Liver Cirrhosis Flashcards
Definition
chronic polyetiological diffuse
progressive disease of the liver, characterized by
• significant decreasing of the amount of functioning
hepatocites,
• increasing fibrosis,
• reconstruction of the normal structure and vascular
network of the liver,
• appearing of the nodes of regeneration, and further
• development of hepatic insufficiency and portal
hypertensio
Causes
– Viral hepatitis (B, C, Delta, G);
– Autoimmune hepatitis;
– Alcohol abuse, the disease develops in 10-15 years from first
use (60 grams/day for men and 20 grams/day for women);
– Metabolic disorders (hemochromatosis, Wilson’s disease,
Konovalov, deficiency of alpha-1-antitrypsin deficiency and
other);
– Chemical toxic substances and drugs;
– Hepatotoxic drugs;
– Diseases of biliary tract obstruction (blockage) of
extrahepatic and intrahepatic bile ducts;
– Long-term venous congestion of the liver (constrictive
pericarditis, venooclusive disease, heart failure
Pathogenesis of liver cirrhosis
portal
hypertension
Portal hypertension is the most important syndrome of cirrhosis of the liver
post-sinusoidal block of blood flow in the liver;
- perisinusoidal fibrosis;
- the presence of arteriovenous anastomoses in intra-lobular connective
tissue septa;
- portal infiltration and fibrosis;
- increased blood flow to the liver;
- reduction of the terminal and larger branches of the portal vein and hepatic
artery as a result of the inflammatory process in the liver;
- narrowing of the sinusoid lumen by proliferating endothelial cells.
The first three of these factors lead to an increase in intrinsic sinusoidal
pressure, contribute to the development of ascites and liver failure.
The last mechanisms are responsible for an increase in presinusoidal pressure
and the development of extrahepatic manifestations of portal hypertension
Complication after portal hypertension
the most important clinical
manifestations of cirrhosis of the liver develop — portocaval
anastomoses, ascites, splenomegaly
Bleeding from the esophageal
varices
Bleeding from the esophageal varices is a critical
condition that occurs when the esophageal veins
wall is stretched and ruptured due to increased
pressure in the portal syste
Hepatic encephalopathy (PE)
Hepatic encephalopathy (HE) is
a complex of potentially
reversible neuropsychiatric
disorders resulting from liver
failure and/or portosystemic
blood bypass
Stages of liver cirrhosis
Cirrhosis consists of 3 distinct prognostic stages.
The compensated stage is defined by the absence of clinically
overt complications and is associated with a median survival
that exceeds 12 years;
the stage of decompensation is marked by the development
of ascites, hepatic encephalopathy, and/or gastroesophageal
variceal hemorrhage and is associated with a median survival
of approximately 2 years.
A third stage of “further” decompensation is characterized by
the development of a second (additional) decompensating
event, recurrent ascites (requiring large-volume [>5 L]
paracentesis), recurrent variceal hemorrhage, recurrent
hepatic encephalopathy, spontaneous bacterial peritonitis,
acute kidney injury/ hepatorenal syndrome, and/or jaundice
Functions of the liver
Symptoms of LC
pain in the right hypochondrium and epigastric region, non-
intense, pulling, often disturbed by a feeling of heaviness in the
right hypochondrium;
• nausea, sometimes vomiting
• bloody vomiting is possible with bleeding from varicose veins
of the esophagus and stomach
• feeling of bitterness and dry mouth;
• itchy skin (with cholestasis and accumulation of large amounts
of bile acids in the blood);
• fatigue, irritability;
• frequent loose stools (especially after eating fatty foods);
• bloating;
• weight loss;
• sexual weakness (in men), menstrual irregularity (in women
Characteristic appearance of patients
with cirrhosis of the liver
emaciated face,
• unhealthy subicteric skin color,
• bright lips,
• prominent zygomatic bones, erythema of the
zygomatic region,
• dilation of the capillaries of the facial skin;
• muscular atrophy (thin limbs);
• enlarged abdomen (due to ascites);
• swelling of the lower extremities
Examination of patients
• xanthelasmas (yellow lipid spots in the upper eyelid
area);
• fingers in the form of drumsticks with hyperemia of the
skin at the nail holes;
• in case of fluffiness of joints and adjacent bones (mainly
in case of biliary cirrhosis of the liver — “biliary
rheumatism”);
• dilation of the veins of the abdominal and chest walls
When examining internal organs, pronounced
functional and dystrophic changes are found.
Myocardial dystrophy is manifested by palpitations,
expansion of the heart border to the left, deafness of
tones, shortness of breath, on an ECG - a decrease in
the ST interval, a change in the T wave (decrease, two-
phase, in severe cases - inversion). Hyperkinetic type
of hemodynamics is often detected (increased minute
blood volume, pulse pressure, fast, full puls
Small signs of cirrhosis
“spider naevi (vascular asterisks)” on the skin of the upper half of the trunk —
telangiectasia in the form of spiders. It is characteristic that the “vascular
asterisks” are never located below the navel, they are most pronounced with an
exacerbation of cirrhosis, and their reverse development is possible during
remission;
- angiomas at the edge of the nose, in the corner of the eyes (they may bleed);
- erythema of the palms — bright red lingonberry coloration of warm palms spilled
either in the thenar or hypothenar area, as well as in the area of the fingertips
(“liver palms”, “hands of beer lovers”);
- varnished, edematous, uncoated lingonberry-colored tongue;
- carmine-red coloration of the mucous membrane of the mouth and lips;
- gynecomastia in men;
- atrophy of the genitals;
- decrease in the severity of secondary sexual characteristics (decrease in the
severity of hair loss in the armpits, in the pubic area).
Complications of the liver cirrhosis
Thrombosis at portal vein system
• Carcinoma of the liver
• Infectious complications (pneumonia, «spontaneous»
peritonitis at ascites )
• Sepsis
• Encephalopathy with the development of hepatic coma;
• Profuse bleeding from varicose veins of the esophagus and
stomach;
• Bleeding from a varicose inferior hemorrhoidal vein;
• Portal vein thrombosis;
• Secondary bacterial infection (urinary tract infection,
pneumonia, sepsis, peritonitis);
• Transformation into cirrhosis-cancer,
• Progressive liver and kidney failure
Laboratory diagnostic tests
a general (clinical) blood test (to assess the level of
hemoglobin, platelets, and leukocytes).
• a biochemical general therapeutic blood test,
including such indicators as total protein, albumin,
total bilirubin, direct bilirubin, creatinine, alanine
aminotransferase, aspartate aminotransferase,
alkaline phosphatase,
gammaglutamintranspeptidase, glucose ( to assess
necroinflammatory activity, cholestasis, liver and
kidney function)
• ammonia determination (for the diagnosis of
hepatic encephalopathy
t is recommended to evaluate the level of vitamin D
in patients with cirrhosis of the liver, especially if
osteopenia or osteoporosis is suspected
urine analysis is
recommended for patients with LC to exclude
urinary infection,
recommended to study markers of viral hepatitis
(hepatitis B virus antigen (HBsAg) in blood,
determination of total antibodies of classes M and G
laparocentesis(as cites present or absent recommended to count the number of neutrophils in ascitic
fluid. The neutrophil content > 250 cells /mm3 (0.25 x 109/l) is a
criterion for SBP in the absence )
ultrasound(etermine the size and ultrasound characteristics of
the liver, diagnose portal hypertension (detection of
ascites, measurement of the diameter)
• Esophagogastroduodenoscopy (EGDS) is
recommended for patients with LC in order to assess
the size of the veins of the esophagus and stomach
and exclude spots of vasculopathy as stigmas of high
risk of bleeding
computed
tomography (CT) of the abdominal cavity with
intravenous contrast in patients with LC with
suspected thrombosis in the veins of the portal
system or with focal liver changes on ultrasound
Mir
recommended for patients with CP to calculate BMI (kg/m2) to
assess body weight deficiency or the degree of obesity for
subsequent correction of nutritional stat
Liver cirrhosis classifications
Morphological variants of the LC
• Micronodular (small nodular) – regularly located
small nodes 1-3 mm in diameter, separated by a
network of scar tissue
• Macronodular – irregularly located large nodes up to
5 cm in diameter, separated by cords of connective
tissue of various widths
• Mixed
Child–Pugh score classification
Child–Pugh score
is used to assess the prognosis of
chronic liver disease, mainly cirrhosis.
Measure 1 point 2 points 3 points
Total bil
μmol/L (mg/dL) <34 (<2) ,34–50 (2–3) ,>50 (>3)
Serum albumin,
g/dL. >3.5 ,2.8–3.5, <2.8
Prothrombin
time,
prolongation
(s)
<4.0 , 4.0–6.0 , > 6.0
OR
INR
<1.7 ,1.7–2.3, >2.3
Ascites None
Mild (or
suppressed with
medication)
Moderate to
severe (or
refractory)
Hepatic
encephalopathy None Grade I–II Grade III–IV
METAVIR scoring system classification of liver cirrhosis
The fibrosis stages range from F0 to F4:
• F0: no fibrosis
• F1: portal fibrosis without septa
• F2: portal fibrosis with few septa
• F3: numerous septa without cirrhosis
• F4: cirrhosis
EVOLUTION OF CIRRHOSIS
The evolution can be assessed on degree of fibrosis and nodule formation. Liver cirrhosis classification
1-INCOMPLETE SEPTAL
(Incomplete bridging fibrosis, no nodules)
2-EARLY
(Thin bridging fibrosis with dissecting nodules)
3-MODERATELY ADVANCED
(Thick bridging fibrosis with dissecting nodules)
4-ADVANCED
(Wide septa with regenerative hyperplastic nodules
ACTIVITY OF CIRRHOSIS classifications
Activity is assessed by extent of cell damage, inflammatory reaction
within the scar tissue, necrosis along fibrous septa, edema of the
septa and changes in the parenchymal nodules such as necrosis and
cholestasis.
Activity indicates the progression of the cirrhotic process and is graded
as:
INACTIVE No inflammation and intact limiting plates around septa
which are fibrotic
SLIGHT Mild inflammation; segmental erosion of limiting plates
MODERATE Moderate inflammation and damage of limiting plates
SEVERE Marked inflammation, extensive damage of limiting plates,
piecemeal necrosis and parenchymal damage, i.e.: necrosis,
cholestasis, dysplasia, malignant transformation
Treatment of LC
Principles of diet therapy and nutritional
support may be advised to
avoid hypomobility and gradually increase physical
activity to prevent and/or reduce the degree of
sarcopenia
