PBL 3b Human Structure

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PBL Group 3B Medical Faculty of Airlangga University

Human Structure Module

General Instructional Objective
After completing this module based on Problem Based Learning, the 2
nd

semester students of Medical Faculty of Airlangga University will be able to:
1. Identify the human body structure
2. Identify the growth and development of the human body
3. Identify the relation between the structures of the human body with a clinical
problem

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CHAPTER ONE
FIRST TUTORIAL
Brain Storming and Cognitive Strategy

1.1 SCENARIO
In the first tutorial, we were given a case or scenario regarding the
module. The scenario is as follows:

1.2 MAIN PROBLEM
From the scenario given, we concluded that the main problem for this
scenario is Vomiting blood and Black stools

1.3 KEYWORDS
1.3.1 Man
1.3.2 58 years old
1.3.3 Vomiting blood
1.3.4 Black stools

1.4 EARLY HYPOTHESIS
1.4.1 Vomiting of blood occurs due to rupture of esophageal varices
A man 58 years old, escorted by his family to the Emergency Room
because of vomiting of blood and black stools

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1.4.2 Black stools occurs because the feces mixed with blood due to rupture
of varicose veins in the rectum

1.5 COGNITIVE STRATEGY
Steps to solve the problem scenario,
1. Group discussion without tutor, suggest idea between students.
2. Group discussion in tutorial, tutor as facilitator.
3. Self learning at library from text books, journal, internets information
or other audiovisual facilities.
4. Arrange group discussions conclusion.
5. Attend plane discussion with informant and present discussions
conclusion if the group chosen as presenter.

1.6 ADDITIONAL QUESTIONS OR INFORMATION
No. Question Reason Answer
1 How is the
endoscopy-test
result?
We assume the
presence of
cirrhosis.
Ask the tutor on the
next meeting
2 What is the Liver
Function Test (LFT)
result?
We assume the
presence of cirrhosis
caused by alcohol.
Not yet done
3 Is there any ascites? We assume the
vomiting blood is
caused by cirrhosis.
Ask the signs.

4 What is the
composition of
traditional medicine
(jamu) that Mr. A
We assume the
is causing Mr. As
sickness.
Traditional medicine
for stomach ache.

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Additional Information :
Patients personal information :
Name : Mr. A
Address : Wonokromo, Surabaya
Age : 58 years old
Occupation : Pedi cab driver
Family status : -
Case :
Vomiting blood (hematemesis) 3 hours before being hospitalized as much as
1 small bucket containing dark-blood colored fishy-smell liquid. No food
left over because since several days, Mr. A doesnt eat.
Complains :
Vomiting blood (hematemesis)
Since 10 days earlier, Mr. A defecate with mushy dark-colored stool
(Melena)
Weaken body
Couldnt get up from bed
Headache
Habits :
Defecate everyday
Refuse treatment
Lose of apptit
Drink sweet tea
consumed?

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Drink traditional medicine (jamu)
Family report :
Other family member never had this kind of illness
Social report :
Was a public transportation driver for 10 years
Enough nutrition (with meat, chicken, and fish diet)
Consume alcohol since teenager until now
Medical history :
Diabetic, hypertension, hepatitis are denied
If Mr. A feels stomachache, he consume traditional medicine (jamu)
Feel prop on his top left stomach since several months earlier

1.7 LEARNING ISSUES 1
1. How about the normal anatomical and histological structure of digestive
system?
2. How was the normal development of the gastrointestinal tract?
3. How about the pathophysiology, etiology and clinical manifestations of
Melena and Hematemesis?
liver cirrhosis?
5. Explain the relationship between liver cirrhosis with esophageal varices
and black stools?
6. How does alcohol and traditional medicine really can cause cirrhosis of
the liver?

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CHAPTER TWO
SECOND TUTORIAL
Problem Analysis

2.1 LEARNING METHODS AND STEPS
2.1.1 Search all the information related to the learning issues from the
internet, text books, and journals.
2.1.2 Critically appraise the information sources to determine which sources
are valid, important, and applicable to answer the learning issues.
2.1.3 Answer the learning issues based on all sorted information.

2.2 ANSWER OF LEARNING ISSUES 1
1. How about the normal anatomical and histological structure of digestive
system?
Answer:
Human digestive system consists of several organs which is
esophagus, Gaster (stomach), intestinum tenue (small intestine), and
intestinum crassum (colon).
(Drake, Vogl & Mitchell, 2012)
A. ESOPHAGUS
The first organ is the esophagus. Esophagus is the channel
formed by the muscles that runs from the pharynx in the neck heading
to the stomach in the abdomen. Location of eshopagus started in
vetebra C VI and ends at vetebra T XI. In the thoracic region

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eshopagus passing on the midsection, right in front of the vetebra. But
when approached diaphragm eshopagus cross the aorta and walk in
front of it, and then passes through the hiatus eshopagus in the
diaphragm in TX and headed to ostium cardiacum of gaster. At the
left of eshopagus there is Aorta Thoracica (descenden). At the anterior
of esophagus there are thrachea and cor. And at the porterior there are
ductus thoracicus, vena hemiazygoz, and posterior intercostalis blood
vessel dextra. (Drake, Vogl & Mitchell, 2012)
Arterial supply of esophagus comes from aorta thoracica, arteriae
bronchiales, rami ascendens of gastrica sinitral artery, rami
eshopageales of gastrica sinitral artery (from coeliacus trunk) and rami
esophageales of phrenica inferior sinitral artery. Vein system of
eshopagus heading to azygoz vein, hemiazygoz vein and rami
esophageales of gastrica sinitral vein. Nervous system of eshopagus is
complex, but generally originated from Vagus nerve, and Sympathetic
trunk. Vagus nerve also form plexus esophageus that divided to two

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(Reinhard & Reinhard 2006)
trunks : Anterior vagalis trunks and posterior vagalis trunks.(Drake,
Vogl & Mitchell, 2012)

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B. GASTER
Gaster is part of gastrointestinal tract that can be dilated the most. Having
a shape like J letter. Lies at epigastrium, umbicalis, and hypochondrium
sinitral region of abdomen. It divided into 4 region : pars cardiaca, pars
gastricus, corpus gastricum, pars pylorica that divided to antrum
pyloricum and canalis pyloricus. There are several features of gaster :
curvatura gastrica major, curvatura gastrica minor, incisura cardiaca and
incisura angularis. Arterial supply of gaster comes from gastrica sinistral
artery, gastrica dextra artery, gastro omentalis dextra artery, gastro
omentalis sinistra artery and gastrica posterior (accessory).

C. INTESTINUM TENUE
This is the longest part of digestive system. The lenght of this part up to
6-7 meters. Its a cannel that narrowed in diameter from the beginning to
the end. Its start from ostium plorus of gaster and ends at plica
illeocaecale. Intestinum tenue divided into three parts : duodenum,
jejenum and ileum.

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Duodenum

This is the first part of intestinal tenue. Its shaped like C letter, near the
head of the pancreas. Duodenum length is about 20-25 cm. Lies at the top
of umbili1cus and has the widest lumen than the rest of intestinum tenue.
Duodenum divided into four parts. They are pars superior, pars
descendens, pars inferior and pars ascenden.
Pars superior clinically called as ampulla or duodenal cap or ulcus
duodenalis. Started from ostium pyloricum gaster and ends at
collum vesicae fellea. Lies at the right of the body of vetebra LI.
Pars decendens started from collum vesica fellea until bottom
edge of vetebra LIII. Papilla duodeni major and minor are found
in this part of duodenum.
Pars Inferior or called pars horizontalis is the longest part of
duodenum.
Pars ascendens runs up until top edge of vetebra LII and ends as
flexura duodenojejunalis.

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Arterial suplly for duodenum are from branches of gastroduodenal artery,
supraduodenalis artery, rami duodenales from several artery and first
branch of jejunales artery. (Drake, Vogl & Mitchell, 2012)

Jejenum
Jejenum is 2/5 proximal part of the rest of intestinum tenue. Its lies at
upper left of the abdomen. Jejenum has wider and thicker lumen than
ileum. Jejenum has more plicae circulares than ileum. Arcade arteriae of
jejenum can not be seen or unclear to be seen. Jejenum also has longer
vasa recta than ileum. Arterial supply of jejenum are from jejunales and
mesentrica superior artery. (Drake, Vogl & Mitchell, 2012)

Ileum
Ileum is 3/5 distal part of the rest of intestinum tenue. Its lies at the
lower right of the abdomen. Ileum has thinner lumen than jejenum. Its
also had lesser plicae circulares. Ileum has more arcade arteriae than the
jejenum, but has shorter vasa recta. At the end, ileum form plica
ileocaecale and furthermore form a sphincter at the meeting of ileum and
intestinum crassum. Arterial supplyof ileum is from ileales artery and a
branch of ileocolica artery. (Drake, Vogl & Mitchell, 2012)

INTESTINUM CRASSUM

The length of intestinum crassum is about 1.5 meters on man. Intestinum
crassum has wider lumen than intestinum tenue. Its function is mainly to
absorbs liquids and salts. Starts from ends of illeum and ends at anus.
Intestinnum crassum is consist of caecum, appendix vermiformis, colon,
rectum, and analis channel. (Drake, Vogl & Mitchell, 2012)

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Caecum is the first part of intestinum crassum. Lies at fossa
illiaca dextra and intraperitoneale. Arterial supply for caecum are
from caecalis anterior artery and caecalis posterior artery.

Appendix vermiformis is narrow tube structure and has a dead
end. Its arterial supply is appendicularis artery.

Colon is divided into colon ascendens, colon transversum and
colon sigmodium. Beetween ascendens colon and transversum
colon lies flexura coli dextra. Between transversum colon and
desendens colon lies flexura coli
sinistra. At lateral of ascendens
and descendens colon there is sulci paracolici dextra and sinistra.
Colon sigmoideum start at apetura pelis superior, and ends at
vetebra SIII. Atreial supply of colon is diferent each parts.

Rectum and analis channel ususally meeting between rectum
and colon sigmoideum is on vetebra SIII. (Drake, Vogl &
Mitchell, 2012)

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LIVER

Liver is the bigest Viscera organ in human Body. It lies mostly on
hypochondrium region. It Fcies divided into two parts, facies
diaphragmatica and facies visceralis.
Liver has a structure called hepatic port. Its main role as the
entrance for hepatica artery and hepatic porta veins. Thos structure also
used as gateaway for hepatic duct.
Liver got its arterialitation from hepatica dextra and hepatica
sinistra artery from hepatica prpria artery. (Drake, Vogl & Mitchell,
2012)

L
i
e
s

a
t

t
h
e
(Netter, 2010)
(Netter, 2010)

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right side of abomen cavity, under the diaphragm, had a spongy
consistency, had a smooth surface, has a brownish red color, consists of 4
lobes: right, left, caudate, and quadrate. Right lobe is the largest lobe,
bound by falciforme and triangular hepatic ligament, covered by a thin
fibrous capsule that Glisson's capsules were continued until the porta
hepatic.
In the posterior ligament venosum there, attached to the left portal
vein and attached to the top of the inferior vena cava. At birth, the
umbilical vein and ductus closed and menjadipita venosum fibrosum, at
the bottom there gallbladder, serves to emulsify fat and channeled
through the cystic duct (fitriani, 2008)
The Liver had a very important role because the hepatic porta veins
is entering liver. This veins is carrying blood contains of rich nutrients
form digestive system. In the liver these nutrient is selected and
neutralized to avoid harmful substance harm the body. Many enzymes
and drugs also being activated in this organ. So when distributed within
the body, these subtance could work efectively.

P
A
N
C
R
E
A
S
N
o
r
m
a
(Netter, 2010)

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lly pancreas lies at the back of gaster. It divided into caput pancreatic,
processus uncinatus, collum pancreatic, corpus pancreatic and cauda
pancreatic.
Pancreas will form ductus pancreaticus that starts from the cauda
pancreatic and ends at the duodenum. Ductus pacreaticus will form
papilla duodeni mayor and minor. Papilla duodeni mayor is inserted by
ampulla hepatopancreatica that formed by ductus pancreaticus and ductus
choledochus. Differs with pailla duodeni mayor, papilla duodeni minor is
inserted only by ductus pancreaticus accesorius. Ductus pancreaticus
mayor and minor ussually connected.

T
her
e
are
ma
ny
art
ery
tha
t
su
ppl
y
the
pancreas such as Gastroduodenal artery, pancreatic duodenal artery,
pancreatic duodenalis superior posterior artery, pancreatica
dorsalisnartery, and many more. (Drake, Vogl & Mitchell, 2012)
SPLEEN
Spleen is developed as part of vascular system of the body. In
mature man lien lies at the front of diaphragm, its about beetween costae
(Netter, 2010)

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9 and costae 10. Its located at hypochondroium sinistra region of
abdomen.
Spleen is connected to curvatura mayor of gaster by gastrolienale
ligament and ren sinister by splenorenale ligament. Those two ligament
are part of omentum majus. Spleen is surrounded by peritoneum viscerale
except on the hillum area at the medial face of the lien.

There are some circumstance that the spleen could swell very big.
This patological circumstances called by splenomegally. It occur at many
clinical circumstances, such as infection, cancer, hematological
malignancy, and in mr. As case caused by portal hypertension.
2. How was the normal development of the gastrointestinal tract?

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Answer:
In the development of digestive system, the gastrointestinal tract
could be divided in three part by its arteries. These parts are foregut,
midgut and hindgut. Viscera that included in foregut start from
esophagus until the cranial part of duodenum. Foregut is arterialized by
celiac artery. In the midgut, it is arterialized by Mesenteric Superior
artery and the viscera are descending part of duodenum until two-third of
transversal colon. The mid gut is arterialized by Mesenteric Inferior
artery, and the viscera are start from last one-third of transversal colon
until superior part of rectum.

All of the viscera of the gastrointestinal tract are fixated to the
wall of abdomen. This fixator is called mesentery. By this mesentery that
covered them, the viscera could be divided as retroperitoneal or
intraperitoneal. An organ is called retroperitoneal if half of the surface or
less of the organ is covered with the mesentery. And, the organ is called
intraperitoneal if two-third or all of its surface are covered up with the
mesentery.

Foregut
The viscera that included in the foregut are esophagus, stomach,
cranial part of duodenum, pancreas, liver, gallbladder and spleen.
Foregut is the only part of gastrointestinal tract which is almost all of its
viscera are fixated at the dorsal and ventral wall of abdomen by dorsal
mesentery and ventral mesentery.
The foregut starts from the gut tube. The anterior part of the gut
tube will rise gallbladder and liver bud and the ventral pancreatic bud
into the ventral mesentery. And, the posterior part of the gut tube will

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rise dorsal pancreatic bud and spleen bud into the dorsal mesentery. As
the rapid grow of the organ the position of them are change too, they are
move clockwise. As the dorsal mesentery lengthen and the clockwise
movement of the organs remain a room that called omental bursa (Lesser
sac). Leaving the spleen at the left side at the body. The dorsal bud of
pancreas become the body ant tail of pancreas and the ventral bud of
pancreas become the head of pancreas, because of this movement there
be a fusion in this two part of pancreas to becoming one and the fusion of
its mesentery with the dorsal wall of abdomen, remain pancreas to be
retroperitoneal except the tail of pancreas. Because of this movement too,
the stomach remain at the left side of the body, anteromedial from the
spleen and remain intraperitoneal. The duodenum moves to the right and
fuses with the dorsal wall of abdomen except the cranial part leaving an
opening way called epiploic foramen (omental foramen). The liver and
gallbladder remain at the right side of the body and intraperitoneal except
the bare area of liver that meets with the diaphragm and the neck of
gallbladder that meets the liver.
The mesenteries that covered up all of the organs making a room
called greater sac. And, the ventral mesentery becomes the falciform
ligament, the dorsal mesentery between the liver and stomach and the
cranial part of duodenum becomes the lesser omentum, and the dorsal
mesentery between dorsal wall of abdomen and stomach creating a
doubled layer of peritoneum with an apron-like structure called greater
omentum.

Midgut
The viscera of the midgut are distal part of duodenum, jejunum,
ileum caecum, ascending colon and two-third of transversal colon. At the

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first development of the midgut, there are a connection between the
intestinal loop with the yolk sac via vitelline duct, anteriorly.
In the sixth week of development, the gastrointestinal tract grows
rapidly, resulting the mid gut to herniating out to the extraembryonic
cavity. The midgut doing a movement too, counterclockwise from the
longitudinal axis. While the movement happens, the body grows in size,
the connection with the yolk sac is lost and the midgut entering back to
the abdominal cavity. The part of the intestinal loop which reenter firstly
to the abdominal cavity will lie at the left side and the last part will lie on
the right side of the abdominal cavity. The cecal, which is the last part of
the loop that reenter to the cavity, lies at the right side, and descended to
the inferior right of the abdomen cavity. (Sadler, 2004)

The jejunum and ileum remains intraperitoneal until cecum, from
dorsal mesentery. Ascending colon remains retroperitoneal because a
fusion of its mesentery with the dorsal wall of abdomen. Meanwhile, the
transversal colon remains intraperitoneal too with its mesentery, and the
greater sac fuses with the mesentery of transversal colon and overlying
them.

Hindgut
The viscera that included in the hindgut are last one-third of
transversal colon, descend colon, colon sigmoid and superior part of
rectum. The hindgut moves to the right side of the cavity. The dorsal
mesentery of descended colon fuses with the posterior wall of abdomen,
remains it retroperitoneal. While the sigmoid colon retain its mesentery
and remains intraperitoneal. (Drake, Vogl and Mitchell, 2009)

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Melena and Hematemesis?
Answer:
Hematemesis was vomiting of blood, while Melena is black
bowel movements that resemble asphalt, usually due to upper tract
bleeding started the esophagus to the duodenum. Dark red / black comes
from the conversion of hemoglobin into hematin by bacteria after 14
hours.
Signs and symptoms of common
Vomiting blood, bowel movements dark red (Melena), bleeding from the
rectum (hematoskezia) rapid pulse, low blood pressure, cold and wet
acral palpable, abdominal pain, decreased appetite, in case of prolonged
bleeding can lead to anemia , fatigue, pallor, pain, and dizziness.
Arise after patients taking drugs that cause stomach irritation, before
vomiting, patients usually complain of pain, the patient experienced
dispesi include nausea, vomiting, pain, and before hematemesis preceded
pain or pain in the epigastrium associated with food (Muhammad, 2012)

liver cirrhosis?
Answer:
Cirrhosis of the liver is a condition that diffuse destruction of the
structure of the liver caused by regeneration of hepatic parenchymal cells
has occurred, in which diffuse increase in connective tissue has resulted
in disorganization of the lobular architecture. A complete liver cirrhosis
is a disease in which the microcirculation , vascular anatomy and whole
liver system architecture has been changed into irregular connective
tissue as well as the addition ( fibrosis ) in the surrounding liver

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parenchyma regenerated . In the evolution of many chronic liver
diseases, cirrhosis is a stage that is considered to be irreversible.
Cirrhosis can be stabilized by controlling the primary disease but its
presence implies consequences such as portal hypertension, intrahepatic
shunting of blood, impaired parenchymal function affecting protein
synthesis, hormone metabolism and excretion of bile and bile salts.
(Gunnarsdttir, 2008) Patients with liver cirrhosis more prevalent in men
compared with women of about 1.6 : 1 with the largest age between the
ages of 30-59 years . (Danastri, 2013) The main causes of cirrhosis are:
alcoholic liver disease (ALD), hepatitis B (HBV), hepatitis C (HCV),
non-alcoholic steatohepatitis (NASH), haemochromatosis, auto-immune
hepatitis (AIH), primary biliary cirrhosis (PBC) and primary sclerosing
cholangitis (PSC). The natural history of cirrhosis can be divided into a
preclinical and a subsequent clinical phase. The preclinical phase is
usually prolonged over several years; once clinical events occur, such as,
ascites, encephalopathy, variceal bleeding or the development of
hepatocellular carcinoma the remaining course of the disease is much
shorter and usually fatal. (Gunnarsdttir, 2008)

5. Explain the relationship between liver cirrhosis with esophageal varices
and black stools?
Answer:
Liver cirrhosis is a liver disease that is irreversible and serious.
The disease is characterized by the formation of connective tissue with
nodules. Cirrhosis of the liver is also characterized by inflammation of
extensive necrosis of liver cells, connective tissue formation and
regenerrating nodules. Distortion of the liver architecture will lead to
changes in the circulation micro and macro become irregular due to the
addition of the connective tissue and nodules. Cirrhosis can also cause

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progressive liver dysfunction, and is a major cause of mortality and
morbidity in the world. In early cirrhosis of the liver is usually enlarged,
palpable rubbery, blunt edge, and feels pain when pressed. Cirrhosis of
the liver causes liver damage sustained.
It is known that this disease is the last stage of Chronic liver disease and
hardening of the liver which will cause deterioration of liver function and
normal heart shape will change with the emphasis on blood vessels and
disruption of the portal venous blood flow eventually lead to portal
hypertension (Universitas Sumatera Utara, nd).

Portal hypertension is an increase in blood pressure in the
vascular system called the portal venous system. Normally, blood vessels
originating from the stomach, intestine, spleen, and pancreas, merge into
the portal vein , which then branched into the small blood vessels and
moves through the heart . If the blood vessels in the liver is blocked ,
blood flow will be difficult , thus causing high pressure in the portal
system . When the pressure becomes too high , the blood will find other
ways to flow back to the heart , which pumps blood to the lungs , where
it can eliminate waste products and take oxygen . Blood can travel to the
deep veins/esophageal varices of the esophagus (National Cardiovascular
Center Harapan Kita, 2011).

Esophageal varices was visibly protruded veins ranging from
proximal to distal esophagus due to portal hypertension . The blood
vessels of the intestines will also flow into the portal vein in the liver . If
there is a blockage in the heart (Universitas Sumatera Utara, nd) .
There will be increasing pressure on the small intestine and colon.
So that would eventually lead to bleeding . Black stool ( mixed blood )

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and foul smelling is the end result . This disease is called melena
(Hastings, 2005) .

6. How does alcohol and traditional medicine really can cause cirrhosis of
the liver?
Answer:
Negative effect of the traditional medicine
Currently there are still many Indonesian people who believe in
traditional medicine, traditional medicine is one of the inexpensive and
easily obtained is by eating herbs for traditional medicine. It is not
wrong, because herbal medicine is a traditional medicine that is
improving the overall tissue damage. (Susanti, 2014)
In contrast to chemical drugs, chemical drugs and improving the
overall network are not yet working directly on the target pain. (Susanti,
2014) This causes it takes a little time to heal and the results are only for
temporary even just to ease the pain. As in traditional medicine takes a
long time to be able to repair all the damaged tissue.
Herein lies the weakness of traditional medicine than chemical
drugs, but people prefer drugs that can instantly cure and minimal side
effects. This is why many manufacturers of herbal medicine (traditional
medicine) that started adding some chemicals behind the traditional
word. Long-term use of these chemicals can impair organ function.
According to Susanti (2014), some of the chemicals found in traditional
medicine, namely:
Sildenafil Citrate: can cause headaches, dizziness, nausea,
abdominal pain, visual disturbances, rhinitis (inflammation of the nose),
and death.
Fenilbutason: may cause nausea, vomiting, skin rash, edema,

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stomach bleeding, stomach pain, hypersensitivity reactions, hepatitis,
renal failure.
Mefenamic acid: may cause drowsiness, diarrhea, skin rashes,
and seizures, and is contraindicated for people with peptic ulcers
/ gut, asthma, and kidney.
Prednisone: may cause moon face (round face = like the moon,
chubby); gastrointestinal disturbances such as nausea and
stomach ulcers; bone loss, etc..
Metampiron: can cause gastrointestinal disturbances such as
nausea, stomach bleeding, burning, and nervous system
disorders such as tinnitus (ringing in the ears) etc..
Paracetamol: the long-term use can cause liver damage.

Negative effect of the alcohol

Ethanol or ethyl alcohol, or better known as alcohol is an ingredient
contained in some beverages, like beer. Drinks that contain certain levels
of alcohol can lead to hangovers. This is because alcohol including
'sedative hypnotic' drug, alcohol in high levels can reduce the work of the
central nervous system. (ALAC, 2012)
Consumption of alcohol at high levels and in a long period of time
can cause some bad effects on the organs of the body. Alcohol not only
the impact of physical health, alcohol can also adversely affect the
mental health of a person.
Consumption of alcohol in high levels is one of the causes of death
at this time, either directly or indirectly. The cause of death that caused
by alcohol, can be a chronic disease such as cancer or diseases of alcohol
poisoning. While the cause of death by alcohol indirectly is suicide,

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because alcohol has affected the mental health of a person so as to cause
harm to the person himself.
According to ALAC (2012), alcohol is absorbed into the body by
the blood, 80% through the small intestine and the remaining 20% is
absorbed through the stomach. Alcohol has been absorbed by the blood
will be taken to all organs in the body. However, 90% occur in the
process of alcohol metabolism in the liver and 10% more alcohol
metabolism process through the lungs and kidneys. The process of
alcohol metabolism in the liver in the form of the decomposition of
alcohol in the form of toxic substances into the water and then elaborated
further up into carbon dioxide. However, the liver can break down
alcohol only in certain levels every hour.

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Adapted from : Alcohol Advisory Council of New Zealand. Alcohol the Body &
Health Effects : A Brief Overview

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Consumption of alcohol at high levels and the long periods of time can
lead to several chronic diseases of the liver, chronic disease is steatosis
(fatty liver), acute alcoholic hepatitis, and cirrhosis.
Steatosis or fatty liver disease is the first stage of cirrhosis is
alcohol, this is caused by the buildup of fat (triglycerides) in the liver as a
result of excessive alcohol metabolism. (Corwin, 2009) At this stage is
reversible, with no symptoms, and can be cured within a few months if
the consumption of alcohol is stopped. Steatosis can occur in 90-100% of
alcohol abusers. (ALAC,2012)
The second stage of the disease hepatitis cirrhosis alcohol is
alcohol, which is inflammation of the liver cells. Hepatitis is caused by
alcohol toxicity results of alcohol metabolism in the liver which
promotes liver cell inflammation and stimulate apoptosis in liver cells.
(Corwin, 2009) Because apoptosis is the one that cause scarring and
fibrous tissue in the liver cells. This disease affects an estimated 10-35%
of alcohol addicts, this stage is reversible if the consumption of alcohol is
stopped. (ALAC, 2012) Symptoms that occur in this stage may include
malaise, tiredness, jaundice (yellow skin and eyes), swelling of the
abdomen, and an enlarged liver.
According to ALAC (2012), approximately 40% of patients with
hepatitis alcohol leads to liver cirrhosis. Cirrhosis is an end-stage liver
cirrhosis and alcohol is irreversible. At this stage apoptotic tissue will
turn into scar tissue. Chronic inflammation causing swelling and
interstitial edema, swelling can cause the collapse of the small blood
vessels and increases the resistance to blood vessels that pass through the
liver, which causes the portal vein hypertension and assists. It can also
arise esophageal varices, rectum, abdomen, and hepatocellular Icterus.
(Corwin, 2009)

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Adapted from : Table 1 in Jackson, P. and Gleeson, D. (2010). Alcoholic
liver disease. Continuing Education in Anaesthesia, Critical Care &
Pain, [online] 10(3), pp.66-71.

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Adapted from : Table 1 in Jackson, P. and Gleeson, D. (2010). Alcoholic
liver disease. Continuing Education in Anaesthesia, Critical Care &
Pain, [online] 10(3), pp.66-71.

2.3 OBSTACLES
- Having difficulties in knowing the aim of the issue
- Having difficulties in finding the valid websites
- Having difficulties in finding the reliable and relevant websites
- Having difficulties to determine the main idea
- Having difficulties to determine the main problem
- Having difficulties in finding the early concept mapping
- Having difficulties in finding the right answers for learning issues

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2.4 EARLY CONCEPT MAPPING

Alkohol LIVER
Hepatitis B
Hepatitis C
Parenchyma cells
damaged
Liver function
damaged
Portal vein clogged up
Portal hypertension
Liver cirrhosis
Esophageal varices
Melena Hematemesis

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2.5 ANALYSIS
Consumption of alcohol at high levels and the long periods of time can lead
to several chronic diseases of the liver, chronic disease is steatosis (fatty liver),
acute alcoholic hepatitis, and cirrhosis. Alcohol could harm the veins and
artery, this is caused by the build up of fat (triglycerides) in the liver In this
case.
In this case, we believe that Mr. A got cirrhosis diasese. Cirrosis is a disease
of the liver that characterized by formation of conective tissue and nodules to
replace demaged liver tissue and it will lead to the hardening of the liver. That
means that Mr. As liver is badly damaged and can no longer functioning
properly. In this case the vascularization of the liver will disturbed. Especially
bllood vessel that lead to liver, such as porta hepatica veins.
Veins that comes from gaster, pancreatic, intestinum tenue and intestinum
crassum all ends up in portal vein in liver. But, because of portal veins is
blocked up by buildn up of fat (triglycerides) it makes its liver got portal
hypertension. Portal hypertension is an increase in blood pressure in the
vascular system called the portal venous system. Blood which is, it should
normally go through portal venous, it will find other ways to flow back to the
liver. Blood will flow to the deep vein or oesophagical varices.
In Mr. As case his eshophagical varices cause massive bleeding. The blood
flowing down to gaster and trigger vomiting of blood. In gaster, the blood
mixed with gastric acid will produce black paste. This event will result to
production of black feces or melena.
2.6 LEARNING ISSUES 2
1. Describe the signs and symptoms of what is obtained in the additional
information coherently (Head/Neck, Thorax, Abdomen and Extremity)

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2. Based on the signs and symptoms that occur, which structures are
changing?
2.7 ADDITIONAL QUESTION OR INFORMATION

A
namn
esis
result
:
a. V
ital sign :
Weight : 60 kg
Height : 155 cm
Pulse : 112 times/minute
RR : 24 times/minute
Temperature : 38.7 C
Tension : 90/60

b. Head/neck :
Anemia
Icterus
Cyanosis

c. Thorax :
Symmetrical, No retraction
Lung : Vesicular breath sound, no additional sound
Heart : No noisy sound

No. Question Reason Answer
1 How is the
endoscopy-test
result?
We assume the
presence of
cirrhosis.
Ask the tutor
2 What is the Liver
Function Test(LFT)
result?
Liver function test
result is yet
unknown.
SGOT = 87 IU/L
SGPT = 96 IU/L

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d. Extremities :
Cold, pale, and wet
Pitting edema presence on feet and leg

e. Abdomen :
Convex abdomen
Collateral veins are visible
Protruding umbilicus
Auscultation sound louder
Shifting dullness
Lien is palpable on S2 (Splenomegaly)
Presence of spider naevi

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CHAPTER THREE
THIRD TUTORIAL
Problem Solving
3.1 ANSWER OF LEARNING ISSUES 2
1. Describe the signs and symptoms of what is obtained in the additional
information coherently (Head/Neck, Thorax, Abdomen and Extremity)
2. Based on the signs and symptoms that occur, which structures are
changing?
Answer :
Head / Neck
Jaundice is a yellowing of the sclera, skin or other tissues due to the
accumulation of bilirubin in the body or accumulation of bilirubin in the
blood of more than 5 mg / dl within 24 hours, which indicates the
occurrence of functional disorders of the liver, biliary system, or
hematologic system Symptoms of jaundice, such as: skin color is yellow,
the observation well with little sunlight and pressing to eliminate skin color
due to the influence of blood circulation. The degree of jaundice is
determined by looking at the direct and indirect bilirubin levels, or clinically
by Kremer under ordinary light (day-light). Kern-clinical symptoms of
jaundice in the beginning is not clear, among other things: the baby will not
suck, latergi, eyes spinning, erratic movements (involuntary movements),
seizures, elevated muscle tone, stiff neck and epistotonus
(Khairunisak,2013)

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Anemia was defined as a decrease in hemoglobin levels or the number of
red blood cells in the blood in which the decrease in hemoglobin level is
usually accompanied by a decrease in red cell count and hematocrit. Anemia
is not a diagnosis, but a collection of symptoms of a disease. Anemia is
often regarded as an ordinary disease. When experiencing symptoms of
anemia such as fatigue, lethargy, pale, and cold sweats (Margarina S,
Herawati, & Yasa, 2012)
Thorax
Spider naevi
Spider naevi is cutaneous manifestations, is located near the surface of the
skin and looks like a collection of abnormal blood vessels . They appear as a
red dot in the center, reddish extensions that reach out from the center, and
most often found on the face and neck. But they can appear in other part of
body, such as thorax, arms, shoulder, and hands. Spider naevi will dissapear
when the pressure is applied. If the pressure is removed, they will reappear.
(Medlineplus, 2012)
Spider naevi occur in pregnant women and also can be seen in healthy
children. Spider naevi appears more commonly in patients with chronic liver
disease. (Detry & Roover, 2009)
Spider naevi is related to liver disease. It is created from dilatation of an
arteriole with multiple radiating vessels coming out from it. Pressure on the
central arteriole make the entire lesion will disappear and will reappear
when the pressure is removed. We usually can see the lesions in the area of
superior vena cava. The lesions varies but more than a couple must concern
about underlying liver disease. Histologically, it composed by central
arteriole with radial branching of telangiectasia in the periphery. The other
theories have given different explanation, such as increased levels of
vascular endothelial growth factor, basic fibroblast growth factor,

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estrogen/testosterone ratio and substance P as reason for their development.
In majority subjects, spider naevi is usually asymptomatic. (Sharma et al.,
2012)
Abdomen
HARD DISTENDED ABDOMEN AND COLLATERAL VEIN

In patients with abdominal symptoms appear hard distended
abdomen and looks collateral vein. It seems collaterall vein indicates that
the presence of portal vein obstructed in patients, either outside or inside the
liver.
Hard distended abdomen with very stretched skin, protruding hips
and umbilicus enter a description of ascites. This text can view in
Departement of Academic Affairs
James H. Quillen College of Medicine Site(n.d.)
The main abdominal vein pattern with the direction of flow away
from the umbilicus is often a reflection of portal hypertension; the collateral
venous flow away from the lower abdomen to the umbilicus support the
inferior vena cava obstruction; flow downward toward the umbilicus
showed superior vena cava obstruction (Harrison, 1999)
Portal system is the coverage of all the veins that carry blood from
the abdominal part of the digestive tract of the spleen, pancreas and gall
bladder. Entering the portal vein to the liver at the hepatic portal, there are
two main branches that each have lobes, and there are no valves in the larger
branches.Portal vein is formed from the union of upper mesenteric vein and
splenic vein posteriorly in the lumbar spine II. It extends slightly right of the
center line for a distance of 5.5 to 5.8 cm into the hepatic portal. Intrahepatic
portal vein has a segmental distribution accompany with hepatic artery .The
superior vena mecentrica formed by the small intestine, colon and
pancreatic head, and the irregularity of the vein gartroepiploic . Splenic vein
consists of 5-15 channels derived from splenic hilum and joined near the tail

37 | P a g e


of the pancreas with gastric short channel of the main splenic vein . The
inferior mesenteric vein carries blood of the left colon and rectum , usually
enters the medial part , but he entered in junction of the superior mesenteric
and splenic veins .
Portal blood flow around the human body 1000 - 1200 mL / min. Portal
pressure was 7 mmHg.
Inhibition of the portal vein can occur outside the liver or in the liver.
(Andrew K, 2011)

Intrahepatic obstruction
Actually, portal venous blood flow 100 % recovered from the
hepatic vein , which in kirosis only 13 % were stunted . The rest goes
collateral channels which divided four groups: Group I: where protective
epithelium adjoins absorptive epithelium; Group II : in the falciform
ligament through the paraumbilical veins, relics of the umbilical circulation
of the fetus; Group III : where the abdominal organs are in contact with the
retroperitoneal tissues or adherent to the abdominal wall . These collaterals
run from the liver to the diaphragm and in the splenorenal ligament and
omentum. They include lumbar veins and veins developing in scars of
previous operations or in small or large bowel stomach; Group IV: portal
venous blood is Carried to the left renal vein . This may be through directly
entering the blood from the splenic vein or via diaphragmatic , pancreatic ,
gastric or left adrenal veins (Andrew K, 2011)

Extrahepatic obstruction
If there is inhibition in extrahepatic, the addition of collateral form
and return blood to enter the portal vein liver These in the hepatic portal
beyond the block . They include the veins at the hilum, venae comitantes of
the portal vein and hepatic arteries , veins in the suspensory ligaments of the
liver and diaphragmatic and omental veins . Lumbar collaterals may be very
large Collaterals usually imply portal hypertension , although occasionally if

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the collateral circulation is very extensive portal pressure may fall .
Conversely , portal hypertension of short duration can exist without a
demonstrable collateral circulation . A large portal - systemic shunt may
lead to hepatic encephalopathy, septicaemias due to intestinal organisms ,
and other circulatory and metabolic effects .(Andrew K, 2011)
Portal hypertension is the term used because of the pressure in the
portal vein system. Portal hypertension may be caused by intrinsic liver
disease, obstruction, or a structural change that may result in an increase in
portal venous flow. (Hopkins, n.d.)

PROMINENT UMBILICUS

Prominent collateral veins radiating from the umbillicus are termed caput
medusa. This is one of result of portal hypertension. This is rare and usually
only one or two veins, frequently epigastric. Normally abdominal veins are
invisible or barely visible. (Hopkins, n.d.) Loss of abdominal wall fatt or
increased pressure in the superior vena cava (SVC), inferior vena cava
(IVC) or portal vein can make the vessels visible, particularly in the red or
infrared spectrum. The normal direction of blood flow in abdominal veins is
upward above the umbilicus, and downward below the umbilicus. In portal
hypertension the direction of flow is normal; in SVC obstruction, the flow is
all downward; and in IVC obstruction the flow is all upward. (Quillen, n.d)

THE AUSCULTATION OF ABDOMEN

In the patient's abdomen showed increased auscultation, lively sound. It was
suspected because of the increase in fluid and air in the dilated viscus
concave. Careful auscultation over the enlarged liver sometimes harsh bruit,
that indicates vascular tumors, especially hepatoma, or friction rub rough
surface of the nodules. Venous Hurn on umbilicus may indicate portal

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hypertension and increased collateral blood flow in vicinity of the liver.
(Harrison, 1999)

Shifting dullness

Shifting dullnes is a physical examination for detection of ascites. The steps
of shifting dullness are when the patient is supine, percuss across the
abdomen as for flank dullness, with the point of transition from tympany to
dullness signed. Then, te patient is rolled on side away from the examiner,
and percussion from the umbilicus to flank area is repeated.The result is
positive and ascites is present if the area of dullness will shift to the
dependent site and the area of tympany will shift toward the top. We must
note that the shift in zone of tympany with position change will usually be at
least 3 cm when ascites is present.(University of Washington Department of
Medicine, n.d.)
Ascites is the excessive accumulation of fluid in the abdominal cavity, space
between the lining of abdomen and organs in abdomen. Liver damage,
including hepatitis C or B infection and alcohol abuse can causes ascites.
(University of Maryland Medical Center, 2014) The symptoms of ascites are
abdomen gradually becomes distended, nausea, vomiting, early satiety,
dyspnea, lower extremity edema, weight gain and reduced mobility. Ascitic
fluid give pressure on the diaphragm and causes shortness of breath. Ascites
is related to portal hypertension, which is usually related to liver cirrhosis.
(Saif et al., 2009)
The development mechanism of ascites in cirrhosis is multifactorial. The
initial factors are portal hypertension, decrease in colloid osmotic pressure
due to hypoalbuminemia, the retention of sodium and water, and increased
synthesis of liver and lymph flow. They make a nonfuctional circulatory.

40 | P a g e


There are some characteristic of circulatory dysfunction, such as arterial
vasodilation, arterial hypotension, high cardiac output and hypervolemia
and to renal sodium and water retention.The increase synthesis of local
vasodilatory proven that arterial vasolidation in cirrhosis occurs in the
splanchnic circlulation. The vascular resistance in vascular territories, such
as kidney, muscle, skin, and brain can be normal or increased. Splanchnic
arterial vasodilation also triggers hemodynamics in the splanchnic
microcirculation. The main factor increasing hydrostatic pressure in the
splanchnic capillaries that leads to an excessive production of splanchnic
lymph over lymph return are the rapid and high inflow of arterial blood into
the splanchnic microcirculation. Lymph leakage from the liver and other
splanchnic organs causes fluid accumulation in the abdominal cavity.
Constant renal sodium and water retention preserves ascites formation.
(Arroyo, 2002)

Lien is in the sacral 2

From some of the literature, it was found that patients with liver cirrhosis
often showed the characteristics of splenomegaly and thrombocytopenia. In
a study conducted by Madhotra et al., (2002) found that patients with
esophageal varices liver cirrhosis thrombocytopenia and splenomegaly are
inferred to be a predictor of the occurrence of esophageal varices.

Splenomegaly

Splenomegaly is a pathological condition in which the structure of the
spleen enlargement. The structure of the spleen, which is located in the
abdomen region is the largest lymphoid glands and located on the front and
near the back of the abdominal cavity between the diaphragm and the

41 | P a g e


stomach. Spleen is an organ could be categorized as RES
(Retichuloendothelial System) that are anatomically normal along the costa
IX, X, and XI and the left inferior limb goes forward as far as the linea
axilaris media. Spleen or lien also an intra-peritoneal organs. The function
of spleen is accumulates lymphocytes and macrophages, degradates
erythrocytes, as blood reservoirs, and as an organ of defense against
infection of foreign particles into the blood.
A physical examination is done to determine the existence of a lien
splenomegaly. To determine whether there is splenomegaly, can be done
with palpation examination and percussion.
In case of splenomegaly, the spleen enlarges in caudomedioanterior
direction. Therefore, palpation of the spleen is done along the schuffers
line, the line extending from Spina Ischiadica Anterior Superior (SIAS)
dextra , passing through the umbilicus to the left of arcus costae
Meanwhile, to do percussion on lien, can be done in the Traube area,
which is a place located in the ICS (intercostalis space) and axillaries media
line. Normally it sounds like timpani (after first percussion), and then
patients are asked to breathe in and hold, and then do the second percussion.
If it is sound like timpani again, like the first percussion, the spleen is in
normal condition, but if it sounds dim, it could be guess that the spleen in
splenomegaly condition, ehich is larger than a normal spleen.
According to research whic is done by Andriana (2013), it is obtained
that splenomegaly can be one of the predictor in occurrence of esophageal
varices with p = 0.000, which means there is a significant relationship
between splenomegaly with esophageal varices.
Splenomegaly which is caused of portal hypertension occurs as a result
of retrograt pressure in the spleen. In portal hypertension, spleen is
enlarging in line with retrograt pressure on the portal vein and then the
spleen vein. Splenomegaly in cirrhosis can be explained by chronic passive
congestion due to obstruction and increased blood pressure in the splenic
vein, which is a branch of the portal veins.

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Trombocytopenia

Thrombocytopenia is a disorder associated with the presence of
splenomegaly, which is also one of esophageal varices signs.
Trombocytopenia is a condition in which the number of platelets in the body
is low or below normal.
Research conducted by Arulprakash et al. concluded that the
thrombocytopenia and spleen size can be used as predictors of the
occurrence of esophageal varices. Later research by Prihatini et al. in
Indonesia shows the number of platelets can be used as predictors of the
occurrence of esophageal varices.
Meanwhile, the research done by Andriana (2013) found the relationship
between trombocytopenia with esophageal varices. The obtained data shows
that thrombocytopenia is more common in patients with Esophageal varices
(63.8 %) compared with patients without esophageal varices (36.2 %).
Therefore, it could be concluded that trombocytopenia is one of indicator of
presence of esophageal varices. Moreover, could be said as a good indicator
one (Madhorta et al., 2002).
The splenomegaly could be underwent because the accumulation platelet
in the spleen counts more than 80 %, which is normally just about 30%, so
that the examination of the circumstances found in peripheral
thrombocytopenia . In addition to inadequate production of TPO in
advanced liver disease is the cause of thrombocytopenia.

Hypoalbuminemia

The other indicator of the presence of esophageal varices in patients is
undergoing hypoalbuminemia. Hypoalbuminemia is a condition which is
below normal or low in albumin levels. Sarwar et al, found that in 65
patients who had hepatic cirrhosis esophageal varices who examined 50

43 | P a g e


patients had acquired thrombocytopenia and hypoalbuminemia. Patients
with serum albumin < 2.95 g / dl, platelet count < 88 x 103/muL and portal
vein diameter > 11 mm are more likely to have high grade varices.
Obtained data from Yenni (2013) showed that hypoalbuminemia occurs
more frequently in patients with Esophageal varices (52.2 %) compared
with patients without esophageal varices (47.8 %).
The humans liver produces about 12 grams of albumin per day which is
25 % of total liver protein synthesis and half the amount of protein secreted.
In patients with liver cirrhosis, the level of serum albumin decreases, and
named as hypoalbuminemia, due to decretion in synthesis, due to hepatic
parenchymal cell necrosis.
With the onset of the scar tissue to secrete albumin liver function
progressively reduced as well as increased collateral flow to the portal
hypertension that caused esophageal varices.

Extremity
Edema is a swelling because of an increase of interstitial fluid volume
(Ely, Osheroff, Chambliss and Ebell, 2006). Edema that exist on leg usually
has two types: venous edema and lymphedema. W Peter Gorman (2000)
said that venous edema consists of overage low viscosity, lack of protein in
interstitial fluid that produced from the increase of capillary filtration that
cannot be accommodated by a normal lymphatic system. While
Lymphedema consists of overage protein-rich interstitial fluid within the
skin and subcutaneous tissue that produced from lymphatic dysfunction
(Mortimer, 2000)
Cutaneous edema is referred to as "pitting" when, after pressure is
applied to a small area, the indentation persists after the release of the
pressure. Peripheral pitting edema, as shown in the illustration, is the more
common type, resulting from water retention. It can be caused by systemic
diseases, pregnancy in some women, either directly or as a result of heart

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failure, or local conditions such as varicose veins, thrombophlebitis, insect
bites, and dermatitis. Non-pitting edema is observed when the indentation
does not persist. It is associated with such conditions as lymphedema,
lipedema, and myxedema (Reviews, 2013).
The pitting edema begins when capillary hypertension results in the
movement of protein-poor fluid into the interstitial spaces, reducing the
concentration of tissue proteins and decreasing tissue colloid osmotic
pressure. Because solute is excluded from a large portion of gel water in the
extracellular matrix, the rapidity of the decrease in tissue protein
concentration that occurs in response to increased interstitial fluid volume is
enhanced (Joshua Scallan, 2014). This capillary hypertension generally
caused by the blockage of veins draining a specific set of capillaries (in this
case lower extremities capillaries) that caused by the increased of portal
venous pressure which we can connect with cirrhosis if it appear with
ascites as well.
3.2 ADDITIONAL QUESTION OR INFORMATION
Additional information:
Endoscopy-test result :
Lot of big esophageal varices, especially on 1/3 distal esophagus near
gastric esophagus junction.
Gastric mucosal hyperemia with some small reddish spots

Blood test result :
SGPT : 96 IU/L
SGOT : 87 IU/L
HBSAG : non reactive
Anti HCV : non reactive
Hb : 5,1 g/dl hypo (normal : 12 g/dl)

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Leukocyte : 8900 cells/mmnormal
Thrombosis : 63000 cells/mmhypo (normal : 150000-450000
cells/mm)
Albumin : 2,3 g/dl hypo (normal: 3,4-5,4 g/dl)

USG abdomen-test result :
Narrow liver
Liver contour nodular
Rough surface with eco image heterogeneously increased
Presence of fluid in peritoneum cavity
Swelling lien with eco image roughly increased
Widening of portal veins and upper mesenterical veins

3.3 FINAL HYPOTHESIS
3.3.1 Vomiting of blood caused by rupture of esophageal varices due to
liver cirrhosis
3.3.2 Black stools occur because the blood that goes through the stomach
caused by rupture of esophageal varices due to liver cirrhosis

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3
.
4

F
I
N
A
L

C
O
N
C
E
P
T

M
A
P
P
I
N
G

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3.5 ANALYSIS OF FINAL CONCEPT MAPPING
From this scenario , Mr. A 58 years old and working as a pedicab driver was
rushed to the Emergency Room by his family because he was vomiting
blood 3 hours before being taken to the hospital and 10 days earlier he has
black stools . With the additional information and the results of that history
has been given from the tutor , we suspect that liver cirrhosis in Mr . A.
Actually, cirrhosis of the liver can be caused by many things , but there are
3 main things that act as the cause like hepatitis B , C and alcohol . In this
case it is known that he has a habit of drinking alcohol since his teenager .
Hepatitis B and C be denied as the cause for the blood test results because
the result obtain negative HBsAg and anti- HCV. So the major cause of
liver cirrhosis in Mr. A is alcohol .
If a person often consume alcohol in large quantities , it would interfere the
hepatic metabolism. Alcohol itself has properties that can damage liver
tissue and cause impaired hepatic function. If it impair hepatic function that
may occur some complication like anemia or ascites . Allegations of liver
cirrhosis is reinforced by the results of abdominal ultrasound examination
test which showed that narrow liver , liver contour nodular and have some
rough on the liver surface .
Liver cirrhosis is a disease characterized by the presence of diffuse and
chronic inflammation of the liver, followed by proliferation of connective
tissue , degeneration and regeneration , causing damage to the liver
parenchyma arrangement . The main result of liver cirrhosis is the blockage
of the portal vein leading to the liver and resulting in portal hypertension
and blood in the portal vein will automatically find the collateral way that
can cause vasodilation of collateral veins in the esophagus and the umbilical
region and can cause splenomegaly as well .

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Vasodilation of veins in the esophagus region can cause esophageal varices
and our expectation is strengthened by the data showing from endoscopic
test of the esophagus walls are red and have many bulge , the results of
these tests further confirmed that indeed happened in Mr.As esophageal
varices . If the esophageal varices widened continuously, it will burst and
cause vomiting of blood and blood from the esophagus it will come down to
the gastric area which can cause black stools due to feces mixed with blood .
3.6 GROUP OPINION
In this module, we were given the scenario A. The scenario is "A man 58
years old, escorted by his family to the Emergency Room because of
vomiting of blood and black stools". At the first tutorial, we made our main
problem, early hypothesis, and learning issues. We thought that the main
problems are vomiting blood and black stools. And our hypothesis are
vomiting of blood occurs due to rupture of esophageal varices and black
stools occurs because the feces mixed with blood due to rupture of varicose
veins in the rectum.
During group discussions, from the answers of our learning issues, we
concluded that vomiting of blood caused by rupture of esophageal varices
due to liver cirrhosis and black stools occur because the blood that goes
through the stomach caused by rupture of esophageal varices due to liver
cirrhosis.
3.7 CONCLUSION
From this scenario, Mr. As habit who like to drink alcohol since teenager
may cause damage to the liver tissue and the result is cirrhosis of liver that
can damage heart function and it all ended in the portal vein blockage that
causes vasodilation in the veins of the esophagus causing esophageal
varices. When these varices rupture, it can make blood vomiting
(hematemesis) and black stools (melena)

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CHAPTER FOUR
Critical Appraisal
4.1 REFERENCES
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N., Poturoglu, S., Badur, S. and Okten, A., 2007. The role of thrombopoietin and spleen
volume in thrombocytopenia of patients with noncirrhotic and cirrhotic portal
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Andriana, Y., 2013. Hubungan Trombositopenia, Hipoalbuminemia, dan Splenomegali sebagai
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April 2014].
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2014].

Detry, Oliver & Roover, Aunard De., 2009. Spider Angiomas. The New England Journal of
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2014].
Dooley, James S., Lok, Anna S.F & Burroughs, Andrew K., 2011, Sherlocks Diseases
of the Liver and Biliary System. 12th ed, Blackwell Production Publishing.
Drake, R. L., Vogl, A. and Mitchell, A., 2009. Gray's Anatomy for Student. 2nd ed.
London: Elsevier Health Science., pp.256-259.
Dugdale, D., 2014. Splenomegaly. [online] MedlinePlus. Available at: http://Non-
endoscopic prediction of presence of esophageal varices in cirrhosis [Accessed 28 April
2014].
Ely, J., Osheroff, J., Chambliss, M. and Ebell, M., 2006. Approach to leg edema of unclear
etiology. The Journal of the American Board of Family Medicine, 19(2), pp.148--160. [ebook]
Available at: http://www.jabfm.org/content/19/2/148.full [Accessed 27 April 2014].
Ferdaus, M., 2012. Asuhan keperawatan nyeri pada tn. p dengan hematemesis melena
di ruang mawar I RSUD KARANGANYAR. DIII. Surakarta: STIEKES Kusuma Husada
Surakarta. Available at: http://digilib.stikeskusumahusada.ac.id/files/disk1/5/01-gdl-
muhferdaus-207-1-muhammad-2.pdf [Accessed 27 April 2014].

51 | P a g e


Gunnarsdttir, S. A., 2008. Liver cirrhosis Epidemiological and Clinical Aspects.
[online], Sweden: Department of Internal Medicine The Sahlgrenska Academy at
Gteborg University. Available at:
https://gupea.ub.gu.se/bitstream/2077/10132/1/Ramen-Avh-SAG.pdf . [Accesed 30
April 2014].
Harrison, 2010. Prinsip Prinsip Ilmu Penyakit Dalam. Vol.1, 13th ed. Indonesia: Penerbit
Buku Kedokteran EGC. Hastings, G. E., 2005. Hematemesis & Melena, [online] pp1-7.
Available at: http://wichita.kumc.edu/hastings/hematemesis.pdf [Accessed 26 April 2014].
Jackson, P. and Gleeson, D., 2010. Alcoholic liver disease. Continuing Education in
Anaesthesia, Critical Care & Pain, [online] 10(3), pp.66-71. Available at:
http://ceaccp.oxfordjournals.org/content/10/3/66.full [Accessed 27 April 2014].

James H. Quillene of Medicine, n.d. Caput Medusa. Available at:
http://www.etsu.edu/com/medicalmystery/CAPUTMEDUSA.aspx [Accessed 27 April
2014].

Joshua Scallan, R.,2014. Pathophysiology of Edema Formation - Capillary Fluid Exchange -
NCBI Bookshelf. [online] Ncbi.nlm.nih.gov. Available at:
http://www.ncbi.nlm.nih.gov/books/NBK53445/ [Accessed 28 April 2014].
Khairunisak., 2013. breastfeeding relationship with the occurrence of jaundice newborn
in 0-7 days in hospital regional general dr. abidinabidinbandaaceh. Available at:
http://simtakp.stmikubudiyah.ac.id/dockti/KHAIRUNNISAK-kti_pdf.pdf. [Accessed 30
April 2014].
Lumonggo, F., 2008. Struktur liver. [e-book] Medan: Fakultas kedokteran universitas
sumatera utara. Available at:
http://repository.usu.ac.id/bitstream/123456789/2052/1/09E01467.pdf [Accessed 1
May 2014].

52 | P a g e


MedlinePlus, 2012. Spider Angioma [Online] (Updated November 20 2012) Available at:
http://www.nlm.nih.gov/medlineplus/ency/article/001095.htm [Accessed 27 April 2014].

Mortimer, P., 2000. ABC of arterial and venous disease: Swollen lower limb2:
Lymphoedema. BMJ: British Medical Journal, [online] 320(7248), p.1527. Available at:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1118110/ [Accessed 27 April 2014].

National Cardiovaskular Center Harapan Kita, 2011. Portal Hipertensi [online] pp.1-3.
Available at:
http://www.pjnhk.go.id/index2.php?option=com_content&do_pdf=1&id=3446 [Accessed
26 April 2014].

Netter F. H., 2010. Atlas of Human Anatomy. USA: Elsevier.

Prihartini, J., Lesmana, L., Manan, C. and Gani, R., 2005. Detection of esophageal varices in
liver cirrhosis using non-invasive parameters. portal, [online] 37(3). Available at:
http://www.ncbi.nlm.nih.gov/pubmed/16110174 [Accessed 28 April 2014].Reinhard, P.
&Reinhard, P., 2006. Sobotta Atlas of Human Anatomy, vol. 2 14
th
ed. German: Elsevier.

Reviews, C.,2013. Studyguide for bates guide to physical examination and history taking by. 1st
ed. [S.l.]: Cram101 Incorporated.
Saif, Muhammad W. et al.,2009. Management of ascites due to gastrointestinal
malignancy. Annals of Saudi Medicine. [Online], 29(5), pp.369-377. Available at:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3290049/ [Accessed 27 April 2014].
Sadler, T., 2004. Langman's Medical Embryology. 9th ed. Philadelphia: Lippincott
Williams &Willkins, pp.285-316.

53 | P a g e


Sarwar, S., Khan, A., Alam, A., Butt, A., Shafqat, F., Malik, K., Ahmad, I. and Niazi,
A., 2005. Non-endoscopic prediction of presence of esophageal varices in cirrhosis.
Journal of the College of Physicians and Surgeons--Pakistan: JCPSP, [online] 15(9),
pp.528--531. Available at: http://www.ncbi.nlm.nih.gov/pubmed/16181569 [Accessed
28 April 2014].
Sharma, Vishal et al., 2012. Spiders on the skin: Spider angioma. Journal of Symptoms
and Signs. [Online], 1(1), pp.15-19. Available at:
http://www.academia.edu/4920794/Spiders_on_the_skin_Spider_angioma
[Accessed 27 April 2014].
Sophia Margina, D., Herawati, S. and yasa, S., 2012. laboratory diagnosis of iron
deficiency anemia. Available at:
http://ojs.unud.ac.id/index.php/eum/article/download/7719/5808 [Accessed 30 April
2014].
Universitas Ahmad Dahlan Yogyakarta, 2014. BahayaJamuBerbahan Kimia
Obat(online) Available at: http://uad.ac.id/id/bahaya-jamu-berbahan-kimia-obat
University of Maryland Medical Center, 2014. Ascites. [Online] (Updated April 14
2014) Available at: http://umm.edu/health/medical/ency/articles/ascites [Accessed
27 April 2014].
University of Ronchester, 2014. Portal Hypertension. Available at:
http://www.urmc.rochester.edu/Encyclopedia/Content.aspx?ContentTypeID=134
&ContentID=179 [Accessed 30 April 2014].

University of Washington Department of Medicine, n.d. Techniques: Liver and Ascites
[Online] (Updated n.d.) Available at:
http://depts.washington.edu/physdx/liver/tech.html [Accessed 27 April 2014].

54 | P a g e


V, Arroyo., 2002. Pathophysiology, diagnosis and treatment of ascites in cirrhosis. National
Center for Biotechnology Information. [Online], 1(2), pp.72-9. Available at:
http://www.ncbi.nlm.nih.gov/pubmed/15115971 [Accessed April 27].

W Peter Gorman, R., 2000. ABC of arterial and venous disease: Swollen lower limb1:
General assessment and deep vein thrombosis. BMJ: British Medical Journal, [online]
320(7247), p.1453. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1127644/

55 | P a g e


4.2 TABLE OF REFERENCE
Source For Answering Searching Information
Validity

Importance

Applicability

Questions Method Type Foundation Result Foundation Result Foundation Result
Drake, R. L., Vogl, A. and
Mitchell, A., 2009. Gray's
Anatomy for Student. 2nd ed.
London: Elsevier Health
Science., pp.256-259.
1.6.1 How is the
normal anatomical
structure and
histological
strucuter of
Digestive system?
Open the
contents, then
read chapter
4: regio
abdominales
Textbook idea valid
Content of
Information
yes
Is it
applicable ?
yes
Reinhard, P. &Reinhard, P.,
2006. Sobotta Atlas of Human
Anatomy, vol. 2 14
th
ed.
German: Elsevier.

1.6.1 How is the
normal anatomical
structure and
histological strucuter
of Digestive system?
Open the
contents, then
read chapter
10: thorax,
11:
abdominal
viscera
Atlas idea valid
Content of
Information
yes
Is it
applicable ?
yes

56 | P a g e


Netter F. H., 2010. Atlas of
Human Anatomy. USA:
Elsevier
1.6.1 How is the
normal anatomical
structure and
histological structure
of Digestive system
?
Open the
contents, then
read chapter
3 : thorax, 4 :
abdomen
Atlas idea valid
Content of
Information
yes
Is it
applicable ?
yes
Lumonggo, F., 2008. Struktur li
ver. [e-book] Medan: Fakultas
kedokteran universitas sumate
ra utara. Available at: http://re
pository.usu.ac.id/bitstream/
123456789/2052/1/09E01467.
pdf [Accessed 1 May 2014].
1.6.1 How is the
normal anatomical
structure and
histological structure
of Digestive system
?
Type
www.google.
com, then
type struktur
liver
Electronic
books
idea valid
Content of
Information
yes
Is it
applicable ?
yes
Drake, R. L., Vogl, A. and
Mitchell, A., 2009. Gray's
Anatomy for Student. 2nd ed.
London: Elsevier Health
Science., pp.256-259.
1.6.2. How was the
normal development
of the
gastrointestinal
tract?
Read chapter:
Abdomen
page 256-259
Textbook idea valid
Content of
Information
yes
Is it
applicable ?
yes

57 | P a g e


Sadler, T., 2004. Langman's
Medical Embryology. 9th ed.
Philadelphia: Lippincott
Williams &Willkins, pp.285-
316.
1.6.2. How was the
normal development
of the
gastrointestinal
tract?
Read chapter:
Digestive
system page
285-316
Textbook idea valid
Content of
Information
yes
Is it
applicable ?
yes
Ferdaus, M., 2012. Asuhan
keperawatan nyeri pada tn.p
dengan hematemesis melena di
riangmawar I RSUD
KARANGANYAR. DIII.
Surakarta: STIEKES Kusuma
Husada Surakarta. Available
at:
http://digilib.stikeskusumahu
sada.ac.id/files/disk1/5/01-
gdl-muhferdaus-207-1-
muhammad-2.pdf [Accessed
27 April 2014].
1.6.3 How about the
pathology, etiology,
and manifestation of
melena and
hematomesis
Open
google.com
type:
hematemesis
dan melena
Final Report
(HTML)
idea valid
Content of
information
yes
Is it
applicable?
yes

58 | P a g e


Gunnarsdttir, S. A., 2008.
Liver cirrhosis
Epidemiological and Clinical
Aspects. [online], Sweden:
Department of Internal
Medicine The Sahlgrenska
Academy at Gteborg
University. Available at:
https://gupea.ub.gu.se/bitstre
am/2077/10132/1/Ramen-
Avh-SAG.pdf . [Accesed 30
April 2014].
1.6.4 How about the
pathophysiology,
etiology and clinical
manifestations of
liver cirrhosis?

Open
Scholar.googl
e.com type
cirrhosis of
the liver
Thesis idea valid
Content of
information
yes
Is it
applicable?
yes
Danastri, C., 2013. Sirosis
Hepatis pada Pasien dengan
Riwayat Mengkonsumsi
Alkohol Kronik. Medula
Unila,[online]1(2), pp. 19-26.
Available at:
http://juke.kedokteran.unila.
1.6.4 How about the
pathophysiology,
etiology and clinical
manifestations of
liver cirrhosis?

Open
scholar.googl
e.com type
sirosishati
Online
journal
idea valid
Content of
Information
yes
Is it
applicable?
yes

59 | P a g e


ac.id/index.php/medula/articl
e/view/93/91 . [Accesed 26
April 2014].

Anon, n.d. Medan: Universitas
Sumatera Utara [online]
Diaksesdari:
http://repository.usu.ac.id/bit
stream/123456789/33917/4/C
hapter%20II.pdf [Accessed
26 April 2014].

1.6.5 Explain the
relationship between
liver cirrhosis with
esophageal varices
and black stools?
Type
www.google.
com, then
type the
connection
between liver
cirrhosis and
varices of the
esophagus

Online
journal
idea valid
Content of
Information
yes
Is it
applicable ?
yes
National Cardiovaskular
Center Harapan Kita, 2011.
Portal Hipertensi [online]
pp.1-3. Available at:
http://www.pjnhk.go.id/index
1.6.5 Explain the
esophageal varices
Type
www.google.
com, then
type the
connection
Online
journal
idea valid
Content of
Information
yes
Is it
applicable ?
yes

60 | P a g e


2.php?option=com_content&
do_pdf=1&id=3446

and black stools? between liver
cirrhosis and
varices of the
esophagus

Hastings, G. E., 2005.
Hematemesis & Melena,
[online] pp1-7. Available at:
http://wichita.kumc.edu/hasti
ngs/hematemesis.pdf[Accesse
d 26 April 2014].

1.6.5 Explain the
esophageal varices
and black stools?
Type
www.google.
com, then
type the
connection
between liver
cirrhosis and
varices of the
esophagus

[e-book] Idea valid
Content of
Information
yes
Is it
applicable ?
yes
Alcohol Advisory Council of
New Zealand, 2012. Alcohol
the Body & Health Effects: A
Brief Overview (e-book)
1.6.6 How does
alcohol and
really can cause
Type
www.google.
com, then
type alcohol
e-book
(HTML)
idea valid
Content of
Information
yes
Is it
applicable ?
yes

61 | P a g e


Available at:
http://www.alcohol.org.nz/sit
es/default/files/useruploads/R
esourcepdfs/HealthEffects.pd
f [Accessed 26 April 2014]
cirrhosis of the
liver?

and cirrhosis
Jackson, P. and Gleeson, D.,
2010. Alcoholic liver disease.
Continuing Education in
Anaesthesia, Critical Care &
Pain, [online] 10(3), pp.66-71.
Available at:
http://ceaccp.oxfordjournals.
org/content/10/3/66.full[Acce
ssed 27 April 2014]
1.6.6 How does
alcohol and
really can cause
cirrhosis of the
liver?
Type
www.google.
com, then
type alcohol
and cirrhosis
Online
journal
(HTML)
idea valid
Content of
Information
yes
Is it
applicable ?
yes
Corwin, Elizabeth J., 2009.
BukuSakuPatofisiologi. 3
rd
ed.
Jakarta: EGC Available at:
http://books.google.co.id/boo
1.6.6 How does
alcohol and
really can cause
Type
books.google.
com, then
type alcohol
e-book
(HTML)
idea valid
Content of
Information
yes
Is it
applicable ?
yes

62 | P a g e


ks?id=0b-
MJ2p9GdAC&printsec=fron
tcover&hl=id#v=onepage&q
&f=false [Accessed 27 April
2014]
cirrhosis of the
liver?
and cirrhosis.
Universitas Ahmad Dahlan
Yogyakarta, 2014.
BahayaJamuBerbahan Kimia
Obat(online) Available at:
http://uad.ac.id/id/bahaya-
jamu-berbahan-kimia-obat
[Accessed 27 April 2014]
1.6.6 How does
alcohol and
really can cause
cirrhosis of the
liver?
Type
www.google.
com, then
type bad
effect of
herbal
Online
review
(HTML)
idea valid
Content of
information
yes
Is it
applicable?
yes
Sophia Margina, D., Herawati,
S. and yasa, S.,
2012. laboratory diagnosis of
iron deficiency
anemia. Available at:
http://ojs.unud.ac.id/index.p
2.6.1 Describe the
signs and symptoms
of what is obtained
in the additional
information
coherently
Type
www.google.
com, then
type anemia
symptom.pdf
Online
journal
(HTML)
idea valid
Content of
Information
yes
Is it
applicable ?
yes

63 | P a g e


hp/eum/article/download/771
9/5808[Accessed 30 April
2014]
(head/neck)

Khairunisak.,
2013. breastfeeding
relationship with the
occurrence of jaundice
newborn in 0-7 days in
hospital regional general dr.
abidinabidinbandaaceh. Avail
able at:
http://simtakp.stmikubudiyah.a
c.id/dockti/KHAIRUNNISAK-
kti_pdf.pdf. [Accessed 30
April 2014]
2.6.1 Describe the
signs and symptoms
of what is obtained
in the additional
information
coherently
(head/neck)
Type
www.google.
com, then
type ikterus
symptom.pdf
Online
journal
(HTML)
Idea valid
Content of
Information
yes
Is it
applicable ?
yes
MedlinePlus, 2012. Spider
Angioma [Online] (Updated
November 20 2012) Available
2.6.1 Describe the
signs and symptoms
of what is obtained in
Type
www.google.
com, then
Online
publication
Idea Valid
Content of
infromation
?
Yes
Is it
applicable?
Yes

64 | P a g e


at:
http://www.nlm.nih.gov/medl
ineplus/ency/article/001095.h
tm [Accessed 27 April 2014].

the additional
information
coherently (Thorax)
type spider
nervi
Detry, Oliver &Roover,
Aunard De., 2009. Spider
Angiomas. The New England
Journal of Medicine. [Online],
360, p.280. Available at:
http://www.nejm.org/doi/full/
10.1056/NEJMicm0706361#t
=article[Accessed 27 April
2014]

2.6.1 Describe the
signs and symptoms
the additional
information
coherently (Thorax)
Type
www.google.
com, then
type spider
nervi
Online
journal
Idea Valid
Content of
information
Yes
Is it
applicable?
Yes
Sharma, Vishal et al., 2012.
Spiders on the skin: Spider
angioma. Journal of Symptoms
2.6.1 Describe the
signs and symptoms
Type
www.google.
com, then
Online
Journal

Idea Valid
Content of
information
?
Yes
Is it
applicable?
Yes

65 | P a g e


and Signs. [Online], 1(1),
pp.15-19. Available at:
http://www.academia.edu/49
20794/Spiders_on_the_skin_
Spider_angioma[Accessed
27April 2014]
the additional
information
coherently (Thorax)
type spider
nervi
University of Washington
Department of Medicine, n.d.
Techniques: Liver and Ascites
[Online] (Updated n.d.)
Available at:
http://depts.washington.edu/
physdx/liver/tech.html

2.6.1 Describe the
signs and symptoms
of what is obtained
in the additional
information
coherently
(Abdomen)
Type
www.google.
com, then
type shifting
dullness and
ascites
Online
publication
idea valid
Content of
Information
yes
Is it
applicable ?
yes
University of Maryland
Medical Center, 2014. Ascites.
[Online] (Updated April 14
2014) Available at:
2.6.1 Describe the
signs and symptoms
of what is obtained
in the additional
Type
www.google.
com, then
type shifting
Online
publication
idea valid
Content of
Information
yes
Is it
applicable ?
yes

66 | P a g e


http://umm.edu/health/medic
al/ency/articles/ascites[Acces
sed 27 April 2014].
information
coherently
(Abdomen)
dullness and
ascites
V, Arroyo., 2002.
Pathophysiology, diagnosis
and treatment of ascites in
cirrhosis. National Center for
Biotechnology Information.
[Online], 1(2), pp.72-9.
Available at:
http://www.ncbi.nlm.nih.gov/
pubmed/15115971 [Accessed
April 27].

2.6.1 Describe the
signs and symptoms
the additional
information
coherently
(Abdomen)
Type
www.google.
com, then
type shifting
dullness and
ascites
Online
journal
Idea valid
Content of
Information
yes
Is it
applicable ?
yes
Akyuz, F., Yekeler, E.,
Kaymakoglu, S., Horasanli, S.,
Ibrisim, D., Demir, K., Aksoy,
N., Poturoglu, S., Badur, S.
2.6.1 Describe the
signs and symptoms
the additional
Type
ncbi.nlm.nih.
gov/, then
type
Online
journal
idea valid
Content of
information
yes
Is it
applicable?
yes

67 | P a g e


and Okten, A., 2007. The role
of thrombopoietin and spleen
volume in thrombocytopenia
of patients with noncirrhotic
and cirrhotic portal
hypertension. Turk J
Gastroenterol, [online] 18(2),
pp.95--9. Available at:
http://www.ncbi.nlm.nih.gov/p
ubmed/17602356 [Accessed
28 April 2014].
information
coherently
(Abdomen)
cirrhotic
Arulprakash Sarangapani, J.,
2010. Noninvasive Prediction
of Large Esophageal Varices
in Chronic Liver Disease
Patients. Saudi Journal of
Gastroenterology : Official
Journal of the Saudi
Gastroenterology Association,
2.6.1 Describe the
signs and symptoms
the additional
information
coherently
(Abdomen)
Type
ncbi.nlm.nih.
gov/, then
type
esophageal
varices
Online
journal
idea valid
Content of
information
yes
Is it
applicable?
yes

68 | P a g e


[online] 16(1), p.38. Available
at:
mc/articles/PMC3023101/?rep
ort=reader [Accessed 28 April
2014].

Dugdale, D., 2014.
Splenomegaly. [online]
MedlinePlus. Available at:
http://Non-endoscopic
prediction of presence of
esophageal varices in cirrhosis

2.6.1 Describe the
signs and symptoms
the additional
information
coherently
(Abdomen)
Type
www.google.
comthen type
splenomegal
y
Website idea valid
Content of
information
yes
Is it
applicable?
yes
Prihartini, J., Lesmana, L.,
Manan, C. and Gani, R., 2005.
2.6.1 Describe the
signs and symptoms
Type
ncbi.nlm.nih.
Online
journal
Idea valid
Content of
information
yes
Is it
applicable?
Yes

69 | P a g e


Detection of esophageal
varices in liver cirrhosis using
non-invasive parameters.
portal, [online] 37(3).
Available at:
28 April 2014].
the additional
information
coherently
(Abdomen)
gov/, then
type
cirrhosis
Sarwar, S., Khan, A., Alam,
A., Butt, A., Shafqat, F.,
Malik, K., Ahmad, I. and
Niazi, A., 2005. Non-
endoscopic prediction of
presence of esophageal varices
in cirrhosis. Journal of the
College of Physicians and
Surgeons--Pakistan: JCPSP,
[online] 15(9), pp.528--531.
Available at:
2.6.1 Describe the
signs and symptoms
the additional
information
coherently
(Abdomen)
Type
ncbi.nlm.nih.
gov/, then
type
cirrhosis
Online
journal
idea Valid
Content of
information
Yes
Is it
applicable?
yes

70 | P a g e


28 April 2014].
Andriana, Y., 2013. Hubungan
Trombositopenia,
Hipoalbuminemia, dan
Splenomegali sebagai
Prediktor Varises Esofagus
Pada Pasien Sirosis Hati di
RSUD Dr. Soedarso
Pontianak. Jurnal Mahasiswa
PSPD FK Universitas
Tanjungpura, 2(1).
2.6.1 Describe the
signs and symptoms
the additional
information
coherently
(Abdomen)
Type
www.scholar
.google.com,
then type
spelnomegal
i
Online
journal
idea valid
Content of
information
yes
Is it
applicable?
yes
University of Ronchester,
2014. Portal Hypertension.
Available at:
http://www.urmc.rochester.e
du/Encyclopedia/Content.asp
x?ContentTypeID=134&Con
2.6.1 Describe the
signs and symptoms
the additional
information
coherently

Open the web
and click it
on the link
that contains
the
Website idea valid
Content of
information
yes
Is it
applicable?
Yes

71 | P a g e


tentID=179 [Accessed 30
April 2014].
(Abdomen) information
Harrison, 2010. Prinsip
PrinsipIlmuPenyakitDalam.
Vol.1, 13th ed. Indonesia:
PenerbitBukuKedokteranEGC.
2.6.1 Describe the
signs and symptoms
the additional
information
coherently
(Abdomen)

Opening in
page 269
Textbook idea valid
Content of
information
yes
Is it
applicable?
yes
Dooley, James S., Lok, Anna
S.F & Burroughs, Andrew K.,
2011, Sherlocks Diseases of
the Liver and Biliary System.
12th ed, Blackwell Production
Publishing.
2.6.1 Describe the
signs and symptoms
the additional
information
coherently
(Abdomen)
Opening
chapter 9:The
Hepatic
Artery, Portal
Venous
System and
Portal
Hypertension
: The Hepatic
veins and
Textbook idea valid
Content of
information
yes
Is it
applicable?
yes

72 | P a g e


Ely, J., Osheroff, J.,
Chambliss, M. and Ebell, M.,
2.6.1 Describe the
sign and symptom of
Type
www.scholar
Online
journal
idea valid
Content of
Information
yes
Is it
applicable ?
yes
Liver in
Circulatory
Failure
James H. Quillene of
Medicine, n.d. Caput Medusa.
Available at:
http://www.etsu.edu/com/me
dicalmystery/CAPUTMEDU
SA.aspx [Accessed 27 April
2014].

2.6.1 Describe the
signs and symptoms
the additional
information
coherently
(Abdomen)
Opening in
page chapter
9:The
Hepatic
Artery, Portal
Venous
System and
Portal
Hypertension
: The Hepatic
veins and
Liver in
Circulatory
Failure
Website idea valid
Content of
information
yes
Is it
applicable?
yes

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2006.Approach to leg edema
of unclear etiology.The
Journal of the American Board
of Family Medicine, 19(2),
pp.148--160. [ebook]
Available at:
http://www.jabfm.org/content/
19/2/148.full [Accessed 27
April 2014]

what is obtained in
the additional
information
coherently
(Extremity)
.google.com,
then type
Leg edema
W Peter Gorman, R., 2000.
ABC of arterial and venous
disease: Swollen lower limb
1: General assessment and
deep vein thrombosis. BMJ:
British Medical Journal,
[online] 320(7247), p.1453.
Available at:
2.6.1 Describe the
sign and symptom of
what is obtained in
the additional
information
coherently
(Extremity)
Type
www.scholar
.google.com,
then type
Swollen
lower limb

Online
journal
idea valid
Content of
Information
yes
Is it
applicable ?
yes

74 | P a g e


mc/articles/PMC1127644/
Mortimer, P., 2000. ABC of
arterial and venous disease:
Swollen lower limb2:
Lymphoedema. BMJ: British
Medical Journal, [online]
320(7248), p.1527. Available
at:
mc/articles/PMC1118110/

2.6.1 Describe the
sign and symptom of
what is obtained in
the additional
information
coherently
(Extremity)
Type
www.scholar
.google.com,
then type
Swollen
lower limb

Online
journal
Idea valid
Content of
Information
yes
Is it
applicable ?
yes
Reviews, C.,2013. Studyguide
for bates guide to physical
examination and history taking
by. 1st ed. [S.l.]: Cram101
Incorporated.
2.6.1 Describe the
sign and symptom of
what is obtained in
the additional
information
Opening:
Bates Guide to
Physical
Examination
and History-
e-book
(HTML)
Idea valid
Content of
Information
yes
Is it
applicable ?
yes

75 | P a g e


coherently
(Extremity)

Taking
Joshua Scallan, R.,2014.
Pathophysiology of Edema
Formation - Capillary Fluid
Exchange - NCBI Bookshelf.
[online] Ncbi.nlm.nih.gov.
Available at:
http://www.ncbi.nlm.nih.gov/b
ooks/NBK53445/ [Accessed
28 April 2014].

2.6.1 Describe the
sign and symptom
of what is obtained
in the additional
information
coherently
(Extremity)
Type
ncbi.nlm.nih.
gov/, then
type
Capillary
fluid.

Online
journal
idea valid
Content of
information
yes
Is it
appllicable?
yes

76 | P a g e


4.3 APPRAISAL
SCIENTIFIC PAPER APPRAISAL SHEET

Name/Group : 3B
Papers Title : Noninvasive Prediction of Large Esophageal Varices in Chronic Liver
Disease Patients

1. APPRAISAL OF PAPERS FORMAT COMPLETENESS

Items Availability
Title Available (page 1)
Abstract and or Summary Available (page 1)
Introduction, background Available (page 1)
Methods Available (page 1-2)
Result Available (page 2)
Discussion Available (page 2-3)
Reference Available (page 3-4)

Conclusion :This journal has complete contents.

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2. APPRAISAL OF RESEARCHS VALIDITY

Aim of research : This prospective study was conducted to evaluate noninvasive predictors of large
varices (LV).

Methods:
Item telaah Temuan
Design Prospective Study
Rank on hierarchy of evidence 4
Sample Patients with liver diseases
Sample size 106 patients with liver disease between August 2007
December 2008 at Departement of Digestive Health and
Disease, Government peripheral hospital, Anna Nagar,
Chennai.
Eligibility criteria Relevant history and physical characteristics including
symptoms and signs of liver failure, hepatomegaly,
spleenomegaly, and abdominal vein collaterals.
Exclusion criteria Patients with evidence of hepatocellular carcinoma on
ultrasonography, or previous or current treatment with
beta-blockersm nitrates and diuretics., and patients who
have receive endoscopic or surgical intervention for
portal hypertension previously.
Sampling frame -
Measurement and or assesment Ascites graded as none, mild, moderate, or severe
Hepatic encelopathy was graded o to IV
Instrument Blood tests, ultrasound Doppler, Endoscopic Evaluation
All calculations were made using SPSS software
(version 11 for windoes; SPSS, Chicago, Il, USA)
Randomization -
Intervention -

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Analysis method Performed using Student t test for continous variables
and chi square tests for categorical variables.

Compatibility between design and objective of the research : compatible
Compatibility between asessment and measurement and instrument : compatible

Conclusion: This research is valid based on two criterias above.

3. IMPORTANCE OF RESEARCH STUDY

OR/PR/RR : -
Confidence Interval : 95% (0,81 0,91)
P value : 0,02

4. APPLICABILITY

Applicability criteria :

Items Keputusan
Burden of illness Same / not same
barriers to treatment Same / not same
behaviours needed
It should be a lot of changes
in behavior / It shoulnt be a
lot of changes in behavior
Balance Advantage / Disadvantage

How about the applicability of this research appropriate in to your case?
Applicable / not applicable

PBL 3b Human Structure

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PBL Group 3B Medical Faculty of Airlangga University

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