Pemicu 3

“MEDICAL CHECK-UP”
Mishael Octaviany Jireh
405130097
CIRRHOSIS
• Cirrhosis is defined as a diffuse process characterized
by fibrosis and the conversion of normal liver
architecture into structurally abnormal nodules.
• Its major causes include chronic viral infections,
alcoholic or nonalcoholic steatohepatitis (NASH),
autoimmune diseases affecting hepatocytes and/or
bile ducts, and iron overload.
• Cryptogenic cirrhosis : unknown cirrhosis.
• Fibrous septa in the form of delicate bands or
broad scars around multiple adjacent lobules.
• Parenchymal nodules, ranging in size from
very small (less than 3 mm in diameter—
micronodules) to large (over 1 cm—
macronodules), encircled by these fibrous
bands.
Alcoholic Cirrhosis
Postnecrotic Cirrhosis
 Passive Congestion

Cardiac Cirrhosis
Billiary Cirrhosis
 Macronodul Cirrhosis Micronodul Cirrhosis
(Hep B n C, Wilson, a1 antitrypsin def) Chronic Alcoholism, Hemokromatosis
 Complications
• Hepatic failure
• Portal hypertension
• Ascites
• Bacterial peritonitis
• Esophageal varices
• Encephalopathy hepaticum
• Increased risk for development of hepatocellular
carcinoma
 Portal hypertension
• Increased resistance to portal blood flow may develop
from prehepatic, intrahepatic, and posthepatic.
• The dominant intrahepatic cause is cirrhosis,
accounting for most cases of portal hypertension.
• Portal hypertension in cirrhosis results from :
– Compression of central veins by perivenular fibrosis and
expanded parenchymal nodules  Increased resistance to
portal flow at the level of the sinusoids.
Ascites
 Diagnosis Ascites
• Inspeksi = perut buncit, umbilikus
bergerak seolah ke arah kaudal
mendekati symphisis os pubis, sering
dijumpai hernia umbilikalis akibat
tekanan intrabdomen.
• Perkusi = pekak, shifting dullness +
• Pemeriksaan khusus = pudle sign 
untuk menemukan asites.
• Pemeriksaan penunjang = USG
• Pemeriksaan cairan asites :
– Asites hemoragik : kemerahan, sering
dihubungkan dengan keganasan. (
ruptus kapiler peritoneum yang
menyebabkan sirosis hati)
– Chillous ascites  ruptur pembuluh
limfe.
– Serum-ascites albumine gradient :
untuk membedakan asites hipertensi
porta atau asites eksudat. Jika gradien
tinggi (>1,1gr/dL)  hipertensi porta.
– PMN >250mm3 = Peritonitis bakteri
spontan. MN = Peritonitis tuberkulosa /
karsionmatosis.
– Polimikroba = asites akibat perforasi
usus. Monomikroba = peritonitis
bakteri spontan.
Portosystemic Shunt
Hepatorenal sydrome
Prognosis
HCC
 Epidemiology
• The highest incidences of HCC are found in Asian countries
(southeast China, Korea, Taiwan) and sub-Saharan African
countries in which HBV is transmitted vertically.
• Aflatoxin, which when combined with HBV infection
increases the risk of hepatocellular carcinoma dramatically.
• In Western countries the incidence of hepatocellular
carcinoma is rapidly increasing, largely owing to the
hepatitis C epidemic.
 Morphology
(1) Unifocal, usually massive tumor
(2) Multifocal tumor made of nodules of variable size.
(3) Diffusely infiltrative cancer, permeating widely and
sometimes involving the entire liver, blending imperceptibly
into the cirrhotic background.
★ Extensive intrahepatic metastases are characteristic, and
occasionally snakelike masses of tumor invade the portal vein
(with occlusion of the portal circulation) or inferior vena cava,
extending even into the right side of the heart.
Well-differentiated hepatocellular carcinoma has distortions of normal
structures: Liver cell plates are markedly widened, and frequent
“pseudoacinar” structures (arrows)—abnormal bile canaliculi—often contain
bile.
Acidophilic hyaline inclusions within the cytoplasm may be present,
resembling Mallory bodies.
 Sign and symptoms
• Rapid increase in liver size, sudden worsening
of ascites, or the appearance of bloody
ascites, fever, and pain call attention to the
development of a tumor.
• The most commonly used marker is serum
alpha-fetoprotein level, but it rises only with
advanced tumors and only in 50% of patients.
• Radiologic screening of patients with cirrhosis
at 6-month intervals, looking for dysplastic
nodules or early, small hepatocellular
carcinomas, is the current clinical frontier.
FATTY LIVER DISEASE
 FATTY LIVER DISEASE

• Three categories of liver alterations are

observed in fatty liver disease.
• They can be present in any combination:
– Steatosis (fatty change)
– Hepatitis (alcoholic or steatohepatitis)
– Fibrosis.
 Hepatocellular Steatosis
• Hepatocellular fat accumulation typically begins in
centrilobular hepatocytes.
• Lipid droplets range from small (microvesicular) to
large (macrovesicular), the largest filling and expanding
the cell and displacing the nucleus.
• As steatosis becomes more extensive, the lipid
accumulation spreads outward from the central vein to
hepatocytes in the midlobule and then the periportal
regions
Fatty liver disease. Macrovesicular steatosis is most prominent around the central vein and
extends outward to the portal tracts with increasing severity. The intracytoplasmic fat is seen
as clear vacuoles. Some fibrosis (stained blue) is present in a characteristic perisinusoidal
“chicken wire fence” pattern. (Masson trichrome stain.)
 Steatohepatitis
• These changes typically are
more pronounced with
alcohol use than in NAFLD.
– Hepatocyte ballooning
– Mallory-Denk bodies
– Neutrophil infiltration
 Steatohepatitis with fibrosis
• Fibrosis appears first in the centrilobular region as central vein
sclerosis. Perisinusoidal scar appears next in the space of Disse of
the centrilobular region and then spreads outward, encircling
individual or small clusters of hepatocytes in a chicken wire fence
pattern
• Fibrosis link to portal tracts and then begin to condense to create
central-portal fibrous septa  cirrhosis.
• Early in the course, the liver is yellow-tan, fatty, and enlarged.
However, with persistent damage, over the course of years the liver
is transformed into a brown, shrunken, nonfatty organ composed of
cirrhotic nodules that are usually less than 0.3 cm in diameter
Steatohepatitis leading to cirrhosis. Small nodules are entrapped in blue-staining
fibrous tissue; fatty accumulation is no longer seen in this “burned-out” stage.
(Masson trichrome stain.)
 Alcoholic Liver Disease
Excessive ethanol consumption
causes more than 60% of chronic
liver disease in Western countries
and accounts for 40% to 50% of
deaths due to cirrhosis.

From 90% to 100% of heavy drinkers develop fatty

liver (i.e., hepatic steatosis), and of those, 10% to
35% develop alcoholic hepatitis, whereas only 8% to
20% of chronic alcoholics develop cirrhosis.
• Short-term ingestion of as much as 80 g of
ethanol per day (5–6 beers or 8–9 ounces of
80-proof liquor) generally produces mild,
reversible hepatic changes, such as fatty liver.
Metabolism of ethanol
• Alcoholic hepatitis can occur after
just weeks or months of consistent
use. The onset is typically acute and
often follows a bout of particularly
heavy drinking.
• Malaise, anorexia, weight loss, upper
abdominal discomfort, tender
hepatomegaly, and fever.
• Typical laboratory findings include
hyperbilirubinemia, elevated alkaline
phosphatase, and neutrophilic
leukocytosis. SGPT and SGPTare
elevated but usually remain below
500 U/mL.
• The first signs of cirrhosis relate to
complications of portal hypertension.
• The stigmata of cirrhosis (e.g., an abdomen
grossly distended with ascites, wasted
extremities, caput medusa) may be the
presenting features.
• Insidious onset of malaise, weakness,
weight loss, and loss of appetite 
jaundice, ascites, and peripheral edema.
• A patient may first present with life-
threatening variceal hemorrhage or hepatic
encephalopathy.
• Laboratory findings reflect the developing
hepatic disease, with elevated serum
aminotransferase, hyperbilirubinemia,
variable elevation of alkaline phosphatase,
hypoproteinemia (globulins, albumin, and
clotting factors), and anemia.
 Complication
End-stage alcoholic liver disease, the immediate causes of
death are :
• Hepatic failure
• Massive gastrointestinal hemorrhage
• Intercurrent infection (to which affected persons are
predisposed)
• Hepatorenal syndrome
• Hepatocellular carcinoma in 3% to 6% of cases
 Nonalcoholic Fatty Liver Disease (NAFLD)
NAFLD is consistently associated with insulin resistance and the
metabolic syndrome:
• Type 2 diabetes (or family history of the condition)
• Obesity, primarily central obesity (body mass index greater
than 30 kg/m2 in whites and greater than 25 kg/m2 in Asians)
• Dyslipidemia (hypertriglyceridemia, low high-density
lipoprotein cholesterol, high low-density lipoprotein
cholesterol)
• Hypertension
• Metabolic syndrome is defined as having at least two of the
following: obesity, insulin resistance, dyslipidemia, and
hypertension.
• In patients with metabolic syndrome, the presence of type 2
diabetes and obesity is the best predictor of severe fibrosis and
disease progression.
• Insulin resistance results in the accumulation of triglycerides in
hepatocytes by at least three mechanisms:
– Impaired oxidation of fatty acids
– Increased synthesis and uptake of fatty acids
– Decreased hepatic secretion of very-low-density lipoprotein
cholesterol
 Damage
Fat-laden Oxidative Lipid
mitochondrial and Apoptosis
hepatocytes stress peroxidation
plasma membranes
• Most persons with steatosis are asymptomatic;
patients with active steatohepatitis or fibrosis may
also be asymptomatic, but some may have fatigue,
malaise, right upper quadrant discomfort.
• The frequency of progression from steatosis to active
steatohepatitis and then from active steatohepatitis
to cirrhosis seems to be low.
• Liver biopsy is required for diagnosis.