CHAPTER I

INTRODUCTION

1.1 Issue Background

Digestif system is the eleventh block in the fourth semester of the Medical
Education Competency Based Curriculum in the Faculty of Medicine,
Muhammadiyah Palembang. Tutorial is an implementation of Problem Based
Learning (PBL). The tutorial process is divided into 10 groups of 11 people
who are guided by a lecturer / tutor as a facilitator to solve existing cases.
From the Problem Based Learning (PBL) program, students are able to
learn actively and independently, also design learning processes effectively.
The tutorial process is divided into 2 sessions and 1 tutorial plenary
discussion. In session 1, students are asked to classify terms, to find
hypotheses. Then, in session 2, students were asked to be able to submit
arguments and make conclusions together. At the end of the week, a plenary
tutorial will be held where students are given the opportunity to express their
opinions in front of experts in their fields.

1.2 Purpose and Objectives

The purpose and objectives of this case study tutorial, namely:
1. As a report task group tutorial that is part of KBK learning system at the
Faculty of Medicine, Muhammadiyah University of Palembang.
2. Can solve the case given in the scenario with the method of analysis and
learning group discussion.
3. Achieving the objectives of the tutorial learning method.
 CHAPTER II
DISCUSSION

2.1 Tutorial Data

Tutor : dr. Wieke Anggraini
Moderator : M. Amaruna Sahona
Secretary of table : Tasya Salsabila
Secretary of board : Mutiara Irma Khairunnisa
Day and Date : Monday, March 30th 2020
13.00 – 14.45 pm
Wednesday, April 01th 2020
13.00 – 14.45 pm
Rule of Tutorial :
1. Mutual respect among fellow tutorial participants
2. It is forbidden to eat and drink during the tutorial
3. Using good and proper communication

2.2 Case Scenario

“YELLOWISH EYE”

Ms. F, a 45 years old female came to the emergency department with a

chief complain of yellowish eyes since 7 days ago. The complain also followed
with an urine that colored like dark tea, but it was not followed with white fecal
matter and itchy skin since two weeks ago. Ms. F also complains of feeling limp,
epigastric pain and reduced appetite. Since two month ago, Ms. F also
experiencing a pain on her right upper abdomen that radiates to the right shoulder,
that was felt especially after consuming fatty food, with a pain duration lasting
about 10-15 minutes and dissapear all by itself.

Ms. F didnt have history of consuming drugs on a long period of time, and
Ms. F have medical history of contracting Hepatitis B since birth.
Physical Examination:

General Appearance: looks moderately sick, conciousness compos mentis.

Vital Sign: BP 110/80 mmHg; Pulse 80x/m; RR 22x/m, Temp 36,8oC.

BW 75 kg, BH 158 cm.

Specific Examination:

Head : Pale conjungtive (-/-), Icteric Sclera (+/+)

Neck : JVP 5-2 cmH2O, theres no enlargement on the neck

Thorax :

Thorax wall: Spider Naevy (+)

Pulmo:

- Inspection: symetric static and dynamic

- Palpation: same stem fremitus left and right
- Percussion: sonor on the whole lung
- Auscultation: vesikuler (+/+). Ronkhi (-/-), wheezing (-/-)
Cor:

- Inspection: flat, ictus cordis (-)

- Palpation: ictus cordis were not palpable
- Percussion; normal heart border
- Auscultation: HR 80x/m, reguler, heart sound I-II normal
Abdoment :

- Inspection: flat, caput medusa (-).

- palpation: supple, Murphy sign (-), hepar were not palpable, lien S1,
ballotement (-)
- Percussion: shifting dullness (+)
- Auscultation: normal bowel sound
Ekstremity : edema pretibia (+), palmar eritem (+).

Laboratory Examination:

- Hb 12,3 g/dl
- Ht 36 vol %
- Leukosit : 8.600/mm3
- Trombosit 90.000/mm3
- LED : 10 mm/hour
- Bil tot : 8,2 mg/dl
- Bil direk : 7,6 mg/dl
- Bil indirek : 0,6 mg/dl
- SGOT : 102 u/L
- SGPT : 115 u/L
- Fosfatase alkali : 110 u/L
- HBs Ag (+)
- Albumin 2,8 mg/d

Urinalysis: bilirubin urin (+)

USG Examination:
2.3 Clarification of Terms
No. Term Meaning
1 Spider naevy A dilation of arteiol arteries in an outward
direction
2 Ballotement A sign that an object is floating or floating in
liquid
3 Icteric Sclera Yellowish color of the eyeball due to
hyperbilirubinemia and deposition of bile
pigments
4 Murphy sign A inspection at quadrant right above abdominal
for diagnose kolesistitis
5 Albumin A plasma protein that is soluble in water and
also in a salt solution of moderate concentration
6 White fecal The absence of a color of bile that is coloring
matter fecess
7 Hepatitis Hepatitis is inflammation of the liver usually
transmitted through oral ingestion but can also
be transmitted parenterally
8 Yellowish eyes A white part of eye which called as sklera turn
on become yellow color because of excessively
high level of bilirubin in the blood
9 Palmar eritemia Redness of the skin of the palm of the hand
produced by capillary congestion
10 Caput medusa A plexus of dilated veins around the umbilicus,
seen in patients with portal hypertension
(usually as a result of cirrhosis of the liver)
11 HBs Ag HBs Ag or hepatitis B Supace antigen is the
hepatitis B virus surface antigen
12 SPGT Glutamic transmilase serum is an enzyme that is
normally found in serum and body tissue

5
 especially in the liver.
13 SGOT SGOT or serum gluamic oxaluasetic
transaminase is an enzyme that is usually
present in body tissues, especially in the heart
and liver, this enzyme is released into the serum
as a result of tissue injury
14 Edema pretibia Abnormal fluid collection in the intercellular
space of the body in the pretibia.
15 Bilirubin Bile pigments resulting from heme breakdown
and biliverdin reduction.
16 LED Sedimentation rate (LED) is the speed of red
blood cells settling in the test tube in units of
mm / hour.
17 Lien S1 Enlarged spleen that is palpated in the schuffner
line 1
18 Composmentis Fully aware
19 Bilirubin total The result of direct billirubin and indirect
bilirubin
20 Bilirubin indirek Bilirubin that has not been conjugated by the
liver with glucoranic acid
21 Shifting dullness A sign of free peritoneal fluid where in abdomen

2.4 Identification of Problem

1. Ms. F, a 45 years old female came to the emergency department with a
chief complain of yellowish eyes since 7 days ago. The complain also
followed with an urine that colored like dark tea, but it was not followed
with white fecal matter and itchy skin since two weeks ago. Ms. F also
complains of feeling limp, epigastric pain and reduced appetite.
2. Since two month ago, Ms. F also experiencing a pain on her right upper
abdomen that radiates to the right shoulder, that was felt especially after

6
 consuming fatty food, with a pain duration lasting about 10-15 minutes
and dissapear all by itself.
3. Ms. F didnt have history of consuming drugs on a long period of time, and
Ms. F have medical history of contracting Hepatitis B since birth.
4. Physical Examination:
General Appearance: looks moderately sick, conciousness compos mentis.
Vital Sign: BP 110/80 mmHg; Pulse 80x/m; RR 22x/m, Temp 36,8oC. BW
75 kg, BH 158 cm.
Specific Examination:

Head : Pale conjungtive (-/-), Icteric Sclera (+/+)

Neck : JVP 5-2 cmH2O, theres no enlargement on the neck

Thorax :

Thorax wall: Spider Naevy (+)

Pulmo:

- Inspection: symetric static and dynamic

- Palpation: same stem fremitus left and right
- Percussion: sonor on the whole lung
- Auscultation: vesikuler (+/+). Ronkhi (-/-), wheezing (-/-)
Cor:

- Inspection: flat, ictus cordis (-)

- Palpation: ictus cordis were not palpable
- Percussion; normal heart border
- Auscultation: HR 80x/m, reguler, heart sound I-II normal
Abdoment :

- Inspection: flat, caput medusa (-).

- palpation: supple, Murphy sign (-), hepar were not palpable, lien
S1, ballotement (-)

7
 - Percussion: shifting dullness (+)
- Auscultation: normal bowel sound
Ekstremity : edema pretibia (+), palmar eritem (+).

5. Laboratory Examination:
- Hb 12,3 g/dl
- Ht 36 vol %
- Leukosit : 8.600/mm3
- Trombosit 90.000/mm3
- LED : 10 mm/hour
- Bil tot : 8,2 mg/dl
- Bil direk : 7,6 mg/dl
- Bil indirek : 0,6 mg/dl
- SGOT : 102 u/L
- SGPT : 115 u/L
- Fosfatase alkali : 110 u/L
- HBs Ag (+)
- Albumin 2,8 mg/d

Urinalysis: bilirubin urin (+)

USG Examination:

8
2.5 Priority of problem
The priority problem is in the 1st identification, the reason is if this case not
managed quickly and properly will increase mortality and mordibity

2.6 Analysis and Synthesis of Problem

1. Ms. F, a 45 years old female came to the emergency department with a
chief complain of yellowish eyes since 7 days ago. The complain also
followed with an urine that colored like dark tea, but it was not followed
with white fecal matter and itchy skin since two weeks ago. Ms. F also
complains of feeling limp, epigastric pain and reduced appetite.
a. What is the system and organs in this case?
Answer :
Hepatobiliary system
Organs involved:
- Hepar
- Gallbladder
- Biliary tract
b. What is the anatomy, physiology and histology of the case ?
Answer :
Anatomy

Picture 1. Anatomy Gallblader

(Snell, 2014)

9
The gallbladder is entirely surrounded by peritoneum, and is in direct
relation to the visceral surface of the liver.
It lies in close proximity to the following structures:
Anteriorly and superiorly – inferior border of the liver and the anterior
abdominal wall.
Posteriorly – transverse colon and the proximal duodenum.
Inferiorly – biliary tree and remaining parts of the duodenum.
The gallbladder has a storage capacity of 30-50ml and, in life, lies
anterior to the first part of the duodenum. It is typically divided into
three parts:
Fundus – the rounded, distal portion of the gallbladder. It projects into
the inferior surface of the liver in the mid-clavicular line.
Body – the largest part of the gallbladder. It lies adjacent to the
posteroinferior aspect of the liver, transverse colon and superior part of
the duodenum.
Neck – the gallbladder tapers to become continuous with the cystic
duct, leading into the biliary tree.
The neck contains a mucosal fold, known as Hartmann’s Pouch.
This is a common location for gallstones to become lodged, causing
cholestasis.

Picture 2. Anatomy Gallblader

(Snell, 2014)

10
The Biliary Tree
The biliary tree is a series of gastrointestinal ducts allowing newly
synthesised bile from the liver to be concentrated and stored in the
gallbladder (prior to release into the duodenum).
Bile is initially secreted from hepatocytes and drains from both lobes
of the liver via canaliculi, intralobular ducts and collecting ducts into
the left and right hepatic ducts. These ducts amalgamate to form
the common hepatic duct, which runs alongside the hepatic vein.
As the common hepatic duct descends, it is joined by the cystic duct –
which allows bile to flow in and out of the gallbladder for storage and
release. At this point, the common hepatic duct and cystic duct
combine to form the common bile duct.
The common bile duct descends and passes posteriorly to the first part
of the duodenum and head of the pancreas. Here, it is joined by the
main pancreatic duct, forming the hepatopancreatic
ampulla (commonly known as the ampulla of Vater) – which then
empties into the duodenum via the major duodenal papilla. This papilla
is regulated by a muscular valve, the sphincter of Oddi.

11
 Picture 3. Anatomy Liver (Ventral and Dorsal )

(Drake et.al, 2012)

The liver is the largest organ in the body. Textured hepar soft and
supple, also located at the top of the abdominal cavity just below the
diaphragm. Most of the located under the arcus costalis dexter, and
diaphragm right half of liver broken from pleura, lung pericardium and
heart. The liver is stretching left to reach the left half diaphragm. Top
surface the curved liver under the arched diaphragm dome.The
posteroinferior, or visceral, surface forms the mold attractive viscera,
therefore the shape becomes irregular. This surface is related to pars
esophageal abdominal, gastric, duodenal, flexura coli dextra, ren
dexter and derartra suprarenalis glands, and vesica biliaris (Snell,
2014).

12
The liver can be divided into large dexter lobes and lobes small sinister
by attachment of the peritoneum by the ligament falciforme. The
dexter lobes are subdivided into lobes quadratus and lobes caudatus by
the presence of vesica biliaris, fissura for ligament teres hepatis,
inferior vena cava, and fissure for the ligamentum venosum. Research
shows that at in fact the quadratus lobe and the caudatus lobe
constitute functional part of the sinister hepatic lobe. So the dextra
branch and sinistra arteria hepatica and portal vein, and ductus
hepaticus dexter and sinister take care of the dexter and lobes
respectively sinister (including the quadratus lobe and caudatus lobe).
Porta hepatis, or hepatic hilar, is on the surface.

posteroinferior, and is located between the caudatus lobe and lobe

quadratus. The top of the free tip is omentum minus attached to the
edge of the hepatic port. In this place, there is ductus hepatlcus dexter
and sinister, dextra branch and sinistra.

artery hepatica, portal vein, and sympathetic nerve fibers and

parasympathetic Here are a few liver lymph glands. This gland holds
liver lymph fluid and gallbladder, and send efferent fibers to nodi
lymphoidei celiaci (Snell, 2014).

The whole liver is surrounded by fibrous capsules, only partially

covered by peritoneum. The liver is composed of lobules hepatic. The
central vein in each lobule empties to the vein hepaticae. In the room
between the lobules there are hepal canal, which contains branches of
arteria hepatica, portal vein, and a branch of the ductus choledochus
(hepatic triad). Arterial and venous blood travel between cells the liver
through the sinusoid and flow into the central vein (Snell, 2014).

The falciform ligament, which is a double fold of the peritoneum, runs

upwards from the umbilicus to the liver. This ligament has a free
shaped edge crescent and contains lepament teres hepatis which is the

13
umbilical vein side. The falciform ligament travels to the surface of the
anlgrior and then to the superior surface of the liver and finally divides
into two layers. The right layer forms the upper layer of the coronary
ligament; left layer forms the upper layer of the triangulare ligament
synistrum. The right portion of the coronary ligament is known as the
triangulare dextrum ligament. The hepatic ligarnentum runs into the
fissures found in the hepatic visceralis facies and joins the branches of
the portal venous hepatic sinistra (Snell, 2014).

Ligamentum venosum (ligamentum of Arantius), a fibrous band which

is a remnant of the ductus venosus, attaches to the portal venous
sinistra branch and travels upwards in the fissure on the hepatic
visceral surface, and above attaches to the inferior vena cava (Snell,
2014).

Liver are supply by Arteria hepatica propria, arteria celiaca branch

(truncus celiacus), ends by branching into ramus dexter and sinister
that entered into the porta hepatis. Liver also supply portal vein The
portal vein ends by branching into a dexter branch and sinister that
enters the hepatic porta behind the arteries. Venae hepaticae (three or
more) arise from the posterior surface hepatic and empties into the
inferior vena cava (Snell, 2014).

Physiology
The gallbladder is a pear-shaped, hollow structure located under the
liver and on the right side of the abdomen. Its primary function is to
store and concentrate bile, a yellow-brown digestive enzyme produced
by the liver. The gallbladder is part of the biliary tract.
The gallbladder serves as a reservoir for bile while it’s not being used
for digestion. The gallbladder's absorbent lining concentrates the
stored bile. When food enters the small intestine, a hormone called

14
cholecystokinin is released, signaling the gallbladder to contract and
secrete bile into the small intestine through the common bile duct.

Histology

The inner surface of the gall bladder is covered by the mucosa. The
sufrace is made up of a simple columnar epithelium. The epithelial
cells have microvilli, and look like absorptive cells in the intestine.
Underneath the epithelium is the lamina propria. The wall of the
bladder does not have a muscularis mucosae and submucosa.

The muscularis externa (muscle layer) contains bundles of smooth

muscle cells, collagen and elastic fibres. Underneath this, on the
outside of the gall bladder is a thick layer of connective tissue, which
contains large blood vessels.

Cells in the liver include: hepatocytes, endothelial cells, and

macrophage cells which are referred to as kuppfer cells, and ito cells
(fat storage cells). Hepatocyte cells radiate in the liver lobules and
form layers of 1-2 cells similar to a brick arrangement. This cell plate
leads from the edge of the lobules to its center and anastomoses freely
forming labyrinthine and foam structures. The gaps between these
plates contain capillaries called liver sinusoids (Junquiera et al., 2017).

Liver sinususoid is a winding and widened channel, irregular in

diameter, coated with multilevel endothelial cells that are not intact.
Sinusoid is limited by 3 kinds of cells, namely endothelial cells
(majority) with dark flat nuclei, phagocytic kupffer cells with ovoid
nuclei, and stellate cells or Ito cells or hepatic lipocytes that function to
store vitamin A and produce extracellular matrix and collagen. Blood
flow in sinusoids comes from the terminal branches of the portal vein
and hepatic arteries, carrying nutrient-rich blood from the digestive
tract and also rich in oxygen from the heart (Eroschenko, 2012;
Junqueira et al., 2017).

15
 Portal tracts are located in hexagonal corners. In the portal tract, blood
from the portal vein and hepatic artery is directed to the central vein.
The portal tract consists of 3 main structures called portal triads. The
largest structure is the terminal portal venules bounded by flat
endothelial cells. Then there are arterioles with thick walls which are
the terminal branches of the hepatic artery. And the third is the bile
ducts that drain bile. In addition to the three structures, lymphatics are
also found (Junqueira et al., 2017).

Picture 4. Histology of Liver

(Junqueira et al., 2017).

c. What is the relation between age and gender?

Answer :

16
 Gender :
Women have a 3-fold risk of getting gallstones compared to men. This
is because the hormone estrogen influences the increase in cholesterol
excretion by the gallbladder. Pregnancy, which increases estrogen
levels also increases the risk of gallstones. The use of contraceptive
pills and hormone therapy (estrogen) can increase cholesterol in the
gallbladder and decrease the activity of emptying the gallbladder.
Age :
The risk of getting gallstones increases with age. People> 60 years are
more likely to get gallstones than younger people. Bile becomes more
lithogenic as you get older (Balzer et al., 2017).
d. What the meaning Ms. F, a 45 years old female came to the emergency
department with a chief complain of yellowish eyes since 7 days ago?
Answer :
The meaning is, in this case Ms. F had jaundice or icteric which is a
yellow discoloration of the body tissue resulting from the
accumulation of an excess of bilirubin in the blood circulation. Sclerae
have a high affinity for bilirubin due to their high elastin content.
e. What is patophysiology of yellowish eyes ?
Answer :
Distruption of the formationa bilirunin → Increase bilirubin in the
blood vessels → Change the color of the elastin tissue → Yellowish
eye (Price, 2012).
f. What possibly disease of yellowish eye?
Answer :
1. Cirrhosis of the liver
Liver serosis is scar tissue in the liver caused by long-term and
continuous liver damage. Scarring replaces healthy tissue in the
liver and prevents the liver from working properly.

17
 2. Gallstones
The liver produces bile that is collected in the gallbladder and
flowed through the bile ducts. The gallbladder is responsible for
releasing bile to help the body digest fat. A person can experience
jaundice if the bile duct is blocked. The blockage can be caused by
several things, including gallstones
3. Pancreatic disorders
Pancreatic ducts and bile ducts unite to flow into the small intestine.
If the pancreatic duct is blocked, bile may not flow properly and
jaundice can occur. Pancreatic cancer and inflammation of the
pancreas can cause this blockage to occur
4. Blood disorders
Yellow eyes can also be caused by abnormalities in red blood cells
so they break easily. Blood disorders that can make yellow eyes
include hemolytic anemia (early destruction of red blood cells),
which can be caused by drugs, reactions due to mismatched blood
transfusions, or sickle cell anemia (Sudoyo, 2014).
g. What the etiology of the yellowish eye?
Answer :
- Prehepatic phase, the main cause of increased formation of
bilirubin. Usually found in infectious diseases (malaria, typhus,
etc.), defects from erythrocytes (familial hemolytic, sickle cell
anemia, pernicious anemia, etc.).
- Intrahepatic phase, the causes of hepatic jaundice include hepatitis
(due to viruses, bacteria, parasites), liver cirrhosis, tumors (primary
and secondary carcinomas, sarcomas, etc.), chemicals (phosphorus,
arsenic, syncope), etc.
- Post hepatic phase, the cause is gallstones, carcinoma of the
gallbladder, or carcinoma of the ampulla Vateri. As a result of the
blockage above, there is bile retention in the gall bladder. Over

18
 time the bile will enter the bloodstream resulting in increased
(conjugated) plasma bilirubin.
- Production of bilirubin. The increasing
Increased production of bilirubin often occurs due to excessive
destruction of red blood cells .
Decreased speed of absorption of bilirubin by sel liver cells
Some genetic agility such as Gilbert syndrome and some types
of medications can lead to decreased absorption of bilirubin by
sel livercells.
- Bilirubin conjugation disorder
The disruption of the bilirubin jonjugation may occur when there
is a deficiency or absence of a transkoronyl transferase
mislanya enzyme , such as the effect of drugs or on kelaianan
Genetic insufficiency such as Crigler-Najjar syndrome .
- Gengguan bilirubin expenditure
Bilirubin spending disorders can occur in liver or hepatic cell
damage or bile duct obstruction in the liver or outside the liver.
(kanoko,2012)
h. What the meaning of The complain also followed with an urine that
colored like dark tea, but it was not followed with white fecal matter
and itchy skin since two weeks ago?
Answer :
Urine like the old shows the occurrence of conjugated
hyperbilirubinemia so that one of the compensation of the body to
reduce the number of conjugated bilirubin is by removing renal
dysfunction in the form of urine. This is what caused the old color of
the urine to arise.
While not followed by a such as Putty shows 2 possibilities, namely
the absence of ductus choledocus or there is a partial blockage in the
ductus choledocus. The most possible in this case is that there is partial
blockage in the ductus choledocus. Because blockages are partial,

19
 bilirubin from the gallbladder can still enter the gastrointestinal tract so
that it can be converted into Sterkobilin and give color to the stool.
i. What is correlation between yellowish eyes since 7 days ago followed
by colored urine like black tea but it was not followed with white fecal
matter and itchy skin since two weeks ago?
Answer :
Ms. F didn’t have total obstruction bile tract, Ms. F only have icterus
intrahepatic. If obstruction happend Ms. F have sign with fecal matter
and itchy skin because there are blockage of bile duct like
choledocolitiasis, cholecystitis and etc. And also no strecobilin
coloring the stool and there are pruritus (itchy skin) (Price, 2012).
j. What is the etiology urine that colored like dark tea?
Answer :
Drug, pregnancy, operation, cystic fibrous, infection or sepsis, gilbert
sindrome, dubin-johnson syndrome and rotor syndrome, autoimun
disease, hepatocecullar disease, biliary tract disease, intra or extra
cholestasis, hepatitis virus or alkaholic.
k. How is the patophisiology of urine that colored like dark tea, feeling
limp, epigastric pain and reduced appetite?
Answer :
Risk Factor Infection of Chronic injury to the
Hepatitis B Virus hepatocytes cell in hepar

Cirrhosis Hepatic Fibrosis and Scarring

Decreased intrahepatic Portal Hypertension Metabolic disorder

excretion of billirubin (metabolism of carbohydrates,
proteins, and lipids)
Increase in splenic blood
Accumulation of an flow
excess of bilirubin in the Energy produced will
blood circulation perifer not be maximal
+ albumin
20
 Splenomegaly

Feeling
Secreted through urine Supress gastric limp

Epigastric Reduced
Urine colored like dark pain appetite
tea

(Huether, 2017)

l. What is possibly disease of feeling limp, epigastric pain and reduced

appetite in the case?
Answer :
The possibly disease of symptoms are clinical manifestation of
cirrhosis hepatic. The symptom include feeling limp, epigastric pain,
reduce appetite, vomitting and nausea, dyspepsia, anorexia and change
pattern of defecation (Nurdjanah, 2017).
m. What is possible disease with all complaint?
Answer :
- Hepatic cirrhosis
- Cholestasis intrahepatic
- Extrahepatic choestatis

2. Since two month ago, Ms. F also experiencing a pain on her right upper
abdomen that radiates to the right shoulder, that was felt especially after
consuming fatty food, with a pain duration lasting about 10-15 minutes
and dissapear all by itself.
a. what the meaning of Since two month ago, Ms. F also experiencing a
pain on her right upper abdomen that radiates to the right shoulder, that
was felt especially after consuming fatty food, with a pain duration
lasting about 10-15 minutes and dissapear all by itself.?
Answer :

21
 The meaning these complaints are clinical manifestations of
cholelithiasis, and complaints are felt when consuming fatty foods
because in the duodenal mucosa, there is the hormone peptide
cholecystokinin (CCK). This hormone is released from the duodenal
mucosa in response to ingestion of fats and amino acids, and indicates
it is chronic (Anthony, 2008).
b. how is the pathophysiology of pain on her right upper abdomen that
radiates to the right shoulder?
Answer:
Pain on her right upper abdoment, shoulder usually called as biliarry
colic, the gallbladder contraction in response to some from of
stimulation , forcing a stone through the gallbladder into the cysctic
duct opening, leading to increased gallbladder wall tension and
pressure which often result in pain, pain radiates the right shoulder
because of it’s dermatome nerves in T7 and T10 side nerves.

Pain (There is a gallstone clogging the ductus sisticus, the duct biliaris
comunis temporary) → pressure biliaris duct ↑ → ↑peristaltic
contractions in place of blockage → inflammation and irritation of
peritoneum Parietale Subdiafragmaticus by N. Phrenicus (C 3, 4, 5)
→ Viscera in the epigastric region → the interluding to the back
(Nervi supraclavikularis C 3.4) (Price, 2012).

Partial → blockages in the duct distention → of the duct increase in

the in or intraduktal pressure in the proximal → side of the smooth
muscles in contraction duct to remove the stone from the duct
→ damaged or depressed cells due to increased in pressure removing
substance P (bradikinin, prostaglandins, or peptide compounds) →
trigger free nerves (n. Frenikus and Splanknicus) to awaken potential
→ Action potential actions forwarded to The section Cornu tabes
dorsalis cord spinal cord by the nerve fibers of the afferent → fibers of

22
 the afferent nerve is associated with other spinal cord fibers (skin, etc.)
→ Pain response is transmitted to the brain → pain perception in
disturbed visceral organs and dermatomics → upper right quadrant
pain that propagated to the right Shoulder (Kowalak, 2017).

c. What the relationship of the main complaint with the experiencing a

pain on her right upper abdomen that radiates to the right shoulder in
the case?
Answer :
The relationship of eating fatty foods with complaints of upper right
abdominal pain that spreads to the back is the occurrence of biliary
colic. Where if the cystic duct or communist bile duct is blocked for a
moment by a stone, the pressure increases in the bile duct and
increased peristaltic contractions in the obstruction region cause severe
visceral pain in the epigastric region, possibly spreading to the back,
and vomiting (Silbernagl, 2017).
d. What is the risk factor of a pain on right upper abdomen?
Answer :
A pain on right upper abdomen can caused by formed gallstone. Some
risk factor for the development of cholesterol gallstones are obesity,
age, female gender, pregnancy, genetic, total parentral nutrition, rapid
weight loss and certain medication ( oral contraceptives , clofibrate and
somatostatin anlogs) (Chung and duck, 2018).
e. What the etiology experiencing a pain on her right upper abdomen that
radiates to the right shoulder?
Answer :
- Organ strain / distension (intestine obstruction, gallstone, liver
swelling due to hepatitis).
- Colic pain (obstruction of the ductus choledocus or
coledocholithiasis)
- Neoplasm

23
 - Infection
- Stress
- Trauma
(Katz, J. 2016).
f. What are the possible disease with a chief complain of pain on her
right upper abdomen that radiates to the right shoulder?
Answer :
- Gallstone
- Liver or Pancreas issues
- Gastritis
- Muscle Pain
- Appendicitis
- Bowel Obstruction
- Diverticular disease
(Jennifer, 2015).
- Vesicca fellea (cholecystitis, cholangitis, cholestasis,
cholesterolothesis, choletiasis)
- Liver (Hepatitis, Liver abscess, Liver cirrhosis, Neoplasm)
- Pancreas (Pancreatitis)
(Greenberger NJ & Gustav P, 2015).
g. How pathofisilogy of pain will increase, especially after consuming
fatty food?
Answer :
Pain on her right upper abdoment, shoulder usually called as biliarry
colic, when consume fatty food so in normally body will increase CCK
hormone and through it out to the duodenum lumen after that it will
stimulate muscle of gallbladder with directly as a positif feedback in
normally condition because of compensation. When in the gallbladder
has one or some stone so the gallbladder contraction forcing a stone
through the gallbladder into the cysctic duct opening, leading to
increased gallbladder wall tension and pressure which often result in

24
 pain, pain radiates the right shoulder because of it’s dermatome nerves
in T7 and T10 side nerves (Snell, 2014).

3. Ms. F didnt have history of consuming drugs on a long period of time, and
Ms. F have medical history of contracting Hepatitis B since birth.
a. What the meaning of Ms. F didnt have history of consuming drugs on
a long period of time, and Ms. F have medical history of contracting
Hepatitis B since birth ?
Answer :
The meaning of Ms. F didnt have a history of consuming drugs on a
long period of time is to exclude the etiology of the complaints are the
result of the consumption of drugs in the long term that will cause
disruption through the membrane of hepatocytes bilirubin transferes
that cause bilirubin retention in the cell (Price, 2012).
The meaning of Ms. F have medical history of contracting Hepatitis B
since birth is intoxication Hepatitis B can be the etiology of
inflamation in liver cells that cause necrosis covering a wide area
(hepatocellular) (Kowalak, 2017).
b. What the relationship of the main complaint with the history of
consuming drugs on a long period of time, and Ms. F have medical
history of contracting Hepatitis B since birth. ?
Answer :
possible symptoms / illness experienced due to a history of chronic
hepatitis b virus (HBV) infection which can cause cirrhosis of the
liver. under normal circumstances, damaged liver cells will be
replaced with scar tissue. the more severe the damage, the greater the
scar tissue that forms and the less the number of healthy liver cells, so
that there can be a decrease in liver function (Sjamsuhidayat & De
Jong. 2014).
c. how the transmission of hepatitis ?
Answer :

25
 In highly endemic areas, hepatitis B is the most commonly spread
from mother to child at birth (perinatal transmission), or through
horizontal transmission (exposure to infected blood), especially from
an infected child to an uninfected child during the first 5 years of life.
The development of chronic infection is very common in infants
infected from their mothers or before the age of 5 years.
Hepatitis B is also spread by needlestick injuries, tattooing, piercing
and exposure to infected blood and body fluids, such as saliva and,
menstrual, vaginal, and seminal fluids. Sexual transmission of
hepatitis B may occur, particularly in unvaccinated men who have sex
with men and heterosexual persons with multiple sex partners or
contact with sex workers.
Infection in adulthood leads to chronic hepatitis in less than 5% of
cases, whereas infection in infancy and early childhood leads to
chronic hepatitis in about 95% of cases. Transmission of the virus
may also occur through the reuse of needles and syringes either in
health-care settings or among persons who inject drugs. In addition,
infections can occur during medical, surgical and dental procedures,
through tattooing, or through the use of razors and similar objects that
are contaminated with infected blood (WHO, 2019).

4. Physical Examination:
General Appearance: looks moderately sick, conciousness compos mentis.
Vital Sign: BP 110/80 mmHg; Pulse 80x/m; RR 22x/m, Temp 36,8oC. BW
75 kg, BH 158 cm.
Specific Examination:

Head : Pale conjungtive (-/-), Icteric Sclera (+/+)

Neck : JVP 5-2 cmH2O, theres no enlargement on the neck

Thorax :

26
 Thorax wall: Spider Naevy (+)

Pulmo:

- Inspection: symetric static and dynamic

- Palpation: same stem fremitus left and right
- Percussion: sonor on the whole lung
- Auscultation: vesikuler (+/+). Ronkhi (-/-), wheezing (-/-)
Cor:

- Inspection: flat, ictus cordis (-)

- Palpation: ictus cordis were not palpable
- Percussion; normal heart border
- Auscultation: HR 80x/m, reguler, heart sound I-II normal
Abdoment :

- Inspection: flat, caput medusa (-).

- palpation: supple, Murphy sign (-), hepar were not palpable, lien
S1, ballotement (-)
- Percussion: shifting dullness (+)
- Auscultation: normal bowel sound
Ekstremity : edema pretibia (+), palmar eritem (+).

a. How is the physical examination and specific interpretation?

Answer :
NO The case normal level Interpretation
1 General Painless Hypoxia
appearance : looks Compos mentis Normal
moderately sick,
conciousness
composmentis.
2 BP : 110/80 Sistole : 90-120 Normal
mm/Hg mmHg

27
 Diastole : 60-90
mmHg
3 Pulse : 80 x/menit 60-100 x/menit Normal
4 RR : 22 x/menit 16-24 x/menit Normal
5 T : 36,80C. 36,5 – 37,5oC Normal
6 BW : 75 kg Hyperlipidemia or
BH : 158 cm over weight
IMT : 30,04
7 Head :
Pale conjungtive Pale conjungtive (-/-) Normal
(-/-)
Icteric sclera (+/+) Icteric sclera (-/-) Hyperbilirubinemia
8 Neck :
JVP 5-2 cmH2O, JVP 5-2 cmH2O, Normal
Theres no Theres no
enlargement on the enlargement on the
neck neck
9 Thoraks:
Thorax wall : Abnormal
spider nevi (+), spider nevi (-)
Pulmo :
Inspection : Inspection : symetric
symetric static and static and dynamic Normal
dynamic
Palpation : same Palpation : same
stem fremitus lef stem fremitus lef and
and right right
Percussion : sonor Percussion : sonor on
on the whole lung the whole lung
Auscultation : Auscultation :

28
 vesikuler (+/+), vesikuler (+/+),
ronkhi (-/-), ronkhi (-/-),
wheezing (-/-) wheezing (-/-)

10 Cor :
Inspection : flat, Inspection : flat,
ictus cordis (-) ictus cordis (-) Normal
Palpation : ictus Palpation : ictus
cordis were not cordis were not
palpable palpable
Percussion : Percussion : normal
normal heart heart border
border
Auscultation : HR Auscultation : HR
80x/m, reguler, 80x/m, reguler, heart
heart sound I-II sound I-II normal
normal
11 Abdomen :
Inspection : flat, Inspection : flat, Normal
caput medusa (-) caput medusa (-)
Palpation : supple, Palpation : supple, Normal
murphy sign (-), murphy sign (-),
hepar were nor hepar were nor
palpable, lien S1, palpable, lien S0, Splenomegali
ballotement (-) ballotement (-)

29
 Percussion : Percussion : shifting Acites
shifting dullness dullness (-)
(+)
Auscultation : Auscultation : Normal
normal bowel normal bowel sound
sound

12 Ekstremity :
Edema pretibia (+) Edema pretibia (-) Edema
Palmar eritem (+) Palmar eritem (- ) Palmar eritem

b. How the abnormal mechanism of physical examination and specific?

Answer :

Risk factor (high profile lipid/ and high lipid consumption diet → BMI
overweight (Price, 2012).

Ichteric sclera

History of hepatitis B → Progression of liver hepatocyte cell damage

→ disorder absorption and secretion so bilirubin direct in plasma →
change the color of elastine tissue → icteric sclera (Price, 2012).

Shiffting dullnes

Disorder absorption and secretion so bilirubin direct in plasma increase

→ albumin binds to bilirubin → secretion billirubin in kidney so
albumin come out → disorder plasma osmotic pressure →
extravasation of intavascular fluid to interstitial → acites → shiffting
dullness (Price, 2012).

Edema Pretibia

Infected hepatitis B virus - immune response to hepatocytes damaged

hepatocytes (necrosis) → release of paracrine factors → activation of

30
 collagen-producing stelate cells port → portal venous hypertension →
edema pretibia (Price, 2012).

Palmar ertiema and Spider Naevi

History of hepatitis B → Progression of liver hepatocyte cell damage

→ lipid and hormone metabolisme disorder → estrogen in the blood
vaskular → vasodilatation certain blood vessel → in hand ( Palmar
eritema ) in thorax ( Spider naevi) (Price, 2012).

5. Laboratory Examination:
- Hb 12,3 g/dl
- Ht 36 vol %
- Leukosit : 8.600/mm3
- Trombosit 90.000/mm3
- LED : 10 mm/hour
- Bil tot : 8,2 mg/dl
- Bil direk : 7,6 mg/dl
- Bil indirek : 0,6 mg/dl
- SGOT : 102 u/L
- SGPT : 115 u/L
- Fosfatase alkali : 110 u/L
- HBs Ag (+)
- Albumin 2,8 mg/d

Urinalysis: bilirubin urin (+)

USG Examination:

31
a. How is the interpretation of Laboratory Examination ?
Answer :
No The case Normal level Interpretation
1 Hemoglobin 12,3 Lk : 13-16 g/dl Normal
g/dl Pr : 12- 14 g/dl
2 Hematokrit 36 36%-48% Normal
vol%
3 Leukosit 8.600 5.000 – 10.000 mm3 Normal
mm3
4 Trombosit 90.000 150.000 – 450.000 Trombositopenia
mm3 mm3
5 LED 10 mm/hour Lk : <10 Normal
Pr : <15
6 Bil total 8,2 mg/dl 0,25 – 1,0 mg/dl There’s
hepatocellular
disease
7 Bil direk 7,6 mg/dl 0.1 - 1.0 mg/dl There’s disturbing
of conjugated
bilirubin
8 Bil indirek 0,6 0,2 - 0,9 mg/dl Normal
mg/dl
9 SGOT 102 u/L 5 – 40 u/L (+) Broken of
10 SGPT 115 u/L 5 – 35 u/L cellular of liver
11 Fosfatase alkali 15 – 69 u/L There’s biliary
110 u/L obstruction
12 HBs Ag (+) HBs Ag (-) Hepatitis B
13 Albumin 2,8 mg/dl 3,7 – 5,2 mg/dl There’s problem in
cell of liver
14 Urinalysis : bilirubin urin (-) Bilirubin in urine
bilirubin urin (+)

32
 USG Examination: Hyperechoic lesion with posterior shadowing =
Cholelithiasis.

b. How the abnormal mechanism of Laboratory Examination?

Answer :
The hepatitis virus enters the body parenterally → from the
bloodstream, Dane particle enters the liver → the virus replicates →
the virus secretes HBsAg and HBeAg → an inflammatory process
occurs → activation of CD 8+ and CD 4+ cells → hepatocellular
necrosis → stellate cells will form collagen → activation of liver
fibrosis → formation of scar tissue and regenerative nodules →
cirrhosis of the liver → impaired liver function → clotting factor
disorders → thrombocytopenia (Price, 2012).

HbsAg (+)
History hepatitis B since birth → hepatitis infected → HbsAg (+)
(Price, 2012).

SGOT, SGPT, Alkaline posfatase increase

Progression hepar cell damage → enzyme, mineral and hepatocit cell
leave the cell → accumulation to the sinusoid → spread systemic
through the blood vessels → SGOT, SGPT, alkaline posfatase increase
(Price, 2012).

33
 Bilirubin direct and total increase, bilirubin urine (+)
Progression hepar cell damage → disorder absorption bilirubin direct
→ bilirubin in plasma → bilirubin direct increase → secretion in
kidney → bilirubine urine (Price, 2012).

Hipoalbumin
Progression hepar cell damage → disorder absorption bilirubin direct
→ billirubin direct secretion in kidney, billirubin can’t accumulation in
blood except bind with albumin → albumin also secretion in kidney →
hipoalbumin (Price, 2012).

Cholelithiasis
There’s viral infection of the liver → inflamation in cell of liver
→fibrous cells increased → excreation of conjugated bilirubin
decreased → accumulating direct bilirubin serum → increasing
bilirubin pigmen → supersaturated in / bladder → Cholelithiasis
(Price, 2012).

6. How to diagnose the case?

Answer :
At the stadium the perfect compensate sometimes very difficult diagnosis
of liver cirrhosis. In a further process stage compensate can be enforced
with the help of careful clinical examination, laboratory biochemical /
serological and other imaging tests. In the decompensated stage diagnosis
is not too difficult because the clinical signs and symptoms usually appear
with their complications. Golden point for the diagnosis of liver cirrhosis
is a liver biopsy, through a percutaneous, transjugular, laparoscopic, or
with a fine needle biopsy. Biopsy is not required if the clinical, laboratory
examination, and radiology to show tendency liver cirrhosis. Although
liver biopsy risk is small, but can be fatal for example, bleeding and death
(Sudoyo, Aru W. Dkk, 2014).

34
7. What is the Differential Diagnosis in the case?
Answer :
Clinical Cirrhosis Cirrhosis hepatic Cirrhosis
Manifestation hepatic + + choledolitiasis hepatic +
Cholelitiasis cholesistisis
Fever - - +
Epigastrium pain + + -
Icterus + + -
Murphy sign - - +
Acites + + +
Varises - - +
Edema pretibia + + +
Pruritus - + -
Palmar eritema + + +
Spider nervi + + +
Splenomegali + + +
Urobilinogen urine Less - Less
fecal pigment Normal /Less - Less
Phospatase alkali Normal Decrease Decrease

8. How is the Supporting examination the case?

Answer :
1. Ultrasonography
It has a high degree of specificity and sensitivity to detect gallstones of
the intrahepaattic and extrahepatic bile duct widening. Also can be
seen the wall of gall bile that thickened because of fibrosis or edema
because of inflammation and other reasons. The stone found in the
ductal duct is difficult to detect, because the air is blocked in the
intestine With ultrasonography can be moved in accordance with

35
 gravitational force. With ultrasound maximum punctum pain in a
gangrene.
2. Endoscopic Retrograde Cholangiopancreatography (ERCP)
Useful for stone inspection in the Koledokus duct. The indicative is the
gallbladder stone with impaired liver function that cannot be detected
by ultrasonography (Sudoyo, Aru W. Dkk, 2014).

9. What is the working diagnosis of the case?

Answer :
Cirrhosis hepatic decompensated e.c Chronic Hepatitis B and accompanied
with cholelithiasis.

10. How is the Treatment of the case?

Answer :
a. Low salt diet, high in protein 1gram / kg / day -> protein 2,000-3,000
kcal / day
b. Treat the etiology: liver cirrhosis with carasteroid and hepatitis B
vaccine
c. Treat complications (choledolithiasis) by surgery
d. Treat the complications (portal hypertension) by diuresis and serum
albumin, spironolactone, dose 50 -200 mg / day
e. Treat yellowish eye complications with UDCA dose 15-20 mg / kg bw
(Longo and Fauci, 2013).
11. What are the complications in the case?
Answer :
Complications that occur in hepatic cirrhosis that can occur are
gastrointestinal bleeding, ascites, hepatorenal, hepatic encephalopathy,
spontaneous bacterial peritonitis and hepatocellular carcinoma (Arief,
2011).

36
12. What is the prognosis for the case?
Answer :
Quo ad vitam : dubia ad bonam
Quo ad fungsionam : dubia ad malam
Quo ad sanasionam : dubia ad bonam

13. What is Medical Doctor Competences of this case?

Answer :
Liver cirrhosis and cholelitiasis
Capability Level 2: diagnosing and referring physician graduates capable
of making a clinical diagnosis of the disease based on history and physical
examination and determine the most appropriate referral for further patient
management. Graduates are also able to follow up after the doctor returned
from a referral.

14. How is the islamic point of view of this case?

Answer :
Qs. Al-Baqarah : 219

That means :
They question thee about strong drink and games of chance. Say: In both is
great sin, and (some) utility for men; but the sin of them is greater than
their usefulness. And they ask thee what they ought to spend. Say: that
which is superfluous. Thus Allah maketh plain to you (His) revelations,
that haply ye may reflect

37
2.7 Conclusion
Ms. F, 45-year-old woman complaining of icteric sclera, urine that is
colored like dark tea, ascites, colic pain, feeling limp, due to experiencing
cirrhosis hepatic decompensated e.c Chronic Hepatitis B and accompanied
with cholelithiasis.

38
 2.8 Conceptual Framework

Risk Factor Infection of Hepatitis B Virus

Chronic injury to the hepatocytes cell in hepar

Fibrosis and Scarring

Cirrhosis Hepatic

Portal Hypertension Hepatocelluar disorder

Edema Estrogen Hepatocellular Metabolic

Pretibia Metabolic icterus disorder
Disorder (metabolism of
carbohydrates,
Ascites Hyperbilirubinemia proteins, and
Palmar lipids)
eritema
Icterus
Splenomegaly Sclera
Spider Feeling
naevy limp
Urine like
dark tea
Epigastric Reduced
pain appetite
Cholelithiasis

39
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