II Ultrastructural changes associated with some biochemical lesions: accumulation of water, fat,
and damage to DNA
A biochemical lesion can be defined as the biochemical change or defect which directly
precedes pathological change or dysfunction
Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases
and conditions, such as hepatitis and chronic alcoholism. Cirrhosis occurs in response to
damage to the liver. Each time the liver is injured, it tries to repair itself. In the process, scar
tissue forms. As cirrhosis progresses, more and more scar tissue forms, making it difficult for
the liver to function. The specific complications resulting from the changes brought on by
cirrhosis is termed decompensated cirrhosis and is life-threatening.
Complications of cirrhosis include edema, ascites, spontaneous bacterial peritonitis, bleeding
from varices, hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome,
and liver cancer.
1. Ascites
Ascites is an abnormal buildup of fluid in the abdomen, specifically the peritoneal cavity. It
occurs when the body makes more fluid than it can remove. Ascites can occur with disease as
cancer and liver disorders, such as severe alcoholic hepatitis without cirrhosis, chronic hepatitis,
and obstruction of the hepatic vein (Budd-Chiari syndrome). When ascites is due to cancer, or
if the fluid in the abdomen contains cancer cells, it is often called malignant ascites or malignant
peritoneal effusion.
a- Types of ascites
Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to 35 liters are
possible.
Transudates are a result of increased pressure in the hepatic portal vein, e.g. due to cirrhosis,
while exudates are actively secreted fluid due to inflammation or malignancy. As a result,
exudates are high in protein, high in lactate dehydrogenase, have a low pH (<7.30), a
low glucose level, and more white blood cells. Transudates have low protein (<30 g/L), low
LDH, high pH, normal glucose, and fewer than 1 white cell per 1000 mm³. Clinically, the most
useful measure is the difference between ascitic and serum albumin concentrations (albumin
usually leaks from blood vessels into the abdomen. Normally, albumin, the main protein in
blood, helps keep fluid from leaking out of blood vessels. When albumin leaks out of blood
vessels, fluid also leaks out.). A difference of less than 1 g/dl (10 g/L) implies an exudate.
a- Formation of ascites
Ascites tends to occur in long-standing (chronic) rather than in short-lived (acute) liver
disorders. Ascitic fluid leaks from the surface of the liver and intestine and accumulates within
the abdomen. A combination of factors is responsible:
-Portal hypertension—high blood pressure in the portal vein (the large vein that brings blood
from the intestine to the liver) and its branches. Portal hypertension plays an important role in
the production of ascites by raising capillary hydrostatic pressure. It mostly results from
cirrhosis
-Fluid retention by the kidneys
-Alterations in various hormones and chemicals that regulate body fluids
c- Complications of ascites
Regardless of the cause, sequestration of fluid within the abdomen leads to additional fluid
retention by the kidneys. The sympathetic nervous system is also activated,
and renin production is increased. Extreme disruption of the renal blood flow can lead
to hepatorenal syndrome. Spontaneous bacterial peritonitis (SBP), due to decreased
antibacterial factors in the ascitic fluid such as complement can also occur.