LO:

1. Vena renalis bermuara kemana

2. Eryhtopoietin diproduksi dimana

3. All about cirrhosis

4. Ascites

Ascites is defined as the pathological accumulation of excess fluid in

the peritoneal cavity. Normally, the peritoneal cavity contains 25–50
mL of ascitic fluid, which allows for the movement of bowel loops past
one other and helps hydrate serosal surfaces. With ascites, this fluid is
not static within the peritoneal cavity, but is rather in a continuous
exchange with the circulation through a large capillary bed under the
visceral peritoneum, with about half the volume entering and leaving
the peritoneal cavity every hour. Furthermore, the constituents of the
fluid are in dynamic equilibrium with those of the plasma. However,
the daily absorption of fluid from the peritoneal cavity back to the
circulation is limited, and the maximum absorption of fluid out of the
peritoneum is approximately 850 mL/d. Thus, the development of
clinically significant ascites occurs when the rate of ascites formation
exceeds the rate of ascites reabsorption. For easily‐controllable ascites,
on the other hand, the volume of fluid that spills into the peritoneal
cavity can be reduced below this absorption threshold. This is the case
 at the early stages of hepatic decompensating when ascites is
responsive to a reduced intake of dietary sodium and to moderate doses
of diuretics.

Cirrhosis is the most common cause of ascites, representing 85% of all

cases of ascites [1]. In patients with cirrhosis, ascites due to portal
hypertension (PHT) is primarily related to an inability to excrete adequate
amounts of sodium into urine, leading to a positive sodium balance. Other
causes of ascites include malignancy, heart failure, tuberculosis, alcoholic
hepatitis, Budd‐Chiari syndrome, and nephrogenic ascites

5. All about hepatoma

Anatomy
A complete understanding of the surgical and interventional approach to the liver
requires a comprehensive understanding of its anatomy and vascular
supply. [6, 7] The liver is the largest internal organ, representing 2-3% of the total body
weight in an adult. It occupies the right upper quadrant of the abdomen, surrounding
the inferior vena cava, and attaches to the diaphragm and parietal peritoneum by
various attachments that are commonly referred to as ligaments.
The vascular supply of the liver includes two sources of inflow that travel in the
hepatoduodenal ligament, as follows:
 Hepatic artery
 Portal vein
The hepatic artery is generally derived from the celiac axis, which originates on the
ventral aorta at the level of the diaphragm. Common variations include a replaced
right hepatic artery, which originates from the superior mesenteric artery, a replaced
left hepatic artery, which is derived from the left gastric artery, or a completely
replaced common hepatic artery, which can originate from the superior mesenteric
artery or the aorta. The hepatic artery supplies 30% of the blood flow to the normal
liver parenchyma but greater than 90% to hepatic tumors, including both HCC and
metastatic lesions.
The other major inflow vessel is the portal vein which carries 70-85% of the blood
into the liver. The portal vein is confluence of the splenic vein and the superior
mesenteric vein, which drain the intestines, pancreas, stomach, and spleen.
The primary venous drainage of the liver is through three large hepatic veins that
enter the inferior vena cava adjacent to the diaphragm. The right hepatic vein is
generally oval in shape, with its long axis in the line of the vena cava. The middle
and left hepatic veins enter the inferior vena cava through a single orifice in about
60% of individuals. In addition, there are 10-50 small hepatic veins that drain directly
into the vena cava.
The biliary anatomy of the liver generally follows hepatic arterial divisions. The
common bile duct gives off the cystic duct and becomes the hepatic duct. The
hepatic duct then divides into two or three additional ducts draining the liver. There is
significant variation in the biliary anatomy, and thus, careful preoperative imaging is
vital before any major hepatic resection. [6]
The vascular anatomy of the liver defines its functional segments. Bismuth
synthesized existing knowledge and new insight into the anatomy of the
liver. [8] Bismuth defined the right and left hemilivers, which are defined by a line
connecting the gallbladder fossa and the inferior vena cava, roughly paralleling the
middle hepatic vein that is slightly to the left. [8]
The right hemiliver (lobe) is divided into four segments (ie, 5, 6, 7, 8), each of which
is supplied by a branch of the portal vein. The right hemiliver drains via the right
hepatic vein. The left hemiliver (lobe) is composed of three segments (ie, 2, 3, 4).
Segment 4 is the most medial and is adjacent to the middle hepatic vein. Segments
2 and 3 make up the left lateral section, are to the left of the falciform ligament, and
drain via the left hepatic vein. Finally, segment 1 (caudate lobe) is located behind the
porta hepatis and adjacent to the vena cava.
In general, resection of the liver is divided into the following two main categories [9] :
 Nonanatomic (wedge) resections are generally limited resections of a small
portion of liver, without respect to the vascular supply
 Anatomic resections involve removing one or more of the eight segments of the
liver
Commonly, a right hepatectomy refers to the removal of segments 5-8, an extended
right hepatectomy (right trisectionectomy) includes segments 4-8, a left hepatectomy
includes segments 2-4, and an extended left hepatectomy (left trisectionectomy)
includes segments 2, 3, 4, 5, and 8. A left lateral sectionectomy includes only
segments 2 and 3. The caudate lobe can be removed as an isolated resection or as
a component of one of the more extensive resections noted above. The extent of
resection that can be tolerated is based upon the health of the remnant liver.
Pathophysiology
The pathophysiology of HCC has not been definitively elucidated and is clearly a
multifactorial event. In 1981, after Beasley linked hepatitis B virus (HBV) infection to
HCC development, the cause of HCC was thought to have been
identified. [10] However, subsequent studies failed to identify HBV infection as a major
independent risk factor, and it became apparent that most cases of HCC developed
in patients with underlying cirrhotic liver disease of various etiologies, including
patients with negative markers for HBV infection and who were found to have HBV
DNA integrated in the hepatocyte genome.
Inflammation, necrosis, fibrosis, and ongoing regeneration characterize the cirrhotic
liver and contribute to HCC development. In patients with HBV, in whom HCC can
develop in livers that are not frankly cirrhotic, underlying fibrosis is usually present,
with the suggestion of regeneration. By contrast, in patients with hepatitis C virus
(HCV), HCC invariably presents, more or less, in the setting of cirrhosis. This
difference may relate to the fact that HBV is a DNA virus that integrates in the host
genome and produces HBV X protein that may play a key regulatory role in HCC
development; [11] HCV is an RNA virus that replicates in the cytoplasm and does not
integrate in the host DNA.
The disease processes, which result in malignant transformation, include a variety of
pathways, many of which may be modified by external and environmental factors
and eventually lead to genetic changes that delay apoptosis and increase cellular
proliferation (see the image below).
Hepatocellular carcinoma: pathobiology.
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Efforts have been made to elucidate the genetic pathways that are altered during
hepatocarcinogenesis. [12] Among the candidate genes involved, the p53,
PIKCA, and β-catenin genes appear to be the most frequently mutated in patients
with HCC. Additional investigations are needed to identify the signal pathways that
are disrupted, leading to uncontrolled division in HCC. Two pathways involved in
cellular differentiation (ie, Wnt-β-catenin, Hedgehog) appear to be frequently altered
in HCC. Upregulated WNT signaling appears to be associated with preneoplastic
adenomas with a higher rate of malignant transformation.
Additionally, studies of inactivated mutations of the chromatin remodeling
gene ARID2 in four major subtypes of HCC are being performed. A total of 18.2% of
individuals with HCV-associated HCC in the United States and Europe
harbored ARID2 inactivation mutations. These findings suggest that ARID2 is a
tumor suppressor gene commonly mutated in this tumor subtype. [13]
Whereas various nodules are frequently found in cirrhotic livers, including dysplastic
and regenerative nodules, no clear progression from these lesions to HCC occurs.
Prospective studies suggest that the presence of small-cell dysplastic nodules
conveyed an increased risk of HCC, but large-cell dysplastic nodules were not
associated with an increased risk of HCC. Evidence linking small-cell dysplastic
nodules to HCC includes the presence of conserved proliferation markers and the
presence of nodule-in-nodule on pathologic evaluation. This term describes the
presence of a focus of HCC in a larger nodule of small dysplastic cells. [14]
Some investigators have speculated that HCC develops from hepatic stem cells that
proliferate in response to chronic regeneration caused by viral injury. [15] The cells in
small dysplastic nodules appear to carry markers consistent with progenitor or stem
cells.
Etiology
Cirrhosis
In general, cirrhosis of any etiology is the major risk factor for HCC. [16, 17] About 80%
of patients with newly diagnosed HCC have preexisting cirrhosis. Major causes of
cirrhosis in the United States are nonalcoholic fatty liver disease (NAFLD), alcohol
abuse, hepatitis C infection, and hepatitis B infection. [3]
Metabolic factors
Obesity and diabetes have been implicated as risk factors for HCC, most likely
through the development of nonalcoholic steatohepatitis (NASH). [18, 19, 20] In the
analysis of a large managed care database, the incidence of HCC linked
to nonalcoholic fatty liver disease rose by 10 times from 0.03-0.46 per 100,000
between the years 1997 and 2005. [12] Currently, HCC non-alcoholic fatty liver
disease has the greatest proportion of the burden of the main risk factors for HCC in
the United States. [3, 4, 21]
Alcohol
In the United States, about 30% of HCC cases are thought to be related to excessive
alcohol use. Chronic alcohol use (> 80 g/d or > 6-7 drinks per day) for more than 10
years increases risk of HCC 5-fold.
Approximately 50% of US HCC patients have histories of alcohol abuse. As many as
50% of alcoholics may have subclinical HCC at autopsy.
Alcohol abusers are at increased risk of HCC if they stop drinking alcohol, because
heavy drinkers typically do not survive long enough to develop cancer. The risk of
HCC in patients with decompensated alcoholic cirrhosis is approximately 1% per
year.
Hepatitis B virus infection
The global prevalence of chronic hepatitis B virus (HBV) infection is estimated to be
257 million persons [22] ; chronic HBV infection is the most common cause of HCC
worldwide. In the United States, about 20% of HCC cases are thought to be related
to chronic HBV infection. Chronic HBV infection in the setting of cirrhosis increases
the risk of HCC 1000-fold. The mechanism by which HBV causes HCC is thought to
be from a combination of chronic inflammation and integration of the viral genome
into the host DNA.
It is anticipated that with implementation of worldwide vaccination, the incidence of
hepatitis B–related HCC will decrease. In a study from Taiwan, where universal
hepatitis B vaccination in newborns and children was instituted in 1984, the average
annual incidence of HCC per 100,000 children age 6-14 years declined from 0.70 in
1981-1986 to 0.36 in1990-1994 (P< 0.01). [23] By the end of 2018, hepatitis B
vaccine for infants had been introduced nationwide in 189 countries.; in addition,109
countries had introduced one dose of hepatitis B vaccine to newborns within the first
24 hours of life, and the global coverage is 42%. [24]
Hepatitis C virus infection
Hepatitis C virus (HCV) infection is a global pandemic affecting 71 million
persons. [22] Approximately 80% of individuals infected with HCV develop chronic
infection; this rate is higher than occurs with HBV infection.
HCV infection has become the most common cause of HCC in Japan and Europe,
and it is also responsible for the recent increased incidence in the United
States. [7] More than 3 million Americans have chronic HCV infection. In the United
States, about 30% of HCC cases are thought to be related to HCV infection. Some
5-30% of individuals with HCV infection develop chronic liver disease. In this group,
about 30% progress to cirrhosis, and in these, about 1-2% per year develop HCC.
The lifetime risk of HCC in patients with HCV is approximately 5%, appearing 30
years after infection. However, studies suggest that antiviral treatment of chronic
HCV infections may significantly reduce the risk of HCC. [25]
Co-infection with HBV further increases the risk; many patients are co-infected with
both viruses. Alcohol use in the setting of chronic HCV doubles the risk of HCC
compared with HCV infection alone.
Hemochromatosis
Patients with hemochromatosis, especially in the presence of cirrhosis, are at an
increased risk of developing HCC. About 30% of all iron-related deaths in
hemochromatosis are due to HCC.
Aflatoxin
This hepatic carcinogen is a byproduct of fungal contamination of foodstuffs in sub-
Saharan Africa and East and Southeast Asia. Aflatoxin causes DNA damage and
mutations of the p53 gene. Humans are exposed through the ingestion of moldy
foods found in susceptible grains. Dietary levels in endemic areas correlate directly
with incidence of hepatocellular carcinoma.
Rare associations
These include the following:
 Primary biliary cirrhosis
 Androgenic steroids
 Primary sclerosing cholangitis
 Alpha1-antitrypsin deficiency
 Thorotrast radioactive contrast
 Oral contraceptives
 Porphyria cutanea tarda.

6. Natural history Hep B and Cirrhosis

7. Spider naevi and palmar erythema
Ada increased vascularity