FAKULTAS KEDOKTERAN

UNIVERSITAS MUSLIM INDONESIA

BLOK GASTROENTEROHEPATOLOGI Makassar,29Desember2018
MODULE 2
“ YELLOW SKIN”
SCENARIO 2

ARRANGED BY:
GROUP 14
MASITHA (11020170002)
DEWI DHARMA PUTRI ALIM (11020170005)
USI TRIS SEPTIA NINGSIH (11020170029)
HUMAIRAH SHALEH (11020170057)
AMALIAH FILDZAH ASILAH HIDAYAT (11020170067)
KASMA (11020170087)
SANISKA AYU KARTINIVA ISKANDAR (11020170114)
JIHAN RANA MARDHIYAH (11020170115)
KARISMAN (11020170129)
RATU DINI FAUZIAH (11020170156)

TUTOR: dr.FarahEkawati

FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
MAKASSAR
2018/2019
FOREWORD

Praise we present the presence of Allah SWT for His mercy and guidance
so that this tutorial report can be completed on time. Aamiin.We realize that there
are still many shortcomings in this tutorial report, therefore constructive criticism
and suggestions are always expected to encourage us to create better works.

Finally, we would like to thank all those who have provided assistance in the
preparation of this paper, especially to:

1. Dr.FarahEkawati

2. Friends who have supported and provided motivation in completing this tutorial
report.

May Allah SWT be able to give a reward for all goodness and sacrifice with an
abundance of mercy from Him.Aamiin is RobbalA'lamiin.

Makassar, 29Desember 2018

Group 14
 SCENARIO 2 :

A 45-year-old woman comes to the out patient clinic with complaints of yellow
all over the body that have been experienced for the past 3 days, complaints of
right abdominal pain over loss arising from the last 1 month. History of frequent
consumption of fatty foods

 HARD WORD :
-
 KEYWORDS :
 A 45-year-old woman
 yellow all over the body that have been experienced for the past 3 days
 complaints of right abdominal pain over loss arising from the last 1
month
 History of frequent consumption of fatty foods

 QUESTION :
1. How could the skin become yellow?
2. How is bilirubin formed normally?
3. what is the relationship between fatty foods and the disease they suffer ?
4. How is the patomechanisme of right upper abdominal pain in the scenario?
5. explain the differential diagnosis of the scenario?
6. explain prevention according to the scenario?
7. Islamic perspective on the scenario?
 ANSWER :
1. How could the skin become yellow?
Jaundice occurs when there is too much bilirubin (a yellow
pigment) in the blood a condition called hyperbilirubinemia. Bilirubin is
formed when hemoglobin (the part of red blood cells that carries oxygen)
is broken down as part of the normal process of recycling old or damaged
red blood cells. Bilirubin is carried in the bloodstream to the liver, where it
binds with bile. Bilirubin is then moved through the bile ducts into the
digestive tract, so that it can be eliminated from the body. Most bilirubin is
eliminated in stool, but a small amount is eliminated in urine. If bilirubin
cannot be moved through the liver and bile ducts quickly enough, it builds
up in the blood and is deposited in the skin. The result is jaundice.Many
people with jaundice also have dark urine and light-colored stool. These
changes occur when a blockage or other problem prevents bilirubin from
being eliminated in stool, causing more bilirubin to be eliminated in urine.
If bilirubin levels are high, substances formed when bile is broken down
may accumulate, causing itching all over the body. But jaundice itself
causes few other symptoms in adults.
Jaundice is defined as yellow discoloration due to increased serum
bilirubin level. This is usually found in the skin, sclerae (the white part of
eye) and mucus membranes. The image displayed shows marked
discoloration of the patient’s sclera, called scleral icterus. This sign may be
present before discoloration of the skin is noticed and is used to clarify the
presence of jaundice. Jaundice In simple terms, normally bilirubin is
released as a byproduct when the red blood cells in the blood are
destroyed. The liver then needs to process the bilirubin so that it can be
excreted as bile into the gut and passed out through the stools or urine.
Thus, jaundice occurs when(1)

 Increased bilirubin production due to increased red blood cells being

destroyed (this is known as this is known as hemolysis): collection of
 blood in the tissue, increased red blood cells destruction leading to
tiredness, lethargy, etc (also known as hemolytic anaemia).
 Failure of the liver to process the bilirubin to be excreted: many diseases
that affect the liver such as viral infection, genetic diseases, excessive
accumulation of chemicals (copper and iron), or tumor can cause jaundice
by this means. A disease known as Gilbert’s syndrome is a common but
harmless genetic disease that causes jaundice through this method.
 Blockage of the passage of bile into the gut: this include gallstones and
cancer of the bile duct or liver.
Jaundice has various variants including pre-hepatic jaundice (due to
hemolysis of red blood cells), hepatic jaundice (due to defect in capture,
conjugation and excretion of bilirubin by liver) and post hepatic jaundice
(due to the obstruction of extra hepatobiliary system). The causes of
various variants of Jaundice is either acquired or congenital. High plasma
bilirubin level can cause various manifestations involving satiety,
gastrointestinal bleeding, diarrhea, anemia, edema, weight-loss and can be
fatal because it can cause psychosis, lethargy, seizures, coma or even
death. High bilirubin level can help in the diagnosis of Jaundice(1)
2. How is bilirubin formed normally?

Bilirubin is an orange-shaped crystal pigment of jaundice which is

the final form of the breakdown of heme catabolism through an oxidation-
reduction reaction process. Bilirubin is derived from catabolism of heme
protein, of which 75% comes from the destruction of erythrocytes and
25% comes from the destruction of immature erythrocytes and other heme
proteins such as hemoglobin, cytochrome, catalase and peroxidase.

Metabolism bilirubin includes formation of bilirubin, transport of

bilirubin, intake of bilirubin.The first oxidase step is biliverdin which is
formed from the hem with the help of the enzyme hemeoxygenase, an
enzyme that is mostly available in liver cells and other organs. Biliverdin
which dissolves in water will then be reduced to bilirubin by the enzyme
biliverdinreductase. Bilirubin is lipophilic and is bound to hydrogen and at
normal pH is insoluble. The formation of bilirubin that occurs in the
reticuloendothelial system, then released into circulation which binds to
albumin. Bilirubin which is bound to serum albumin is insoluble in water
and will then be transported to liver cells.
When the bilirubin-albumin complex reaches plasmahepatosit membranes,
albumin will bind to cell surface receptors. Then the bilirubin is
transferred through membrane cells that bind to ligandin (Y protein),
possibly also with other cytotoxic bond proteins. Reduced hepatic taking
capacity of unconjugated bilirubin influences the formation of
physiological jaundice.

 differences in indirect bilirubin and direct bilirubin :

a. Indirect conjugated bilirubin / bilirubin is non-conjugated bilirubin with
glucoronic acid. This bilirubin can react with diazo and Ehrlich reagents
after the addition of alcohol. Bilirubin is fat soluble, non-polar, and
insoluble in water.
b. Conjugated bilirubin / direct bilirubin is bilirubin which has been
conjugated with glucoronic acid. This bilirubin can react directly with
the diazio and Ehrilch reagents without the addition of alcohol, is not
fat soluble, polar, and soluble in water. Therefore, direct bilirubin can
be found in urine.(2)

Unconjugated bilirubin is converted to bilirubinconjugasi which dissolves

in water in the endoplasmic reticulum with the help of the enzyme
uridinediphosphateglucoronosyltransferase (UDPG-T). This bilirubin is
then excreted into the bile canaliculus. While one unconjugated bilirubin
 molecule will return to the reticulum for the next reconjugation. After
undergoing a conjugation process, bilirubin will be excreted into the gall
bladder, then enter

Once in the small intestine, indirect conjugated bilirubin can be

absorbed, unless converted back into a form not conjugated by the beta-
glucoronidase enzyme found in the intestine. Restoring bilirubin from the
gastrointestinal tract and returning to the liver for conjugation is called the
enterohepatic circulation.

 Pre-hepatic jaundice is caused by conditions that heighten your blood’s

rate of hemolysis. This is the process through which red blood cells are
broken down, releasing hemoglobin and converting into bilirubin.Because
the liver can only process so much bilirubin at once, bilirubin overflows
into bodily tissues.
The most common causes of pre-hepatic jaundice are:

 malaria, a blood infection caused by a parasite

 sickle cell anemia, a genetic condition in which red blood cells
become crescent-shaped rather than the typical disc shape
 spherocytosis, a genetic condition of the red blood cell membrane
that causes them to be sphere-shaped rather than disc-shaped
 thalassemia, a genetic condition that causes your body to make an
irregular type of hemoglobin that limits the number of healthy red
blood cells in your bloodstream

Common symptoms of pre-hepatic jaundice include:

 abdominal pain, fever, including chills or cold sweats, abnormal

weight loss, feeling itchy, dark urine or pale stool

Some risk factors for this type of jaundice include:

 drug use, having a family member with a blood disorder, traveling

to malaria-endemic regions

for diagnose pre-hepatic jaundice, your doctor will likely order the
following tests:

 a urinalysis to measure the amount of certain substances in your

urine
 blood tests, such as a complete blood count (CBC) or liver function
tests to measure bilirubin and other substances in the blood
 imaging tests, such as an MRI or ultrasound, to examine your liver,
gallbladder, and bile ducts to rule out other forms of jaundice
 a HIDA scan to help find blockages or other issues in the liver,
gallbladder, bile ducts, and small intestine.(8)
 Hepatic jaundice happens when your liver tissue is scarred (known as
cirrhosis), damaged, or dysfunctional. This makes it less effective at
filtering out bilirubin from your blood.Since it can’t be filtered into your
digestive system for removal, bilirubin builds up to high levels in your
blood.

The most common causes of hepatic jaundice are:

 liver cirrhosis, which means that liver tissues are scarred by long-
term exposure to infections or toxic substances, such as high levels
of alcohol
 viral hepatitis, an inflammation of the liver caused by one of
several viruses that can get into your body through infected food,
water, blood, stool, or sexual contact
 primary biliary cirrhosis, which happens when bile ducts are
damaged and can’t process bile, causing it to build up in your liver
and damage liver tissue
 alcoholic hepatitis, in which your liver tissues are scarred by the
heavy, long-term drinking of alcohol
 leptospirosis, is a bacterial infection that can be spread by infected
animals or infected animal urine or feces
 liver cancer, in which cancerous cells develop and multiply within
liver tissues

Common symptoms of hepatic jaundice include:

 loss of appetite, bloody nose, skin itching ,weakness, abnormal

weight loss ,swelling of your abdomen or legs ,dark urine or pale
stool, pain in your muscles or joints, darkening skin, feeling sick,
throwing up
 Some risk factors for this type of jaundice include:

 drug use, drinking a lot of alcohol over a long period of time, use
of medications that can cause liver damage, such as acetaminophen
or certain heart medications, previous infections that affected your
liver

To diagnose hepatic jaundice, your doctor will likely order the following tests:

 a urinalysis to measure levels of substances in your urine related to

your liver function
 blood tests, such as a complete blood count (CBC) and antibody
tests, or liver function tests to measure bilirubin in the blood and
levels of substances that indicate that your liver may not be
processing bilirubin properly
 imaging tests, such as an MRI or ultrasound, to examine your liver
for damage or for the presence of cancerous cells
 an endoscopy, which involves inserting a thin, lighted tube into a
small incision to look at your liver and take a tissue sample
(biopsy) if necessary for analysis for cancer or other conditions

 Post-hepatic, or obstructive jaundice, happens when bilirubin can’t be

drained properly into the bile ducts or digestive tract because of a
blockage.

The most common causes of post-hepatic jaundice are:

 gallstones, hard calcium deposits in the gallbladder that can block

bile ducts
 pancreatic cancer, the development and spread of cancer cells in
the pancreas, an organ that helps produce digestive substances
 bile duct cancer, the development and spread of cancer cells in
your bile ducts
  pancreatitis, an inflammation or infection of your pancreas
 biliary atresia, a genetic condition in which you have narrow or
missing bile ducts

Common symptoms of post-hepatic jaundice include:

 feeling sick, throwing up, dark urine or pale stool, abdominal pain,
diarrhea, abnormal weight loss, skin itching, abdominal swelling,
fever

Some risk factors for this type of jaundice include:

 being overweight, eating a high-fat, low-fiber diet, having diabetes

mellitus, having a family history of gallstones, being femaleaging,
smoking tobacco products ,drinking a lot of alcohol ,having a
previous pancreas inflammation or infection, being exposed to
industrial chemicals

To diagnose post-hepatic jaundice, your doctor will likely order the

following tests:

 a urinalysis to measure levels of substances in your urine

 blood tests, such as a complete blood count (CBC) and antibody
tests for cancer, or liver function tests to rule out hepatic jaundice
 imaging tests, such as an MRI or ultrasound, to examine your liver,
gallbladder, and bile ducts for obstructions like gallstones or
tumors
 an endoscopy, which involves inserting a thin, lighted tube down
the esophagus to look at your liver, gallbladder, or bile ducts and
take a tissue sample if necessary for analysis for cancer or other
conditions.(8)
3. what is the relationship between fatty foods and the disease they
suffer?
Free cholesterol is in rapid equilibrium between serum lipoproteins
and red cells. The level of red cell cholesterol is influenced by bile salts,
which shift the serum/cell partition of free cholesterol to the cell phase and
which inhibit the cholesterol-esterifying mechanism. During incubation in
normal serum possessing an active cholesterol-esterifying mechanism, red
cells lose cholesterol and surface area and thereby become more
spheroidal and less resistant to osmotic lysis. When exposed to serum from
patients with obstructive jaundice or to normal serum with added bile salts,
red cells accumulate cholesterol and increase their surface area, thereby
acquiring a flattened shape and an increased resistance to osmotic lysis.
The described gains and losses of red cell cholesterol and surface area do
not involve metabolic injury and occur with no significant change in
phospholipid content.
The red cells of patients with obstructive jaundice are flat and
osmotically resistant and have an increased cholesterol:phospholipid ratio.
When transfused into normal subjects these “target cells” rapidly lose their
osmotic resistance. Similarly, normal cells acquire osmotic resistance in
the circulation of patients with obstructive jaundice. These reversible
changes in shape occur with half-times of about 9 and 24 hr, respectively,
and occur without impairing cell viability.These studies indicate that the
red cell membrane accumulates cholesterol in obstructive jaundice as a
consequence of the elevated levels of bile salts. The resulting increment in
red cell surface area is responsible for the physical properties and
appearance of target cells. These observations substantiate Murphy's
findings in vitro indicating that cholesterol is an important determinant of
red cell shape and that its content in the cell membrane may vary
independently from the phospholipids. Presumably any process or disorder
affecting cholesterol exchange in vivo is capable of critically modifying
the shape and behavior of red cells.(3)
4. How is the patomechanisme of right upper abdominal pain in the
scenario?
a. Understanding Pain
Pain as a subjective sensory and emotional experience not fun that
is related to tissue damage acute nature that is felt in the events where it
occurs damage. Pain is a sensory pain and emotional experience that is
not fun related to actual and networkdamage potential.

b.Pain Classification Based On the duration

1)Acutepain
Acute pain is pain that occurs after acute injury, disease, or
surgical intervention and has a fast process with intensity which varies
(mild to severe). Acute pain is short duration (approximately 6 months)
and will disappear without treatment after the damaged area has
recovered.
2)Chronicpain
Chronic pain is a constant, intermittent pain that persists over a
period of time, this pain lasts long with the intensity varies and usually
last smore than 6 months.

Pathomechanism Nociceptive Pain

a. Transduction. Is a change in pain stimulation (noxious stimuli) into
electrical activity in sensory nerve endings. Algesic substances
such as prostaglandin, serotonin, bradykinin, leukotriene, substance
P, potassium, histamine, lactic acidand pain receptors. Pain
receptors are woven edges free afferent fibers A-delta and C. These
receptors are often found in the skin tissue, periosteum, in the
dental pulp and tissues another body. Afferent nerve fibers A-delta
and C are nerve fibers sensory function has the function of
continuing sensory pain from peripheral to central to the central
nervous system. Interaction between algesic substances and
receptors pain causes the formation of pain impulses. Transduction
is the process of pain stimulation is configured in forms that can be
accessed by brain. The transduction process starts when the
nociceptor is the receptor function to receive activated pain stimuli.
Activation of this receptor (nociceptors) is a form of response to a
stimulus come like network damage. Transmission / Transmission.
Transmission is a series of neural events that carry electrical
impulses through the nervous system to the area of the brain.
b. The transmission process involves afferent nerves formed from
small to medium-diameter nerve fibers and large-diameter ones.
Afferent nerves will accuse the dorsal horn in the spinal cord.
Furthermore this transmission is continued through the
contralateral spinalthalamic system through the lateral ventral of
the thalamus to the cerebralcortex..Modulation / Modulation.
c. The modulation process refers to neural activity in an effort to
control the nociceptor transmission line. The modulation process
involves a complex neural system. When pain impulses reach the
nerve center, the transmission of pain impulses will be controlled
by the central nervous system and transmit these pain impulses to
other parts of the nervous system such as cortex section.
 Furthermore this pain impulse will be transmitted through descend
nerves to the spine to modulate effectors.
d. Perception / Perception. Perception is a subjective process. This
perception process is not only related to physiological processes or
anatomical processes, but also includes cognition and memory.
Therefore, psychological, emotional, and berhavioral (behavioral)
factors also appears as a response in perceiving the experience of
the pain. This process of perception is also what makes the pain a
phenomenon which involves multidimensional(4).

The splanchnic and the cerebrospinal are the two neural pathways
available for transmission of abdominal pain. Pacinian corpuscles and free
nerve endings in the walls of the viscera are the splanchnic afferent nerve
receptors. They are sensitive only to stretch and spasm. By contrast,
receptors of the cerebrospinal nerves are sensitive to pressure, friction,
cutting, burning, and any other stimulus that can be appreciated by skin. In
the dorsal root ganglia the splanchnic and cerebrospinal cell bodies are
side by side. Their proximal fibers also terminate in close proximity within
the spinal cord. The close relationship of these anatomic pathways may
account for the fact that severe visceral pain, such as rapid distention of a
viscus, may "spill over" into somatic segments (viscerosensory and
visceromotor reflexes) in the absence of somatic nerve irritation.
Understanding of "spillover" pain is essential for accurate diagnosis of
abdominal pain.Since the embryonic gut and its appendages arise as
midline organs, their splanchnic innervation is bilateral, and accordingly,
visceral pain is perceived in the midline. Cerebrospinal nerves to the
parietal peritoneum (T6 through T12) have the same segmental
arrangement as the lower thoracic dermatomes. There are no nerve fibers
in the visceral peritoneum.Upper abdominal organs have anatomic features
that make pain patterns emanating from them far more complex than those
of the appendix. Painful lesions of the gastroesophageal junction, the
fundus and lesser curvature of the stomach, the biliary tract, and proximal
portions of the duodenum commonly produce pain in the interscapular
zone corresponding to the sixth thoracic segment, since the somatic
innervation of the lesser omentum is supplied by that thoracic nerve.
Pancreatic pain is often perceived in the same location one segment
lower.The stomach is so situated that portions of its surface are in contact
with the diaphragm, the gastrohepatic ligament, the lesser sac, the
pancreas, the parietal peritoneum, the splenic hilus, the gastrocolic
ligament, the transverse mesocolon, and the transverse colon.
Inflammatory or neoplastic lesions of the stomach that involve any of
these surfaces may irritate somatic nerves from several different spinal
segments. Accordingly, pain may be(7).
5. Explain the differential diagnosis of the scenario?

1.CHOLELITHIASIS

 Definition
Gallstone disease (cholelithiasis) is an important health problem in the
West while in Indonesia it is only getting clinical attention, while the
publication of gallstone research is still limited. Most patients with
gallstones have no complaints. The risk of having gallstones to experience
symptoms and complications relative to small pathogens. However, once
gallstones begin to cause specific attacks of colic pain, the risk of
experiencing problems and complications will continue to increase.
Gallstones are commonly found inthe gallbladder, but they can migrate
through the cystic duct into the bile duct into a bile duct stone and are
called as secondary bile duct stones D1 Western countries 10-15% of
patients with gallbladder stones are also accompanied by bile duct stones.
In some circumstances, bile duct stones can form primary in the intra-or
extra-hepatic bile duct without involving the gallbladder. Primary bile duct
stones are more common in patients in the Asian region compared to
patients in Western countries. The course of secondary bile duct stones is
not yet clear, but complications will be more frequent and severe than
asymptomatic gallbladder stones.
 Etiology
There are three main pathways in the formation of gallstones:
1.Cholesterolsupersaturation: Normally, bile can dissolve the amount of
cholesterol excreted by the liver. But if the liver produces more cholesterol
than bile can dissolve, the excess cholesterol may precipitate as crystals.
Crystals are trapped in gallbladder mucus, producing gallbladder sludge.
With time, the crystals may grow to form stones and occlude the ducts
which ultimately produce the gallstone disease.
 2.Excess bilirubin: Bilirubin, a yellow pigment derived from the
breakdown of red blood cells, is secreted into bile by liver cells. Certain
hematologic conditions cause the liver to make too much bilirubin through
the processing of breakdown of hemoglobin. This excess bilirubin may
also cause gallstone formation.

3.Gallbladderhypomotility or impaired contractility: If the gallbladder

does not empty effectively, bile may become concentrated and form
gallstones.Depending on the etiology, gallstones have different
compositions. The three most common types are cholesterol gallstones,
black pigment gallstones, and brown pigment gallstones. Ninety percent of
gallstones are cholesterol gallstones.Each stone has a unique set of risk
factors. Some risk factors for the development of cholesterol gallstones are
obesity, age, female gender, pregnancy, genetics, total parenteral nutrition,
rapid weight loss, and certain medications.Approximately 2% of all
gallstones are black and brown pigment stones. These can be found in
individuals with high hemoglobin turnover. The pigment consists of
mostly bilirubin. Patients with cirrhosis, ileal diseases, sickle cell anemia,
and cystic fibrosis are at risk of developing black pigment stones. Brown
pigments are mainly found in Southeast Asian population and are not
common in the United States. Risk factors for brown pigment stones are
intraductal stasis and chronic colonization of bile with bacteria.

 Epidemiology

Cholelithiasis is quite common and can be found in approximately 6% of

men and 9% of women. The highest prevalence of cholelithiasis arises in
Native American populations. Gallstones are not as common in Africa or
Asia. The epidemic of obesity has likely magnified the rise of
gallstones.Despite how prevalent gallstones may be, more than 80% of
people remain asymptomatic. Biliary pain, however, will develop annually
in 1% to 2% of individuals previously asymptomatic.
 Pathogenesis

According to the macroscopic definition and chemical composition, bile

duct stones can reach three categories of mayors, namely: 1) cholesterol
stones in which cholesterol content increases by 70%, 2) brown pigment
stones or calcium bilirubinate stones containing Ca-bilirub as a rich
component non-extracted black residues ma, and 3) black pigment stones
that in Western societies the main composition of gallstones is cholesterol,
while studies in Jakarta 51 patients found pigment stones in 7396 patients
and cholesterol stones in 27% of patients. There are three important factors
that play a role in the pathogenesis of cholesterol stones: 1) cholesterol
hypersaturation in the gall bladder, 2) acceleration of crystallization of
cholesterol and 3) gall motility and intestinal motility disorders The
presence of pigments in cholesterol stone nuclei associated with
gallbladder mud in the early stages of formation stone Pathogenesis of
pigment stones involves bile duct infection, bile stasis, malnutrition, and
dietary factors Excessive activity of bacterial and biological human B-
glucuronidase enzymes (endogenous) plays a key role in the pathogenesis
of pigment stones in patients in eastern countries Hydrolysis of bilirubin
by these enzymes will form non bilirubin conjugated which will
precipitate se calcium bilirubinate. The p-enzyme comes from the germ E
coli and other germs in the bile glucuronidase bacteria. This enzyme can
be inhibited by glucaro, whose concentration increases in patients with
low protein and low fat

 Diagnosis

Before the development of advanced imaging such as ultrasound (US), a

number of patients with gallstone disease were often misdiagnosed as
recurrent gastritis or hepatitis, as well as 60% of studies in Jakarta which
included 74 patients with bile duct stones. Today US is the first choice
imaging for diagnosing gallbladder stones with a high sensitivity
exceeding 95% while for detection of bile duct stones the sensitivity is
relatively low ranging from 18-74%. In a study in Jakarta involving 325
patients with suspected biliary disease, the diagnostic value of ultrasound
in diagnosing bile duct stones had bile ducts with a sensitivity of 90%, a
specificity of 98%, it causes complications of pancreatitis and cholangitis
which can still be fatal compared to endoscopic retrograde
cholangiopancreatography (ERCP) as a standard reference method for
direct cholangiography. Overall the accuracy of ultrasound for bile duct
stones is 77% ERCP is very useful in detecting stones and 96% accuracy,
but this procedure is invasive and can cause. Patients with gallstone
disease typically present with symptoms of biliary colic (intermittent
episodes of constant, sharp, right upper quadrant (RUQ) abdominal pain
often associated with nausea and vomiting), normal physical examination
findings, and normal laboratory test results. It may be accompanied by
diaphoresis, nausea, and vomiting.Acutecholecystitis occurs when
persistent stone dislodged the cystic duct causes the gallbladder to become
distended and inflamed. The patient may also present with fever, pain in
the right upper quadrant and tenderness over the gallbladder (this is known
as Murphy's sign).When fever, persistent tachycardia, hypotension, or
jaundice are present, it requires a search for complications of
cholelithiasis, including cholecystitis, cholangitis, pancreatitis, or other
systemic causes.Choledocholithiasis is a complication of gallstones when
stones obstruct the common bile duct it impedes the flow of bile from the
liver to the intestine. Pressure rises resulting in elevation of liver enzymes
and jaundice.Cholangitis is triggered by colonization of bacteria and
overgrowth in static bile above an obstructing common duct stone. This
produces purulent inflammation of the liver and biliary tree. Charcot's
triad consists of severe RUQ tenderness with fever and jaundice and is
classic for cholangitis. Surgical removal of stone obstruction with
intravenous antibiotics is required to treat this condition.
 Anamnesis
halfto two thirds of patients with cholelithiasis are asymptomatic.
Complaints that may arise are dyspepsia which is sometimes accompanied
by intolerance to fatty foods. Symptomatically, patients usually present
with a major complaint in the form of pain in the epigastric or pain / colic
in the right upper abdomen or pericondrium which may last more than 15
minutes, and sometimes several hours. The onset of pain is mostly slow
but in 30% cases arise suddenly patients with yellow eyes and body, body
itching, colored urine like tea, colored stools such as putty and the spread
of pain in the middle back, scapula, or shoulder peak, accompanied by
nausea and vomiting. More or less a quarter of sufferers reported that pain
was reduced after using antacids. If cholelithiasis occurs, pain complaints
persist and increase when breathing deeply
 Physical examination
Patients with lithogenic or asymptomatic stones do not have abnormalities
in physical examination. During biliary colic attacks, especially during
acute cholelithiasis, the patient will experience palpation / tenderness with
maximum punktum in the area of the anatomy of the gallbladder. It is
known by the presence of a positive Murphy sign when tenderness
increases when the patient takes a deep breath because the inflamed
gallbladder is touched by the examiner's fingertip and the patient stops
breathing. History of jaundice and cutaneous jaundice and sclera and can
be felt by the liver.(13).
 Laboratory examination
Asymptomatic gallstones generally do not show abnormalities on
laboratory tests. If acute inflammation occurs, leukocytosis can occur. In
the case of the mirizzi syndrome, a mild increase in serum bilirubin will be
found due to suppression of the ductal koledokus by stone. High serum
bilirubin levels may be caused by stones in the koledokus duct. Serum
alkaline phosphatase levels and possibly also serum amylase levels usually
increase moderately every time an acute attack occurs
 Supporting investigation
1..Ultrasound examination has a high degree of specificity and sensitivity
for detecting gallbladder stones and widening of the intrahepatic and extra
hepatic bile ducts. With ultrasound it can also be seen that the gallbladder
wall is thickened due to fibrosis or edema caused by inflammation or other
causes. Stones found in the duct of the distal coledokus are sometimes
difficult to detect because they are blocked by air in the intestine. With
maximum punktum ultrasound the pain in gangrene gallstones is clearer
than with normal palpation.
2.Plain Abdomen Photographs of photos that have not shown a typical
picture because only about 10-15% of gallbladder stones are radiopaque.
Sometimes bile containing high calcium levels of bile can be seen with
plain photos. In acute inflammation with an enlarged gallbladder or
hydrops, the gallbladder is sometimes seen as a soft tissue mass in the
right upper quadrant that suppresses the air in the large intestine, in the
flexura hepatica

3.Cholecystography For certain patients, contrast cholecystography is

quite good because it is relatively inexpensive, simple, and accurate
enough to see radiolucent stones so that the number and size of stones can
be calculated. Oral cholecystography will fail under paralytic ileus,
vomiting, serum bilirubin levels above 2 mg / dl, pylorus obstruction and
hepatitis, because in these conditions contrast cannot reach the liver.
 Examination of oral cholecystography is more significant in assessing
gallbladder function.
 Treatment
Most patients with asymptomatic stones will not experience complaints
and the number, size and composition of stones will not be related to the
onset of complaints during monitoring. Even if complaints arise later, they
are generally mild so that handling can be elective.Laparoscopic
cholecystectomy is a minimally invasive surgical technique in the
abdominal cavity using a pneumoperitoneum, endocamera system and
special instruments through the monitor screen without seeing and
touching the gallbladder directly. Since it was first introduced, this
laparoscopic surgical technique has shown a significant advantage
compared to conventional surgical techniques. Minimal pain, rapid
recovery, short duration of treatment and very minimal scarring are the
advantages of laparoscopic surgery In Indonesia itself, especially in
Jakarta, the method of laparoscopic cholecystectomy was initiated in 1991
and over a period of four years (1991-1994) later surgery followed by
other flashlights. laparoscopic treatment in 2687 patients in four flashlights
in Indonesia and sensitivity laparoscopic cholecystectomy was the most
common indication with a total of 2201 cases. Converting to conventional
cholecystectomy is needed in 27-62% of patients. This is mainly due to
difficulties in recognizing anatomy. Today in some hospitals, laparoscopic
cholecystectomy has become a standard procedure for the removal of
symptomatic gallbladder. The advantages obtained by patients with this
technique include small surgical wounds (2-10 mm) so that postoperative
pain is minimal. In addition, in terms of cosmetics the small scar that will
be hidden in the umbilicus area has made laparoscopic a more patient
friendly surgery. Complications of bile duct injuries from this technique
which generally occur at the learning stage can be overcome largely by
cases of stenting or nasobilier catheter with ERCP..(10)
2. CHOLECYSTITIS

 Acute cholecystitis
inflammation of the gallbladder (acute cholecystitis) is an acute
inflammatory reaction of the gallbladder wall accompanied by complaints
of right upper abdominal pain, tenderness, and fever. until now the
pathogenesis of this disease that is quite often encountered is still unclear.
although there are no epidemiological data on the population, the
incidence of cholecystitis and gallstones (cholelithiasis) in our country is
relatively lower compared to western countries.
 Chronic cholecystitis
Chronic cholecystitis is more common in clinical settings, and is very
closely related to litiasis and more often arises slowly.
Clinical Symptoms
the diagnosis of chronic cholecystitis is often difficult to enforce because
the symptoms are very minimal and not prominent such as dyspepsia, full
feeling in the epigastrium and nausea especially after eating high-fat foods,
which sometimes disappear after belching. History of gallstones in the
family, recurrent jaundice and colic, local pain in the gallbladder area with
positive Murphy signs, can support the diagnosis.Differential diagnoses
such as fat intolerance, peptic ulcer, spastic colon, right colon carcinoma,
chronic pancreatitis, and koledokus duct abnormalities need to be
considered before deciding to do cholecystectomy.
 Etiology and pathogenesis
factors that influence the onset of attacks of acute cholecystitis are bile
stasis, bacterial infections, and gallbladder wall ischemia. the main cause
of acute cholecystitis is a gallbladder stone (90%) located in the cystic
duct which causes static bile, while a small number of cases arise without
the presence of gallstones (acute calculus cholecystitis). how static static
cystic duct can cause acute cholecystitis, is still unclear. it is estimated that
many influential factors, such as bile density, cholesterol, lysolesitin and
 money prostaglandins damage the mucous lining of the gallbladder wall
followed by inflammatory reactions and suppuration.Acute calculus acute
cholecystitis can occur in patients who are treated long enough and receive
nutrition parenterally, in obstruction due to gallbladder malignancy, stones
in the bile duct or is one of the complications of other diseases such as
typhoid fever and diabetes mellitus.
 Clinical Symptoms
a rather typical complaint for attacks of acute cholecystitis is the right
upper or epigastric stomach colic and tenderness and increase in body
temperature. sometimes the pain radiates to the right shoulder or scapula
and can last up to 60 minutes without subsiding. the severity of complaints
varies greatly depending on the presence of mild inflammatory
abnormalities up to gangrene or gallbladder perforation.on physical
examination palpable during the gall bladder, tenderness, accompanied by
signs of local peritonitis (Murphy's sign).jaundice is found in 20% of
cases, generally mild (bilirubin <4.0 mg / dl). if the bilirubin level is high,
it is necessary to think about adanta stones in the extra hepatic bile
duct.Laboratory examination shows the presence of leukocytosis and the
possibility of elevation of serum transaminases and alkaline phosphotase.
if complaints of pain increase with high temperature and shivering and
leukocytosis, the possibility of empyema and gallbladder perforation needs
to be considered.
 Diagnosis
Plain abdominal photographs cannot show a picture of acute cholecystitis.
only in 15% of patients is it possible to see opaque stones (radiopaque)
because they contain enough calcium.oral cholecystography cannot show
the gallbladder if there is obstruction so that this examination is not useful
for acute cholecystitis.ultrasound examination (USG) should be done
routinely and is very useful to show the size, shape, thickening of the
gallbladder wall, stones and extra hepatic bile ducts. the value of
sensitivity and accuracy of USG reaches 90% -95%.Bile duct scintigraphy
 uses radioactive substances HIDA or 99n Tc6 Iminodiaceticacied has a
value slightly lower than ultrasound but this technique is not easy. the
appearance of the choledococcal duct without the presence of gallbladder
in the examination of oral cholecystography or scintigraphy strongly
supports acute cholecystitis. abdominal CT scan is less sensitive and
expensive but is able to show the presence of a small pericolescopic
abscess that may not be seen on an ultrasound examination.a differential
diagnosis for sudden right upper abdominal pain that needs to be
considered such as spinal nerve pain, organ abnormalities under the
diaphragm such as the retrosecal appendix, intestinal obstruction,
perforation of the peptic ulcer, acute pancreatitis and myocardial
infarction.
 Anamnesis
Complaint of patient Severe pain in your upper right or center abdomen,
Pain that spreads to your right shoulder or back, Tenderness over your
abdomen when it's touched,Nausea, Vomiting, Fever.
 Physical Examination
On physical examination you can find fever, tachycardia, and pain in the
epigastric or right upper quadrant, often with a typical body position (as if
trying to protect a painful organ). Murphy sign can be found, the test is
specific but not sensitive for cholecystitis, where as a result of pain, an
inspiring pause occurs when the gallbladder touches the examiner's finger
during palpation of the right upper quadrant. The palpable gallbladder or
fullness of the right upper quadrant is found in 30-40% of cases. Jaundice
can be found in about 15% of patients.
 Supporting investigation
Oral cholecystography examination, ultrasonography and
colloangiography can show cholelithiasis and gallbladder function.
endoscopie retrograde choledochopancreaticography (ERCP) is very
useful for showing the presence of gallstones in the gallbladder and
koledokus duct.
 Treatment
Common treatments include complete rest, parenteral nutrition, a mild
diet, painkillers such as pethidine and antispasmodics. Antibiotic
administration in the early cloud phase is very important to prevent
complications of perionitis, cholangitis, and septicema. ampicillin,
cephalosporins and metronidazole are sufficient to kill germs that are
common in acute cholecystitis such as E. Coli, Strep. faecalis, and
klabsiella.when when the action of cholecystectomy is carried out it is
debatable whether it should be done as soon as possible (3 days) or waited
6-8 weeks after conservative therapy and the patient's general condition is
better as many as 50% of cases will improve without surgery. surgeons
who are pro-early surgery state that the emergence of gangrene and the
complications of failure of conservative therapy can be avoided, the
duration of hospital stay is shorter and costs can be reduced. while those
who disagree stated, early surgery will cause the spread of infection to the
peritoneal cavity and early surgical techniques will cause the spread of
acute inflammation around the duct to obscure anatomy.
 Prognosis
Spontaneous healing is found in 85% of cases, even though the gallbladder
becomes thick, fibrotic, full of stones and no longer functioning. not
infrequently recurrent cholecystitis. Sometimes acute cholecystitis
develops rapidly into gangrene, empyema, and perforation of the
gallbladder, fisistel, liver abscess or general peritonitis. This can be
prevented by providing adequate antibodies at the beginning of the attack.
Acute surgery in patients aged (> 75 years) has a poor prognosis in
addition to the possibility of many postoperative complications.
3.CHOLANGITIS
 Definition
Acute cholangitis is a morbid condition with acute
inflammation and infection in the bile duct.
 Pathophysiology
The onset of acute cholangitis involves two factors: (1)increased
bacteriain the bile duct, and (2) elevated intra-ductal pressure in the bile
duct allowing translocation ofbacteria or endotoxin into the vascular
and lymphatic system (cholangio-venous/lymphatic reflux). Because of its
anatomical characteristics, the biliary system is likely to be affected by
the elevated intraductal pressure. In acute cholangitis, bile ductules tend
to become more permeable to the translocation of bacteria and toxins with
the elevated intraductal biliary pressure. This process results in serious and
fatal infections such as hepatic abscess and sepsi.Historical aspect of
terminologySigns of hepatic feverHepatic fever was a term used forthe
first time by Charcot in his report published in 1887 [3].Intermittent fever
accompanied by chills, right upper quadrant abdominal pain, and
jaundice have been estab-lished as Charcot’s triad.Acute obstructive
cholangitis Acute obstructive cholan-gitis was defined by Reynolds and
Dargan [4] in 1959 as a syndrome consisting of lethargy or mental
confusion and shock, as well as fever, jaundice, and abdominal pain
caused by biliary obstruction. They indicated that emer- gency
surgical biliary decompression was the only effec-tive procedure for
treating the disease. These five symptoms were thus called Reynold’s
pentad.
 Causes and symptoms
As noted above, the two things that are needed for cholangitis to occur are:
1) obstruction to bile flow, and 2) presence of bacteria within the bile
ducts. The most common cause of cholangitis is infection of the bile ducts
due to blockage by a gallstone. Strictures (portions of ducts that have
become narrow) also function in the same way. Strictures may be due to
 congenital (birth) abnormalities of the bile ducts, form as a result of injury
to the bile duct (such as surgery, trauma), or result from inflammation that
leads to scar tissue and narrowing.The bacterium most commonly
associated with infection of the bile ducts is Escherichia coli (E. coli)
which is a normal inhabitant of the intestine. In some cases, more than one
type of bacteria is involved. Patients with AIDS can develop infection of
narrowed bile ducts with unusual organisms such as Cryptosporidium and
others.The three symptoms present in about 70% of patients with
cholangitis are abdominal pain, fever, and jaundice. Some patients only
have chills and fever with minimal abdominal symptoms. Jaundice or
yellow discoloration of the skin and eyes occurs in about 80% of patients.
The color change is due to bile pigments that accumulate in the blood and
eventually in the skin and eyes.Inflammation due to the autoimmune
disease primary sclerosing cholangitis leads to multiple areas of narrowing
and eventual infection. Tumors can block the bile duct and also cause
cholangitis, but as noted, infection is relatively infrequent; in fact
cholangitis occurs in only about one in six patients with tumors.Another
type of bile duct infection occurs mainly in Southeast Asia and is known
as recurrent pyogenic cholangitis or Oriental cholangitis. It has also been
identified in Asians immigrating to North America. Most patients have
stones in the bile ducts and/or gallbladder, and many cases are associated
with the presence of parasites within the ducts. The role of parasites in
causing infection is not clear. Many researchers believe that they are just
coincidental, and have nothing to do with the stones or infection.
 Diagnosis
The above symptoms alone are very suggestive of cholangitis; however, it
is important to determine the exact cause and site of possible obstruction.
This is because attacks are likely to recur, and different causes require
different treatments. For example, the treatment of cholangitis due to a
stone in the CBD is different from that due to bile duct strictures. An
elevated white blood count suggests infection, but may be normal in 20%
 of patients. Abnormal or elevated tests of liver function, such as bilirubin
and others are also frequently present. The specific bacteria is sometimes
identified from blood cultures.
 Anamnesis:
Previous biliary disorder cholangitis are asymptomatic. Complaints of
patiens Jaundice Fever, chills, and rigors,Abdominal pain, Pruritus,
Acholic or hypocholic stools, Malaise
 Physical examination :
Physical Examination In general, patients with cholangitis are quite ill and
frequently present in septic shock without an apparent source of the
infection : Fever (90%), although elderly patients may have no fever,
RUQ tenderness (65%), Mild hepatomegaly, Jaundice (60%),Mental status
changes (10-20%) Sepsis,Hypotension (30%),Tachycardia, Peritonitis
(uncommon, and should lead to a search for an alternative diagnosis).(14)
 Laboratory Examination :
1. CBC: Leukocytosis: In patients with cholangitis, 79% had a WBC
greater than 10,000/mL, with a mean of 13.6. Septic patients may be
leukopenic. Electrolyte panel with renal function may be performed.
2. Calcium level is necessary to check if pancreatitis, which can lead to
hypocalcemia, is a concern.
3. Expect liver function test results to be consistent with cholestasis,
hyperbilirubinemia (88-100%), and increased alkaline phosphatase
level (78%).
4 Aspartate aminotransferase (AST) and alanine aminotransferase (ALT)
levels are usually mildly elevated.
5. C-reactive protein level and erythrocyte sedimentation rate are typically
elevated. [5]
6. Blood cultures (2 sets): Between 20% and 30% of blood cultures are
positive. Many exhibit polymicrobial infections.
7. Biliary cultures (not performed in the ED): Send biliary cultures if the
patient has biliary drainage by interventional radiology or endoscopy
 Treatment
The first aim is to control the bacterial infection. Broad-spectrum
antibiotics are usually used. If the infection does not come under control
promptly, as noted by decrease in fever and pain, then other methods to
relieve the obstruction and infection will be needed. Either way, definitive
treatment of the cause of bile duct infection is the next step, and this has
undergone revolutionary changes in the past decade. Endoscopic,
radiographic and other techniques have made it possible to successfully
remove stones and dilate strictures that previously required surgical
intervention, often with high morbidity and mortality.
 Prognosis
The outlook for those with cholangitis has markedly improved in the last
several years due in large part to the development of the techniques
described above. For those patients whose episode of infection is caused
by something other than a simple stone, the future is not as bright, but still
often responsive to treatment. Some patients with autoimmune disease will
need liver transplantation.
 Prevention
This involves eliminating those factors that increase the risk of infection of
the bile ducts, mainly stones and strictures. If it is medically possible,
patients who have their gallbladder and suffer a bout of cholangitis should
undergo surgical removal of the gallbladder and removal of any stones.For
other patients, a variety of therapies as outlined above, including
dissolving small stones with bile acids are also available. A combination
of several of these methods is needed in some patients. Patients should
discuss the risks and alternatives of these treatments with their physicians.
(9)
6. explain prevention according to the scenario?
Prevention :
 Providing adequate antibiotics at the beginning of the attack to
prevent complications of peritonitis, cholangitis, and septicemia.
 Complete rest
 Parenteral nutrition
 Light diet
 Painkillers such as pethidine and antispasmodics
 Reduce eating foods containing betacarotine (such as squash,
melon, papaya, and carrots). (6)
Handling:
a. Exchange transfusion
reduce bilirubun levels and replace hemolytic blood.Indications: in
the case of indirect bilirubin levels ³ 20 mg / dL or if it cannot be
treated with phototherapy, rapid increase in biirubin is 0.3 -1 mgz /
hour, severe anemia in neonates with symptoms of heart failure, or
infants with Hb levels 14 mgz umbilical cord and positive direct
coombs test.
7.islamic perspective on the scenario?

Prophet Muhammad sallallaahu 'alaihi wa sallam said:

(‫البردة )البردة داء كل صل‬: ‫التخمة‬: ‫الصغير الجامع في السيوطي الحافظ أخرجه‬
"The source of all diseases is al-baradah." Al-baradah: at-Tukhmah (Poor
digestion of food) (narrated by Imam al-Hafizh as-Suyuthi rahimahullah in
al-Jaami 'ash-Shaghiir)
Basically, self-originating diseases do not originate from viruses, bacteria,
germs, mosquitoes, cell mutations and other viruses or bacteria that are
rampant in the body when sick are not as a result.So the source of the
disease is human actions themselves through our daily behavior that is less
praiseworthy before Allah SWT, unfavorable character makes the angel
Ratib record and report it before Allah SWT. where it has been going on
for years or even decades so that finally Allah decreases disaster in the
form of a disease as a warning to his people to immediately return to its
path Word of Allah swt
"And whatever changes happen to you are caused by the creation of your
own hands and Allah forgives as much of your mistakes. And you do not
let go (of the punishment of Allah) on the face of the earth and you do not
get a protector or helper besides Allah ".
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Hyperbilirubinemia. Field. University of Northern Sumatra(2)

4. https://www.ncbi.nlm.nih.gov/pmc.(3)

5. [price,sylvia Anderson.2015.patofisiologi.jakarta:egc].(4)

6. Figure 1. Flow of management of acute cholangitis according to Tokyo

Guidline 2013].(5).

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edition V. Jakarta: Interna Publishing.(6)

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10. https://medical-dictionary.thefreedictionary.com/cholangitis.(9)

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