Hepatitis A | Podcast

Added: 2026-05-28

[00:00:08]Welcome back to the Ninja podcast. Today we're talking about hepatitis A. And we're going to break up hepatitis into into individual lectures. So it's a little more bite-sized pieces. So we're going to do A, B, C. D is kind of with B and then we'll do hepatitis E.

[00:00:22]>> Yep. Sounds good.

[00:00:23]>> All right. So first up is hepatitis A.

[00:00:25]Let's get right into it. If you had to say the most important thing about hepatitis A and really the population that we have to be careful with, what would you say about hepatitis A?

[00:00:35]>> I say like it's it's so it's it's a fecal oral transmission. And that sounds like what it sounds like. It's it's people who have let's say been infected with hepatitis A. It's actually shed through their intestinal lining. So generally it's biliary secreted. And so then the virus gets into the intestines.

[00:00:54]You poop it out. If someone then takes and let's say that they didn't clean themselves or sanitize themselves appropriately and they touch something and that other person touches that same thing and then they eat something that has some of that feces like that material that has the virus sounds absolutely revolting when you think about it like that. But that's really the the logic behind it. They ingest it.

[00:01:16]They can get hepatitis. And so that fecal oral transmission comes from usually I'd say the biggest kind of like risk factors is probably like any contaminated like water source or probably even like you know raw undercooked like foods is is really a big one. And I'd say just any kind of like higher like risk behaviors kind of put you in generally in that concept. So generally like maybe IV drug abusers, men who have sex with men that those are kind of things that potentially bring about that risk of that fecal kind of oral transmission. But >> and it's unfortunate with hepatitis A because this is like you always hear maybe it's like some it's it's badly sanitization or the food where it's like food trucks which are my favorite. I love I love food trucks. So this is something where it's like be careful where you get your food.

[00:02:04]>> Yeah. Yeah, a lot of the times it's like traveling is going to be in the clinical vignette where they travel to some particular area where maybe it's a little bit more like of an endemic area where their sanitation areas are a little bit like not as good and and so that puts some of the food and water sources maybe at a contaminated risk.

[00:02:19]I'd say those are probably the biggest things. And then obviously since it's a close contact kind of thing, like if you live in like a dorm or you live in a I don't know some kind of institutionalized like like a nursing home or a household member that has it, you guys are sharing certain types of things that can easily take and transmit that again that virus via the fecal oral route. So those are the biggest ways that I think you can get it is that fecal oral transmission from contaminated food, water sources or being in like an area where there's a lot of close contact exposure from those who are infected. Daycare centers is another one because kids can actually be pretty much like asymptomatic. They can show like no symptoms of it, but they can just pass it around like wild for fire because they're, you know, digging and rumaging around back there and they're saying, "All right, here give me my my Rugrat toy." And oh, you and then that that kid goes and sucks on the tip of it and say, "There you go." Yeah.

[00:03:08]>> So, that's a very common way that they can pass it along.

[00:03:11]>> Let's get into some cases. Here we have case one. A 26-year-old man comes in with one week of fatigue, low-grade fever, nausea, and diffuse myalgas. Over the last 48 hours, they developed dark urine, yellow eyes, and mild right upper quadrant discomfort. They recently returned from traveling and mentioned eating street food and raw vegetables.

[00:03:34]They have no history of chronic liver disease. overall they're just relatively healthy. They're younger. What are you thinking about? Obviously, we're talking about hepatitis A. So, what are some of the red flags that you're hearing with this patient? Well, generally hepatitis A obviously there we talked about the fecal oral transmission. Whenever you ingest that virus and it gets into your esophagus, your stomach, it crosses the intestinal mucosa, gets into the apatic portal circulation, goes to your liver.

[00:03:59]You go through two phases. So, first one is called a prodal phase. So it generally appears like let's say maybe I don't know probably like one to two weeks after you first were exposed. And so the symptoms that you get is usually the kind of the viral attack on the liver. It's the apatite infection itself. So once the virus gets into the apatite it replicates sheds itself into this the actual stool where again it can be transmitted to the other individual.

[00:04:23]But from that you also get kind of like a your cuper cells which are like they're like hpatic macrofasages essentially. They kind of sense this and they release some cytoines and the cytoines can cause like localized apatic edema that can cause some of the right upper quadrant pain. Maybe the liver can get a little bit bigger or we can get a padomegaly. On top of that those cytoines can also cause things like activation of the chemotrigger zone. So they can get nausea they can get anorexia they can have decreased appetite vomiting and they can get low-grade fever from activation of the hypothalamus. And then the myalgia is it may just be that the some of that TNF alpha tends to actually cause a little bit of an effect on the muscles. So that's probably the phase that they start off with is the is the prodrome phase and then about maybe a week or two weeks after that then they progress into what's called the ectctor phase and the ectaric phase is essentially the virus doesn't actually damage the cell itself.

[00:05:13]It doesn't actually like cause lis of the hpatocytes. It triggers it takes a piece of the virus and puts it on its MHC1 complex and then cytotoxic tea cells natural killer cells they come and they recognize it and they trigger cell death. So they actually cause apoptosis and sometimes get secondary necrosis where you actually your immune system kills the apatocytes. When you kill and damage those apatocytes, anything that's inside of those cells leak out. ALT leak out. So I would expect that they would have some increased liver enzymes. Any kind of like mixture of unconjugated and conjugated Billy Rubin can leak out into the bloodstream that can cause a hyperbillarenemia that can actually contribute to jaundice. And on top of that, if your hpatocytes are damaged, you get inflammation. Inflammation.

[00:06:00]Think about this. Here's two cells.

[00:06:03]Right in between them is a biliary canaliculi. If your cells are inflamed and you get inflammation, what are you going to do to that biliary canaliculi?

[00:06:10]You're going to squeeze on it. And then your bile which contains billy rubin and bile salts. They can't flow. So that's called intrahypatic choleistasis. And that causes Billy Rubin and bile salts to backflow out of the bile and into the blood. And so then that Billy Rubin goes up and it can cause jaundice which is the you know yellowish orangish discoloration of like the hands, the palms and hands, soles of the feet, other areas of the skin and then ictus which is the yellowish discoloration of the eyes. And then because of that Billy Rubin being high in the blood, it gets secreted into the urine and that causes the dark urine. And then if Billy Rubin isn't in the stool, it's what gives the dark, you know, brown pigment to that, you know, to that that turd. And so you lose that and so you're pooping out like palish whitish turds, you know. So that's kind of the things that are probably going on here is that they started off with the produm phase and then a little bit later they progressed into the ectaric phase. Most patients with hepatitis A, they resolve. If they have a good immune system, they pretty much clear it on their own. You don't have to give them anything. But in this patient, we don't know, have they completely cleared it yet? But they're probably in that ectctor phase right now is what I'm expecting.

[00:07:22]acute versus chronic.

[00:07:24]>> Again, I would say that hepatitis A rarely ever ever ever if at all becomes chronic because most of the time, as long as the patient's relatively immunompetent, their CD8 cells and natural killer cells eliminate the virus on its own. And so, it rarely ever becomes chronic in these particular scenarios like things like hepatitis E virus, which we'll talk about, it can become chronic. But the big ones that we talk about a lot of the times is like hepatitis B and hepatitis C. All right, perfect. We don't have to kind of go into that anymore. Now, with this patient, we have a good idea of what's going on. You have some suspicions and you hear the history and there's some red flags there. Travel, street food, raw food, things like that. So, you're thinking, how do I go ahead and do my diagnostic approach? What system, what systematic approach will you take for this patient?

[00:08:11]>> Yeah. So, I think any patient that came in and let's say that I didn't have like a good history, but in this case, I do.

[00:08:17]When a patient comes in jaundest, pale stools, dark urine, and they have right upper quadrant pain, they have apatomegaly and some other non-specific signs, the next best thing is to just get some labs. So obviously you'll do a basic kind of workup, but probably the most important one in this canar scenario is getting some LFTs. So that's probably what I'd start off with. You can add like a a coagulation panel onto that. It's never a bad thing like a PTINR and a PTT and things of that nature. But I think the most important thing is the LFTs. If you see the LFTs, the key thing about that is it's looking at what kind of injury is it. Is it predominantly an increased A and ALT more so than the Billy Rubin and the ALC Foss? If that's the case, it suggests more of a padellular injury, which is what you see more often than not in patients with viral hepatitis. You can get a little bit of a bump in the Billy Rubin like we talked about, but the AD and the ALT are going to be the really, really big things. They're probably going to be super high. If it's acute, you'd expect it to be greater than like a thousand.

[00:09:15]>> Wow.

[00:09:16]>> So that's the first thing I would look at. Now, anytime a person has a super high a and they have an elevated billy rubin, you cannot exclude a gall stone or some type of like, you know, kidocaliasis, ascending colonitis, something of that nature. And so it is extremely crucial that I rule out a biliary obstruction. And so a right upper quadrant ultrasound if they had super elevated LFTs and and Billy Rubin as well and they're a jaundice I would check that to just make sure I rule out an obstruction because that's something I can actually do something with immediately.

[00:09:47]If that came back with no obstruction then I start to say okay my injury seems more hpatoscellular I don't have an obstruction that means that this is a potential hepatitis that could be autoimmune related it could be viral it could be es schemic it could be from right heart failure there's so many different reasons it could be from Tylenol that's when you start looking at their history a lot their history suggests an acute onset they had some travel I start to think could this be a viral hepatitis that's when you send off the viral hepatitis panel. In this case, I'm looking, you know, we're talking about hepatitis A, but guess what?

[00:10:21]You'll send off hepatitis A, you'll send off C, you'll send off B. E is like an add-on. We don't often do that unless they have like specific risk factors, but it's an add-on to your normal viral panel for hepatitis. So, I would definitely do a viral corology if I had risk factors, apatosellar injury, and no bilary obstruction. And then from there, that's going to tell me if they have acute viral hepatitis due to HE. Other than that, that's probably the at least initial startup that I would do for this patient.

[00:10:49]>> Perfect. And then how do you determine whether this should be really an outpatient case or inpatient? What are your differences?

[00:10:56]>> Well, I think outpatient case for these is if I had a patient that probably presented with like a very, let's say, a mild case, maybe they had some LFTs, but they weren't significantly jaundist.

[00:11:10]they weren't showing a lot of signs of I'd say the biggest thing is like a like fulminant hpatic failure. That's really what would concern me to say that this patient needs to be admitted and monitored. So fulminate hypatic failure would be one and so that would be super high LFTs. They're bleeding or they have a coagulopathy. So I checked their PTINR let's say and it was like greater than 1.5 they're bleeding. They have evidence of hyperammia. So maybe they're confused. They have asterexis that would concern me. Also, when you have hepatitis, you get nausea and vomiting, and they can vomit a lot. And if they get like pretty like hypoalmic or dehydrated sometimes, that might make me consider admitting them as well. If they're particularly if they're hypoalmic and they can't keep up with their fluid intake. I'd say those are reasons why I would say this patient probably should be watched as if they have signs of encphylopathy, coagulopathy, or significant dehydration. I would probably admit them. But for our patient, for the most part, they're 26. It's mild. We're going to probably say, "Hey, you're good to go. Outpatient. This will this is self-limiting. It will get better on its own. Your body will clear it. Maintain hydration. All the good stuff."

[00:12:18]>> Yeah. Yeah. That's probably the key thing for these patients. Yep.

[00:12:21]>> Perfect. Well, then that is case one. I feel pretty good about that one. I hope you do, too.

[00:12:26]>> Yeah. Yeah.

[00:12:26]>> Awesome. Well, then let's move on to case two. This is the red flag case.

[00:12:29]This is the one we're really worried about. And honestly, I'm pretty sure it's a such a small percentage of patients that actually can turn from hepatitis A into something like acute liver failure.

[00:12:38]>> Yeah, it's pretty low. Probably like one, maybe less than that.

[00:12:42]>> Wow.

[00:12:42]>> Percentwise. I mean, it's it's just not like one of the common ones obviously, but it can happen. It's still something to definitely keep an eye out, but probably lower on the likelihood.

[00:12:50]>> And this one will make it even more so because they have Well, let's hear it.

[00:12:54]The we have a 68-year-old female with chronic hepatitis C comes in with one week of malaise right upper quadrant pain and now has jaundice family reports that the patient is acting confused and had an episode of a near fall on exam you do note asteris so with this patient we have a chronic hepatitis C comes in with some new findings this isn't her normal her normal self and she's confused asterixis >> yeah so anytime a patient That's the only time where it really becomes more likely. So like we said acute liver failure or fulman hypatic failure from hepatitis A is pretty rare but it increases in incidence whenever you have a chronic liver disease especially if you have a co- infection. So if they have hepatitis C that definitely increases your risk of developing acute liver failure because you already have a diseased or damaged or chronic liver disease in that nature. So having a chronic liver disease especially a co- infection with another hepatitis virus increases the risk more so for acute or fullman hepatic failure. So, seems like that's what they're in.

[00:13:55]>> And let's not forget advanced age as well. I mean, she's 68.

[00:13:58]>> Yeah. Yeah. But this one definitely she's I'd say concern for fulment hypatic failure is a pretty big one here. And based upon the presence of, you know, confusion and asterexis, I mean, you'd probably check maybe an ammonia level, it would probably be elevated. I would also again check the PTINR and see if there's any evidence of bleeding from this patient because they would probably have some increased risk of bleeding. And so coagulopathy and sephylopathy with predominantly elevated A and ALT in this clinical context would concern me for acute liver failure.

[00:14:28]>> And then also the confusion with you're thinking potentially ammonia levels.

[00:14:32]Yep. High elevated. Yep.

[00:14:34]>> And then with this patient, would you then go ahead and say let's do a right upper quadrant ultrasound >> for this one? If I had this patient, again, I think the the big thing is is if a person came in and they had signs of like acute liver failure like this, which they would present with, they probably present with signs of jaundice.

[00:14:51]That would be the biggest thing.

[00:14:52]Probably have right upper quadrant pain.

[00:14:54]They would have increased LFTs. Again, I would still you always rule out the bilary obstruction with the right upper quadrant ultrasound. Same concept for that one. Do the viral corology. If I confirm that this is hepatitis A kind of acute liver failure or at least acute viral hepatitis due to type A the next thing that comes into mind is like we said are they in fulminant hpatic failure fulminant hpatic failure really comes from looking at the evidence of coagulopathy so is that PTINR really high and do they have incphylopathy and that's the more particular thing you prefer to go off the symptoms so if they have asteris they have confusion alteration seizures that's going to be more valuable than the ammonia level but I could still get the ammonia level and add that on. But again, it's more symptoms. And so the presence of the liver, the viral hepatitis plus the evidence of coagulopathy and encphylopathy that puts them into the acute liver failure bucket. And let's say we go through some results just to give you a little bit more of this information. Her ASL to ALT is greater than 2,000. Total Billy Rubin is 10. INR is 2.6. Ammonia is highly elevated. So we we are thinking then acute liver failure in the setting of acute viral hepatitis.

[00:16:06]>> Yeah.

[00:16:06]>> And of course she has underlying hepsi.

[00:16:09]>> So for this patient I'm wondering what you do with treatment. Where do you start first?

[00:16:14]>> Well for this one it's again it's usually like for for this patient it's it's a little bit more aggressive. So obviously supportive care will only get you so far. If they're dehydrated you can give them some fluids. if they're, you know, having puritis and things like that, you can do the choleisteramine and and a lot of a lot of this really is kind of the that's that's really maybe the only mildly beneficial for the patient who's not going to get admitted.

[00:16:38]In this kind of patient who's getting admitted, they they're they're going to probably need a liver transplant.

[00:16:43]There's only so much that you can do supportively for this patient. Maybe for the hyperammia, I can give something like lactolose to try to lower that ammonia level.

[00:16:52]Sometimes you can add in refaxamin if you really need to. For the coagulopathy, I can just try and correct their INR and give them things like PCC, which is a prothroin complex concentrate, and that may help to give them some of the coagulation factors that the liver is no longer producing to prevent them from like bleeding. But eventually, that's just putting a band-aid on a problem that is going to only need to be fixed with a liver transplant, unfortunately.

[00:17:19]>> All right. Well, that was our case two and you we don't like to see that, but luckily it is very rare.

[00:17:26]>> Yeah.

[00:17:27]>> All right. So, for the last part of this episode on HEP A, I want to talk just briefly about prevention because there are ways that we can do prevention, especially when you know you're traveling to endemic areas.

[00:17:39]>> So, this is where boards kind of love to hit you with a postexposure type question.

[00:17:44]>> So, what can you do with hepatitis A?

[00:17:45]Talk a little bit about the vaccines we can do. Well, if most people get routine vaccines, so you know, for preexposure, prophylaxis, pretty much, I mean, me and you when we were younger, you get two doses of Havris, which is the hepatitis A vaccine. And so that's pretty much routine, like standard vaccination process, at least get two of those doses >> and that's for children greater than one year.

[00:18:08]>> Yeah. Yeah. So that that's pretty much routine. Other scenarios where you give it is in those patients who are kind of like in high-risisk scenarios. So, like you said, they're traveling, they have high-risisk behaviors, things of that nature would probably trigger me to give that hepatitis A vaccine. And again, it's more as a preexposure. You're giving it to them so that they have the antibodies. they ever became exposed from those high risk or exposures from again maybe they're traveling men who have sex with men certain types of like areas that you're going to that are a little bit more high risk close contact or things of that nature then yes I would probably say that they should get the hepatitis A vaccine as well but again that's going to be a different scenario so most people they're going to get the hepatitis A vaccine routinely two doses as a preexposure prophylaxis if you get it other than that time it's because you're going to be putting yourself in a high-risisk scenario. And then I think the classic example is you're getting ready to travel over to an area that is it's more endemic to that.

[00:19:03]>> And then potentially even if they do have like HEP B or HEP C, I would guess that they would get this vaccine as well.

[00:19:10]>> So for this one, yeah. Yeah. Same thing because in that scenario, they're pretty high risk. And so if they ended up getting hepatitis A and they already had that co- infection, especially if they had something like hepatitis C, they're a high risk for fulminant hepatic failure. So yeah, >> how about post-exposure prophylaxis? The the classic case of daycare outbreak, let's say.

[00:19:30]>> Yeah. So I I think this one depends. A lot of the times again I think if you got a healthy individual like I think the age is like one to 40 years old, you can probably just give them the hepatitis A vaccine if even if they were in that kind of like scenario where it was a a close contact exposure. And so they had exposure. You want to give this to them pretty early though. So once you once you turn yellow, there's no point in giving this thing. I'm not kidding.

[00:19:55]Like at that point, it's like why even give it?

[00:19:58]>> Let the body do its thing.

[00:19:59]>> Yeah. Exactly. You're trying to prevent the actual problems from this. And so ideally, you want to try to give this like pretty soon, at least two weeks.

[00:20:09]Yeah. Like you know, at least less than two weeks since they're like their exposure because once they get to that that that ectaric phase, it's like all right, it's it's kind of a little bit too late to be honest with you.

[00:20:18]>> Gotcha. So yeah, giving this one is really for that close contact exposure.

[00:20:24]Giving it as soon as you possibly can is desirable. If they're pretty healthy, relatively within that one to fouryear range, I think you can just give them the vaccine. But I think if they're like, you know, generally in those patients who probably are a little bit more like immuno compromised, it's it's they're not as good at being able to probably like respond to a vaccine. So maybe they don't have the immune system capable of producing those antibodies and those ones I probably would give them not necessarily the vaccine. I would I probably give them like some form of a the actual amunoglobulin. So we actually do have like hepatitis A amogloabbulins.

[00:21:01]I'd probably give them something like that. And sometimes you can still give the vaccine as well, but you're mainly giving the imunoglobulin because you're not sure if that hepatitis A vaccine will give them the pure response that they need.

[00:21:12]>> Awesome. So healthy ages 1 to 40, they can be given the vaccine. They should respond well to that. If they're less than one year or they have a vaccine contraindication, we can give them the HIV immune globulin. Or if they're greater than 40, immuno compromised, or a chronic liver disease, we're probably going to do a vaccine plus the immunoglobulin.

[00:21:32]>> Yeah. Yep. Exactly.

[00:21:33]>> All right. Perfect. That was it. Short and sweet. This isn't a crazy high yield topic, but we got the information that we needed.

[00:21:40]>> Yeah. And I think that's the key for viral hepatitis is that it's obviously a a preventable illness in certain scenarios. And if you get it, it's not to say that it's not important, but it'll probably go away on its own without having to give any kind of like antivirals or the chances of it developing acute liver failure is pretty low. Obviously, if you have underlying co- infections from things like hepatitis C, it puts you at risk. But for the most part, this will work its course and eventually it'll resolve.

[00:22:09]Unlike other kinds of infections like hepatitis C and B, those may stick around and increase your risk for a lot of problems, which we'll talk about eventually. But hey, I hope that you guys like this podcast. I hope you learned a lot about hepatitis A and I hope that you feel confident about it.

[00:22:23]And if you guys do, you guys know the deal. Hit the like button, subscribe, comment, keep listening to this. Give us think any suggestions that you guys have. And I just hope that you guys are learning a lot and just staying hungry.

[00:22:33]And I love you. I thank you. And as always, until next time.