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THE LIVER
Introduction
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The liver is the largest internal organ in the body
and is situated in the right hypochondrium.
Functionally, it is divided into right and left lobes by
the middle hepatic vein.
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The liver has the enormous task of maintaining the
body`s metabolic homeostasis. This includes the
processing of dietary amino acids, carbohydrates,
lipids and vitamins; synthesis of serum proteins
including coagulation factors; and detoxification and
excretion into bile of endogenous waste products .
Viral hepatitis
 Viral
hepatitis is caused mainly by hepatitis
viruses A(HAV), B (HBV), C (HCV), D
(HDV), and E (HEV).
 These viruses and their infections have
distinct features.
Hepatitis A virus
Hepatitis A usually is a benign, self-limited disease.
 It is a single stranded RNA virus with incubation period
of 2 to 6 weeks.
 HAV does not cause chronic hepatitis or a carrier state.
 Rarely there is fulminant hepatitis; fatalities occur at a
rate of only 0.1%.
 Occurs worldwide & is endemic in places with
substandard hygiene (people may have detectable
antibodies by age of 10y).
 Spread is by contaminated water & food (fecal-oral).
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Hepatitis A virus
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Virus is shed in stool for 2-3 wks before & 1 wk
after onset of jaundice.
HAV is not shed in any significant quantities in
saliva, urine, or semen.
Because HAV viremia is transient, blood-borne
transmission of HAV occurs only rarely; therefore,
donated blood is not routinely screened for this
virus.
Detection of anti-HAV IgM antibody is the best
diagnostic marker for the disease.
IgG antibody persists for years and is the primary
defense against reinfection.
Hepatitis B

DNA virus.
 Incubation period 4-26 wks
 Clinicopathological
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syndroms:
Acute hepatitis with recovery
Nonprogressive chronic hepatitis
Progressive chronic disease>cirrhosis
Fulminant hepatitis
Asymptomatic carrier state (presence of HBsAg in
serum for 6 months or longer).
Modes of transmission
 whereas
blood and body fluids are the
primary vehicles of transmission, virus also
may be spread by contact with body
secretions such as semen, saliva, tears, breast
milk, and pathologic effusions.
 In endemic regions, vertical transmission
from mother to child during birth
constitutes the main mode of transmission.
Prevention
Vaccination
 Screening of donor blood & tissues
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Hepatitis C
 Single
stranded RNA.
 Incubation period 2-26 weeks
 Most common chronic blood-borne
infection
 Routes of transmission
• Inoculations
• Blood transfusions
• Sexual intercourse
• Perinatal
Clinicopathological syndroms
1. Acute hepatitis (rarely fulminant).
2. Chronic hepatitis.
3. Cirrhosis in 20%-30% of patients with
chronic infection after 5-20y of acute
infection.
Hepatitis D Virus

HDV is a unique RNA virus that is replicationdefective, causing infection only when it is
encapsulated by HBsAg
 .Delta hepatitis arises in two settings:
(1) acute coinfection after exposure to serum
containing both HDV and HBV.
(2) superinfection of a chronic carrier of HBV with
a new inoculum of HDV
Hepatitis E Virus
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Single stranded RNA
Incubation period 6 weeks
Water-borne infection affecting young to middle-aged
adults (oral route)
the disease is self-limited; HEV is not associated
with chronic liver disease or persistent viremia
A characteristic feature of the infection is the high
mortality rate among pregnant women, approaching
20%.
Morpholpgy of acute and chronic
viral hepatitis
Grossly :
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liver involved by mild acute hepatitis appears normal or
slightly mottled.
in massive hepatic necrosis the liver may shrink to
and become transformed into a limp, red organ
covered by a wrinkled, baggy capsule.
Microscopical changes in acute viral
hepatitis
The first is swelling (ballooning degeneration), producing
cells with emptyappearing pale cytoplasm.
• Necrosis (cytolysis), the necrotic cells appear to
have dropped out, leaving collapsing sinusoidal collagen.
• Apoptosis, in which hepatocytes shrink, become
intensely eosinophilic, and have fragmented nuclei;
• In severe cases, bridging necrosis (central-central,
portal-portal, central-portal).
• Inflammation (mononclear), spillover into adjacent
parenchyma.
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Microscopical changes in chronic
viral hepatitis
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Changes shared with acute hepatitis,hepatocytes injury,
necrosis,apoptosis.
Dense mononuclear portal infiltrates of variable
prominence are the defining lesion of chronic hepatitis.
Fibrosis
Ground-glass hepatocytes (HBV)
Lymphoid aggregate formation (HCV)
Fulminant viral hepatitis
Chronic HBV hepatitis, ground-glass
hepatocytes
Chronic HCV hepatitis
Primary Biliary Cirrhosis
 Primary
biliary cirrhosis (PBC) is a chronic,
progressive, and sometimes fatal cholestatic
liver disease.
 PBC is primarily an immune disease of middleaged women.
 Peak incidence between the ages of 40 and 50
years.
Primary Billiary Cirrhosis
Characterized by:
 Destruction of intrahepatic bile ducts(The
cardinal feature of PBC is a nonsuppurative
destruction of small and medium-sized
intrahepatic bile ducts).
 Portal inflammation
 Scarring
 Development of cirrhosis.
 Liver failure over years to decades
Clinical Course
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The onset of PBC is insidious.
Common early symptoms:
Fatigue
Pruritis
Dry eyes and mouth
Later signs and symptoms:
Jaundice(is an indication of how far the disease has progress)
Skin hyperpigmentation and xanthoma.
Edema
Ascites
Musculoskeletal pain, arthritis.
Renal stone and gallstone.
Morphology
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Stage1: Interlobular bile ducts are actively destroyed by
lymphocytic or plasmacytic inflammation with or
without granulomas (the florid duct lesion).
Stage2: periportal fibrosis and/or inflammation.
stage3: fibrous septa formation.
Stage4: nodules formation.
Hepatic Failure
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The most severe clinical consequence of liver
disease is hepatic failure.
The patterns of injury that cause liver failure fall
into three categories:
Acute liver failure with massive necrosis : Most
often caused by drugs or viral hepatitis, or toxins.
Chronic liver disease (chronic hepatitis,cirrhosis)
Hepatic dysfunction without overt necrosis
(tetracycline, fatty liver in pregnancy
Clinical Features

Jaundice is invariable finding.
 Coagulopathy, attributable to impaired hepatic
synthesis of blood clotting factors.
 Hypoalbuminemia that predispose to edema.
 palmar erythema (local vasodilatation).
 Hypogonadism, gynecomastia (due to
hyperestrogenemia)
 Hyperammonemia due to defective hepatic urea
cycle function.
 Spider angiomas.
Complications
Hepatic encephalopathy
 Hepatorenal syndrome (renal failure)
 Hepatopulmonary syndrome
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Cholelithiasis(gallstones)
Affect 10%-20% of adults
 Types
-cholesterol-containing stones, (80%)
-bilirubin-containing stones, (20%)
 Risk factors
I. cholesterol stones
.old age
.female sex hormones (oral contraception,pregnancy)
.obesity & metabolic syndrome(insulin resistence)
.rapid weight reduction
.gallbladder stasis
.inborn errors of bile acid metabolism
.dyslipidemia syndromes.
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II. Pigment stones
.chronic hemolytic syndromes(sickle cell
anemia).
.biliary infection
.gastro-intestinal disorders (Crohns
disease, cystic fibrosis).
Pathogenesis
Cholesterol stones
Super-saturation of bile with bilirubin &
cholesterol
Pigment stones
Disorders associated with elevated levels of
unconjugated bilirubin in bile
 Hemolytic syndromes
 Severe ileal dysfunction.
 Bacterial contamination of biliary tree
Morphology
Cholesterol stones
 Ovoid and firm.
 Multiple mostly.
 Pure cholesterol stones are: pale yellow,and
(radiolucent)
 Mixed stones (calcium carbonate, phosphates,
& bilirubin) are: gray-white to black, (radioopaque)
 Pigment stones
.Black-sterile bile (radio-opaque)
.Brown-infected bile (all radiolucent)
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Gall bladder, cholesterol stones
Gall bladder, pigment stones
Clinical features:
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asymptomatic
Biliary colic
Complication in gall bladder
(empyema,Perforation, fistulas, cholecystitis,
carcinoma)
 Cholangitis & cholestasis
 Pancreatitis
 Intestinal obstruction