Liver Disease: The Explanation
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Liver Disease: The Explanation
I notice that there is a lot of concern and questions about liver disease lately. Being that I'm in veterinary medical school and liver disease is the same whether it's in an animal or a person, I thought try to give a simple as possible explanation of what it is and how it happens. Hopefully it will help answer your questions and maybe spark an intesting disscussion.
First, here are a few "doctor terms" so you can sound like your MD:
"hepatic" - medicine has a latin based root word for every organ. Hepatic is the medical term for "liver".
"hepatitis" - We associate hepatitis with a sexually transmitted disease, but all it really means is "inflammation of the liver". The suffix "itis" is the medical term for "inflammation" and "itis" at the end of anything means it's inflammed. (Like conjunctivitis. The "conjunctiva" is the outer skin of the eye and when it gets red and inflammed and itchy, we have "conjuntivitis".)
So if a doctor says you have "hepatitis", she simply means, your liver is inflammed. They haven't told you why it's happening though. Hepatitis is a symptom of something - always. So if a doctor says "you have hepatitis" the next thing you say is "what is the cause?"
"necrosis" - death of cells. Cells can die for a lot of reasons: but the main reasons are either because they are damaged in some way or because the body is done using them (for example all human red blood cells die after 120 days).
"fibrosis" - what the body does when there's too much necrosis. If an organ, such as the kidney or the heart, loses too many cells due to necrosis, the body will replace these missing cells with a material called "fibrin". This process is called fibrosis.
On type of fibrosis we can see is scars on our skin. Like a scar isn't as strong as the skin as it replaced, nor does it have the same functionality or strength.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Okay, that's the start. I'm going to make a new post for each section to make it easier to ask questions.
-e
First, here are a few "doctor terms" so you can sound like your MD:
"hepatic" - medicine has a latin based root word for every organ. Hepatic is the medical term for "liver".
"hepatitis" - We associate hepatitis with a sexually transmitted disease, but all it really means is "inflammation of the liver". The suffix "itis" is the medical term for "inflammation" and "itis" at the end of anything means it's inflammed. (Like conjunctivitis. The "conjunctiva" is the outer skin of the eye and when it gets red and inflammed and itchy, we have "conjuntivitis".)
So if a doctor says you have "hepatitis", she simply means, your liver is inflammed. They haven't told you why it's happening though. Hepatitis is a symptom of something - always. So if a doctor says "you have hepatitis" the next thing you say is "what is the cause?"
"necrosis" - death of cells. Cells can die for a lot of reasons: but the main reasons are either because they are damaged in some way or because the body is done using them (for example all human red blood cells die after 120 days).
"fibrosis" - what the body does when there's too much necrosis. If an organ, such as the kidney or the heart, loses too many cells due to necrosis, the body will replace these missing cells with a material called "fibrin". This process is called fibrosis.
On type of fibrosis we can see is scars on our skin. Like a scar isn't as strong as the skin as it replaced, nor does it have the same functionality or strength.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Okay, that's the start. I'm going to make a new post for each section to make it easier to ask questions.
-e
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The Normal Liver
The normal human liver weighs about 1200 grams, has a smooth surface and is a nice mahogany brown color.
The internal architecture is based upon zonal patterns called "lobules". (A lobule is outlined in the microscopic picture below.) Each lobule has a central vein at the center and "portal triads" at each corner. These are the basis for the flow of blood and bile - it is how the liver filters the blood and metabolizes drugs and toxins.
The liver has several types of cells but the most important is the "hepatocyte" or "hepatic cell" (cyte is the medical term for "cell".). It is the most numerous and the cell that defines the fundamental lobule architecture. When the liver is damaged by toxins etc. it is the hepatocytes that show signs of damage first and ultimately suffer necrosis.
Here I've attached images of a normal liver: both a gross image of a human liver and the internal cellular architecture showing the hepatocytes and several lobules.
-e
The internal architecture is based upon zonal patterns called "lobules". (A lobule is outlined in the microscopic picture below.) Each lobule has a central vein at the center and "portal triads" at each corner. These are the basis for the flow of blood and bile - it is how the liver filters the blood and metabolizes drugs and toxins.
The liver has several types of cells but the most important is the "hepatocyte" or "hepatic cell" (cyte is the medical term for "cell".). It is the most numerous and the cell that defines the fundamental lobule architecture. When the liver is damaged by toxins etc. it is the hepatocytes that show signs of damage first and ultimately suffer necrosis.
Here I've attached images of a normal liver: both a gross image of a human liver and the internal cellular architecture showing the hepatocytes and several lobules.
-e
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The basic functionality of the liver
Thanks for the responses already. I figure by doing this, everybody wins. I review the subject (it will be on an upcoming exam for me), get to practice disscussing the subject with clients, and hopefully I can help others out with their questions, concerns, etc... Thanks for providing the opportunity. 
This is how the liver functions, which is the basis of how the liver gets damaged.
First : the liver is probably the coolest organ in the body besides the brain. At any given time 25% of the blood in your body is in your liver! That's because your liver has the critical job of maintaining the body's "metabolic homeostasis". What does this mean? "Homeostasis" is the term for balance. Everything you ingest whether it is eaten, drank, inhaled, or even absorbed through the skin needs to be metabolized and is therefore processed by the liver. Without it, you would shift from extreme to extreme everytime you ate, drank, or encountered anything.
The list of things that the liver processes includes dietary amino acids, carbohydrates, lipids, and vitamins; in addition it's responsible for the removal of microbes (bacteria and viruses that can make you sick) and toxins (drugs and alcohol fall under this catagory as far as the liver is concerned). While it is doing that, it is also responsible for the synthesis of many of the proteins in our blood used for coagulation (so people with liver disease often have bleeding problems too). In addition it assists in the breakdown of complex sugars into glucose (our body's primary energy source), storage of excess glucose for use later, and can even make blood (usually the job of the bone marrow). And if you aren't a fan of the liver yet - it can regenerate up to 60% of its mass when damaged.
If the above was a little too much to follow - basically what it's saying is that everything that passes into the body goes through the liver. Anything toxic to the body is neutralized by the liver. These "metabolites", or neutralized toxins, are carried away in the bile. This will be important later when we start talking about cirrhosis
It should be obvious that hepatic disorders, therefore, have far-reaching consequences. Symptoms aren't just things like pain in the left side (where the liver is), they are problems with the skin, the kidneys, with the stomach and bowels, and with the nervous system.
The attached image is a very nice drawing of how the lobular architecture works. The blood arrives at the liver via both the portal vein and hepatic artery. There are several of these in each lobule because each lobule has a number of portal triads (see above for a reminder) and there are hundreds of thousands of lobules in the liver. The blood then flows across the hepatocytes like a filter and exits at the central vein. All the central veins for all the lobules for the whole liver all hook up together and the blood flows back to the heart.
Any toxins filtered out and processed by the liver enters the bile which flows in the opposite direction of the blood and leaves via the digestive tract.
The reason I've bothered to explain this in such detail is that it is the fundamental mechanism by which liver disease occurs. When the flow of bile is blocked, it is very serious. However, the redundant nature of the liver and its regenerative properties mask the early impact of disease.
I'll talk about what happens when things go wrong next.
Thanks
-e
This is how the liver functions, which is the basis of how the liver gets damaged.
First : the liver is probably the coolest organ in the body besides the brain. At any given time 25% of the blood in your body is in your liver! That's because your liver has the critical job of maintaining the body's "metabolic homeostasis". What does this mean? "Homeostasis" is the term for balance. Everything you ingest whether it is eaten, drank, inhaled, or even absorbed through the skin needs to be metabolized and is therefore processed by the liver. Without it, you would shift from extreme to extreme everytime you ate, drank, or encountered anything.
The list of things that the liver processes includes dietary amino acids, carbohydrates, lipids, and vitamins; in addition it's responsible for the removal of microbes (bacteria and viruses that can make you sick) and toxins (drugs and alcohol fall under this catagory as far as the liver is concerned). While it is doing that, it is also responsible for the synthesis of many of the proteins in our blood used for coagulation (so people with liver disease often have bleeding problems too). In addition it assists in the breakdown of complex sugars into glucose (our body's primary energy source), storage of excess glucose for use later, and can even make blood (usually the job of the bone marrow). And if you aren't a fan of the liver yet - it can regenerate up to 60% of its mass when damaged.
If the above was a little too much to follow - basically what it's saying is that everything that passes into the body goes through the liver. Anything toxic to the body is neutralized by the liver. These "metabolites", or neutralized toxins, are carried away in the bile. This will be important later when we start talking about cirrhosis
It should be obvious that hepatic disorders, therefore, have far-reaching consequences. Symptoms aren't just things like pain in the left side (where the liver is), they are problems with the skin, the kidneys, with the stomach and bowels, and with the nervous system.
The attached image is a very nice drawing of how the lobular architecture works. The blood arrives at the liver via both the portal vein and hepatic artery. There are several of these in each lobule because each lobule has a number of portal triads (see above for a reminder) and there are hundreds of thousands of lobules in the liver. The blood then flows across the hepatocytes like a filter and exits at the central vein. All the central veins for all the lobules for the whole liver all hook up together and the blood flows back to the heart.
Any toxins filtered out and processed by the liver enters the bile which flows in the opposite direction of the blood and leaves via the digestive tract.
The reason I've bothered to explain this in such detail is that it is the fundamental mechanism by which liver disease occurs. When the flow of bile is blocked, it is very serious. However, the redundant nature of the liver and its regenerative properties mask the early impact of disease.
I'll talk about what happens when things go wrong next.
Thanks
-e
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Cirrhosis is not the end of the world...
One thing I've observed personally is that people who abuse alcohol or who have a history of abusing alcohol worry about cirrhosis of the liver more than anything. Yes, cirrhosis is serious, but it's not the end of the world; liver failure is.
Liver failure is the consequence of any form of severe liver damage and cirrhosis is not the only form of damage that chronic alcohol abuse can cause. So I thought that before I talked about the diseases that were reversible I'd talk about the end result of NOT reversing liver damage.
Hepatic Failure is the end point of all forms of damage to the liver and there are 2500 new human cases per year in the US. Liver disease is by nature progressive (remember how the structure of the liver is redundant?) so the point of hepatic failure is reached either by some kind of insidious destruction of hepatocytes (the pattern seen in an infectious type of hepatitis or by toxins) or by repetitive damage (the pattern of alcohol and drug abuse).
Now this is important. 80% to 90% of functional capacity must be shut down before hepatic failure ensues. Remember once again the redundancy and the regenerative capability of the organ - you have to work very very hard to reach this point by the "repetitive damage" sequence. And when you reach this point, your chances of survival without a liver transplant are around 10%. Not very good odds.
The two most common alterations of liver function that lead to failure are the following:
#1 is Massive Hepatic Necrosis. You know all these words now. Basically - all the cells got killed off. The usual cause of this is direct toxic damage. Alcohol does not cause this type of toxic damage, for neither alcohol itself, nor its metabolites (one of which is in the same family as formaldehyde) is toxic to hepatocytes. The number one cause of this toxic damage is... Tylenol (acetomeniphen). That's right, Tylenol is responsible for 40% of the cases of hepatic failure by massive hepatic necrosis in this country.
And it's important to know that the way the liver processes Tylenol is made more toxic by the combined presence of alcohol metabolites. So if you are still drinking, avoid taking Tylenol for a hangover and chose aspirin or ibuprophen instead.
And #2 is Chronic Liver Disease. This is where cirrhosis falls and it is the most common route to hepatic failure in this country. Always, the end point of relentlessly chronic cirrhosis (the number one cause of which is chronic alcoholism) will be liver failure.
What does hepatic failure look like?
Regardless of the cause it looks the same on everyone: Jaundice or yellowing of the skin, eyes, and gums (due to lack of functioning of that blood/bile filter I talked about above - the bile can't leave the liver and backs up into the blood. Bile itself is toxic.). Since the liver is responsible for maintaining our "homeostasis" - that will be lost and the result will be dysfunction of other organ systems. These are:
"Coagulopathies" - the term for bleeding disorders due to the fact that all the blood clotting factors are no longer being made. Bleeding in the stomach and intestines is a common complication of liver failure.
"Hyperproteinemia" - the term for too much protein in the blood. Protein balance is important for maintaining our blood pressure in places like the brain and extremities - the result will be brain dysfunctions as well as swelling in hands and feet.
Body Odor - due to the out of whack metabolites. Described as "musty" or "sour"
Impaired Estrogen Metabolism - Men grow breasts. (The term is "gynomastia".)
Kidney dysfunction - This is once again due to the lack of homeostasis. The kidneys require a proper elecrolyte balance to function - the result is the inability to make urine. Once this stage is reached life expectancy is approximately 2 weeks.
Scary stuff. So I will leave you with these um... sobering thoughts for now and post next about how you get to this point because the good news is that nearly all liver disease is reversible.
Sorry there aren't any pictures.
-e
Liver failure is the consequence of any form of severe liver damage and cirrhosis is not the only form of damage that chronic alcohol abuse can cause. So I thought that before I talked about the diseases that were reversible I'd talk about the end result of NOT reversing liver damage.
Hepatic Failure is the end point of all forms of damage to the liver and there are 2500 new human cases per year in the US. Liver disease is by nature progressive (remember how the structure of the liver is redundant?) so the point of hepatic failure is reached either by some kind of insidious destruction of hepatocytes (the pattern seen in an infectious type of hepatitis or by toxins) or by repetitive damage (the pattern of alcohol and drug abuse).
Now this is important. 80% to 90% of functional capacity must be shut down before hepatic failure ensues. Remember once again the redundancy and the regenerative capability of the organ - you have to work very very hard to reach this point by the "repetitive damage" sequence. And when you reach this point, your chances of survival without a liver transplant are around 10%. Not very good odds.
The two most common alterations of liver function that lead to failure are the following:
#1 is Massive Hepatic Necrosis. You know all these words now. Basically - all the cells got killed off. The usual cause of this is direct toxic damage. Alcohol does not cause this type of toxic damage, for neither alcohol itself, nor its metabolites (one of which is in the same family as formaldehyde) is toxic to hepatocytes. The number one cause of this toxic damage is... Tylenol (acetomeniphen). That's right, Tylenol is responsible for 40% of the cases of hepatic failure by massive hepatic necrosis in this country.
And it's important to know that the way the liver processes Tylenol is made more toxic by the combined presence of alcohol metabolites. So if you are still drinking, avoid taking Tylenol for a hangover and chose aspirin or ibuprophen instead.
And #2 is Chronic Liver Disease. This is where cirrhosis falls and it is the most common route to hepatic failure in this country. Always, the end point of relentlessly chronic cirrhosis (the number one cause of which is chronic alcoholism) will be liver failure.
What does hepatic failure look like?
Regardless of the cause it looks the same on everyone: Jaundice or yellowing of the skin, eyes, and gums (due to lack of functioning of that blood/bile filter I talked about above - the bile can't leave the liver and backs up into the blood. Bile itself is toxic.). Since the liver is responsible for maintaining our "homeostasis" - that will be lost and the result will be dysfunction of other organ systems. These are:
"Coagulopathies" - the term for bleeding disorders due to the fact that all the blood clotting factors are no longer being made. Bleeding in the stomach and intestines is a common complication of liver failure.
"Hyperproteinemia" - the term for too much protein in the blood. Protein balance is important for maintaining our blood pressure in places like the brain and extremities - the result will be brain dysfunctions as well as swelling in hands and feet.
Body Odor - due to the out of whack metabolites. Described as "musty" or "sour"
Impaired Estrogen Metabolism - Men grow breasts. (The term is "gynomastia".)
Kidney dysfunction - This is once again due to the lack of homeostasis. The kidneys require a proper elecrolyte balance to function - the result is the inability to make urine. Once this stage is reached life expectancy is approximately 2 weeks.
Scary stuff. So I will leave you with these um... sobering thoughts for now and post next about how you get to this point because the good news is that nearly all liver disease is reversible.
Sorry there aren't any pictures.
-e
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Originally Posted by lostmdboy 
What about smoking? Can your lungs recover?
Your lungs are the source of oxygen/carbon dioxide exchange and without this, nothing in your body will work - not even your liver
And especially not your brain. So take care of those babies, you only get one set.A veterinary medicine fact: I've personally necropsied* animals that have come from the homes of smokers. Their lungs are full of black carbon deposits from the exposure to cigarette smoke. The only other time you might see this is in an animal that was in a fire. So chronic exposure to second hand smoke is a real issue and not just a conspiracy created by people who don't want you to smoke by the door of the building.
* in veterinary medicine you don't "autopsy" animals, you "necropsy" them. Autopsy means "opening of self" and refers to human cadavers.
-e
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Originally Posted by lostmdboy
my Question. so yousay if I drink fr thirty years pretty Dang heavy my liver, and other body parts can recover some what. What about smoking? Can your lungs recover?
The tough thing about lung cancer is that type of cancer cell is very difficult to detect with diagnostic imaging until they are already at a stage where they can spread rapidly to the rest of the lungs or other parts of the body. Being in the lungs doesn't help since the blood from the lungs gets distributed everywhere through large arteries immediately. In other words, cancer in the lungs goes all over very fast.
Scientists have found similar mutations in these cells in the lungs of marijuana smokers, they just have not conducted long enough longitudinal studies of them to see if pot causes lung cancer.
But, its not like you need to worry about it. If you stopped smoking, good for you! Now you are REALLY drug free and totally sober. You can't re-write history so just deal with what you are doing now.
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Looks like I have a double wammy. Smoked lots of cigs and pot. Been quit cigs for 12 trs, and pot well for the most part 10 yrs. Any way can't go back, and change any thing so I guess just will move foward.
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"The tough thing about lung cancer is that type of cancer cell is very difficult to detect with diagnostic imaging until they are already at a stage where they can spread rapidly to the rest of the lungs or other parts of the body. Being in the lungs doesn't help since the blood from the lungs gets distributed everywhere through large arteries immediately. In other words, cancer in the lungs goes all over very fast."
That's very true - a friend of a good friend of mine, smoker but a very healthy-living woman in every other respect, late thirties, was diagnosed with lung cancer at the end of December - she was dead five or six weeks later.
That's very true - a friend of a good friend of mine, smoker but a very healthy-living woman in every other respect, late thirties, was diagnosed with lung cancer at the end of December - she was dead five or six weeks later.
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Great post St Kurt.
Do you have any information about Alcoholic Cardiomapathy as alcohol probably damages the heart muscle of more people than it damages the liver (hence the high rate of post-weekend-binge related heart failures on a Monday)
Do you have any information about Alcoholic Cardiomapathy as alcohol probably damages the heart muscle of more people than it damages the liver (hence the high rate of post-weekend-binge related heart failures on a Monday)
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Back on the subject of Liver Disease
So the good news about the liver is despite all the cool things that it does, it's amazingly simple when it comes to injury. It only does a few things no matter what's injuring it and most of them are reversible.
One of the earliest signs of injury to hepatocytes is that the cells swell up. Depending on the mechanism of injury, the cells will swell up with different substances. In the case of alcoholic injury, the cells accumulate fat (a condition known as "steatosis"). Hepatic steatosis is another name for "fatty liver" and is a common effect of chronic alcohol abuse. Even though alcoholic fatty liver may demonstrate steatosis in every single cell - this condition is reversible if one stops drinking.
Cell swelling that is allowed to continue however, eventually results in necrosis. Because of the pattern of alcoholic hepatic steatosis - the necrosis that occurs is on a very large scale if allowed to continue. The body's response to necrotic tissue is inflammation, hence the common early diagnosis of "hepatitis" - an inflammed liver. Basically, the liver is experiencing a combination of reversible and irreversible damage - the clean up process to remove the dead cells involves inflammation.
This is where things get interesting because the liver is regenerative. Way back in the first post I mentioned "fibrosis" and then never talked about it again. Fibrosis is the body's response to necrosis and inflammation so when the cells die - they are replaced with fibrin. However, this is where things get cool!
As long as the basic architecture of liver remains intact, fibrosis does NOT occur. Instead, the liver develops "regenerative nodules". This regeneration occurs in all but the most severe liver disease and it involves not the growing of a new smooth piece of liver, but the creation of small, healthy nodules of hepatic tissue. These nodules contain the lobules and bile ducts just like any normal liver tissue does and onces they are connected into the existing hepatic framework - they work just fine.
The liver can literally regrow itself a piece at a time as long as you let it.
I've attached an image of what was a severely damaged liver that is composed mostly of regenerative nodules. At first glance you may think it looks like cirrhosis, but look at the color - though the liver is no longer smooth it is a healthy mahogany color. This is a healthy functioning organ believe it or not and demonstrates the extent of the liver's restorative abilities.
(by the way - it's a dog liver. It's very rare the humans make this kind of recovery. This dog was suffering from viral hepatitis (which has nearly the same mechanism as alcohol) and survived.)
-e
One of the earliest signs of injury to hepatocytes is that the cells swell up. Depending on the mechanism of injury, the cells will swell up with different substances. In the case of alcoholic injury, the cells accumulate fat (a condition known as "steatosis"). Hepatic steatosis is another name for "fatty liver" and is a common effect of chronic alcohol abuse. Even though alcoholic fatty liver may demonstrate steatosis in every single cell - this condition is reversible if one stops drinking.
Cell swelling that is allowed to continue however, eventually results in necrosis. Because of the pattern of alcoholic hepatic steatosis - the necrosis that occurs is on a very large scale if allowed to continue. The body's response to necrotic tissue is inflammation, hence the common early diagnosis of "hepatitis" - an inflammed liver. Basically, the liver is experiencing a combination of reversible and irreversible damage - the clean up process to remove the dead cells involves inflammation.
This is where things get interesting because the liver is regenerative. Way back in the first post I mentioned "fibrosis" and then never talked about it again. Fibrosis is the body's response to necrosis and inflammation so when the cells die - they are replaced with fibrin. However, this is where things get cool!
As long as the basic architecture of liver remains intact, fibrosis does NOT occur. Instead, the liver develops "regenerative nodules". This regeneration occurs in all but the most severe liver disease and it involves not the growing of a new smooth piece of liver, but the creation of small, healthy nodules of hepatic tissue. These nodules contain the lobules and bile ducts just like any normal liver tissue does and onces they are connected into the existing hepatic framework - they work just fine.
The liver can literally regrow itself a piece at a time as long as you let it.
I've attached an image of what was a severely damaged liver that is composed mostly of regenerative nodules. At first glance you may think it looks like cirrhosis, but look at the color - though the liver is no longer smooth it is a healthy mahogany color. This is a healthy functioning organ believe it or not and demonstrates the extent of the liver's restorative abilities.
(by the way - it's a dog liver. It's very rare the humans make this kind of recovery. This dog was suffering from viral hepatitis (which has nearly the same mechanism as alcohol) and survived.)
-e
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Originally Posted by Budfrog
Do you have any information about Alcoholic Cardiomapathy as alcohol probably damages the heart muscle of more people than it damages the liver (hence the high rate of post-weekend-binge related heart failures on a Monday)
However, from my human medicine pathology text:
"Alcohol abuse is also strongly associated with the development of dilated cardiomyopathy, raising the possibility that ethanol toxicity or a secondary nutritional disturbance may be the cause of the myocardial injury. Alcohol or its metabolites (especially acetaldehyde) have a direct toxic effect on the myocardium. Nevertheless, the cause-and-effect relationship with alcohol alone remains uncertain, and no morphologic features serve to distinguish alcoholic cardiomyopathy from DCM of other etiology. Moreover, chronic alcoholism may be associated with thiamine deficiency... [goes on to really technical medical discussion that no long applies to alcohol]."
Robbins and Coltrane, Pathologic Basis of Disease, 7th edition
Translation: They don't know.
I've attached an image of a human heart with dilated cardiomyopathy and it should be obvious that it is a chronic condition and not a result of a weekend binge though. (Ignore the arrow. It's pointing to a little blood clot and has nothing to do with the cardiomyopathy itself.)
I'm learning a lot of human medicine from this thread. How interesting.
In cats cardiomyopathy is quite common and it is associated with thiamine deficiency...-e
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The moment you've all been waiting for
It only took me 5 posts to get to the part about actual alcoholic liver disease. But this way you are educated - which was the whole point. It's easy to go on the internet, google "cirrhosis" or whatever and get a whole bunch of stuff that's either wrong or you don't totally understand. This is right and hopefully it makes sense.
Attached is a drawing of what I've described so far minus the part about cirrhosis. I'm guessing "repeated attacks" is supposed to mean "drinking". Basically it describes how you can go back and forth between a normal liver and a damaged liver by abstinence vs. ... non-abstinence. Notice that the only arrows that move in one direction are the ones to "cirrhosis" which has the word "fibrosis" on it.
First some stats from my human medical text:
Excessive alcohol (ethanol) consumption is the leading cause of liver disease in most Western countries. These U.S. statistics attest to the magnitude of the problem:
- Currently, 67% of the population 18 years of age or older drink alcohol.
- More than 14 million Americans meet criteria for alcohol abuse and/or dependence.
- Alcohol abuse causes 200,000 deaths annually, the fifth-leading cause of death, many related to automobile accidents. Approximately 40% of deaths from cirrhosis are attributed to alcohol-induced liver disease.
- Twenty-five percent to 30% of hospitalized patients have problems related to alcohol abuse, 1.5% as the first-listed diagnosis.
Steatosis was already discussed, but a few points specific to Alcoholic Steatosis are: The liver undergoes some signifigant changes and becomes very large, up to 4 to 6 kg (remember the normal liver was about 1.2 kg). It is now a soft organ that is yellow and greasy (rather than smooth and mahogany colored). Although there is little or no fibrosis at the outset, with continued alcohol intake, fibrous tissue develops. The fatty change is completely reversible if there is abstention from further intake of alcohol.
Alcoholic Hepatitis has some particular features as well. These are:
- Hepatocyte swelling and necrosis from the accumulation of fat and water.
- Mallory bodies: These "inclusions" (or evidence of toxic damage to cells) are a characteristic but not specific feature of alcoholic liver disease, as they also are seen in primary biliary cirrhosis, Wilson disease, chronic cholestatic syndromes, and hepatocellular tumors.
"Neutrophilic" reaction: Neutrophils are a type of white blood cells and a cause of the inflammation.
Fibrosis: Alcoholic hepatitis will result in fibrosis, particularly with repeated bouts of heavy alcohol intake.
You are probably beginning to guess by now that the big problem is fibrosis. And you would be right - fibrosis destroys normal liver tissue and eliminates it's regenerative capabilities. The characteristic appearance of cirrhosis is actually regenerative nodules gone wrong due to the destruction of the normal liver architecture due to fibrosis and the result is quite catastrophic.
I'll post that next since I have gruesome images.
-e
Attached is a drawing of what I've described so far minus the part about cirrhosis. I'm guessing "repeated attacks" is supposed to mean "drinking". Basically it describes how you can go back and forth between a normal liver and a damaged liver by abstinence vs. ... non-abstinence. Notice that the only arrows that move in one direction are the ones to "cirrhosis" which has the word "fibrosis" on it.
First some stats from my human medical text:
Excessive alcohol (ethanol) consumption is the leading cause of liver disease in most Western countries. These U.S. statistics attest to the magnitude of the problem:
- Currently, 67% of the population 18 years of age or older drink alcohol.
- More than 14 million Americans meet criteria for alcohol abuse and/or dependence.
- Alcohol abuse causes 200,000 deaths annually, the fifth-leading cause of death, many related to automobile accidents. Approximately 40% of deaths from cirrhosis are attributed to alcohol-induced liver disease.
- Twenty-five percent to 30% of hospitalized patients have problems related to alcohol abuse, 1.5% as the first-listed diagnosis.
Steatosis was already discussed, but a few points specific to Alcoholic Steatosis are: The liver undergoes some signifigant changes and becomes very large, up to 4 to 6 kg (remember the normal liver was about 1.2 kg). It is now a soft organ that is yellow and greasy (rather than smooth and mahogany colored). Although there is little or no fibrosis at the outset, with continued alcohol intake, fibrous tissue develops. The fatty change is completely reversible if there is abstention from further intake of alcohol.
Alcoholic Hepatitis has some particular features as well. These are:
- Hepatocyte swelling and necrosis from the accumulation of fat and water.
- Mallory bodies: These "inclusions" (or evidence of toxic damage to cells) are a characteristic but not specific feature of alcoholic liver disease, as they also are seen in primary biliary cirrhosis, Wilson disease, chronic cholestatic syndromes, and hepatocellular tumors.
"Neutrophilic" reaction: Neutrophils are a type of white blood cells and a cause of the inflammation.
Fibrosis: Alcoholic hepatitis will result in fibrosis, particularly with repeated bouts of heavy alcohol intake.
You are probably beginning to guess by now that the big problem is fibrosis. And you would be right - fibrosis destroys normal liver tissue and eliminates it's regenerative capabilities. The characteristic appearance of cirrhosis is actually regenerative nodules gone wrong due to the destruction of the normal liver architecture due to fibrosis and the result is quite catastrophic.
I'll post that next since I have gruesome images.
-e
cunning. baffling. powerful.
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Join Date: Feb 2007
Location: NY
Posts: 183
Okay, I lied. Cirrhosis is Liver Failure. I just wanted to keep your attention.
Cirrhosis is often referred to as "end stage alcoholic liver disease". That is because it is - as made obvious from the above, the point that the liver cannot regenerate from. It is the finally and irreversible for the alcoholic liver takes and it is a chronic condition that takes a many years to develop.
As I described earlier - a liver with hepatic steatosis can weigh up to 6 kg, however a cirrhotic liver will be shrunken, brown and weigh less than 1 kg (less than a normal liver). In very extreme cases of alcoholic hepatitis, these changes can occur in less than 2 years and the cause is fibrosis.
The development of fibrous tracts combined with the development of the regenerative nodules described above creates a situation in which the new nodules become trapped within the damaged fibrous tissue and are unable to function properly. As the liver fights to continue to regenerate and develop more nodules, the problem is only compounded - the nodules are there, but they are not connected into the biliary system.
Compare the gross liver and it's microscopic image to the normal ones I posted above. This liver is no longer smooth or mahogany colored. The greenish tint is due to the trapped bile. (And remember how I said bile was toxic? Note the bulging mass on the lower left of the liver - that's cancer caused by the presence of excess bile.) The microscopic image no longer is a uniform pink with hexagonal lobules - now they are trapped and isolated within the dark purple bands of fibrin. You can see for yourself how this isn't going to function right, now that you know how it's supposed to work.
So, you're probably wondering how you know if you have any of these conditions. Here's what to look for. Please don't use this to diagnose yourself. Please do use this to take the hint and see a doctor though.
Hepatic steatosis will generally show up as an enlarged liver. A blood test may show a mild elevation of serum bilirubin and alkaline phosphatase* levels. Alcohol withdrawal and the provision of an adequate diet are sufficient treatment.
On the other hand, alcoholic hepatitis tends to appear relatively acutely, usually following a bout of heavy drinking. Symptoms and laboratory results may be minimal or those of impending hepatic failure. So, you really have no idea what's wrong. The symptoms of hepatitis are very vague: lethary, anorexia, weight loss, upper abdominal discomfort, and a tender and enlarged liver. A blood test might show hyperbilirubinemia (too much bile in the blood), elevated alkaline phosphatase*, and an elevated white blood cell count. The outlook is unpredictable; each bout of hepatitis incurs about a 10% to 20% risk of death. With repeated bouts, cirrhosis appears in about one third of patients within a few years. Alcoholic hepatitis also may be superimposed on established cirrhosis. With proper nutrition and total cessation of alcohol consumption, the alcoholic hepatitis may clear slowly. However, in some patients, the hepatitis persists despite abstinence and progresses to cirrhosis.
Commonly, the first signs of cirrhosis relate to complications of high blood pressure, including life-threatening hemorrhage. Alternatively, lethargy, weakness, weight loss, and loss of appetite precede the appearance of jaundice, swelling of the belly, and swelling of the hands and feet. The stigmata of cirrhosis (e.g., grossly distended abdomen (ascites), wasted extremities...) may be dramatically evident. Laboratory results reflect the developing hepatic compromise, with elevated alkaline phosphatase*, hypoproteinemia (too little proteins in the blood) , and anemia (too few red blood cells).
*Alkaline Phosphatase is an important liver enzyme. Its elevation is a clue to doctors that something is wrong.
The long-term outlook for alcoholics with liver disease is variable. Five-year survival approaches 90% in abstainers who are free of jaundice, ascites, or hematemesis (vomiting blood); it drops to 50% to 60% in those who continue to imbibe.
In the end-stage alcoholic, the proximate causes of death are (1) hepatic coma, (2) a massive gastrointestinal hemorrhage, (3) an infection (to which these patients are predisposed), (4) kidney failure following a bout of alcoholic hepatitis, and (5) liver cancer in 3% to 6% of cases.
Short-term ingestion of up to 80 gm of alcohol (eight beers or 7 ounces of 80-proof liquor) over one to several days generally produces mild, reversible hepatic changes, such as fatty liver. Daily intake of 80 gm or more of ethanol generates significant risk for severe hepatic injury, and daily ingestion of 160 gm or more for 10 to 20 years is associated more consistently with severe injury. In the absence of a clear understanding of the factors influencing liver damage, no "safe" upper limit for alcohol consumption can be proposed,
Statitistics from Robbins and Coltrane Pathologic Basis of Disease, 7th ed
And there you have it. You are now experts in alcohol related liver disease. Congratuations and may you use your knowledge well.
-e
As I described earlier - a liver with hepatic steatosis can weigh up to 6 kg, however a cirrhotic liver will be shrunken, brown and weigh less than 1 kg (less than a normal liver). In very extreme cases of alcoholic hepatitis, these changes can occur in less than 2 years and the cause is fibrosis.
The development of fibrous tracts combined with the development of the regenerative nodules described above creates a situation in which the new nodules become trapped within the damaged fibrous tissue and are unable to function properly. As the liver fights to continue to regenerate and develop more nodules, the problem is only compounded - the nodules are there, but they are not connected into the biliary system.
Compare the gross liver and it's microscopic image to the normal ones I posted above. This liver is no longer smooth or mahogany colored. The greenish tint is due to the trapped bile. (And remember how I said bile was toxic? Note the bulging mass on the lower left of the liver - that's cancer caused by the presence of excess bile.) The microscopic image no longer is a uniform pink with hexagonal lobules - now they are trapped and isolated within the dark purple bands of fibrin. You can see for yourself how this isn't going to function right, now that you know how it's supposed to work.
So, you're probably wondering how you know if you have any of these conditions. Here's what to look for. Please don't use this to diagnose yourself. Please do use this to take the hint and see a doctor though.
Hepatic steatosis will generally show up as an enlarged liver. A blood test may show a mild elevation of serum bilirubin and alkaline phosphatase* levels. Alcohol withdrawal and the provision of an adequate diet are sufficient treatment.
On the other hand, alcoholic hepatitis tends to appear relatively acutely, usually following a bout of heavy drinking. Symptoms and laboratory results may be minimal or those of impending hepatic failure. So, you really have no idea what's wrong. The symptoms of hepatitis are very vague: lethary, anorexia, weight loss, upper abdominal discomfort, and a tender and enlarged liver. A blood test might show hyperbilirubinemia (too much bile in the blood), elevated alkaline phosphatase*, and an elevated white blood cell count. The outlook is unpredictable; each bout of hepatitis incurs about a 10% to 20% risk of death. With repeated bouts, cirrhosis appears in about one third of patients within a few years. Alcoholic hepatitis also may be superimposed on established cirrhosis. With proper nutrition and total cessation of alcohol consumption, the alcoholic hepatitis may clear slowly. However, in some patients, the hepatitis persists despite abstinence and progresses to cirrhosis.
Commonly, the first signs of cirrhosis relate to complications of high blood pressure, including life-threatening hemorrhage. Alternatively, lethargy, weakness, weight loss, and loss of appetite precede the appearance of jaundice, swelling of the belly, and swelling of the hands and feet. The stigmata of cirrhosis (e.g., grossly distended abdomen (ascites), wasted extremities...) may be dramatically evident. Laboratory results reflect the developing hepatic compromise, with elevated alkaline phosphatase*, hypoproteinemia (too little proteins in the blood) , and anemia (too few red blood cells).
*Alkaline Phosphatase is an important liver enzyme. Its elevation is a clue to doctors that something is wrong.
The long-term outlook for alcoholics with liver disease is variable. Five-year survival approaches 90% in abstainers who are free of jaundice, ascites, or hematemesis (vomiting blood); it drops to 50% to 60% in those who continue to imbibe.
In the end-stage alcoholic, the proximate causes of death are (1) hepatic coma, (2) a massive gastrointestinal hemorrhage, (3) an infection (to which these patients are predisposed), (4) kidney failure following a bout of alcoholic hepatitis, and (5) liver cancer in 3% to 6% of cases.
Short-term ingestion of up to 80 gm of alcohol (eight beers or 7 ounces of 80-proof liquor) over one to several days generally produces mild, reversible hepatic changes, such as fatty liver. Daily intake of 80 gm or more of ethanol generates significant risk for severe hepatic injury, and daily ingestion of 160 gm or more for 10 to 20 years is associated more consistently with severe injury. In the absence of a clear understanding of the factors influencing liver damage, no "safe" upper limit for alcohol consumption can be proposed,
Statitistics from Robbins and Coltrane Pathologic Basis of Disease, 7th ed
And there you have it. You are now experts in alcohol related liver disease. Congratuations and may you use your knowledge well.
-e
Last edited by St_Kurt; 03-30-2007 at 04:20 PM. Reason: I didn't define "ascites". --SK
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Join Date: Mar 2007
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That is very interesting Kurt and thank you for including info on alcoholic hepatitis. In my own case, the doctor saying that my bilirubin count was high but not dangerously high the main problem was with something that the pancreas was producing that was many times higher than it should have been, maybe alkaline phosphatase. Thanks again.
And like you said I won't use the info to diagnose myself I realize now that I should not have asked for medical advice here and I apologize.
And like you said I won't use the info to diagnose myself I realize now that I should not have asked for medical advice here and I apologize.
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