Ep16: Cirrhosis | Pathophysiology, treatments, causes

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This podcast covers cirrhosis or end stage liver disease.  I discuss the causes, labs associated with, and pathophysiology of cirrhosis.  This is a fun review of treatments and patient care for patients suffering from this terminal condition.  Great review for or clinical nursing.

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Podcast Transcription

Welcome to the nrsng.com podcast – the podcast created by nurses for nurses. Are you ready to

take your learning to the next level? Sit back and crank up the volume. Here’s your host, Jon


Hello friends, this is Jon with the nrsng.com podcast. Today we’re going to talk about cirrhosis –

what cirrhosis is, some of the causes, some of the signs you’re going to see in your patient and

also some of the available treatments for treatment nowadays. Before we get started though I

wanted to let you know about a new book we have up on Amazon. It is November 2014; we just

published a book on Amazon called “63 Must Know NCLEX Lab Values”. So this is a book that

covers some of the most important lab values that you need to know. It covers everything from

ABGs to BMPs and renal labs and a whole bunch of different labs that are important to know. It

covers the normal values, what causes high and low values and has some charts and downloads

that you can get PDF versions of the chart and things. If you go to www.labvaluebook.com or if

you search in Amazon, just search Jon Haws or NRSNG and you’ll be able to find it. But it’s a

great book, it will be a great help on your studies.

Like I said, today we’re going to talk about cirrhosis. Cirrhosis is an important condition to

understand because it is a terminal condition, meaning it’s incurable. There are piloted[?]

treatments and things that we can do to try to help our patients feel better, but at the current

time there is no cure for cirrhosis. Once a patient progresses to this stage of liver failure, then

there is really no turning back.


First of all, we need to understand what the different functions of the liver are. The liver is

considered a gland and that it secretes different chemicals. It produces bile. Bile is used to digest

fats. So it’s important that we have bile in our system in order to break fats up into smaller

pieces that can then be digested. The liver also detoxifies blood so when different chemicals,

drugs, different alcohol is in the system, the liver actually detoxifies that and tries to pull those;

it’s like a big filter for our blood. It also stores vitamins and iron so it’s very important for the

storage of different vitamins that we’re going need and iron that we’re going to obviously need

in our blood. It also converts stored sugar into usable sugar. As we have our blood sugars, we

actually need our liver to help convert that sugar into something that is usable by our system.

The liver also breaks down hemoglobin and insulin and other hormones. So it actually breaks

apart the heme from the globin and you know that whole process is what can lead to jaundice if

it’s not working appropriately and things. The liver also converts ammonia to urea. So it takes

ammonia and it converts it to urea, which can then be excreted from the system. And the liver

along with the spleen helps in the destruction of red blood cells.

So with those various processes in mind, seven or so different functions of the liver in mind, you

can understand what some of the signs of liver damage are going to be. So the liver, like I said, it

plays a part in red blood cell destruction so the process of separating the hemoglobin, the heme

from the globin, that whole process is what leads to having darker stool. So if you start noticing

in your patient’s discoloration of stool that could be a signal of liver damage. If they’re not able

to break the hemoglobin apart, that can actually be a sign of liver damage. Also, jaundice. If you

notice your patient becoming jaundiced – that’s a build up of the bilirubin, that’s a waste

product of the hemoglobin breakdown as well. So if they’re getting jaundiced then they’re not

able to – this bilirubin – this whole breakdown of the hemoglobin system isn’t working



So what is cirrhosis? What happens in cirrhosis is all the functional tissue in our liver, the tissues

that the cells that carry out these different functions that we talked about start becoming

replaced by scar tissue. And this scar tissue inhibits the liver from carrying out these normal

functions. And then blood flow and bile flow is also disrupted because blood can’t flow through

the liver and get back to the inferior vena cava. So because we have all this scar tissue building

up, it constricts the blood flow through the liver and we start having problems there. So that’s

why cirrhosis is such a big deal.

Some of the common causes of cirrhosis? The most common cause is actually alcoholism. With

extensive alcohol use, that can lead to severe liver damage, causing the scar tissue build up. Also

Hep B and Hep C are also common causes. Most common cause again is alcoholism and there

are a couple other possible causes but Hep B and Hep C and alcoholism are the ones that are

going to be the main causes of liver cirrhosis.

Some of the manifestations you’re going to see are you’re going to see a large and tender liver.

Your patient might have dull aching pain in the right upper quadrant as you palpate the

abdomen and in that right upper quadrant, you will most likely feel that liver. You’ll fell them

having that pain. You might notice some weight loss, weakness, anorexia and disrupted bowel

function. And you may start also noticing some of that ascites which is going to be that

abdomen kind of starting to expand out.


Some of the complications associated with cirrhosis are going to be portal hypertension. When

we say portal, we’re referring to the liver. So it’s going to be elevated blood pressure within the

liver itself. So as that happens, as the scar tissue develops, it’s constricting the blood flow

through the liver. And so what happens is blood is forced to find other routes and it becomes

shunted to collateral vessels and it often goes to the esophagus and other places. But what ‘s

going to happen with that is our hydrostatic pressure is going to increase when fluid is pushed

out of the vessels and that’s going to be one of the main causes of this ascites that we’re seeing.

So we know hydrostatic pressure is going to be on the arterial side of the capillaries – of the

blood flow to the capillaries and so what’s going to happen is that force pushing from the heart

and as that portal hypertension begins to develop, as the blood vessels are constricted within

the liver itself, that hydrostatic pressure is going to increase. With that increasing pressure, fluid

is forced out of those vessels and so that’s going to lead to that ascites. We have more pressure

within those vessels on the arterial side and all this fluid is being pushed out because it’s

becoming so greatly constricted that the fluid isn’t able to stay within the vessels and it’s being

forced out leading to that ascites.

You’ll also notice splenomegaly. The spleen enlarges due to the blood shunting. This increases

red blood cell and white blood cell destruction. So as we’re pushing more and more blood to the

spleen, we’re increasing the destruction of those blood cells. And then again we’ll see that

ascites that we’ll see just really, really round, large abdomen. And it’s this fluid accumulation

within the abdominal cavity. And again the portal hypertension is the main cause of that. What

happens is we have decreased serum proteins and we also have increased aldosterone and this

increased aldosterone is going to lead to sodium and water retention. So we’ll have this portal

hypertension, then we’ll have this increased aldosterone, so we’re retaining sodium and water.

So as well as pushing fluid out of the vessels we’re also retaining sodium and water. And we’ll

have these esophageal varices. What happens is blood starts to shunt to try to get back to the

heart, and it will shunt and create these very thin walled sensitive vessels all the way down the

esophagus. And so you’ll see your patient will have these very, very thin vessels up and down

the esophagus. This is due to this hypertension. So what happens is these are called esophageal

varices. What can happen is they’re very, very thin like I said and they’re very sensitive and

they’re very prone to rupture. Again, you have this very high pressure within these vessels and

they’re very thin. So what happens when they rupture is you can lead to massive, massive

hemorrhaging within your patients. Your patient can quickly loose liters of blood if these


We actually had a case of this in our ICU recently where a patient's esophageal varices actually

ruptured and the patient was just spewing blood out of their throat and lost several liters of

blood – three to four liters of blood within a matter of minutes. So what can be done with that is

you can kind of insert a little balloon in there and you try to stop the shunting. You insert the

balloon into the esophagus, press it up against the wall of the esophagus and try to stop this

bleeding as quickly as you can.

Very similar to kind of a stint within the heart, that this balloon goes in there, tries to stop this

bleeding, but this is a very deadly – if these rupture, the amount of blood that can be lost is an

incredibly massive amount of hemorrhaging.

Another issue with cirrhosis is going to be hepatic encephalopathy. So that’s kind of a confusing

term, hepatic encephalopathy, right? But what will happen is due to this accumulation of

neurotoxins in the blood and cerebral edema; what happens is ammonia is not able to be

excreted so ammonia is not able to be converted to urea and you’re not able to get it out of the

system. So what happens is you have this incredible build up of ammonia. And as these

ammonia levels rise, and rise, and rise, it becomes neurotoxic to the brain – neurotoxic, and you

also develop this cerebral edema. So what happens is your patient will start developing severe

neuro changes and they’ll also develop what’s called asterixis and that’s the liver flap. And what

you do is you try to get your patient to flex their wrist up and just kind of lay their arm flat and

just kind of point their wrist directly up at the ceiling. What will happen is they won't be able to

maintain that flex position and their hand will start to bounce down. That is a sign of this hepatic

encephalopathy. A lot of times what will be done is you’ll check your ammonia levels and it will

be incredibly elevated and that can lead to this hepatic encephalopathy. These massive neuro

changes and cerebral edema, which can be severe.


So how do we diagnose cirrhosis? Obviously, one thing we’ll look for is elevated liver functions.

Our AST, our ALT, we’ll look for these labs and determine if they’re elevated. That can be a sign

that we have issues or damage within the liver itself. Also, we’ll check a CBC, our red blood cells

will be decreased as discussed earlier and our platelets will also be decreased. Our coag times

will be up so we’ll check our prothrombin time and that will be increased. As a lot of our

coagulation are created within the liver and maintained within the liver. So as our liver function

decreases, we’re going to have increased prothrombin time. And then our electrolytes – we’ll

have hyponatremia due to this hemodilution. So we have all this fluid within there and so we

may have hyponatremia. We’ll also have an elevated bilirubin, a decreased albumin, again, and

that’s what we discussed about leading to these ascites. Then we will also have elevated

ammonia levels.


To treat some of these things, there're different medications we can give. So with all this fluid

retention we’re having with this ascites, we can give diuretics. A common one to give is

spironolactone. That, of course, is a potassium-sparing diuretic. We don’t want to get rid of all

this potassium, all these electrolytes so we’ll try to preserve some of that with spironolactone.

Another thing we can give is lactulose. What lactulose does is it actually leads to the excision of

ammonia in a kind of a round about way. But what it does is you give it to the patient and what

it does is it helps draw ammonia into the bile and it helps the patient actually be able to get rid

of that ammonia that’s building up within their system. So if you do give lactulose, you obviously

are going to have your patient – you’re trying to get your patient to poop, and that’s the way

that they are able to get rid of this ammonia and to hopefully reverse or slow those neurological

changes and prevent hepatic encephalopathy.

Another thing you can give are beta-blockers. What this is going to do is prevent bleeding of the

esophageal varices. Now we know beta-blockers of course, our beta-2 receptors are going to

lead to esophageal dilation and dilation of the vessels there. What we’re going to do is try to

constrict those. By giving specific beta-blockers, we can help to constrict that. And then, of

course, we’re going to treat the anemia. Another thing we’re going to do is we’re going to

monitor our ammonia. If it’s within range, we actually want to have an appropriate and

adequate protein diet for our patient.

Some of the treatments available for patients with hepatitis are going to be balloon tamponade,

and that’s what I talked about earlier where this balloon is actually inserted into the esophagus

and is inflated. What that’s going to do is it’s going to prevent those varices from rupturing and

bleeding. Another thing you may have heard of is called TIPS, and that’s transjugular

intrahepatic portosystemic shunt. What that is, is a little shunt that’s inserted into the hepatic

vessels. What you do is you actually create a little shunt within the liver for blood to be diverted

around the portal vein. So you kind of just insert that into there, create a little diversion for the

blood around the portal vein and that allows the blood to still go where it needs to go and you

can help relieve some of this portal hypertension and these shunting of the blood.

You can also do a liver transplant. Finding patients and finding livers is always going to be an

issue there but liver transplant is available. One thing that can be done to help patients who

may be on a list for a liver transplant is going to actually be liver dialysis and that’s a pretty new

treatment, but it is available. You can actually dialyze the blood from the liver and kind of help

with some of these functions that the liver needs to carry out with the blood. That is available

and that is a long-term treatment but it can kind of be a short-term holdover for a patient who is

awaiting a liver transplant.

That is, in a nutshell, cirrhosis. If you have a patient with cirrhosis, it can be complicated to take

care of them. There’s a lot of medications, a lot of labs, a lot of things to watch for but you can

really kind of learn a lot with these patients. The best thing to do is kind of help explain to them

what’s going on, why you’re giving everything you’re giving, most of them will have a pretty

good idea of what they’re dealing with is kind of a chronic, long-term condition. But, like I said,

it’s a great condition to learn quite a bit with your patient and understand some of the more

complex anatomies of the body.

So anyway, this is Jon with the nrsng.com podcast. Go to Amazon, check out our books. You can

search my name, Jon Haws on Amazon. I have several books up there to help you with your

studies. Be sure to check us out on YouTube and we love your comments. We actually have

about 5 star ratings on iTunes and we really appreciate that. Hopefully we can help more of you

out and if we have helped you out with some of your studies I would definitely love to see a

review. It would really make my day. Thank you very much! And if you have any comments or

questions, contact me at [email protected]

Thank you for listening to the nrsng.com podcast. Visit us at www.nrsng.com for disclaimer

information and to keep the learning going.