- Radiologic studies include:
- Abdominal ultrasound
- Computed tomography scan
- Magnetic resonance imaging
- Evidence of Portal HTN:
- Abdominal imaging (typically ultrasound) helps:
- Evaluate the liver parenchyma
- Detects extrahepatic manifestations of cirrhosis
- AST to platelet ratio index
- Findings on abdominal imaging are viewed in light of other signs of cirrhosis, such as physical examination or laboratory test findings.
- In addition to evaluating the liver, abdominal imaging may reveal:
- Hepatocellular carcinoma
- Extrahepatic findings suggestive of cirrhosis:
- Hepatic or portal vein thrombosis
- Imaging may indicate etiology of cirrhosis:
- Computed tomography (CT) scanning complements ultrasound imaging.
- Classical appearances in some diseases:
- Haemochromatosis: where the excess iron deposition causes a dramatic increase in hepatic density.
- A hypertrophied caudate lobe discovered on computed tomographic (CT) scanning, for example, suggests Budd-Chiari syndrome.
- Magnetic resonance imaging (MRI):
- determines the nature of focal lesions such as hepatic metastases
- nodular regeneration
- Decreased signal intensity on magnetic resonance imaging may indicate iron overload from hereditary hemochromatosis.
Ultrasonography: routinely used during the evaluation of cirrhosis
- First-line investigation of choice.
- The first radiologic study obtained due to easy availability.
- Provides information about :
- appearance of the liver
- blood flow within the portal circulation
- less expensive than other imaging modalities
- No exposure to intravenous contrast or radiation
- well tolerated
- widely available
- Ultrasound, particularly with colour Doppler imaging : 
- measures changes in blood flow in the presence of portal hypertension
- excludes biliary obstruction in patients who present with jaundice
- Early signs of cirrhosis in B-ultrasonography include:
- inhomogeneity of the hepatic tissue
- Irregularity of the hepatic surface
- enlargement of the caudate lobe
- Splenomegaly due to portal HTN
- The diagnostic evaluation of cirrhosis with ultrasonography is based on the direct relation between the extent of fibrosis and the ultrasonographically determined degree of liver stiffness.
- ultrasonography can rule cirrhosis in or out in over 90% of cases , its findings are less than 100% specific because of occasional in -correct measurements and false-positive findings
- Advanced cirrhosis: liver may appear small and nodular
- Surface nodularity and increased echogenicity with irregular appearing areas are consistent with cirrhosis
- Usually atrophy of the right lobe and hypertrophy of the caudate or left lobes.
- Ultrasonography may also be used as a screening test for hepatocellular carcinoma :nodules on ultrasonography warrants further evaluation
- Findings of portal hypertension:
- increased diameter of the portal vein
- presence of collateral veins
- decreased flow within the portal circulation on Doppler imaging
- Ultrasonography is also useful for detecting splenomegaly, ascites, and portal vein thrombosis.
Computed tomography – not routinely used in the diagnosis of cirrhosis
- It provides similar information to ultrasonography, but at the expense of radiation and contrast exposure.
- CT findings:
- Hepatic nodularity
- Atrophy of the right lobe
- Hypertrophy of the caudate or left lobes
- CT portal phase imaging:
- Patency of the portal vein can be demonstrated
Magnetic resonance imaging:
- The role of magnetic resonance imaging (MRI) in the diagnosis of cirrhosis is unclear.
- Use is limited by expense
- Poor tolerance of the examination
- Ability to obtain information provided by MRI through other means
- reveal iron overload and provide an estimate of the hepatic iron concentration
- Magnetic resonance angiography (MRA) is more sensitive than ultrasonography for diagnosing complications of cirrhosis:
- portal vein thrombosis
- CT portal phase imaging, MRA can determine the volume and direction of blood flow in the portal vein.
- Increasing scarring of the liver is associated with increasing "stiffness" of the tissue.
- Transient elastography and the acoustic radiation force impulse (ARFI) technique are now well-established methods for the staging of fibrosis in various liver diseases 
- Radionuclide testing can be useful in suggesting the diagnosis of cirrhosis:
- 99mTc sulfur colloid is normally taken up by cells of the reticuloendothelial system
- Cirrhosis: heterogeneity in the uptake of 99mTc sulfur colloid by the liver and increased uptake by the spleen and bone marrow
Endoscopic retrograde cholangiopancreatography
- diagnosis of sclerosing cholangitis
- Cirrhosis is primarily a histological diagnosis.
- Percutaneous liver biopsy remains the cornerstone of diagnosis.
- quick and simple to perform in a cooperative patient with a normal INR and platelet count.
- The gold standard for diagnosing cirrhosis is:
- Examination of an explanted liver, either at autopsy or following liver transplantation, because the architecture of the entire liver can be appreciated.
- Sample of the liver is obtained by:
- Laparoscopic radiographically-guided fine-needle approach.
- Liver biopsy is not necessary if the clinical, laboratory, and radiologic data strongly suggest the presence of cirrhosis and if the results would not alter the patient's management.
- Patient with a history of heavy alcohol use who has ascites, severe coagulopathy, and a shrunken, nodular-appearing liver on ultrasonography.
- Liver biopsy may be suggestive of etiology:
- Metabolic causes of cirrhosis include:
- Hereditary hemochromatosis
- Nonalcoholic steatohepatitis
- Wilson disease
- Alpha-1 antitrypsin deficiency
- biliary peritonitis
- perforation of other viscera
- mortality rates of between 0.01% and 0.1%
- Percutaneous biopsy of focal lesions may be performed in combination with either ultrasound or CT imaging.
- normal INR and platelet count.
- May be performed in combination with either ultrasound or CT.
- Patients with moderate coagulopathy:
- Plugged liver biopsy : injection of gelatin sponges or metal coils down the tract after biopsy
- Laparoscopic liver biopsy performed on a sedated patient with moderate coagulopathy
- Advantage: allows direct visualisation of the liver
- Patients with severe clotting disorders:
- Transjugular liver biopsy :
- risk of intraperitoneal bleed is less
- biopsies are small: multiple biopsies required
- taken 'blindly'
- Physical examination of patients with cirrhosis is usually remarkable for: jaundice, spider angiomata, ascites, asterixis, spleenomegaly and palmar erythema.
Appearance of the Patient
- Patients with cirrhosis usually appear weak due to constitutional symptoms such as weight loss, anorexia and muscle atrophy. Yellowish discoloration of skin and abdominal distension may also be present due to ascites.
- Jaundice : yellow discoloration of the skin, eyes, and mucus membranes due to increased bilirubin (at least 2-3 mg/dL or 30 mmol/L). Urine may also appear dark.
- Palmar erythema on the thenar and hypothenar eminences, due to altered sex hormone metabolism.
- Spider angiomata: Increased estradiol levels lead to the formation of vascular lesions consisting of central arterioles surrounded by smaller vessels 
- Telangiectasias or spider veins: small dilated blood vessels near the surface of the skin.
- Abnormalities of the head/hair may include thinning of hair on the scalp due to hyperestrogenism
- Kayser-Fleischer rings : dark rings that appear to encircle the iris of the eye in patients with Wilson's disease.
- Parotid gland enlargement
- Fetor hepaticus: severe portal-systemic shunting leads to increased levels of dimethyl sulfide leads to a sweet pungent smell in the breath
- Flank dullness may be present due to ascites (needs approximately 1500ml for detection)
- Cruveilhier-Baumgarten murmur: venous hum that may be present in patients with portal hypertension.
- Hepatic encephalopathy may have signs of:
- Asterixis (bilateral but asynchronous flapping motions of outstretched, dorsiflexed hands) is seen in patients with hepatic encephalopathy.
- edema of the lower extremities
- Muscle atrophy
- Nail changes:
- Muehrcke nails: paired horizontal white bands separated by normal color due to hypoalbuminemia
- Terry nails: the proximal two-thirds of the nail plate appears white, whereas the distal one-third is red due to hypoalbuminemia
- Clubbing: the angle between the nail plate and proximal nail fold is greater than 180 degrees
- Severe clubbing:
- Dupuytren's contracture may cause flexion deformities of the fingers: This occurs due to shortening and thickening of the palmar fascia, due to collagen deposition and fibroblastic proliferation.
- Asterixis in cases with hepatic encephalopathy
- Past history of abuse
Past Medical history
- History of
- History of
- Family history of:
- History of medication use should be obtained as many drugs such as opioids cause constipation as a side effect.
|Drugs and Toxins||Infections||Autoimmune||Metabolic||Biliary obstruction(Secondary bilary cirrhosis)||Vascular||Miscellaneous|
|Alcohol||Hepatitis B||Primary Biliary Cirrhosis||Wilson's disease||Cystic fibrosis||Chronic RHF||Sarcoidosis|
|Methotrexate||Hepatitis C||Autoimmune hepatitis||Hemochromatosis||Biliary atresia||Budd-Chiari syndrome||Intestinal
bypass operations for obesity
|Isoniazid||Schistosoma japonicum||Primary Sclerosing Cholangitis||Alpha-1 antitrypsin deficiency||Bile duct strictures||Veno-occlusive disease||Cryptogenic: unknown|
|Glycogen storage diseases (such as Galactosaemia, Abetalipoproteinaemia)|
- When an injured issue is replaced by a collagenous scar, it is termed as fibrosis.
- When fibrosis of the liver reaches an advanced stage where distortion of the hepatic vasculature also occurs, it is termed as cirrhosis of the liver.
- The cellular mechanisms responsible for cirrhosis are similar regardless of the type of initial insult and site of injury within the liver lobule.
- Viral hepatitis involves the periportal region, whereas involvement in alcoholic liver disease is largely pericentral.
- If the damage progresses, panlobular cirrhosis may result.
- Cirrhosis involves the following steps: 
- Hepatic stellate cell activation
- Kupffer cells are hepatic macrophages responsible for Hepatic Stellate cell activation during injury.
- The hepatic stellate cell (also known as the perisinusoidal cell or Ito cell) plays a key role in the pathogenesis of liver fibrosis/cirrhosis.
- Hepatic stellate cells(HSC) are usually located in the subendothelial space of Disse and become activated to a myofibroblast-like phenotype in areas of liver injury.
- Collagen and non collagenous matrix proteins responsible for fibrosis are produced by the activated Hepatic Stellate Cells(HSC).
- Hepatocyte damage causes the release of lipid peroxidases from injured cell membranes leading to necrosis of parenchymal cells.
- Activated HSC produce numerous cytokines and their receptors, such as PDGF and TGF-f31 which are responsible for fibrogenesis.
- The matrix formed due to HSC activation is deposited in the space of Disse and leads to loss of fenestrations of endothelial cells, which is a process called capillarization.
- Cirrhosis leads to hepatic microvascular changes characterised by 
- formation of intra hepatic shunts (due to angiogenesis and loss of parenchymal cells)
- hepatic endothelial dysfunction
- The endothelial dysfunction is characterised by 
- insufficient release of vasodilators, such as nitric oxide due to oxidative stress
- increased production of vasoconstrictors (mainly adrenergic stimulation and activation of endothelins and RAAS)
- Fibrosis eventually leads to formation of septae that grossly distort the liver architecture which includes both the liver parenchyma and the vasculature. A cirrhotic liver compromises hepatic sinusoidal exchange by shunting arterial and portal blood directly into the central veins (hepatic outflow). Vascularized fibrous septa connect central veins with portal tracts leading to islands of hepatocytes surrounded by fibrous bands without central veins.
- The formation of fibrotic bands is accompanied by regenerative nodule formation in the hepatic parenchyma.
- Advancement of cirrhosis may lead to parenchymal dysfunction and development of portal hypertension.
- Portal HTN results from the combination of the following:
- Structural disturbances associated with advanced liver disease account for 70% of total hepatic vascular resistance.
- Functional abnormalities such as endothelial dysfunction and increased hepatic vascular tone account for 30% of total hepatic vascular resistance.
Pathogenesis of Cirrhosis due to Alcohol:
- More than 66 percent of all American adults consume alcohol.
- Cirrhosis due to alcohol accounts for approximately forty percent of mortality rates due to cirrhosis.
- Mechanisms of alcohol-induced damage include:
- Impaired protein synthesis, secretion, glycosylation
- Ethanol intake leads to elevated accumulation of intracellular triglycerides by:
- Lipoprotein secretion
- Decreased fatty acid oxidation
- Increased fatty acid uptake
- Alcohol is converted by Alcohol dehydrogenase to acetaldehyde.
- Due to the high reactivity of acetaldehyde, it forms acetaldehyde-protein adducts which cause damage to cells by:
- Trafficking of hepatic proteins
- Interrupting microtubule formation
- Interfering with enzyme activities
- Damage of hepatocytes leads to the formation of reactive oxygen species that activate Kupffer cells.
- Kupffer cell activation leads to the production of profibrogenic cytokines that stimulates stellate cells.
- Stellate cell activation leads to the production of extracellular matrix and collagen.
- Portal triads develop connections with central veins due to connective tissue formation in pericentral and periportal zones, leading to the formation of regenerative nodules.
- Shrinkage of the liver occurs over years due to repeated insults that lead to:
- Loss of hepatocytes
- Increased production and deposition of collagen
- There are four stages of Cirrhosis as it progresses:
- Chronic nonsuppurative destructive cholangitis - inflammation and necrosis of portal tracts with lymphocyte infiltration leading to the destruction of the bile ducts.
- Development of biliary stasis and fibrosis
- Periportal fibrosis progresses to bridging fibrosis
- Increased proliferation of smaller bile ductules leading to regenerative nodule formation.
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Cirrhosis of the liver can be classified using two methods; classification based on etiology, and classification based on morphology. Currently, classifying cirrhosis based on morphology is not used, as it requires an invasive procedure to examine the gross appearance of the liver, and it provides little diagnostic value. Classifying cirrhosis according to etiology is a more accepted form of classification, as it can be attained through non-invasive laboratory testing, and has a higher diagnostic value.
Classification Based on Etiology
Cirrhosis can be classified by its etiology. This is the most widely accepted method of classification.
This is the most common cause of cirrhosis, and is caused by continuous and prolonged alcohol abuse. The American Academy of Family Physicians estimate that 60-70 percent of all cases of cirrhosis are a result of alcohol abuse.
This type of cirrhosis occurs after a massive event causes liver cell death. Viral hepatitis is the most common cause for this type of cirrhosis. Agents that are toxic to the liver can also cause this type of cirrhosis, as well as certain types of carcinomas.
This type of cirrhosis results from any diseases that cause biliary obstruction. There is usually a blockage in the bile duct and there may also be inflammation. The excess bile in the liver causes tissue destruction. It commonly results in jaundice.
This type of cirrhosis is caused by congestive heart failure causing poor circulation of oxygenated blood to the liver. This results in liver cell death, and the subsequent replacement of dead cells by fibrous tissue.
This category contains cirrhosis caused by various forms of malnutrition, particularly chronic starvation.
Classification Based on Morphology
Cirrhosis has historically been classified upon the nodular morphology that is seen on upon the gross appearance of the liver. Accurate assessment of the liver morphology can only be obtained through surgery, biopsy, or autopsy, therefore more recently, more non-invasive means of classifying and determining the causes of cirrhosis are used.
|Micronodular cirrhosis is characterized by nodules that are less than 3mm in diameter||Macronodular cirrhosis is characterized by nodules that are more than 3mm in diameter||Micronodular cirrhosis can often progress into macronodular cirrhosis. During this transformation, a mixed form of cirrhosis may be seen.|
|Mixed nodular cirrhosis is also seen in Indian childhood cirrhosis. |
Video in table
- REDIRECTEsophageal web
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Image and text to the right
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Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas
Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas
Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas
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