REPORT OF PBL 1

“MODUL 1 – YELOW SKIN”

BASIC MECHANISM OF DISEASE (BMD)

TUTOR : dr. Berry Erida Hasbi

GROUP15:

DHIAN HIDAYAT : 110 2011 0100

ANDI MUHAMMAD ARIANSYAH N : 110 2014 0021
AULIA ADI PUTRI MS : 110 2014 0028
MUHAMMAD YATSRIB SEMME : 110 2014 0036
KHANSA LUTHFIYYAH : 110 2014 0042
INDIRA YUNITA ALIE : 110 2014 0061
PUTRI NUR INDAH SARI : 110 2014 0080
MUH. ZUHAL DARWIS : 110 20140085
ANDI NUR CHAMIDAH W : 110 2014 0100
ANGGA NUGRAHA HAMID : 110 2014 0129
SEESARIAH FATIMAH HB : 110 2014 0143

MEDICAL FACULTY
MUSLIM UNIVERSITY OF INDONESIA
MAKASSAR
2015
CASES 2
SCENARIO 1 : YELLOW SKIN WITH HIGH FEVER
A mother of 40th years old was taken to Polyclinic Hospital Care (PHC)
because of high fever accompanied nausea and epigastric pain since three days
ago. Patient also complain of her skin and eyes.

1. Difficult Words
No difficult words.

2. Key Words
1. A mother 40th years old
2. Skin and eye turning yellow
3. Has been sick for a week
4. Weakness of the body, decrease of appetite, urine colour is brown tea

3. Questions
1. How we devide our abdomen region ?
2. Whats connection between high fever and yellow skin ?
3. Which organ that responsible turning yellow skin ?
4. How is the mechanism of bilirubin?
5. What is Reticuloendhotelial System (RES) ?
6. What is the definition of Icterus and how many types ?
7. What age icterus can be happen ?
8. What disease that have icterus symptoms ?
9. How is the mechanism of Jaundice cause by pre-hepatic, Intra-hepatic
and Post hepatic ?
 4. Answers of Questions
1. How to devide our regio abdomen

a. 4 regions:

The abdominal wall has few anatomic landmarks. The flat abdominal
plane is broken up only by the costal margins, anterior superior iliac spines, and
the umbilicus. Thus, many attempts have been made over the years to describe
what surface anatomy cannot.

The most common and widely accepted system for identification of the
various regions of the abdomen is the simple division of the abdomen into 4
quadrants by a vertical and horizontal line bisecting the umbilicus and forming the
right and left upper and lower quadrants (see the image below).

Abdomen Description
Quadrants

Right Doctors often assess this portion to localize pain and

 Upper tenderness.
Quadrant
Organs found in this quadrant include the liver, the
(RUQ)
gall bladder, duodenum the upper portion of the
pancreas and the hepatic flexure of the colon.

The RUQ is commonly tender in cases of hepatitis,

cholecystitis and with the formation of a peptic
ulcer.

Right The right lower quadrant extends from the median

Lower plane to the right side of the body and then from the
Quadrant umbilical plane to the right inguinal ligament.
(RLQ)
Important organs found in the right lower quadrant
include the appendix, the upper portion of the colon,
the right ovary and Fallopian tube in women and the
right ureterpenus.

The right lower quadrant may be assessed when

diagnosing appendicitis in which case this quadrant
would be tender and painful.

Left Upper The left upper quadrant rests alongside the RUQ.
Quadrant The left upper quadrant is formed by the median
(LUQ) plane extending to the left of the patient and with the
umbilical plane to the left rib cage.

Organs found in the left upper quadrant are the

stomach, the spleen, the left portion of the liver, and
the main body of the pancreas. The left portion of
the kidney and the adrenal gland are also found in
this quadrant. The splenic flexure of the colon and
the bottom portion of the colon also sit in the left
 upper quadrant.

The LUQ will be tender and a point of interest in

cases of appendicitis and abnormalities of the
intestines such as malrotation.

Left Lower The left lower quadrant is located below the

Quadrant umbilicus plane. Essential organs found in this
(LLQ) region include the bottom portion of the colon, the
sigmoid colon, the left ovary, Fallopian tube and the
left uterine tube.

The doctors will assess this area if there is

abdominal pain in this region. Abdominal pain in the
LLQ may be a symptom of colitis, diverticulitis, or
ureteral colic. Pain in this region may also be caused
by ovarian cysts or a pelvic inflammation. Tumors
found in this region can be serious determinants of
colon or ovarian cancer.

b. 9 regions :
 Three horizontal lines and two vertical lines create nine regions of the
abdomen. Below is an image of the regions of the abdomen, which are formed
within these planes. “Hypo” refers to “below”, “epi” refers to “above”, “chond”
refers to the cartilage of the rib and “gast” is in reference to the stomach.

9 Regions of Abdomen

The above lines intersect and divide the abdomen into 9 regions:

 Epigastric region (epigastrium)

 Left hypochondrium (LHC)

 Right hypochondrium (RHC)

 Umbilical region

 Left lumbar region

 Right lumbar region

 Hypogastric region

 Right iliac fossa (RIF)

 Left iliac fossa (LIF)

Organs in 9 Regions of Abdomen

Location of various organs in the Abdomen according to the region

Abdomen Organs
Regions

Right Liver, Gallbladder, Right Kidney, Small

Hypochondrium Intestine

Left Spleen, Colon, Left Kidney, Pancreas

Hypochondrium

Epigastrium Stomach, Liver, Pancreas, Duodenum, Spleen,

Adrenal Glands

Right Lumber Gallbladder, Liver, Right Colon

Region

Left Lumber Descending Colon, Left Kidney

Region

Umbilical Umbilicus, Jejunum, Ileum, Duodenum

Region

Right Iliac Appendix, Cecum

Fossa

Left Iliac Fossa Descending Colon, Sigmoid Colon

Hypogastrium Urinary Bladder, Sigmoid Colon, Female

Reproductive Organs
 2. What is the connection between high fever and yellow skin ?

The febrile response, of which fever

is but one component, is a complex
physiologic reaction to disease
involving a cytokine-mediated rise
in body temperature, generation of
acute-phase reactants, and activation
of numerous physiologic,
endocrinologic, and immunologic
systems.1 The temperature of the
body is dependent on maintaining a
balance between the production and
dissipation of heat. Under normal
circumstances, heat is generated
internally during metabolic
processes or when external
environmental temperatures exceed those of the body. Heat can also be produced
by increased skeletal muscle activity, such as that which occurs with shivering.
Heat loss occurs predominantly from the skin via evaporative losses and also, to
some extent, via the lungs.With core body temperature elevations, the sympathetic
system is inhibited, leading to vasodilation of skin vessels and stimulation of the
sweat glands to facilitate evaporative loss. This process prevails until the body
temperature matches the thermal setpoint, when heat production matches heat
loss. Similarly, when body temperature is below the thermal setpoint, a variety of
responses are initiated to conserve and increase production of heat. They include
activation of the sympathetic nervous system to induce vasoconstriction of skin
blood vessels; inhibition of sweating; activation of the shivering center in the
posterior hypothalamus, thereby increasing muscle heat production; and secretion
of neurotransmitters,which increase cell metabolism and, consequently, heat pro-
duction. The hypothalamus also affects behavioral influences in humans, with
individuals changing clothes and/or seeking appropriate shelter to maintain body
temperature. In vivo experiments with rabbits revealed that thermoregulation
requires an intact sympathetic nervous system and can be modulated by various
adrenoceptor antagonists

3. Which organ that responsible turning of yellow skin ?

Liver and vesica billiaris

Liver : The liver is the largest glandular organ in the body and performs many
vital functions to keep the body pure of toxins and harmful substances. One of the
important function is to conjugate the bilirubin, whe heart lose its function it will
produce an accumulation of bilirubin in blood and turning the skin into yellow
Vesica billiaris : After the bilirubin is conjugated by the liver, conjugated bilirubin
go to ductus choledocus and then to ductus cysticis. When there’s a stone in the
ductus it will distrupt the stream of bilirubin to intestine. And in the end it causes
an accumulation of conjugated bilirubin in blood

4. How is the mechanism of the Bilirubin ?

Enzymatic mechanism of bilirubin formation

Haem is a tetrapyrrole, the four pyrrole rings being connected by methane

bridges. The four bridges are not equivalent because the side chains are
asymmetrically distributed (Fig. 1). Haem is cleaved specifically at the amethene
bridge by a reaction catalysed by microsomal haemoxygenases, resulting in the
formation of biliverdin and 1 mole of CO, and the release of an iron molecule.
The reaction consumes three molecules of oxygen and requires a reducing agent,
such as NADPH. The a-methene-bridge carbon is eliminated as CO, and the iron
molecule is released.
There are three known isoforms of haemoxygenase (HO). The ubiquitous
isoform HO-1 is inducible by haem and stress.
HO-2 is a constitutive protein present mainly in the brain and the testis. HO-3 has
a very low catalytic activity and may function mainly as a haem-binding protein.
Subsequently, biliverdin is reduced to bilirubin by the action ofcytosolic
biliverdinreductase. The vasodilatory effect of CO regulates the vascular tone in
the liver, heart and other organs during stress. The other products of haem
breakdown, namely biliverdin and bilirubin, are potent antioxidants, which may
protect tissues under oxidative stress.
Since haem breakdown is by far the most important source of endogenous
CO production, bilirubin formation can be quantified from CO exhaled in the
breath. At steady state, bilirubin formation equals haem breakdown, which in turn
equals haem synthesis. Breath CO excretion increases in haemolytic states. A
small fraction of the CO may be formed by intestinal bacteria. Bilirubin
production can be temporarily inhibited by administering dead-end inhibitors of
haemoxygenase, such as tin-mesoporphyrin. In neonates, a single injection of tin-
mesoporphyrin reduced serum bilirubin levels by 76% and prevented severe
hyperbilirubinaemia in all recipients.

Mecanism of Normal Bilirubin Metabolism

Every haem molecule will produce one molecule of bilirubin.

These molecules are found in haemoglobin and myoglobin. Also, cytochrome

enzymes will also produce one molecule of bilirubin.

The production of bilirubin from haem occurs mainly in the spleen

(macrophages) and liver (Kupfer cells), but also all over the body by
macrophages, and in renal tubular cells. The cells that perform this job are known
collectively as the reticuloendothelial system.

1. Bilirubin-forming molecules (i.e. haem) are taken up by

reticuloendothelial cells.
2. Inside these cells, Haemoxygenase enzymes break down the haem,
removing iron (which is recycled) and carbon monoxide,
leaving biliverdin. The detection of carbon monoxide in breath can be
used to determine how much haem is being turned into
biliverdin. Biliverdin is very water soluble, whilst bilirubin is not.
3. Biliverdin is then converted to bilirubin, whilst still in the
reticuloendothelial cell. This is done by the enzyme biliverdinreductase.
Bilirubin is not just a waste product. It takes up free radicals, and thus is an
antioxidant. This is perhaps the benefit of not directly secreting biliverdin,
but converting it to bilirubin first.
4. After bilirubin is released from reticuloendothelial cells, it travels in the
blood, bound to albumin. This ensures no bilirubin is excreted in the urine.
 At very high concentrations, bilirubin can slowly diffuse into the
peripheral tissues where it is toxic.
5. Bilirubin is then removed from circulation in
the sinusoids by hepatocytes. This is a passive process, which occurs
down a concentration gradient. The fact that hepatocytes are in direct
contact with the sinusoidal fluid helps this process.
6. As soon as bilirubin enters the hepatocyte, it will become bound
to glucuronyltransferase which conjugates the bilirubin ready for
excretion. Bilirubin is joined with glucuronic acid in the conjugation
process. Very small amounts of bilirubin will somehow evade this process
and end up in bile as unconjugated bilirubin.
7. It requires energy to secrete conjugated bilirubin into the canniculi.
The process of conjugation makes the bilirubin water soluble, and
thus easier to excrete.

In situations where the liver cannot excrete conjugated bilirubin, the

kidneys will take over this job, however once plasma concentrations are high
enough (above 600µmol/L) – the kidneys cannot conjugate bilirubin – only
excrete it after this process has occurred.

Bilirubin that is deconjugated by bacteria in the gut will be reabsorbed in

the colon. This process is more likely in the presence of increased bile-acids – i.e.
when there is bile acid malabsorption. Bile acid malabsorption occurs in cases
of intestinal disease and resection. in these patients, as a compensatory
mechanism, the body excretes higher concentrations of bile salts, and
this increases the risk of gallstones.

More bilirubin is also re-absorbed during fasting.

Much of the bilirubin in the colon will also be turned into stercobilogens and
urobilogens. Generally, urobilogens is colourless, and stercobilogens give faeces
its colour.
Some of the urobilogens will be absorbed and enter the circulation, where they
will be removed mainly by the liver, but also by the kidney.

In liver disease and excessive haemolysis, the liver may not be able to remove all
excess urobilogens, and so more is removed by the kidney.

Note that bilirubin will oxidise back to biliverdin after excretion – hence the green
colour of bile.

5. What is Reticuloendhotelial System (RES) ?

Also known as the “mononuclear phagocyte system” (Weinberg and Athens,

1993), the RES is composed of monocytes, macrophages, and their precursor
cells. Monocytes arise from progenitor cells in the bone marrow and are released
into the blood. After migration to different tissues, they differentiate into
macrophages with characteristic morphologic and functional qualities.
 The reticuloendothelial system mainly comprise of phagocytic cells whose
function is to engulf microbes, immune complex from blood and tissues and
participate in inflammation. This way they contribute to non-specific
immunity.These cells also participate in specific immunity by way of antigen
presentation and cytokine secretions. The role of phagocytes was highlighted by
Elie Metchnikoff. The deficiency of phagocytic system can lead to disorders such
as Chronic Granulomatous Disease.
The major phagocytic cells are:
- Polymorphonuclear leucocytes (PMNLs), also called neutrophils, microphages
- Blood and tissue monocytes.
They both are derived form the bone marrow during hematopoiesis.

Neutrophils have short life span. They circulate in the blood for 6-7
hours, then migrate through the endothelial cell junctions and reside in tissue
spaces where they live only for few days and do not multiply. Some neutrophils
may remain attached to endothelial lining of large veins and can be mobilised
during inflammation. The nucleus of a neutrophil is segmented into 3-5 connected
lobes, hence the name polymorphonuclear leukocyte. They are called neutrophils
because their granules stain poorly with the mixture of dyes used in staining
leukocytes. Because of the granules, they are considered as one of the
granulocytes.

Monocytes have rounded or kidney-shaped nuclei with finely granular

cytoplasm, measure 12-15 μm and have half-life of 3 days in circulation.
Monocytes normally make up 2-8% of the WBCs (100-500/mm3 of blood). Once
monocytes leave circulation and enter tissue, they are called macrophages.
Macrophages present in different organs have been given different names. They
are Histiocytes (in tissue), Kupffer cells (in liver), Alveolar macrophages (in
lungs), Peritoneal macrophages (in peritoneum), Microglial cells (in brain),
Mesangial cells (in kidneys) and Osteoclasts (in bone). Functions of macrophage
include killing of microbes, infected cells, tumor cells, secretion of
immunomodulatory cytokines, antigen processing and presentation to T cells.
Macrophages respond to infections as quickly as neutrophils but persist much
longer; hence they are dominant effector cells in the later stage of infection.

Microbial killing by phagocytes:

Phagocytosis involves two steps namely attachment and ingestion.
Following attachment of the organism, invagination of the phagocyte results in the
formation of a phagosome. The phagocytes appear to kill engulfed bacteria by two
pathways, oxygen independent pathway and oxygen dependent pathway. The
microbicidal mechanisms of the respiratory burst are termed oxygen dependent
and phagolysosome formations are termed oxygen independent.
 6. What is the definition of Icterus and how many types ?

If bilirubin is formed more rapidly than it can be excreted, it accumulates in the

body and causes jaundice. Patients with this condition appear yellowish, with this
color being seen most easily in the whites of their eyes. Jaundice can be brought
about in three diff erent ways:
1. Prehepatic (the problem occurs “before the liver”), or hemolytic, jaundice
arises from excessive breakdown (hemolysis) of red blood cells, which results in
the liver being presented with more bilirubin than it is capable of excreting.
2. Hepatic (the problem is the “liver”) jaundice occurs when the liver is
diseased and cannot deal with even the normal load of bilirubin.
3. Posthepatic (the problem occurs “aft er the liver”), or obstructive, jaundice
occurs when the bile duct is obstructed, such as by a gallstone, so that
bilirubin cannot be eliminated in the feces.

Additional information
Bile salts are the most potent stimulus for increased bile secretion. Bile secretion
may be increased by chemical, hormonal, and neural mechanisms: Water-soluble
portion Lipid-soluble portion Water-soluble portion Lipid-soluble portion Lecithin
■ Chemical mechanism (bile salts). Any substance that increases bile secretion
by the liver is called a choleretic. Th e most potent choleretic is bile salts
themselves. Between meals, bile is stored in the gallbladder, but during a meal
bile is emptied into the duodenum as the gallbladder contracts. Aft er bile salts
participate in fat digestion and absorption, they are reabsorbed and returned by
the enterohepatic circulation to the liver, where they act as potent choleretics to
stimulate further bile secretion. Therefore, during a meal, when bile salts are
needed and being used, bile secretion by the liver is enhanced.
■ Hormonal mechanism (secretin). Besides increasing the aqueous NaHCO3
secretion by the pancreas, secretin stimulates an aqueous alkaline bile secretion by
the liver ducts without any corresponding increase in bile salts.
■ Neural mechanism (vagus nerve). Vagal stimulation of the liver plays a minor
role in bile secretion during the cephalic phase of digestion, promoting an increase
in liver bile flow before food ever reaches the stomach or intestine.

7. What age icterus can be happen ?

Neonatal jaundice

Neonatal jaundice is usually harmless: this condition is often seen

in infants around the second day after birth, lasting until day 8 in normal births, or
to around day 14 in premature births. Serum bilirubin normally drops to a low
level without any intervention required: the jaundice is presumably a consequence
of metabolic and physiological adjustments after birth. In extreme cases, a brain-
damaging condition known as kernicterus can occur, leading to significant
lifelong disability; there are concerns that this condition has been rising in recent
years due to inadequate detection and treatment of neonatal hyperbilirubinemia.
A Bili light is often the tool used for early treatment, which often consists of
exposing the baby to intensive phototherapy. Bilirubin count is lowered through
bowel movements and urination so regular and proper feedings are especially
important

Incidence and risk factors:

It is clinically useful to classify jaundice according to the age of the baby when
he/she becomes

visibly jaundiced.

1. Early (days 1-2) - uncommon

oHaemolytic jaundice (Rhesus, ABO, others)

2. Normal (days 3-10) - very common

o Uncomplicated

o G6PD deficiency - especially post discharge home

o Complicated - see below

3. Late (days 14+)

o Breast milk - common

o Conjugated jaundice - uncommon

o Inherited deficiency of glucuronyltransferase enzymes - very rare

Factors likely to make physiological jaundice worse in a given baby include:

• prematurity

• bruising

• cephalohematoma

• polycythaemia • delayed passage of meconium

• breast feeding

• certain ethnic groups, esp Chinese

8. What disease that have icterus symptoms ?

Jaundice, also known as icterus, is a term used to describe a yellowish tinge to the
skin and sclerae (the white part of the eye) that is caused by hyperbilirubinemia
(an excess of bilirubin in the blood). Body fluids may also be yellow. The color of
the skin and sclerae varies depending on levels of bilirubin; mildly elevated levels
display yellow skin and sclerae, while highly elevated levels display brown.
 Bilirubin (bil-ih-ROO-bin) is a yellow colored substance that is
responsible for the yellowing of the skin and sclerae. Bilirubin is a waste product
that remains in the bloodstream after the iron is removed from the hemoglobin,
which is released from the degradation of erythrocytes (cells that contain
hemoglobin and can carry oxygen to the body). When there is an excess of
bilirubin it may leak out into surrounding tissues, saturating them with this yellow
substance.
Bilirubin that is circulating freely in the blood is called unconjugated
bilirubin. One of the liver's functions is to filter out waste, such as bilirubin, from
the blood. Once it is in the liver, other chemicals latch on to the bilirubin, creating
a substance called conjugated bilirubin, which is secreted in bile (a digestive juice
released by the liver) and then excreted. Bilirubin is what gives feces its brown
color.
The modern English word "jaundice" is derived from the middle French
word jaunisse. Jaun means "yellow" and -isse means "-ness"; hence the middle
French word jaunisse, which means "yellowness".

Jaundice is often a sign of a problem with the liver, gallbladder, or pancreas.

Jaundice can occur when too much bilirubin builds up in the body. This may
happen when:

 There are too many red blood cells dying or breaking down and going to
the liver.
 The liver is overloaded or damaged.
 The bilirubin from the liver is unable to properly move into the digestive
tract.

Conditions that can cause jaundice include:

There are three main types of jaundice:

 Hepatocellular jaundice - a type of jaundice that occurs as a result of liver
disease or injury.
  Hemolytic jaundice - a type of jaundice that occurs as a result of hemolysis
(an accelerated breakdown of erythrocytes - red blood cells) leading to an
increase in production of bilirubin.
 Obstructive jaundice - a type of jaundice that occurs as a result of an
obstruction in the bile duct (a system of tubes that carries bile from the
liver to the gallbladder and small intestine), which prevents bilirubin from
leaving the liver.

Jaundice, not to be confused with infant jaundice, is usually a sign of an

underlying disorder. causes of jaundice :
Jaundice most often occurs as a result of an underlying disorder that either
causes tissues to become over-saturated with bilirubin or prevents the liver from
disposing of bilirubin.

Some underlying conditions that may cause jaundice are:

 Acute inflammation of the liver - may impair the ability of the liver to
conjugate and secrete bilirubin, resulting in a buildup of bilirubin.
 Inflammation of the bile duct - may prevent the secretion of bile and
removal of bilirubin, causing jaundice.
 Obstruction of the bile duct - prevents the liver from disposing of
bilirubin, which results in hyperbilirubinemia.
 Hemolyticanemia - Production of bilirubin increases when large
quantities of erythrocytes are broken down.
 Gilbert's syndrome - an inherited condition that impairs the ability of
enzymes (biomolecules that provoke chemical reactions between
substances) to process the excretion of bile.
 Cholestasis-a condition in which the flow of bile from the liver is
interrupted. The bile containing conjugated bilirubin remains in the
liver instead of being excreted.
 Infections of the liver from a virus (hepatitis A, hepatitis B, hepatitis C,
hepatitis D, and hepatitis E) or a parasite
  Use of certain drugs (such as an overdose of acetaminophen) or
exposure to poisons
 Birth defects or disorders present since birth that makes it hard for the
body to breakdown bilirubin (such as Gilbert syndrome, Dubin-
Johnson syndrome, Rotor syndrome, or Crigler-Najjar syndrome)
 Liver damage
 Gallstones or gallbladder disorders
 Blood disorders
 Cancer of the pancreas
 Bile build-up in the gallbladder because of pressure in the belly area
during pregnancy (jaundice of pregnancy)

9. How is the mechanism of Jaundice cause by pre-hepatic, Intra-hepatic and

Post hepatic ?

Jaundice may be caused by several different disease processes. It is helpful to

understand the different causes of jaundice by identifying the problems that
disrupt the normal bilirubin metabolism and/or excretion.

Pre-hepatic (before bile is made in the liver)

 Excessive bilirubin formation by overwhelming destruction of RBC

Jaundice in these cases is caused by rapid increase in the breakdown and

destruction of the red blood cells (hemolysis), overwhelming the liver's ability
to adequately remove the increased levels of bilirubin from the blood.

 Bilirubin uptake disruption

To enter the liver bilirubin must attach with albumin, because unconjugated
bilirubin is so difficult to be soluble in plasm.
 Examples of conditions with increased breakdown of red blood cells include:

 malaria
 sickle cell crisis,
 spherocytosis,
 thalassemia,
 glucose-6-phosphate dehydrogenase deficiency (G6PD),
 drugs or other toxins, and
 autoimmune disorders.

Hepatic (the problem arises within the liver)

Jaundice in these cases is caused by the liver's inability to properly metabolize and
excrete bilirubin. Conjugation of bilirubin disorders

Unconjugated hyperbilirubinemia mild (<12.9 mg / 100ml) arising between the

second and fifth day after birth is called neonatal physiological jaundice. If
unconjugated bilirubin in newborns exceed 20 mg / dl, there is a condition called
kemiukterus. This situation can arise when a hemolytic process with deficient
glucuronyltransfrease. Kerniukterus arising from the accumulation of
unconjugated bilirubin in the basal ganglia region that contains a lot of fat. Three
hereditary disorder that causes deficiency is Gilbert syndrome and Crigler-Najjar
syndrome type 1 and type 2.
Examples include:

 hepatitis (commonly viral or alcohol related),

 cirrhosis,
 drugs or other toxins,
 Crigler-Najjar syndrome,
 Gilbert's syndrome, and
 cancer.

Post-hepatic (after bile has been made in the liver)

Jaundice in these cases, also termed obstructive jaundice, is caused by

conditions which interrupt the normal drainage of conjugated bilirubin in the
form of bile from the liver into the intestines.

Decreased excretion of conjugated bilirubin.

Good excretion of bilirubin disorders caused by functional factors and causes of

obstructive mainly conjugated hyperbilirubinemia. Conjugated bilirubin is water
soluble, so it can be excreted in the urine dark. Changes color ranges from orange-
yellow when young or old trerjadi total obstruction of bile flow. This change is
evidence of cholestatic jaundice. Cholestasis may be intrahepatic or extrahepatic.
The most common causes of intrahepatic cholestasis is hepatocellular disease with
parenchymal liver damage from hepatitis virus or various types of cirrhosis. While
the most common cause of extrahepatic cholestasis is a blockage of gallstones.
Usually at the lower end of the duct choledochal; carcinoma of the head of the
pancreas causes pressure in the duct.

Causes of obstructive jaundice include:

 gallstones in the bile ducts,

 cancer (pancreatic and gallbladder/bile duct carcinoma),
 strictures of the bile ducts,
 cholangitis,
 congenital malformations,
 pancreatitis,
 parasites,
 pregnancy, and
 newborn jaundice.
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