TUTORIAL REPORT

SCENARIO C BLOK XI

GROUP 4

Muhammad Kevin Al Hafidz 702018018

Camelia Panache 702018046
Melenia Rhoma Dona YS 702018041
Mothiara Rezki Ramadhnai 702018053
Muhammad Ridho Amrillah 702018080
Rahmi Nurba Driya Ningsih 702018062
Dennisa Luthfiyah Fadilah 702018074
Coni Barokah 702018091
Amy Ria Annisa 702018084
Zira Rizka Armidia 702018069
Fitriani 702016054

MEDICAL FACULTY
MUHAMMADIYAH UNIVERSITY PALEMBANG
TAHUN AJARAN 2019/ 2020

FOREWORD
1
 Praise the writer praying to Allah SWT for all His graces and gifts so that the author can
complete the tutorial report titled "Report Scenario B Block XI Tutorial" as a group competency
task. Blessings and greetings are always given to our master, Prophet Muhammad, peace be
upon him, with family, friends and followers until the end of time.The author realizes that this
tutorial report is far from perfect. Therefore, the authors expect constructive criticism and
suggestions for future improvement. In completing this tutorial report, the author gets a lot of
help, guidance and advice. On this occasion, the author would like to express respect and thanks
to:
1. Tutor Group 4 dr.Budi Utama M.Biomed
2. Both parents who always provide material and spiritual support.
3. All friend
4. All parties who help the author.
May Allah SWT give gifts for all charities given to all those who have supported the
author and hopefully this tutorial report will benefit us and the development of science. May we
always be protected by Allah SWT. Amen

Palembang, April 2020

Author

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 TABLE OF CONTENTS

Foreword............................................................................................................2

Table of contents...............................................................................................3

CHAPTER I : Introduction

1.1 Background..............................................................................4

1.2 Purpose and Objectives ...........................................................4

CHAPTER II : Discussion

2.1 Tutorial Data ...........................................................................5

2.2 Case Scenario...........................................................................6

2.3 Clarification of Problems.........................................................7

2.4 Identification of Problems .......................................................10

2.5 Priority of Problems.................................................................12

2.6 Analysis of Problems ..............................................................12

2.7 Conclusion...............................................................................39

2.8 Conceptual Framework............................................................39

BIBLIOGRAPHY.............................................................................................40

CHAPTER I

PRELIMINERY

3
1.1 Background
The System Digestif Block is the eleven block in the four semester of the
Competency Based Curriculum of Doctor Education Faculty of Medicine,
Muhammadiyah University of Palembang. In addition, as we know that the learning
program in this UMP FK uses KBK learning system, so it is expected that doctor
graduates from FK UMP become doctors who are able to understand the existing systems
in the human body.

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

4
2.1 Tutorial Data

Tutor : dr. Budi Utama M.Biomed

Moderator : Fitriani

Secretary Desk : Melenia Rhoma Dona YS

Secretary Board: Mothiara Rezki Ramadhani

Run time : Monday , March 30th 2020 (tutorial stage 1)

At 13.00-15.30 PM

Wednesday, April 1th 2019 (tutorial stage 2)

At 13.00-15.30 PM

Rules:

1. Switch the phone off or in silence.

2. Raise your hand when going to argument.

3. Permission when going out of the room.

4. Relax and watch as the tutor gives directions.

5. During the tutorial takes care of attitude and speech

2.2 Case Scenario

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 “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 - Leukosit : 8.600/mm3

- Ht 36 vol % - Trombosit 90.000/mm3
- LED : 10 mm/hour
- Bil tot : 8,2 mg/dl
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 - 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/dl
- Urinalysis: bilirubin urin (+)
USG Examination:

7
2.3 Term of Clarifications :

No Clarifications Meaning
Examination to determine the presense of
11 Murphy Sign cholelithiasis and cholecystitis
(Dorland,2018)
Cutaneous vein dilation around the
2 Caput Medusae umbilicus, especially seen in newborns adn
liver cirrhosis patients (Dorland,2018)
Hepatitis is inflammation of the liver usually
transmitted through oral ingestion but can
3 Hepatitis B
also be transmitted parenterally
(Dorland,2018)
Pain is a distressing feeling often caused by
intense or damaging stimuli. The
International Association for the Study of
Pain's widely used definition defines pain as
4 Pain
"an unpleasant sensory and emotional
experience associated with actual or potential
tissue damage, or described in terms of such
damage (Dorland,2018)
Deaf voice that moves during percussion due
5 Shifting dullness to the free fluid of the abdomen
(Dorland,2018)
Water-soluble protein and also in medium
6 Albumin
concentration salt solutions (Dorland,2018)
Redness due to dilation of blood vessels in
7 Palmar Eritem
the palm of the hand (Dorland,2018)
 HBsAg (Hepatitis B Test is performed as a way to detect hepatitis
8
Surface Antigen) B (Dorland,2018)
Which a person's skin and the whites of the
eyes are discolored yellow due to an
increased level of bile pigments in the blood
9 Yellowish eyes
resulting from liver disease. Jaundice is
sometimes called icterus, from a Greek word
for the condition (Dorland,2018)
Superficial cutaneous artery dilation and
10 Spider Nevi branching appears as a bright red central area
with spider-like branches (Dorland,2018)
Abnormal fluid collection in the anterior
11 Edema Pretibia
tibia (Dorland,2018)
Impaired strength or digestive function,
12 Dyspepsia usually used for discomfort in the
epigastrium after eating (Dorland,2018)
Liquid by-product of metabolism in humans
and in many other animals. Urine flows from
the kidneys through the ureters to the urinary
13 Urine
bladder. Urination results in urine being
excreted from the body through the urethra
(Dorland,2018)
It is an enlargement of the uterus where the
condition is uneven until it is prominent
14 Ballotement
where the direction of the uterus is enlarged
(Dorland,2018)
(Serum glutamate oxaloacetate transaminase)
15 SGOT normal enzymes are in liver cells and other
organs (Dorland,2018)
(Serum glutamic pyruvic transaminase)
enzymes found normally in the liver and
16 SGPT
other organs are higher than the liver
(Dorland,2018)
17 Billirubin Indirect Bilirubin that has been taken up by liver cells

9
 and is conjugated to form water-soluble
diglukluronite billirubin (Dorland,2018)
Protein that is usually produced by the liver
(liver) and yolk sac (yolk sac) during the
18 Alfa Feto Protein
formation of the baby during the pregnancy
process (Dorland,2018)

2.4 Identification of Problems

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
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

10
 - 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 (+).

5. Labority 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/dl
- Urinalysis: bilirubin urin (+)

6. USG Examination:

11
2.5 Priority of Problems
Identification No.1
Because if it is not managed properly it will cause complication that will
increase mortality and morbidity
2.6 Analysis of Problems
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 are the organ involved in this case ?
Answer:
The organ involved are :
1.Liver
2.Pancreas
3.Gallbladder

b. What are the anatomy and physiology in this case ?

Answer:
Anatomy Liver

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 The liver is the largest gland in the human body weighing
approximately 1.5 kg. The liver is the largest visceral organ and is located
under the rib cage.The liver is soft, supple and located at the top of the
abdominal cavity just below the diaphragm. Most of the liver is located in
the deep arcus costalis dextra and hemidiaphragma dextra separating the
liver from the pleura, pulmo, pericardium and cast. The liver extends to
the left to reach hemidiaphragma sinistra.
The liver is composed of hepatic lobules. The central vein in each
lobule empties into the hepatic vein. In the space between the lobules there
is a hepatic canal which contains branches of the hepatic artery, hepatic
portal vein, and a branch of the ductus choledochus (triashepatis). Arterial
blood and veins travel between the liver cells through the sinusoid and
flow into the central vein.
(Snell,2016)

Anatomy Pancreas

The pancreas consists of several parts namely :

1.Head : widest part of the pancreas. It lies within the c-shaped curve
created by the duodenum, and is connected to it by connective tissue.
2.Uncinate process : projection arising from the lower part of the head and
extending medially to lie beneath the body of the pancreas. It lies posterior
to the superior mesenteric vessels.
3.Neck : located between the head and the body of the pancreas. It overlies
the superior mesenteric vessels which form a groove in its posterior aspect.
4.Body : centrally located, crossing the midline of the human body to
lie behind the stomach and to the left of the superior mesenteric vessels.
5.Tail : the left end of the pancreas that lies within close proximity to the
hilum of the spleen. It is contained within the splenorenal ligament with
the splenic vessels. This is the only part of the pancreas that
is intraperitoneal.
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(Snell,2016)

Anatomy Gall Blader

Vesica billiards is a pear-shaped bag located on the bottom of the

porch. Vesica billionaire has the ability to store bile at 30-50 ml, as well as
tighten bile by absorbing water. Vesica billiards comprise the fundus,
corpus, and collum. Fundus vesica biliaris is rounded and usually
protrudes below the inferior margo, the promontory is where the fundus
comes in contact with the anterior wall of the upper abdomen as the
cartilago costalis IX dextra. Corpus vesica biliaris is located and is
associated with the fascies visceralis hepar and its upward, back and left.
Colum vesica biliaris extends as the ductus cysticus, which converts into
the minus omentum and joins the right side of the communist ductus
hepaticus to form the ductus choledochus.Vesica billiards function as bile
storage. vesica biliaris has the ability to bind to bile and to aid in this
process, vesica biliaris mucosa has permanent folds that are interconnected
so that the surface looks like a bee hive The thorax cells located on the
surface of the mucosa have many vials. Emulsions are transported to the
duodenum as a result of contraction and partial evacuation of vesica
biliaris. This mechanism is initiated by the insertion of fatty foods into the
duodenum. Fat causes the production of cholististokinin hormone from the
tunica mucosa duodenum. The hormones then enter the bloodstream and
cause vesica billiards contraction. At the same time the smooth muscle is
located at the distal end of the ductus choledochus and relaxation ampule,
allowing the entry of concentrated bile into the duodenum. Bile salts in
bile fluids are important for emulsifying fat in the intestines and helping
digestion and fat absorptio.
(Sherwood,2017)

Physiology Liver
According to Guyton & Hall , the heart has several functions, namely:
a. Carbohydrate metabolism
The function of the liver in carbohydrate metabolism is storing large
amounts of glycogen, converting galactose and fructose to glucose,

14
gluconeogenesis, and forming many important chemical compounds from
intermediate products of carbohydrate metabolism.
b. Fat metabolism
Liver functions related to fat metabolism, among others: oxidizing fatty
acids to supply energy for other bodily functions, forming most
cholesterol, phospholipids and lipoproteins, forming fat from proteins and
carbohydrates.
c. Protein metabolism
The function of the liver in protein metabolism is the deamination of
amino acids, the formation of urea to remove ammonia from body fluids,
the formation of plasma proteins, and the interaction of various amino
acids and the formation of other compounds from amino acids.
d. Others
Other liver functions include the liver is a storage place for vitamins, the
liver as a place to store iron in the form of ferritin, the liver forms
substances used for blood coagulation in large quantities and the liver
secretes or excretes drugs, hormones and other substances.
(Sudoyo et al,2017)

Bilirubin Metabolism :
About 80% - 85% of bilirubin is formed from the breakdown of old
erythrocytes in the monocyte-macrophage system. The average mass of
erythrocytes is 120 days. Every day about 50 ml of blood is destroyed and
produces 250-350 mg bilirubin. Approximately 15-20% of total bile
pigment does not depend on this mechanism, but comes from the
destruction of mature erythrocyte cells from the bone marrow (ineffective
hematopoiesis) and from other hemoproteins, especially from the liver.
In hemoglobin catabolism (especially in the spleen), globin is first
separated from the heme, after which the heme is changed to beliverdin.
Unconjugated bilirubin is then formed from biliverdin. Biliverdin is a
green pigment formed by oxidation of bilirubin. Unconjugated bilirubin is
fat soluble, insoluble in water, and cannot be excreted in bile or urine.
Unconjugated bilirubin binds to albumin in a water-soluble
complex, then is transported by blood to liver cells. The metabolism of
bilirubin in the liver takes place in three steps: uptake, conjugation, and
excretion. Ambulances by liver cells require two liver proteins, which are
symbolized as proteins Y and Z. The conjugation of bilirubin with
glucuronic acid is catalyzed by the enzyme glucoronil transferase in the
endoplasmic reticulum. Conjugated bilirubin is not soluble in fat, but is
soluble in water and can be excreted in bile and urine. The final step in the
metabolism of liver bilirubin is the transport of conjugated bilirubin
through the cell membrane into the bile through an active process.
Unconjugated bilirubin is not excreted into the bile, except after the photo-

15
oxidation or photoisomerization process.Intestinal bacteria reduce
conjugated bilirubin into a series of compounds called stercobillin or
urobilnogen. These substances that cause brown stool. About 10 to 20% of
urobinilogens undergo interohipatic cycles, while small amounts are
excreted in the urine.
(Setiati et al,2014)

Exocrine pancreas
Pancreas sekitas 20 cm long with its head facing curved bend
duodenum and its tail touched the side of the spleen. Part pancreas corpus
contained inside the abdomen behind the stomach. Pancreatic endocrine
and exocrine function. Releasing hormone endocrine part of the pancreas:
insulin, glucagon, somatostatin and pancreatic polypeptide. Part of the
exocrine pancreas is composed of acinar cells that release enzymes and
tissue alkaline discharge channel. Both have important digestive function.
Acinar cells arranged into spherical surround lobul small sekretorius duct.
The secretion flow into the channel system which then leads to
pancreaticus duct (ductus wirsungi) and empties the bile duct at the
ampulla of Vater and then into the duodenum. Padabeberapa people,
(Kathryn, et al., 2017).
Arterial blood is supplied to the pancreas by a branch of the
superior mesenteric artery and seliaca. Venous blood leaving the head of
the pancreas via the portal vein with the body and tail flowing through the
veins splenica. All pancreatic hormone secretion also through the portal
vein to the liver(Kathryn, et al., 2017).
Nerve supply (innervation) pancreas originate from parasimpatif fibers of
the vagus nerve. These nerves activate post-ganglionic sympathetic nerve
and plexus mensenteri seliaca superior and nerves supplying blood vessels,
causing vasoconstriction, and inhibiting the secretion of the
pancreas(Kathryn, et al., 2017).

c. What is the meaning of Ms.F 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 weks ago?
Answer:
The meaning is that for 7 days ago the yellow eye complained that
the progression of the disease had reached the peripheral tissues as in
the eye, which made the eyes yellow. because of liver hepatocyte cell

16
 damage that will continuously make the accumulation of bilirubin, so
that later will go into the kidneys and come out into the urine so that the
pigment in bilirubin causes the urine to become dark tea. In addition,
the accumulation of bilirubin which accumulates over time will become
a foreign object so that it will be destroyed and cause release of
histamine and NO which will cause wide blood vessels and skin to itch
since 2 weeks ago due to its progression.
(kowalak,2017)

d. What is the relation between sex and age in the case?

Answer:
Sex :
Based on the grouping of decompensated liver cirrhosis patients
accordingly with gender, 128 patients (69.6%) were obtained male and
56 patients (30.4%) were female. Proportion of liver cirrhosis more
common in men with a ratio between men and women 2,3: 1.
Age :
Patients with cirrhosis of the liver more often found along with
increasing age. From this study, the results were obtained in part large
patients were diagnosed with liver cirrhosis in the fourth decade and
fifth (59.3%) with a mean age of 51.5 years and a median of 51 years
(Tambunan,2010)

e. How is the etiolology of yellowish eyes?

Answer:
Yellow eyes can be interpreted as jaundice sclera. Jaundice or
jaundice is yellow or greenish pigmentation on the skin and sclera
caused by hyperbilirubinemia. Hyperbilirubinemia can result from:
1. Increased bilirubin production
Increased bilirubin production often occurs due to excessive destruction
of red blood cells.

17
 2. Decreased rate of absorption of bilirubin by liver cells.
Some genetic disorders such as Gilbert's syndrome and certain types of
drugs can cause a decrease in the absorption of bilirubin by liver cells.
3. Bilirubin conjugate disorders.
Conjugation of bilirubin can occur if there is a deficiency or absence of
the enzyme glucoronil transferase, for example due to the influence of
drugs or on genetic disorders such as Crigler-Najjar syndrome.
4. Disruption of bilirubin secretion
Disruption of bilirubin production can occur in damage to liver cells or
urinary bile in the liver or outside the liver.
(Gondal and Aronsohn, 2016)

f. What is the etiology of urine that colored like dark tea?

Answer:
As a result of obstruction of extrahepatic that conjugated bilirubin
by hepatocytes can not flow through the bile duct because of constraints
that conjugated bilirubin accumulates in the hearts and enter the
bloodstream so that hyperbilirubinemia and icterus. Because the water-
soluble conjugated bilirubin in urine seen the darker color.
(Kathryn, et al., 2017)

g. What is the meaing Ms. F also complains of feeling limp, epigastric

pain and reduced appetite?
Answer:
The meaning is from the progressive progression of hepatocyte cell
damage, in which the liver is one of the central handling of the body, so
that if there is damage it will be hampered, and nutrition increases the
body's cells increase nociseptors (parasympathetic X X) in the liver so
that the stomach will spread reached the liver according to the anatomy
of the liver and decreased appetite.
(Wahyudo,2015)

18
h. What is the etiology complains of feeling limp, epigastric pain and
reduced appetite?
Answer:
The etiology :
1.Inflammation
2.Strain or organ distention
3.Lost of blood supply to organs
4.Abnormal intestine muscle contraction
5.Colic pain
(Longo,2013)

i. How is mechanism of feeling limp, epigastric pain and reduced

appetite?
Answer:
Feeling limp:
Recurrent HBV infection → From blood circulation, dane particles
enter the liver → virus replication → virus secretes HBsAg & HBeAg
→ HBV stimulates the body's immune response → activation of CD 8+
and TCD 4+ cells → liver cell necrosis → stelate cells will form
collagen → disorders of extracellular matrix formation and degradation
disorders → formation of continuous fibrosis → liver tissue replaced by
connective tissue → disruption of metabolic formation →
carbohydrates and fats → feeling limp.
Epigastric pain:
Recurrent HBV infection → from the blood circulation of dane
particles into the liver → viral replication → the virus secretes HBsAg
and HBeAg → hepatitis → liver enlargement → stretching of the liver
fibrous sheath → epigastric pain
Reduced appetite:

19
 recurrent HBV infection → From blood circulation, dane particles enter
the liver → virus replication → virus secretes HBsAg & HBeAg →
HBV stimulates the body's immune response → activation of CD 8+
and TCD 4+ cells → liver cell necrosis → stelate cells will form
collagen → impaired extracellular matrix formation and impaired
degradation → continuous fibrosis formation → liver tissue replaced by
connective tissue → retention of blood flow through the liver and blood
pressure dams in the splenic vein → splenomegaly → suppressing the
vagus nerve → reduced appetite
(Price and Wilson, 2015)

j. What is the relation between main complain with complain in the case?
Answer:
It is the course of the disease in cases of hepatic cirrhosis, darker
urine caused by hyperbilirubinemia in which bilirubin out with urine,
not followed by white fecal indicates that direct bilirubin can still be
distributed to the duodenum, itchy skin is the effect of
hyperbilirubinemia or jaundice that enters the skin tissue, especially the
dermis which stimulates the skin nerves, weakness, epigastric pain and
decreased appetite are the effects of liver disorders themselves due to
disturbed metabolism and inflammation that causes nociceptor
stimulation so that it causes pain.
(Gondal and Aronsohn, 2016)

k. What are the possible disease in this case?

1) Prehepatic:
a) Infection (example: malaria)
b) Genetic abnormalities (example: thalassemia, sickle cell anemia,
spherocytosis)
c) Uremic hemolytic syndrome
2) Intrahepatic:

20
 a) Viral hepatitis (acute or chronic)
b) Alcoholic liver disease
c) Hepatic cirrhosis
d) Neonatal jaundice
e) drug-induced hepatitis
3) Posthepatic:
a) Bile obstruction
b) Pancreatic cancer
c) Strict bile ducts
d) Biliary atresia
e) Pancreatitis
f) Pancreatic pseudocysts
g) Cholangiocarcinoma
(Sjamsuhidajat & Jong, 2014)

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 is the meaning of 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:
The meaning is that this is a clinical manifestation of cholelithiasis.
Symptoms is epigastric pain, that radiates to the right shoulder.
(Bacon,2014)

b. What is the mecanishm of 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?

21
 Answer:
Factors 4F and fatty food >production of bile is increased > bile
crystallization > gallstone > pain on right upper abdomen.
(Price and Wilson,2015)

c. What is the risk factor of this case ?

Answer:
1) Nutrition
Malnutrition can cause damage to the cells of the hepar. Another
important thing is that the consumption of fat that coincides with toxic
substances can also cause a treat in hepar, because Hepar will
prioritize the elimination of toxic substances, so that
metabolismelemak become disturbed.
2) Age
In neonatal cells The Hepar has not been fully mature so that the
metabolism in Hepar is not perfect. In the elderly, there is a decline in
the physiological functions of the body, so that the blood flow to the
hepar decreases and the metabolism is impaired.
3) disease
Diseases such as hepatitis and Reye syndrome and cholestasis will
cause disorders of the metabolism in hepar, especially in the case of
biotransformation of substances.
4) Alcohol and toxic substances
The intermediates in the metabolism of alcohol are acetaldehyde
which can cause a morphological abnormality of 16 in the hepar cells.
The abnormalities are caused by damage to the cell membranes and
their cytoskeleton. Alcohol can also cause a treat in hepar. Some toxic
substances that are harmful to hepar include ethanol, bromobenzen
and carbon tetrachloride. (Setiati,2014)

22
d. What is relation between has experiencing a pain on her right upper
abdomen with that was felt especially after consuming fatty food?
Answer:
Pain episgastrium and right hypochondria and fatty food
intolerance is a major manifestation of cholelithiasis. It is caused by
the discharge of one or more gallstones into the cystic duct or duct
bile communists during contraction katong.
(Kathryn, et al., 2017).

e. What are possible disease with a chief complain of pain on her right
upper abdomen that radiates to the right shoulder?
Answer:
1.Intestinal obstruction
2.Peptic ulcer
3.Hepatitis
4.Cirrhosis hepatis
5.Pancreatitis
6.Kolelitiasis
(Snell, 2016)

f. What is the relation between chief complain (yellowish eyes) and

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:
The relationship is a manifestation of the same etiology, which is
due to a buildup of bile secretion that makes progression from liver
damage resulting in manifestations such as yellow eyes and right
upper quadrant abdominal pain that arise when consuming fat.
(Cotran et al, 2012)

23
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 is the meaning 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:
Do not have a history of long-term drug consumption to remove
the diagnosis of the form of cirrhosis Hepatis EC toksity Drugs, have
a history of the disease has hepatitis since birth indicates that hepatic
cirrhosis experienced by Ny. F is an advanced stage journey of
hepatitis B in which, cirrhosis hepatis is a morphological term that
refers to a particular stage of chronic liver injury of the advanced
phase by specific and cryptogenic causes. Serological evidence
suggests that viral hepatitis (hep. B and C) may be a precursor factor.
(Sandu et al,2017)

b. What is the relation of hepatitis B history with complaints

Answer:
People affected or infected with Hepatitis B causes the liver to
become inflamed and there is necrosis of the liver cells so that there is
continuous liver damage and cause complications such as in that case
hepatic cirrhosis.
(kowalak,2017)

c. What is risk factors of hepatitis disease?

Answer:
1. Health care workers
2. Clients and staff of mental disability
3. hemodialysis patients
4. Male homosexual
5. Intravenous drug use

24
 6. Recipients of blood products chronic
7. Household contact / intercourse with patients with HBsAg career
8. HBV endemic stricken tourists
9. Refugees from HBV-endemic areas
(Khumaedi et al,2017)

d. What is classification of hepatitis disease?

Answer:

Characterist Hepatitis A
Hepatitis Hepatitis Hepatitis Hepatitis
ics B D C E
Virus Virus RNA Virus Virus Virus Virus
27nm DNA RNA RNA 30- RNA 32
42nm 36nm 60nm nm
Antigen or Anti-HAV HBsAg, Anti- Anti-HCV Anti-HEV
antibodi HBcAg, HDV
HBeAg
Incubation 30 days 60-180 30-180 35-60 days 15-60
period days days days
Route Fecal oral Parenteral Parentera Parenteral, Fecal-oral
transmissio (mostly), , sexual, l co- sexual,
n parenteral, plasenta infection plasenta
sexual HBV,
fecal-
oral,
sexual
Early Not Hidden Hidden Hidden Acute
symptoms specific,
acute with
fever
Carrier Negative Positive Positive Positive Negative
condition
Severity Mild severe, severe Unknown Severe in
level long pregnancy
lasting or
chronic
Cronic No yes yes yes No
Hepatitis
Affected Children Everyone Everyone Everyone Children
age group and young and young
adult adult
Prevention Hygiene, Hygiene, Hygiene, Higiene, Hygiene,c

25
disease globulin vaccine vaccine blood lean water
serum HBV, HBV filtration,
immune, blood interferon-
vaccine filtration a
HAV
Pathophysio Hepatosit Virus Co- Hepatosit Virus
logy damage replicatio infection damage replicatio
caused by n, co- with caused by n, liver
sellular infection HBV, immune sitotoxic,
immune with viral severe response, immune
response mutation, damage inflammati response
(cells T, inflammat cells, on, and cause
cells NK ion, and inflamma fibrosis inflammat
and selular tory cause ion and
cytocine) necrotic progressi sirosis colestatis
on to
sirosis
Treatment immunoglo interferon Interferon Interferon- Symptom
bulin within -alfa, -alfa alfa, atic
2 weeks peginterfe peginterfer therapy,
after ron-alfa, om-alfa, same as
exposure, antivirus antivirus HAV
symptomati (lamivudi (ribavirin,
c therapy ne, boceprevir
adefovir, ,
entecavir, telaprevir,
telbivudin simeprevir
e, ,
tenofovir) daclatasvir
,
sofobuvir,
combinati
on
antivirus)
(Setiati,2014)

e. What is patophysilogy of hepatitis B?

Answer:
FR (parenteral or neonates) → HBV virus enters the body →through
blood vessels enter the liver and viral replication occurs in hepatocyte
cells → HBV stimulates the body's immune response (innate immune
response) with the release of inflammatory mediators and the process

26
 of elimination by NK and NK-T cells → if it is not efficient it will
stimulate specific immune responses by activation of T lymphocytes,
B lymphocytes, activation of CD8 + and CD4 + on the surface of the
liver cell wall for virus elimination → liver cell necrosis and other
liver function disorders (chronic hepatitis B because it is persistent).
(Setiati,2014)

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

27
 a. How is the interpretation of physical examination and spesific
examination?
Answer:

Examination Interpretation Medical

referral
1 General appearance: Abnormal
looks moderately sick
2 Conciousness : compos Normal Compos
mentis mentis
2
4 IMT : BH 158 cm, BW IMT = 75/(1,58) = 30,04 IMT = 18,5 -
75 kg. (Obesity 2) 22,9 (Normal)
5 Vital sign : Normal Target for
BP 110/80mmHg Sistole : 100 -
139 mmHg
Diastole :80 -
89 mmHg
6 Pulse : 8 0x/menit Normal 60 - 100
x/minute
7 RR : 22x/m Normal 16 -24 x/m
8 Tempt : 36,8°c Normal 36,5 - 37,5
9 Head :
Pale conjungtive (-/-) Pale conjungtive (-/-) Normal
Icteric sclera (+/+) Icteric sclera (-/-) Abmormal
10 Neck :
JVP 5-2 cmH2O, Theres JVP 5-2 cmH2O, Theres no Normal
no enlargement on the enlargement on the neck
neck
11 Thoraks:
Thorax wall :
spider nevi (+), spider nevi (-) Normal
Pulmo :
Inspection : symetric Inspection : symetric static
static and dynamic and dynamic

28
 Palpation : same stem Palpation : same stem
fremitus lef and right fremitus lef and right
Percussion : sonor on Percussion : sonor on the
the whole lung whole lung
Auscultation : vesikuler Auscultation : vesikuler (+/
(+/+), ronkhi (-/-), +), ronkhi (-/-), wheezing
wheezing (-/-) (-/-)
12 Cor :
Inspection : flat, ictus Inspection : flat, ictus cordis Normal
cordis (-) (-)
Palpation : ictus cordis Palpation : ictus cordis were
not palpable
Percussion : normal heart
border
Auscultation : HR 80x/m,
reguler, heart sound I-II
normal
13 Abdomen :
Inspection : flat, caput Inspection : flat, caput Normal
medusa (-) medusa (-)
Palpation : supple, Palpation : supple, murphy Normal
murphy sign (-), hepar sign (-), hepar were nor
were nor palpable, lien palpable, lien S1,
S1, ballotement (-) ballotement (-)
Percussion : shifting Percussion : shifting
dullness (+) dullness (-) Abnormal
Auscultation : normal Auscultation : normal bowel
bowel sound sound
Normal
14 Ekstremity : Edema pretibia (-) Abnormal
Edema pretibia (+) Palmar eritem (- )
Palmar eritem (+)

29
 b. How is the mecanism abnormal of physical examination and spesific
examination?
Answer:
Icteric sclera:
Infected hepatitis B virus → immune response to hepatocytes →
damaged hepatocytes (necrosis) → impaired bilirubin metabolism →
high bilirubin levels in the elastin (sclera) tissue → icteric sclera
Spider Nevi and Palmar Erythema:
Infected hepatitis B virus → immune response to hepatocytes →
damaged hepatocytes (necrosis) → impaired cholesterol metabolism
→ increased hormone estradiol→ spider nevi and palmar erythema
Edema Pretibia and Lien s1:
Infected hepatitis B virus → immune response to hepatocytes
damaged hepatocytes (necrosis) → release of paracrine factors→
activation of collagen-producing stelate cells port portal venous
hypertension pret edema pretibia and spleen S1.
Ascites:
Infected hepatitis B virus → immune response to hepatocytes
damaged hepatocytes (necrosis) → release of paracrine factors →
activation of collagen-producing stelate cells port portal venous
hypertension spl splanchnic venous pressure → increased plasma
volume expansion and formation of lymphatic → ascites.
(Kowalak,2017)

5. Laboratory examination :
- Hb 12,3 g/dl
- Ht 36 vol %
- Leukosit : 8.600/mm3
- Trombosit 90.000/mm3
- LED : 10 mm/hour

30
- 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/dl
- Urinalysis: bilirubin urin (+)
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 vol Lk : 45-55 vol% Normal
% Pr : 40-50 vol%
3 Leukosit 8.600 5.000 – 10.000 Normal
mm3 mm3
4 Trombosit 90.000 150.000 – Abnormal
mm3 450.000 mm3
5 LED 10 mm/hour Lk : <10 Normal
Pr : <15
6 Bil total 8,2 mg/dl 0,25 – 1,0 mg/dl Hiperbilirubinemia
7 Bil direk 7,6 mg/dl 0.1 - 1.0 mg/dl Hiperbilirubinemia
8 Bil indirek 0,6 0,2 - 0,9 mg/dl Normal
mg/dl
9 SGOT 102 u/L 5 – 40 u/L Abnormal
10 SGPT 115 u/L 5 – 35 u/L Abnormal
11 Fosfatase alkali 110 15 – 69 u/L Abnormal
u/L
12 HBs Ag (+) HBs Ag (-) Abnormal (Hepatitis
B)
13 Albumin 2,8 mg/dl 3,7 – 5,2 mg/dl Abnormal
14 Urinalysis : bilirubin urin (-) Abnormal
bilirubin urin (+)

31
b.How is the mecanism abnormal of laboratory examination?
Answer:
Hb and Ht ↓:
Recurrent HBV infection → From blood circulation, dane particles enter
the liver → viral replication → the virus releases HBsAg & HBeAg →
HBV stimulates the body's immune response → activation of CD 8+
and TCD 4+ cells → liver cell necrosis → clotting factor 5 and 7
production by impaired liver → prolonged prothrombin time → anemia,
hematocrit ↓
Thrombocytopenia:
Recurrent HBV infection → From blood circulation, dane particles enter
the liver → viral replication → the virus releases HBsAg & HBeAg →
HBV stimulates the body's immune response → activation of CD 8+
and TCD 4+ cells → liver cell necrosis → clotting factor 5 and 7
production impaired by the liver → prolonged prothrombin time →
thrombocytopenia
SGOT and SGPT ↑:
Recurrent HBV infection → From blood circulation, dane particles enter
the liver → virus replication → virus secretes HBsAg & HBeAg → HBV
stimulates the body's immune response → activation of CD 8+ and TCD
4+ T cells → liver cell necrosis → SGOT ,SGPT ↑ and alkaline
phosphatase increases.
Hypoalbuminuria:
Recurrent HBV infection → From blood circulation, dane particles enter
the liver → virus replication → virus secretes HBsAg & HBeAg → HBV
stimulates the body's immune response → activation of CD 8+ and TCD
4+ cells → liver cell necrosis → stelate cells will form collagen →
disorders of extracellular matrix formation and degradation disorders
→ formation of continuous fibrosis → liver tissue replaced by
connective tissue → disruption of metabolic formation → protein →
hypoalbuminuria

32
 Total bilirubin and bilirubin reacted ↑:
Recurrent HBV infection → From blood circulation, dane particles enter
the liver → virus replication → virus secretes HBsAg & HBeAg → HBV
stimulates the body's immune response → activation of CD 8+ and TCD
4+ cells → liver cell necrosis → stelate cells will form collagen →
disorders of extracellular matrix formation and degradation disorders
→ formation of continuous fibrosis → liver tissue replaced by
connective tissue → impaired excretion of intrahepatic conjugated
bilirubin → total bilirubin ↑ (direct bilirubin ↑) → conjugated
hyperbilirubinemia in blood
(Kowalak,2017)

6. USG Examination:

a. How is the interpretation of USG examination?

Answer:
On the USG examination, visible hyperechoic gallstone with posterior
shadowing (acoustic shadow).
Interpretation: Kholelithiasis

b. How is the mecanism abnormal of USG examination?

33
 Answer:
Risk factor of F4 ( female, fat body, forty, fat) → increased biliary
cholesterol secretion → Supersaturation of cholesterol → nucleation
of cholesterol crystals → formation of gallstones.
(Price and Wilson,2015)

7. How to diagnose?
Answer:
A. History
Complaints of yellow eyes since 7 days ago.
Urine like old tea.
The body feels weak, heartburn, and decreased appetite.
Suffered from hepatitis B since birth.
b. Physical examination
General conditions: moderate pain
Head: jaundice sclera
Thoracic wall: the presence of spider nevi
Abdomen: shifting dullness (+)
Extremities: pretibia edema (+), palmar erythema (+)
c. Laboratory examination:
Total bilirubin and bilirubin recruited increased
SGOT and SGPT increased
HBsAg (+)
Hypoalbumin

8. What is the differential diagnosis in this case?

Answer:
a. sirosis hepatis ec hepatitis B kronis + kolelitiasis
b. Hepatoma ec hepatitis B kronis + kolelitiasis

9. What is the additional examination to diagnose in this case?

34
 Answer:
a)Radiology: Can see esophageal varices to confirm portal hypertension.
b)Esophagoscopy: Can show the presence of esophageal varices.
c)Angiography: To measure portal venous pressure.
d)Skan / liver biopsy: Detects fat infiltrates, fibrosis, liver tissue damage.
e)Percutaneous transhepatic partography : Shows circulation of the portal
venous system.
(Bacon,2014)

10. What is the working diagnosis in this case?

Answer:
Sirosis hepatis dekompensata ec hepatitis B kronis + kholelitiasis

11. How is the treatment in this case?

Answer:
a.Non pharmacology:
Rest
A low salt Diet
A low calorie Diet
Hepar transplant
b.Pharmacology:
Management for Hepatitis B Chronic:
1.Immunomodulation groups:
Interferon: IFN Alfa : 5-10 MU 3 times per week for 16-24 weeks
2.Antiviral therapy group:
Lamivudin : 100 mg per day (oral) for 1 week
Management for Cholelitiasis (Bladder stone) :
1.Laparoscopic cholecystectomy
2.Endoscopic sphincterotomy

35
 Management for Sirosis:
The management of hepatic cirrhosis by treating the cause of chronic
hepatitis is aimed at reducing the progression of cirrhosis so that it does
not progress and reduce the occurrence of hepatocellular carcinoma.
Management for asites :
1.Antideuretic drugs: spironolactone begins, if the response is inadequate
in combination with furosemide (100-200 mg once daily max 400 mg
and 20-40 mg / day, max 160 mg / day)
2.Parasynthesis when ascites is very large, up to 4-6 liters and protected
with albumin (8 to 10 g IV per liter of parasynthetic fluid (if> 5 L)
3.Fluid restriction (recommended if serum sodium is less than 120-125
mmol / L)
(Gondal and Aronsohn,2016)

12. What is the complication in this case?

Answer:
a.Spontaneous bacterial peritonitis
b.Esophageal varices
c.Hepatoma
d.Hematological disorders
e.Hepatorenal syndrome
f.Liver encephalopathy
(Bacon,2014)

13. How is the prognosis in this case ?

Answer:
Quo ad vitam : dubia ad bonam
Quo ad fungsionam : dubia ad malam (sirosis hepatis) ; dubia ad bonam
(kolelitiasis)

36
 Quo ad sanationam : dubia ad bonam

14. What is the general practitioner’s competence in this case?

Answer:
SKDU 2:
As a general practitioner is able to diagnose and refer the most appropriate
for subsequent patient management. General practitioner can also follow
up on results after referral.

15. What is islamic view in this case?

It means: "O mankind, verily unto dating lessons from your Lord and a
healing for the diseases (that are) in the chest and guidance and mercy for
those who believe." (Qur'an, Yunus: 57)

37
 2.7 Conclusion
Ms. F, a 45 years old female experience yellowish eyes, epigastric pain, urine
that colored like dark tea, itchy skin and spider naevy because suffer to sirosis
hepatis dekompensata ec hepatitis B cronic + kholelitiasis .

2.8 Conseptual Framework

Chronic Hepatitis B

Inflammation of the Sirosis Hepatic Extra Hepatic

Portal Tract Jaundice Obstruction

Canalicullus Billiaris Ductus Biliaris

Liver Fibrosis
Obstruction Obstruction
(kholestasis)

Portal Hypertension Indigestion of Lipid

Splenomegaly thrombocytopenia Indigestion Epigastric Urine Colour

of Bilirubin Darktea
Pain

hematocrit
decreases

38
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