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ABSTRACT
chemistry the definition of alcohol includes many other compounds. Alcoholic beverages are
Ethanol is only slightly toxic compared to other alcohols, but has significant psychoactive
effects. A significant blood alcohol content may be considered legal drunkenness as it reduces
attention and slows reaction speed. Alcoholic beverages can be addictive and the state of
Chronic alcoholism can cause cirrhosis, it’s called Laennec’s cirrhosis. This condition should
be renamed "alcoholic cirrhosis". Laennec's cirrhosis has three stages. The pathologic features of
this form of cirrhosis change with time. Therefore, it is helpful to break the disease down into
three stages, the fatty liver stage, the fibrotic liver stage and, the nodular liver stage.
tissue by fibrous scar tissue as well as regenerative nodules (lumps that occur as a result of a
process in which damaged tissue is regenerated), leading to progressive loss of liver function.
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II. INTRODUCTION
Each year, excessive alcohol consumption kills about 79.000 people in the United States and
do not close the possibility in Indonesia will also be like that. consumption of alcohol will be
increased, particularly among the young. Has been known that consume alcohol frequently will
influence our health condition. alcohol is very toxic to our body organs, especially the Liver.
Alcohol affect the heart condition because all the volume of alcohol that we drink will be
processed there and toxic substances. That substances will accelerate the occurrence of liver
cirrhosis. therefore, I am interested as a writer to create this paper. with the title "The relationship
tissue by fibrous scar tissue as well as regenerative nodules. Cirrhosis is most commonly caused
by alcoholism, hepatitis B and C and fatty liver disease and many other possible causes.
Alcoholism is the first causes of this disease, but now in Indonesia hepatitis B is more often. But
Alcohol users will be increasing from day to day, especially among the young. This claim is
supported by the lifestyle nowdays. Of course this habit is affecting the health of youth in the last
10 years. changes will happen quickly to their liver because the substances that exist in the
alcohol.
Rate of absorption of alcohol depends on several factors. It is quickest, for example, when
alcohol is drunk on an empty stomach. Alcohol is distributed throughout the water in the body, so
that most tissues such as the heart, brain, and muscles are exposed to the same concentration of
alcohol as the blood. The exception is the liver, where exposure is greater because blood is
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received direct from the stomach and small bowel via the portal vein. Alcohol diffuses rather
slowly, except into organs with a rich blood supply such as the brain and lungs.
chemistry the definition of alcohol includes many other compounds. Alcoholic beverages are
The consumption of large doses results in drunkenness or intoxication that may lead to a
hangover as the effect wears off and depending on the dose and regularity of use, can cause acute
respiratory failure or death and with chronic use has medical repercussions, especially to the
liver.
Blood alcohol concentration varies according to sex, size and body build, phase of the
menstrual cycle, previous exposure to alcohol, type of drink, whether alcohol is taken with food
or drugs or not. More than 90% of alcohol is eliminated by the liver, 2-5% is excreted unchanged
in urine, sweat, or breath. The first step in metabolism is oxidation by alcohol dehydrogenases.
Women may have lower levels of alcohol dehydrogenases in the stomach than men, so that less
Chronic alcoholism can cause cirrhosis, it’s called Laennec’s cirrhosis. This condition should
be renamed "alcoholic cirrhosis". Laennec's cirrhosis has three stages. The pathologic features of
this form of cirrhosis change with time. Therefore, it is helpful to break the disease down into
three stages. In early stages the liver is large and fatty, and then the liver becomes scarred
(fibrotic). In the final stage, the liver becomes lumpy (nodular). Substances that contained in the
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III. ALKOHOL
Ethanol is a psychoactive drug that has a depressant effect. Most countries restrict and
regulate its sale and consumption. For example, they place legal drinking-age restrictions upon
the sale of alcoholic drinks to young people. The manufacture and consumption of alcohol
occurs in most cultures and societies of the world, from hunter-gatherer peoples to nation-states.
The drinking of alcoholic beverages is very often an important part of social events in such
Alcoholic beverages that have a lower alcohol content (beer and wine) are produced by
fermentation of sugar or starch containing plant material. Beverages of higher alcohol content
a. Beer
The process of making beer defines the finished product. Beer involves a short (incomplete)
fermentation process and a short aging process (a week or two), typically resulting in an alcohol
b. Wine
Wine involves a longer (complete) fermentation process, and a relatively long aging process
(months or years, sometimes decades) resulting in an alcohol content between 7-18%. Sparkling
wine is generally made by adding a small amount of sugar before bottling, which causes a
c. Spirits
Spirits contain at least 20% ABV. Liqueurs are characterized by the way in which their
flavors are infused and typically have high sugar content. (1)
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Alcoholic content
(ABV), in percentage by weight (sometimes abbreviated w/w for weight for weight), or in proof.
In the USA, the 'proof' measurement is twice the percentage of alcohol by volume at 60 degrees
Fahrenheit (e.g., 80 proof = 40% ABV). Degrees proof were formerly used in the UK where 100
degrees proof was 57.1% ABV (historically, the most dilute spirit which would sustain the
combustion of gunpowder). Common distillation cannot exceed 191.2 proof (USA) because at
that point ethanol is an azeotrope with water. Alcohols of this purity are commonly referred to as
grain alcohol and are not meant for human consumption, with the notable exception of neutral
grain spirits.
Most yeasts cannot grow when the concentration of alcohol is higher than about 18% by
volume, so that is a practical limit for the strength of fermented beverages such as wine, beer,
and sake. Strains of yeast have been developed that can survive in solutions of up to 25% alcohol
by volume, but these were bred for ethanol fuel production, not beverage production. Spirits are
produced by distillation of a fermented product, concentrating the alcohol and eliminating some
of the by-products.
Unsweetened, distilled alcoholic beverages with an alcohol content of more than 30% ABV
are called spirits. Sweetened beverages with a high alcohol content are called liqueurs. Spirits
can be added to wines to create fortified wines, such as port and sherry. (1)
Toxicity
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Alcohols often have an odor described as 'biting' that 'hangs' in the nasal passages. Ethanol in
the form of alcoholic beverages has been consumed by humans since pre-historic times, for a
variety of hygienic, dietary, medicinal, religious, and recreational reasons. The consumption of
large doses results in drunkenness or intoxication (which may lead to a hangover as the effect
wears off) and, depending on the dose and regularity of use, can cause acute respiratory failure or
death and with chronic use has medical repercussions. Because alcohol impairs judgment, it can
Rate of absorption of alcohol depends on several factors. It is quickest, for example, when
alcohol is drunk on an empty stomach and the concentration of alcohol is 20-30%. Thus, sherry,
with an alcohol concentration of about 20% increases the levels of alcohol in blood more rapidly
than beer (3-8%), while spirits (40%) delay gastric emptying and inhibit absorption. Drinks
aerated with carbon dioxide, for example whisky, soda and champagne. They get into the system
quicker. Food, and particularly carbohydrate, retards absorption. Blood concentrations may not
reach a quarter of those achieved on an empty stomach. The pleasurable effects of alcohol are
best achieved with a meal or when alcohol is drunk diluted, in the case of spirits.
Alcohol is distributed throughout the water in the body, so that most tissues such as the heart,
brain, and muscles are exposed to the same concentration of alcohol as the blood. The exception
is the liver, where exposure is greater because blood is received direct from the stomach and
small bowel via the portal vein. Alcohol diffuses rather slowly, except into organs with a rich
Very little alcohol enters fat because of fat's poor solubility. Blood and tissue concentrations
are therefore higher in women, who have more subcutaneous fat and a smaller blood volume,
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than in men, even when the amount of alcohol consumed is adjusted for body weight. Women
also may have lower levels of alcohol dehydrogenases in the stomach than men, so that less
alcohol is metabolised before absorption. Alcohol enters the fetus readily through the placenta
Blood alcohol concentration varies according to sex, size and body build, phase of the
menstrual cycle (it is highest premenstrually and at ovulation), previous exposure to alcohol, type
of drink, whether alcohol is taken with food or drugs, such as cimetidine (which inhibits gastric
Metabolism of Alcohol
More than 90% of alcohol is eliminated by the liver; 2-5% is excreted unchanged in urine,
sweat, or breath. The first step in metabolism is oxidation by alcohol dehydrogenases, of which at
highly reactive and toxic substance, and in healthy people it is oxidised rapidly by aldehyde
The first step in the metabolism of alcohol takes place in the hepatocytes, where conversion to
(ALDH). The toxic substance, acetaldehyde, and its derivatives are implicated in alcoholic
cirrhosis of the liver. The liver alcohol dehydrogenase (ADH), ALDH, and cytochrome
P4502E1(P4502E1) are polymorphic at the ADH2, ADH3, ALDH2 loci, and the 5’-flanking
region of the P4502E1. Further, ethnic variations have been reported. The ß2ß2 enzyme encoded
by ADH2 2*2 is approximately 20-fold more active in ethanol oxidation than the ß1ß1 enzyme.
Individuals who inherit the ADH2*2 allele have homodimeric and heterodimeric ß2-containing
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isozymes and could be expected to have faster rates of alcohol metabolism and possibly higher
attempted to explain susceptibility to alcoholism and alcohol induced liver disease in terms of
in the different alcohol-induced organ-specific diseases, such as those involving the liver,
Alcohol (ethanol) is a drug, and health professionals should know something of its
physiological and pathological effects and its handling by the body. It is a small, water soluble
molecule that is relatively slowly absorbed from the stomach, more rapidly absorbed from the
small intestine, and freely distributed throughout the body. Alcoholic drinks are a major source of
energy, for example, six pints of beer contain about 500 kcal and half a litre of whisky contains
1650 kcal. The daily energy requirement for a moderately active man is 3000 kcal and for a
Heavy drinkers
Two mechanisms dispose of excess alcohol in heavy drinkers and account for "tolerance" in
concentrations of acetate. Secondly, the microsomal ethanol oxidising system is brought into
play; this is dependent on cytochrome P450, which is normally responsible for drug metabolism,
and other cofactors. This process is called enzyme induction, and the effect is also produced by
The two mechanisms lead to a redox state, in which free hydrogen ions build up and have to
be disposed of by several different pathways. Some of the resultant metabolic aberrations can
have clinical consequences: hepatic gluconeogenesis is inhibited, the citric acid cycle is reduced,
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and oxidation of fatty acids is impaired. Glucose production is thus reduced, with the risk of
hypoglycaemia. Overproduction of lactic acid blocks uric acid excretion by the kidneys and
Behavior effect
Alcohol is a sedative and mild anaesthetic. It is believed to activate the pleasure or reward
centres in the brain by triggering release of neurotransmitters such as dopamine and serotonin.
Alcohol produces a sense of wellbeing, relaxation, disinhibition, and euphoria. These feelings are
blood pressure, probably because of stimulation of the hypothalamus and increased release of
sympathomimetic amines and pituitary-adrenal hormones. The kidneys secrete more urine, not
only because of the fluid drunk but also because of the osmotic effect of alcohol and inhibition of
Increasing consumption leads to a state of intoxication, which depends on the amount drunk
and previous experience of drinking. Even at a low blood alcohol concentration of around 6.5
mmol/l (30 mg/100 ml), the risk of unintentional injury is higher than in the absence of alcohol,
although individual experience and complexity of task have to be taken into account. In a
simulated driving test, for example, bus drivers with a blood alcohol concentration of 10.9
mmol/l (50 mg/100 ml) thought they could drive through obstacles that were too narrow for their
vehicles.
People become garrulous, elated, and aggressive at concentrations above 21.7 mmol/l (100
mg/100 ml) and then may stop drinking as drowsiness supervenes. After effects ("hangover")
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If drinking continues, slurred speech and unsteadiness are likely at around 43.4 mmol/l (200
mg/100 ml), and loss of consciousness may result. Concentrations above 86.8 mmol/l (400
mg/100 ml) commonly are fatal as a result of ventricular fibrillation, respiratory failure, or
inhalation of vomit (this is particularly likely when drugs have been taken in addition to alcohol).
(3)
IV. CIRRHOSIS
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The word "cirrhosis" derives from Greek kirrhos, meaning "tawny" (the orange-yellow colour
of the diseased liver). While the clinical entity was known before, it was René Laennec who gave
it the name "cirrhosis" in his 1819 work in which he also describes the stethoscope.(4)
Cirrhosis is most commonly caused by alcoholism, hepatitis B and C and fatty liver disease
and many other possible causes. Some cases are cryptogenic, but most of these are probably due
Ascites (fluid retention in the abdominal cavity) is the most common complication of
cirrhosis and is associated with a poor quality of life, increased risk of infection, and a poor long-
(confusion and coma) and bleeding from esophageal varices. Cirrhosis is generally irreversible
once it occurs, and treatment generally focuses on preventing progression and complications. In
Causes (4,5,6)
Cirrhosis has many possible causes, sometimes more than one cause is present in the same
patient. In the Western World, chronic alcoholism and hepatitis C are the most common causes.
Alcoholic cirrhosis develops in 15% of individuals who drink heavily for more than a decade.
There is great variability in the amount of alcohol needed to cause cirrhosis (as little as 3-4
drinks a day in some men and 2-3 in some women. Alcohol seems to injure the liver by blocking
the normal metabolism of protein, fats, and carbohydrates. Patients may also have concurrent
alcoholic hepatitis with fever, hepatomegaly, jaundice, and anorexia. AST and ALT are both
elevated but less than 300 IU/L with a AST : ALT ratio > 2.0, a value rarely seen in other liver
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diseases. Liver biopsy may show hepatocyte necrosis, Mallory bodies, neutrophilic infiltration
- Chronic hepatitis C
Infection with this virus causes inflammation of and low grade damage to the liver that over
several decades can lead to cirrhosis. Can be diagnosed with serologic assays that detect hepatitis
C antibody or viral RNA. The enzyme immunoassay, EIA-2, is the most commonly used
- Chronic hepatitis B
The hepatitis B virus is probably the most common cause of cirrhosis worldwide, especially
South-East Asia, but it is less common in the United States and the Western world. Hepatitis B
causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D
hepatitis B can be diagnosed with detection of HBsAG > 6 months after initial infection. HBeAG
and HBV DNA are determined to assess whether patient will need antiviral therapy.
In NASH, fat builds up in the liver and eventually causes scar tissue. This type of hepatitis
appears to be associated with diabetes, protein malnutrition, obesity, coronary artery disease, and
treatment with corticosteroid medications. This disorder is similar to that of alcoholic liver
disease but patient does not have an alcohol history. Biopsy is needed for diagnosis.
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antibodies with liver biopsy as confirmation if showing florid bile duct lesions. It is more
common in women.
PSC is a progressive cholestatic disorder presenting with pruritus, steatorrhea, fat soluble
vitamin deficiencies, and metabolic bone disease. There is a strong association with
inflammatory bowel disease (IBD), especially ulcerative colitis. Diagnosis is best with contrast
cholangiography showing diffuse, multifocal strictures and focal dilation of bile ducts, leading to
- Autoimmune hepatitis
This disease is caused by the immunologic damage to the liver causing inflammation and
eventually scarring and cirrhosis. Findings include elevations in serum globulins, especially
gamma globulins. Therapy with prednisone +/- azathioprine is beneficial. Cirrhosis due to
autoimmune hepatitis still has 10-year survival of 90%+. There is no specific tool to diagnose
- Hereditary hemochromatosis
Usually presents with family history of cirrhosis, skin hyperpigmentation, diabetes mellitus,
pseudogout, and/or cardiomyopathy, all due to signs of iron overload. Labs will show fasting
transferrin saturation of > 60% and ferritin > 300 ng/mL. Genetic testing may be used to identify
HFE mutations. If these are present, biopsy may not need to be performed. Treatment is with
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- Wilson's disease
hepatic copper content on liver biopsy. May also have Kayser-Fleischer rings in the cornea and
Autosomal recessive disorder. Patients may also have COPD, especially if they have a history
of tobacco smoking. Serum AAT levels are low. Recombinant AAT is used to prevent lung
- Cardiac cirrhosis
Due to chronic right sided heart failure which leads to liver congestion.
- Other, there are Galactosemia, Glycogen storage disease type IV, Cystic fibrosis, Drugs or
Pathophysiology
The liver plays a vital role in synthesis of proteins (e.g. albumin, clotting factors and
complement), detoxification and storage (e.g. vitamin A). In addition, it participates in the
Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If
the cause is removed at this stage, the changes are still fully reversible.
The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal
parenchyma, blocking the portal flow of blood through the organ and disturbing normal function.
Recent research shows the pivotal role of stellate cell, a cell type that normally stores vitamin A,
in the development of cirrhosis. Damage to the hepatic parenchyma leads to activation of the
stellate cell, which becomes contractile (called myofibroblast) and obstructs blood flow in the
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circulation. In addition, it secretes TGF-β1, which leads to a fibrotic response and proliferation of
connective tissue. Furthermore, it disturbs the balance between matrix metalloproteinases and the
naturally occurring inhibitors (TIMP 1 and 2), leading to matrix breakdown and replacement by
The fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace the
entire liver architecture, leading to decreased blood flow throughout. The spleen becomes
Some of the following signs and symptoms may occur in the presence of cirrhosis or as a
result of the complications of cirrhosis. Many are nonspecific and may occur in other diseases
and do not necessarily point to cirrhosis. Likewise, the absence of any does not rule out the
possibility of cirrhosis.
Vascular lesions consisting of a central arteriole surrounded by many smaller vessels due to
- Palmar erythema
Exaggerations of normal speckled mottling of the palm, due to altered sex hormone
metabolism.
- Muehrcke's nails
Paired horizontal bands separated by normal color due to hypoalbuminemia (low production
of albumin).
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- Terry's nails
Proximal two thirds of the nail plate appears white with distal one-third red, also due to
hypoalbuminemia
- Clubbing
Angle between the nail plate and proximal nail fold > 180 degrees
- Hypertrophic osteoarthropathy
Chronic proliferative periostitis of the long bones that can cause considerable pain.
- Dupuytren's contracture
Thickening and shortening of palmar fascia that leads to flexion deformities of the fingers.
- Gynecomastia
Benign proliferation of glandular tissue of male breasts presenting with a rubbery or firm
mass extending concentrically from the nipples. This is due to increased estradiol and can occur
in up to 66% of patients.
- Hypogonadism
Manifested as impotence, infertility, loss of sexual drive, and testicular atrophy due to
- Liver size
- Splenomegaly
Increase in size of the spleen. Due to congestion of the red pulp as a result of portal
hypertension.
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- Ascites
Accumulation of fluid in the peritoneal cavity giving rise to flank dullness (needs about 1500
ml to detect flank dullness). It may be associated with hydrocele and penile flomation (swelling
- Caput medusa
In portal hypertension, the umbilical vein may open. Blood from the portal venous system
may be shunted through the periumbilical veins into the umbilical vein and ultimately to the
- Cruveilhier-Baumgarten murmur
Venous hum heard in epigastric region (on examination by stethoscope) due to collateral
connections between portal system and the remnant of the umbilical vein in portal hypertension.
- Fetor hepaticus
- Jaundice
Yellow discoloring of the skin, eye, and mucus membranes due to increased bilirubin (at least
- Asterixis
hepatic encephalopathy.
- Other
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Lab findings (4,6)
- Aminotransferases
AST and ALT are moderately elevated, with AST > ALT. However, normal
- Alkaline phosphatase
- GGT
Correlates with AP levels. Typically much higher in chronic liver disease from alcohol.
- Bilirubin
- Albumin
Levels fall as the synthetic function of the liver declines with worsening cirrhosis since
- Prothrombin time
- Globulins
Increased due to shunting of bacterial antigens away from the liver to lymphoid tissue.
- Serum sodium
Hyponatremia due to inability to excrete free water resulting from high levels of ADH and
aldosterone.
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- Thrombocytopenia
Due to both congestive splenomegaly as well as decreased thrombopoietin from the liver.
- Coagulation defects
The liver produces most of the coagulation factors and thus coagulopathy correlates with
Other laboratory studies performed in newly diagnosed cirrhosis may include Serology for
Ferritin and transferrin saturation (markers of iron overload), copper and ceruloplasmin (markers
of copper overload), Immunoglobulin levels (IgG, IgM, IgA), Cholesterol and glucose, Alpha 1-
antitrypsin.
Imaging (4)
- Ultrasound
Ultrasound is routinely used in the evaluation of cirrhosis, where it may show a small and
nodular liver in advanced cirrhosis along with increased echogenicity with irregular appearing
areas. Ultrasound may also screen for hepatocellular carcinoma, portal hypertension and Budd-
Fibroscan is a new type of device, uses elastic waves to determine liver stiffness which
theoretically can be converted into a liver score based on the METAVIR scale. The FibroScan
produces an ultrasound image of the liver (from 20-80mm) along with a pressure reading (in
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kPa.) The test is much faster than a biopsy (usually last 2.5-5 minutes) and is completely
Other tests performed in particular circumstances include abdominal CT and liver/bile duct
MRI (MRCP). Rarely diseases of the bile ducts, such as primary sclerosing cholangitis, can be
causes of cirrhosis. Imaging of the bile ducts, such as ERCP or MRCP (MRI of biliary tract and
pancreas) can show abnormalities in these patients, and may aid in the diagnosis.
Endoscopy (6)
performed in patients with established cirrhosis to exclude the possibility of esophageal varices.
If these are found, prophylactic local therapy may be applied (sclerotherapy or banding) and beta
Pathology (4,5,6)
Macroscopically, the liver may be initially enlarged, but with progression of the disease, it
becomes smaller. Its surface is irregular, the consistency is firm and the color is often yellow (if
associates steatosis). Depending on the size of the nodules there are three macroscopic types:
portal cirrhosis) regenerating nodules are under 3 mm. In macronodular cirrhosis (post-necrotic
cirrhosis), the nodules are larger than 3 mm. The mixed cirrhosis consists in a variety of nodules
septa. In these nodules, regenerating hepatocytes are disorderly disposed. Portal tracts, central
veins and the radial pattern of hepatocytes are absent. Fibrous septa are important and may
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present inflammatory infiltrate (lymphocytes, macrophages) If it is a secondary biliary cirrhosis,
biliary ducts are damaged, proliferated or distended - bile stasis. These dilated ducts contain
inspissated bile which appear as bile casts or bile thrombi (brown-green, amorphous). Bile
retention may be found also in the parenchyma, as the so called "bile lakes."
Diagnosis (4)
The gold standard for diagnosis of cirrhosis is a liver biopsy, through a percutaneous,
micronodular, macronodular, or mixed, but this classification has been abandoned since it is
nonspecific to the etiology, it may change as the disease progresses, and serological markers are
much more specific. However, a biopsy is not necessary if the clinical, laboratory, and radiologic
data suggests cirrhosis. Furthermore, there is a small but significant risk to liver biopsy, and
Grading (4,5)
The severity of cirrhosis is commonly classified with the Child-Pugh score. This score uses
bilirubin, albumin, INR, presence and severity of ascites and encephalopathy to classify patients
in class A, B or C; class A has a favourable prognosis, while class C is at high risk of death. It
was devised in 1964 by Child and Turcotte and modified in 1973 by Pugh et al.[10]
More modern scores, used in the allocation of liver transplants but also in other contexts, are
the Model for End-Stage Liver Disease (MELD) score and its pediatric counterpart, the Pediatric
The hepatic venous pressure gradient, the difference in venous pressure between afferent and
efferent blood to the liver, also determines severity of cirrhosis, although hard to measure. A
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Complications (4,5,)
As the disease progresses, complications may develop. In some people, these may be the first
- Hepatic encephalopathy, the liver does not clear ammonia and related nitrogenous substances
from the blood, which are carried to the brain, affecting cerebral functioning: neglect of personal
- Portal hypertension, blood normally carried from the intestines and spleen through the hepatic
portal vein flows more slowly and the pressure increases. This leads to the following
complications:
a. Ascites, fluid leaks through the vasculature into the abdominal cavity. Fluid in the abdomen
(ascites) may become infected with bacteria normally present in the intestines (spontaneous
bacterial peritonitis).
b. Esophageal varices, collateral portal blood flow through vessels in the stomach and esophagus.
These blood vessels may become enlarged and are more likely to burst.
- Immune system dysfunction, leading to infection. Signs and symptoms of infection may be
aspecific are more difficult to recognize (e.g. worsening encephalopathy but no fever).
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Problems in other organs.
- Hepatorenal syndrome, insufficient blood supply to the kidneys, causing acute renal failure.
- Hepatopulmonary syndrome, blood bypassing the normal lung circulation (shunting), leading
portal hypertension.
Chronic alcoholism can cause cirrhosis, it’s called Laennec’s cirrhosis. This condition should be
renamed "alcoholic cirrhosis". Laennec's cirrhosis has three stages. The pathologic features of this form
of cirrhosis change with time. Therefore, it is helpful to break the disease down into three stages, the fatty
liver stage, the fibrotic liver stage and the nodular liver stage.
lobular, occurs hypoxemia on lobular and make cell injury in areas that far from the flow of blood.
3. Formation of acetaldehyde-protein adducts role as a neoantigen and make limfocyte and specific
antibody actived. Both cells attack hepatosit that have that neoantigen.
In early stages the liver is large and fatty. In this early stage, fat accumulates in the liver cells
around the central vein (fatty change). The liver becomes large, even huge (hepatomegaly). The
normal liver weighs about 1,200 grams. By comparison, fatty livers can weigh in at over 6,000
grams and may, in the living patient, fill the abdominal cavity (remember that the normal liver
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extends 2-3 finger below the right costal margin). At autopsy, the fatty liver is greasy and a cut
surface is yellow. As dramatic as these changes are, the fatty change is reversible.
In later stages, the liver becomes scarred (fibrotic). In this stage, the liver returns to a more
normal size, however, it does not return to normal in any other way. In fact, the changes that
develop during this stage are irreversible. The fatty change subsides and is replaced by fibrosis
(scarring) and some chronic inflammation. No doubt the retreat of fatty change and the shrinking
effect of scar tissue is responsible for the over-all decrease in liver size.
In the final stage, the liver becomes lumpy (nodular). In this stage, the liver shrink even
further. It may not extend below the costal margin at all. Liver cells attempt to regenerate in an
increasingly fibrotic setting. They find it difficult to do so and form "regenerative nodules" that
only partially carry out normal liver function. This shrunken, nodular texture has been dubbed
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