LIVER

It is the largest internal organ in our body, weighing approximately1.37 kg. It lies in
the right epigastric region
The functional unit of liver is –lobule, which is formed by hepatic cells called
hepatocyte’s. Capillaries (sinusoids) between the rows of hepatocytes and are lined
with Kupffer cells which has phagocytic activity. These hepatic cells secretes bile in
to inter lobular bile duct which is known as canaliculi that arise from capillaries
Lobes[edit]
Further information: Lobes of liver

The liver, viewed from above, showing the left and right lobes separated by the falciform ligament

The liver, viewed from below, surface showing four lobes and the impressions
The liver is grossly divided into two parts when viewed from above – a right and a left
lobe, and four parts when viewed from below (left, right, caudate, and quadrate lobes).[12]
The falciform ligament, divides the liver into a left and right lobe. From below, the two
additional lobes are located between the right and left lobes, one in front of the other. A
line can be imagined running from the left of the vena cava and all the way forward to
divide the liver and gallbladder into two halves.[13] This line is called "Cantlie's line".[14]
Other anatomical landmarks include the ligamentum venosum and the round ligament of
the liver (ligamentum teres), which further divide the left side of the liver in two sections.
An important anatomical landmark, the porta hepatis, divides this left portion into four
segments, which can be numbered starting at the caudate lobe as I in an anticlockwise
manner. From this parietal view, seven segments can be seen, because the eighth
segment is only visible in the visceral view.[15

BLOOD SUPPLY.
One third of blood supply from the liver is by hepatic artery and two third is from
portal vein. Hepatic artery is a branch of abdominal aorta and portal vein carries blood
from stomach, intestine, pancreas and spleen to liver. In liver these vessels come in
contact with each lobule. Hepatic vein leaves the liver and carries blood fom liver to
inferior vena cava.
 ENTERO HEPATIC CIRCULATION

RBC’S GENERATED IN BONE MARROW

↓when getting old
Disposed in spleen

↓
Release haemoglobin
↓
Breakdown
 Heam globin
↓
Unconjugated bilirubin(not soluble in water)
↓
Bound to albumin
↓
Reached liver
↓
Unconjugated bilirubin combine with glucoronic acid
↓
Conjugated bilirubin
↓in addition
Hepatic cells secretes bile
↓
Conjugated bilirubin excreted along with bile
↓to
Lobular capillaries
↓
Inter lobular capillaries
↓
Inter lobular bile duct

Right hepatic duct left hepatic duct

Merging and form cystic duct

Common bile duct
↓
Enter duodenum at ampulla of vater recycled in bile
↓in intestine
Bacterial action on bilirubin
↓reduction

Stercobilinogen urobilinogen
↓ ↓
Stool colour insignificant amount excreted in urine

LIVER FUCTION TEST

S.ALBUMIN 3.5-4.8 gm/dl

S. BILIRUBIN 0.3-1.2 mg/dl
DIRECT BILIRUBIN 0.1-0.5 mg/dl
INDIRECT BILIRUBIN 0.2-0.7 mg/dl
ALKALINE PHOSPHATASE 32-91 IU/L
TOTAL PROTIEN 6.3-8.2 gm/dl
ALT 14-54 IU/L
AST 18-41 IU/L
GGT 0-30U/L

System or
Marker Function
function
Aspartate
aminotransferase Catabolises amino acids,
Hepatocyte
permitting them to enter the citric
integrity Alanine acid cycle
aminotransferase
Alkaline Canicular enzyme that plays a role
phosphatase in bile production
Catalyzes transfer of γ-glutamyl
γ-Glutamyl-
group from peptides to other
transferase
Cholestasis amino acids
Breakdown product of haemolysis
Bilirubin(direct and taken up by liver cells and
indirect) conjugated to water-soluble
product excreted in bile
Liver function
Serum albumin Liver synthesises albumin
mass
Bile salts are synthesised in the
Prothrombin time liver and necessary for vitamin K
absorption

 ALT – (alanine aminotransferase) an enzyme involved in the recycling of

the amino acid alanine into glucose (gluconeogenesis). This is the most
specific test for hepatocellular liver injury, although it is present in low
concentrations in other tissues.
 AST – (aspartate aminotransferase) is involved in metabolism of the
amino acid aspartic acid. It is also sensitive for hepatocellular disease, but
is less specific as it is also raised with muscle inflammation and
haemolysis. High levels of liver origin suggest possible alcohol use
(pyridoxine deficiency) and infiltrative liver damage (e.g. malignancy).
 GGT – (gamma glutamyl transferase) is a sensitive marker of liver injury.
Although induced by alcohol and some drugs (e.g. rifampicin), mild
elevation is non-specific and may reflect other liver pathologies (e.g. non-
alcoholic fatty liver disease).
 ALP – (alkaline phosphatase) also mainly reflects hepatobiliary processes
and is raised in cholestasis. ALP is not specific for liver disorders as it is
produced by other tissues including bone, intestine and placenta. These
sources should be considered, especially in patients with isolated
elevation with concurrent elevation of GGT.
 Bilirubin – is a product of red cell (haem) breakdown. Bilirubin is initially
carried loosely attached to albumin as the unconjugated (indirect) form. It
is then taken up into hepatocytes, solubilised to form the smaller
conjugated (direct) form, and excreted by the biliary system. The
unconjugated form is increased by red cell breakdown (e.g. haemolysis) or
reduced uptake and conjugation (e.g. Gilbert’s syndrome). The conjugated
form is increased by impaired liver processing and bile flow (e.g. hepatitis,
bile duct obstruction).
 Total protein – the total of albumin and other plasma proteins (mostly
immunoglobulins). Changes in the total protein are non specific as there
may be increases and decreases in different components. For example
chronic severe inflammatory liver disease may be associated with a low
albumin and other liver globulins, but raised levels of immunoglobulins.
 Albumin – the most abundant plasma protein, produced in adults entirely
by the liver. A falling level may reflect reduced liver production, usually
indicating significant liver damage, but may also reflect increased protein
loss, e.g. nephrotic proteinuria, GI loss. Levels may still be normal in
patients with severe acute liver damage because the half-life of albumin in
plasma is about three weeks.
 INR – a reflection of liver synthesis of vitamin K dependent clotting factors
II, VII, IX, X. Raised INR may indicate decreased liver synthetic ability or
cholestasis with reduced vitamin K absorption. Levels rise quickly with
acute liver disturbance because of the short half-life of the clotting factors.

LIVER BIOPSY
It is the removal of small tissue from liver for diagnostic, to asses severity of known
liver disease and to monitor progress of treatment
APPRAOCHES
 Percutaneous-via needle through skin
 Trans venous-through blood vessel
 Direct-during abdomina; surgery
INDICATIONS
 Liver disease
 Tumour
 Iron over load
 To monitor progress of treatment
  Fatty liver
CONTRAINDICATION
 Severe thrombocytopenia
 Prolonged prothrombin time
 Peritonitis
 Massive ascites
 Enlarged gall bladder
PRE PROCEDURAL PREPARATION
 Asses coagulation studies-BT.CT.PT,PTT,PLT etc
 Cross matching should be done
 Check vital signs and abdominal girth for post procedural comparison
 Prepare skin if excessive hair is present
 Get consent
DURING THE PROCEDURE
 Provide a semi fowlers position
 Keep the patient’s arm over head
 Ask the patient to hold breath when needle is inserted because chest
movement may results in injury to internal organs
PROCEDURE
Percutaneous liver biopsy
Infiltrate the site (6th and 7th) or (8th and 9th) intercostal space on right side. Biopsy
needle is inserted and sample is collected. Often this procedure is doing under USG or
CT guidance
Transvenous
Usually through the jugular vin. Use ultrasound guidance to choose a point on the
skin above vein. Infiltrate local anaesthetics. Aspirate venous blood to ensure position.
Insert guide wire through which insert a metal guide wire and dilator. When it reaches
the hepatic vein remove the guide wire and dilator. Insert the needle through metallic
guide wide and collect biopsy
POST PROCEDURAL CARE
 Keep the patient on right side for minimum 2hrs which will provide a splinting
effect at the puncture site
 Provide strict bed rest for minimum 24 hr because movement increase the risk
of bleeding
 Instruct the patient to avoid coughing and straining that may cause bleeding
 Monitor signs of bleeding
 Monitor vital signs frequently for early detection of haemo dynamic instability
 Monitor abdominal girth, increase in abdominal girth indicates bleeding
 Asses for complications like bile peritonitis, shock and pneumothorax
 Instruct the patient to avoid heavy lifting and strenuous activities for one week