sa type one, low talaga ang B2. Kasi walang makukonjugate. Not unless, magpafototerapi ang ating mga pasyente. Nakakuha. So, that is criggler's nod jar. Type one and type two. Okay. Type one and type two. Now, let's move on to the other two. Okay. The other two, which are your Dubin Johnson syndrome and your rotor syndrome. Sir, bakto sila pinagsama? Magkamukha ba sila? Magkamukha. Tama. Your Dubin Johnson syndrome, your DJ, ay ko, DJ nalang namin saan. Your DJ syndrome and your rotor are characterized by the blockage of blockage of bilirubin excretion into the canaliculi. This is not post-hepatic yet because the problem here is actually kung kanina, hindi makapasok si Bilirubin sa hepatocyte, ngayon naman hindi makalabas si Bilirubin sa hepatocyte. Bakit? Because they lack your multidrag-resistant, multispecific, organic, and ionic transporter protein. Or your MDR2 slash CMOAT. That is your, that is the entire definition of that. Multidrag-resistant, multispecific, organic, and ionic transporter protein. Sir, kailangan ko pa i-memorize. Sige, basta yung MDR2, basta alam mo kung ano ibig kung sabihin sa DJ, John, sa DJ at saka sa rotor. Okay? So, what's the problem here? The problem is this. Okay? Increase ang ating B1 or B2. Which one is increased? B1 or B2. Sa DJ and rotor. B1, B2. Ang O3 and O4 wala nang sumasago. B1 or B2? Okay? The one increase is your B2. Okay? The one increase is your B2. So, in your DJ and rotor, elevated si B2, and of course, si Total Bilirubin. Although for the rest, actually, increase nalaga si Bilirubin, nalala na pag may John, this na. Right? So, this is your lever, the chura of your lever. So, the, what do you call this? The classification on how we would be able to classify DJ and your rotor sendo is by the appearance of an intense dark pigmentation in the lever due to the accumulation, sorry, due to the accumulation of your bilirubin. Okay? Due to the deposition of your bilirubin. And you can actually see that in your rotor syndrome. Okay? So, makikilagay ako nyan, ha? Sineparito na kung sino si DJ kay rotor. Si DJ may problema sa MDR2 si MOT, pero wala nang dark pigmentation sa lever. Si nang meron, si rotor. Okay? Si rotor. Okay? So, moving forward, ang abang sinabi ko. Okay? So, balik'tad. Balik'tad. Si DJ ang may black pigmentation, si rotor ang wala. Okay? Si DJ meron, si DJ ay mai team, si rotor ay wala. Okay? Si DJ Johnson yung meron. Okay? So, paana na lang. Paedit sa notes. Okay? Last is your lucid result, um, syndrome. So, it is a familial form of unconjugated hyperbillerobinemia. Obviously, what type of bilerobin is elevated? B1. Okay? So, um, this is, um, this is most common. Okay? This is most common um, in your babies. Okay? So, in the prehepatic, guys, nakikita yung screen. So, I want you to master this. Okay? So, in the prehepatic, total bilerobin yung increase at unconjugated. Okay? B1. B2. B3. B4. B5. B6. B7. B7. B8. B9. B9. B9. B9. B9. B9. B9. Okay? B1. Sa hepatic, sa Gilberts, lahat mataas, sabi ko sa inyo, di ba? Pero sa Gilberts, wala ang conjugated. Kasi B1, ang, napansin yung arrangement ito, total bilerobin, B2, B1 nyan. So, normal, increase, decrease at regular na jar, kasi wala ng nakokonjugate. There you go. So, Dubin Johnson. Okay? Sir, halap para si Dubin Johnson sa kasi rotor, hanapin yung mai-team kay DJ yung. Okay? So, eto, John dis in the newborn. Okay? John dis in the newborn, halos ka mukha ni Gilberts. Okay? Halos ka mukha ni Gilberts at ka mukha din ni pre-hepatic. So, you need to read the definition kung ano yung problem. Okay? Post-hepatic, sir, lahat mataas, yes, lahat mataas. An example of that is in your cirrhosis. Cirrhosis is a clinical condition in which your scar tissue is normal healthy tissue. Question, how many percent should be abolished in your, in your liver bago siya mag-fail? Okay? How many percent? Ay. Sir, how many percent? Ang sagot dito, 80, 80, 80. May sumagot ng 70. Parang yun, 70 yung kailangan ninyo para pumasa. Okay? 70 yung kailangan ninyo para hindi kayo ma-abolish. Okay? Parang hindi kayo ma-abolish. So, 80 percent, okay, 80 percent yung ating kailangan, 80 percent dapat yung abolish. Okay? So, saan si 16 percent? Ano yung 16 percent na dapat yung tandaang 16 percent? 16 percent, saan siya? Okay, nitrogen content. Very good, nitrogen content. Okay, saan naman siya, no? Gyo ko lang, tama na. Okay, so, moving forward, okay, so, your cirrhosis is most common in mail. Most common in your mail. So, other, this is the most common cost of your cirrhosis is bakt, di ba? Alkoholysem, hepatitis, and your Wilson's disease. Question what? What plasma protein is the problem in your Wilson's disease? Sige nga, what is the problem in your Wilson's disease? What is the problem with your Wilson's disease? Ay, ay hindi po yan. Tama, what plasma protein ng tanong? Tama po, ang tamang sagot ay your okay, 0304. Ano, ang tamang sagot ay your ceruloplasmin. Correct. Ceruloplasmin in cases of Wilson's disease, increase, decrease. What is the matter? Increase, decrease. Okay, what is, anong level? Okay, decrease, very good. So in Wilson's disease, ceruloplasmin is decrease. That's why your copper are deposited in your brain, in your liver, causing your jaundice, eventually your cirrhosis, and also in your eyes. And we call it what? The deposition of your copper in your eyes are called what? What do we call that? Ay, mabubilis ang ating mga keyboard warrior. We call that your 0304. Bakit dilin yung tanong ko sa 0304? Okay, caser, flasher, ring. Okay, caser, flasher, ring. So, that is for your, um, that is in your eyes. Okay, that is in your eyes. So, having said that now, ayan, your caser, flasher, ring is observed in your Wilson's disease, and eventually the deposition of your liver, the deposition of your copper inside your liver to cause your cirrhosis. So, sa cirrhosis kasi your liver can actually regenerate. Kaya niyang gumawa pa ng bagong cells na hepatocytes. It's just that when your, um, your RBS, your, ano ba yun? RBS, naiwan sa hema yung otak ko. In cases of copper deposition, ayan, in cases of cirrhosis, rather, yung scar tissues natin. Hindi na yan nag-regenerate. Okay, ganyan na siya. Okay. So, treatment, ano do treatment sa cirrhosis, number one, actually di treatment, but prevention are abstinence from alcohol. Okay, so tap your back. Okay, tap your back. So, next are interferons for viral hepatitis. And also have corticosteroids if you have autoimmune hepatitis. Okay, autoimmune hepatitis. Moving forward, we go now to your tumor. So, when it comes to your tumor, we have, usually these are tumors with poor prognosis. So, we have the first classification which are the primary or the metastatic tumor. So, around 90 to 95% of all hepatic malignancies are classified as metastatic. So, it can move around or it can be, it can be transferred to other parts of the body. So, the second classification is whether it is benign or malignan. So, ayan. So, your hepatocellular adenoma, your hemangyoma, those are benign. But your hepatocellular carcinoma, your hepatoma and your balda carcinoma, those are malignan. Okay? Those are malignan. So, when we say primary, when we say primary kasi, sa liver talaga nagkumpi sa ang problema. Pag metastatic, nalipat lang sa liver, yung problema. And you would wonder, sir Bakit, if you still remember in your histopath, di ba meron different ways on how your, how your tumor will be, will be transferred. It can be direct contact. I alloy it, dinatanggal yung breast na ipatong doon sa intestine mo. Nalipat, nalipat yung ibang cells. So, makakaroon ng tumor ulit sa intestine naman. Okay. Dahil lang sa pinatong. Direct contact, legit doon doon doon. Uyon. It can also be due to lymphatic o lymphatic na lymphatic metastasis, or it can also be because, ito yun no. May mga tumor cells that are freely circulating on your blood. And remember, remember na in your liver, you are receiving 1.5 liter of blood every single day and you have your portal vein and your hepatic artery that receives 70% and 25% of blood each day. So, there's a possibility talaga na those tumor cells will be deposited, will come across your liver causing now the metastatic cancers, okay? The metastatic tumors in your liver. So, ayon. So, moving forward, after your tumor, we go now to your RAISE syndrome, some call it RAISE syndrome, RAISE syndrome, whichever you want to call it, then yang go. So, ito ayon, ginagawan ko ng palatandaan para yung matatagandaan, RAISE syndrome, mahilig sa mga R. Bakit? So, originally, your RAISE syndrome is actually a group of disorder either by infection, metabolic problem, toxic drugs, toxic drug induced that are almost exclusively found in your children, okay? So, ano yung drugs as perine, R, RAISE as perine. Anong mga infections, varicella, R varicella, what other condition, metabolic conditions, gastroenteritis, okay? And influenza, sir, nasi raya yung ano mo, nasi raya yung palatandaan mo. Walang R sa influenza. Pag may influenza ka, diba? Pag may flu, giniginaw ka. So, basahin yan yung, giniginaw ka. So, may R pa din, sa influenza. So, RAISE syndrome, maipilit lang, varicella, gastroenteritis, influenza, giniginaw, okay? And you're aspirin, okay? So, these are the usual causes of your RAISE syndrome, okay? So, last but not the least, okay? So, we all, ayon. So, ayon pa lang. So, antifalopathy, fatty liver, the generation of liver, entrance urinase, elevation are just secondary, secondary effects ng RAISE syndrome, okay? ng RAISE syndrome. So, alcoholic, alcohol and drug related disorder. So, according to Ms. Katryona Gray, diba? I am for it being, so, are you in favor with the use of marijuana, legalization of marijuana, okay? So, I am for it being for medical use, but not so for recreational use. Ayon. So, paborito yan is rinitan, okay? So, this is the most common cause of immune-mediated injury to your hepatocytes, okay? Immune-related, immune-mediated injury in your hepatocytes. So, where can you see it? You can see it, add na yung ang drugs that can cause it. Your acetaminophen, your ethanol, which is the most common drug, okay? Alcohol is considered to be, actually, they consider it drug as well. So, most common drug, alcohol, ayon. So, alcohol, the hydrogenase, and acetaldehyde, the hydrogenase. So, acetaminophen in your ethanol would induce an immune response. And that immune response would be directed against your, will be directed up to your liver, okay? So, moving on. Okay, moving on. So, acetaminophen, sa nyo nakikita si, acetaminophen? Anyone? Sa nyo nakikita si acetaminophen? Sa parasetamol, okay? Sa parasetamol. Kaya ang sabi ni, janloid, ingat. Okay, hindi niyan sinabi mag-ingat kasi pupuntahan mo, mag-ingat sa parasetamol, okay? So, hindi niyan sinabi mag-ingat kasi pupuntahan mo, mag-ingat sa pag-inom ng parasetamol because it can actually cause, it can actually cause intoxication and eventually liver disease, okay? It can cause liver disease. So, ingat, okay? So, kapag wala naman lag nat wag uminom ng acetaminophen kasi bawal, okay? So, alcohol induce injuries. So, you choose your poison, ano ka ba? Black Clay Bells, Mironov, Hennessy, McCardy, or Jack Daniels, okay? So, pili na po ang mga suki. So, alcoholic, fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. So, all of this are very, all of this are due to alcohol induce, okay? So, you have a risk of having alcohol induce liver injury if you would take 30 grams per day. So, that is three to four drinks per day, okay? Three to four drinks per day. So, imagine that, di ba? Kung three to four drinks ka per day, okay? So, talagang ano na, talagang talagang talag dito. Yung hindi mo na inong nang ilang, nang ilang one, inino mo nang isang ano. Well, di ba? That would cause a liver induce injury eventually. So, when it comes to ano, when it comes to high risk, ayan, so 120 grams per deciliter. So, 12 to 16 drinks per day. So, ang iniinong nila, okay? 12 to 16 drinks per day. So, sabi nga natin, ang highest talaga na risk would be seen if it is greater than 120 drinks, okay? 120 drinks. So, when you reach your toxicology next time, meron tayo dun pag-aaralan na yung alcohol intoxication, nakakatawa yun kasi, based on the characteristic ng lakad ng ano, pag lakad ng, pag lakad ng ano, pag lakad ng isang individual, malalaman mo na kung gano siya intoxicated, okay? So, malalaman mo yung levels ng intoxication ng ano. I don't remember it pa, kasi did not review that. Pero meron gano, okay? So, ayan, dinatawag na po nila si Marb. Si na si Marb? What Marb? Joshua Marvin ka ba? Ah, Marb ba? Okay. Okay. So, moving forward, okay? So, moving forward, ginbulag daw sila mga kapatid, okay? So, alcoholic fatty liver. So, alcoholic fatty liver has a slight elevation, makikisulit ako, has a slight elevation of your AST, ALT, and your Gamaglutamil transferase or your GGT. And a biopsy would show fatty infiltrates in your liver, okay? Fatty infiltrates in your liver. So, I guess I will not be able to discuss na entirely the different test for liver function. But I would, siyempre, re-record ko na lang para ma-aral ninyo, okay? So, alcoholic fatty liver, so, instead na mag-makeup class pa tayo, mag-re-record na lang ako, ha? So, alcoholic hepatitis, ayan. So, moderate, makakikita yung increase na mahayan. So, we have the deritis ratio. So, the deritis ratio is AST, ALT ratio greater than 2. Okay? If it is greater than 2, alcoholic hepatitis siya. Okay. But if it is less than 2, pag less than 2 yung deritis ratio, viral hepatitis siya. Okay, makikisulat ko na. Pag greater than 2, deritis ratio, alcoholic. Pag less than 2, deritis ratio, that is, viral hepatitis. Okay? Viral hepatitis. So, in the scoring system, ayan, meron tayong scoring system na hepatics, alcoholic hepatitis. We have your moderate discriminant function, your Glasgow score, your model for end-stage liver disease or your meld score. Okay? So, ayan, eventually meron din ikaw alcoholic cirrhosis. So, similar to what we were discussing kanina, cirrhosis as the appearance of replacement of your scar tissue induced by alcoholism. Okay? Induced by your alcoholism. So, the time is 11.26 right now. The time is 11.26. So, I'll be cutting this recording para lang meron tayong partition that this video, what we discussed are all about the different diseases related to liver. Okay?