SCENARIO 1

A 35 years old man came to the practice of a general practicioner with a yellow
eye complaint that was realized two days ago. Initially the patient suffered from
fever, nausea, and vomiting since 5 days ago. BAK is coloured like tea and
regular BAB is brown. Patients often consume fatty foods with a history of high
cholesterol. Patient while taking antibiotics because of the fever suffered at this
time.

DIFFICULT WORD

A. KEYWORDS
1. A man 35 years old.
2. a yellow eye complaint that was realized two days ago
3. suffered from fever, nausea, and vomiting since 5 days ago
4. BAK is coloured like tea and regular BAB is brown
5. often consume fatty foods with a history of high cholesterol
6. while taking antibiotics because of the fever suffered at this time

B. QUESTIONS
1. Explain the anatomiy structure and physiology based on the scenario !
2. Explain the patomechanism of the jaundice based on the scenario !
3. Explain the patomechanism of symptoms based on the scenario!
4. What is the corelation of high cholesterol with the jaundice?
5. Explain the early management based on the scenario!
6. What is the diagnostic steps?
7. What is the differential diagnosis based on the scenario ?
8. Explain the Islamic perspective according to the scenario !

C. ANSWERS
1. Explain the anatomy and physiology structure based on the scenario !

Anatomy and Physiology of the Liver

The liver is the largest organ of the human body (Figure 2.1), weighs
approxi- mately 1500 g, and is located in the upper right corner of the abdomen.
The organ is closely associated with the small intestine, processing the nutrient-
enriched ve- nous blood that leaves the digestive tract. The liver performs over
500 metabolic functions, resulting in synthesis of products that are released into
the blood stream (e.g. glucose derived from glycogenesis, plasma proteins,

1
clotting factors and urea), or that are excreted to the intestinal tract (bile). Also,
several products are stored in liver parenchyma (e.g. glycogen, fat and fat soluble
vitamins).

Almost all blood that enters the liver via the portal tract originates from the
gas- trointestinal tract as well as from the spleen, pancreas and gallbladder. A
second blood supply to the liver comes from the hepatic artery, branching directly
from the celiac trunc and descending aorta. The portal vein supplies venous blood
under low pressure conditions to the liver, while the hepatic artery supplies high-
pressured arterial blood. Since the capillary bed of the gastrointestinal tract
already extracts most O2, portal venous blood has a low O2 content. Blood from
the hepatic artery on the other hand, originates directly from the aorta and is,
therefore, saturated with O2. Blood from both vessels joins in the capillary bed of
the liver and leaves via central veins to the inferior caval vein.

2. Anatomy and Physiology

2.1.1 Basic liver architecture

The major blood vessels, portal vein and hepatic artery, lymphatics, nerves
and hepatic bile duct communicate with the liver at a common site, the hilus.
From the hilus, they branch and rebranch within the liver to form a system that
travels together in a conduit structure, the portal canal (Figure 2.2). From this
portal canal, after numerous branching, the portal vein finally drains into the
sinusoids, which is the capillary system of the liver. Here, in the sinusoids, blood
from the portal vein joins with blood flow from end-arterial branches of the
hepatic artery. Once passed through the sinusoids, blood enters the collecting
branch of the central vein, and finally leaves the liver via the hepatic vein. The
hexagonal structure with, in most cases, three portal canals in its corners draining
into one central vein, is defined as a lobule (Figure 2.3). The lobule largely
consists of hepatocytes (liver cells) which are arranged as interconnected plates,

2
usually one or two hepatocytes thick. The space between the plates forms the
sinusoid. A more functional unit of the liver forms the acinus. In the acinus, the
portal canal forms the center and the central veins the corners. The functional
acinus can be divided into three zones: 1) the periportal zone, which is the circular
zone directly around the portal canal, 2) the central zone, the circular area around
the central vein, and 3) a midzonal area, which is the zone between the periportal
and pericentral zone.

2.1.2 Sinusoids

Sinusoids (Figure 2.4) are the canals formed by the plates of hepatocytes. They
are approximately 8-10 μm in diameter and comparable with the diameter of
normal capillaries. They are orientated in a radial direction in the lobule.
Sinusoids are lined with endothelial cells and Kupffer cells, which have a
phagocytic function. Plasma and proteins migrate through these lining cells via
so-called fenestrations (100-150 nm) into the Space of Disse, where direct contact
with the hepatocytes occurs and uptake of nutrients and oxygen by the
hepatocytes takes place. On the opposite side of the hepatocyte plates are the bile
canaliculi situated (1 μm diameter). Bile produced by the hepatocytes empties in
these bile canaliculi and is transported back towards the portal canal into bile
ductiles and bile ducts, and finally to the main bile duct and gallbladder to become
available for digestive pro- cesses in the intestine. The direction of bile flow is
opposite to the direction of the blood flow through the sinusoids.

2.1. Anatomy

3
2.2.1 Pressure distribution

Blood pressure in afferent vessels and pressure distribution inside the

liver, is es- sentially similar for most species. Pressure in the hepatic artery,
originating from the descending aorta and the celiac trunc, is considered to be the
same as aortic pressure. This includes a high pulsatile pressure between 120 and
80 mmHg with a frequency equal to the heart rate. Vessel compliance causes a
gradual decrease in pulsation as the hepatic artery branches and rebranches inside
the liver. Once at the sinusoidal level, pulsation amplitude decreases to virtually
zero and pressure drops to approximately 2-5 mmHg. On the other hand, pressure
in the portal vein, originating from capillaries of the digestive tract, has no
pulsation and a pressure of 10-12 mmHg. In the sinusoids, both portal venous and
hepatic arterial pressure is 3-5 mmHg. Consequently, the pressure drop inside the
liver is much less in the portal venous system than in the arterial system. The
pressure drop from the col- lecting central veins to the vena cava is then
approximately 1-3 mmHg, fluctuating slightly with respiration.

2.2.2 Flow distribution

Total human liver blood flow represents approximately 25% of the cardiac
output, up to 1500 ml/min. Hepatic flow is subdivided in 25-30% for the hepatic
artery (500 ml/min) and the major part for the portal vein (1000 ml/min).
Assuming a human liver weighs 1500 g, total liver flow is 100 ml/min per 100 g
liver. Comparing this normalized flow rate to other species, it can be concluded
that total liver blood flow is 100-130 ml/min per 100 g liver, independent of the
species. The ratio of arterial:portal blood flow, however, is species-dependent.
The hepatic artery orig- inates directly from the descending aorta, and is therefore
saturated with oxygen. It accounts for 65% of total oxygen supply to the liver. The

4
hepatic artery also plays an important role in liver blood vessel wall and
connective tissue perfusion. It also secures bile duct integrity. The blood from the
portal vein is full of nutrients derived from the intestine and allows the
hepatocytes to perform their tasks. Blood from the hepatic artery and the portal
vein joins in the sinusoids. However, recent studies by others as well as our own
observations, have revealed that there are both common and separate channels for
arterial and portal blood. The hepatic artery perfuses the liver vascular bed in a
’spotty’ pattern, while the portal vein perfuses the liver uniformly. The liver is
able to regulate mainly arterial flow by means of so-called sphincters, situated at
the in- and outlets of the sinusoids. One of the most important triggers for
sphincter function is the need for constant oxygen sup- ply. If the rate of oxygen
delivery to the liver varies, the sphincters will react and the ratio of arterial:portal
blood flow alters.

Anatomy and Physiology of the Pancreas

Anatomy of the Pancreas Physiology The pancreas is a marked glandular

compound and its structure is very similar to that of the salivary glands, about 15
cm and 60-100 grams. The pancreas is located in the upper abdomen behind the
stomach in the retroperitoneal space. On the left side of the tail the pancreas
reaches the hilum to the chronio-dorsal and the upper left pan of the pancreas is
connected to the pancreatic corpus by the pancreatic neck which is part of the
pancreas which is usually no more than 4 cm wide, the superior mesentic arteries
and veins are located in the pancreas below the head pancreas. called the
pancreatic unsinatic process. The pancreas consists of two main tissues, namely:

1. Acini, which secretes digestion into the duodenum.

5
2. Langerhans Island, which does not have the means to secrete sap but instead
secretes insulin and glucagon directly into the blood. The human pancreas has 1-2
million langerhans islands, each island is only 0.3 mm in diameter and arranged
around capillaries. Langerhans Island does not have the means to expel its sap but
instead secretes insulin and glucagon directly into the blood. The human pancreas
has 1-2 million langerhans islands, each island is only 0.3 mm in diameter and
arranged around capillaries. Langerhans Island contains four main cell types,
namely alpha, beta, delta and mega cells. Beta cells, which comprise about 60% of
all cells, are located mainly in the middle of each island and secrete insulin. B cell
granules are insulin packets in the cytoplasm of cells. Each package varies from
species to species. In B cells, insulin molecules form polymers that are also
complex with zinc. This difference in packaging may be due to differences in the
size of the polymer or zinc aggregate from insulin. Insulin is synthesized in the B
cell endoplasmic reticulum, then transported to the Golgi device, where it is
wrapped in membrane-bound granules.

These granules move to the cell wall by a process that appears to be cells
that secrete insulin into the outer area by exocytosis. Then insulin crosses the
basement membrane of B cells and adjacent capillaries and endothelial capillary
fenestrata to reach blood flow (Ganong, 1995). Alpha cells, which comprise about
25% of all cells, secrete glucagon. Delta cells which constitute 10% of all cells
secrete somatostatin. There are two functions of the pancreas, then called skeletal
organs, namely:

1. Exocrine function, carried out by lobular secretory cells that form pancreatic
sap containing enzymes and electrolytes. The types of enzymes from the pancreas
are:

A. Amylase; decompose flour into maltose or maltose into polysaccharides and

the polysaccharides used as saccharides are then made into monosaccharides.

B. Trypsin; analyze peptone for polypeptides then to amino acids.

C. Lipase; Decomposes the fat that has been emulsified into fatty acids and
glycerol glycerin.

2. Endocrine function or closed glands function to form hormones in the islands of

langerhans, which are groups of small islands spread between the alveoli and
alveoli of the pancreas and do not have channels. Therefore, the insulin hormone
produced by the island of Langerhans is directly absorbed into the blood
capillaries to be taken to places that need this hormone. Two important hormones
produced by the pancreas are insulin and glucagon.

6
Anatomy and Physiology of the Gall Bladder

The gallbladder is shaped like a bag, a hollow organ about 10 cm long,

located in the fossa that confirms the anatomical boundary between the right and
left lobes of the liver. The extrahepatic portion of the gallbladder is covered by the
peritoneum.

The gallbladder has a fundus, corpus, infundibulum, and column. The

fundus is round, the dead end of the gallbladder extends slightly above the edge of
the liver. The corpus is the largest part of the gallbladder. The column is a narrow
section of the gall bladder that is located between the corpus and the cystic tract
area. The infundibulum, also known as the Hartmann sac, is a small ball of
diverticulum located on the inferior surface of the bladder, which is clinically
meaningful because of its proximity to the duodenum and because stones can be
impregnated into it. Cystic ducts connect the gallbladder to the koledokus channel.
Heister spiral valve is located inside the cystic channel; they are involved in the
entry and exit of bile from gall bladder.

Gall bladder Helps digestion and absorption of fat, not because of the enzymes in
bile that cause fat digestion, but because the bile acids in bile do two things:

-Bile acids help emulsify large fat particles in food into many small particles, the
surface of these particles can be attacked by the lipase enzyme that is secreted in
the pancreas sap.

-Bile acids help absorb the final fat products that have been digested through the
intestinal mucous membranes.

• As a supply of bile sap and make thick bile sap.

• Bile is a liquid that is produced by liver cells every day from every person who
emits 500-1000 ml a day which is used to digest 80% of fat from the pigment bile
(color) of insulin and other substances.

• A place to store bile and concentrate bile in it by absorbing water and

electrolytes. This bile is an electrolyte liquid produced by an agreement. To
eliminate certain body wastes (especially the pigment that results from the
breakdown of red blood cells (hemoglobin) and excess cholesterol) and helps
digestion and absorption of fat.

7
 2. Explain the patomechanism of the jaundice based on the scenario!

Explain the meaning of jaundice in general!

Jaundice is defined as a yellowing of the skin, mucous membranes and sclera due
to the deposition of yellow-orange for example bile pigment bilirubin. The word
Jaundice is actually a derivative of the French word 'Jaune' the which means 'yellow'.
Jaundice indicates the hyper bilirubinemia and that excessive levels of bilirubin may
be in conjugated or unconjugated form. The clinical presentations of jaundice Appear
when bilirubin level exceeds 34.2 mol / L or 2 mg / dL. The substrate for the
production of bilirubin is heme group. The heme is catabolized at the alpha carbon
bridged by an enzyme heme oxygenase and results in the liberation of iron, carbon
monoxide and biliverdin. The biliverdin is further ACTED upon by biliverdin
reductase to form bilirubin. 80% of bilirubin is derived from the heme group of
hemoglobin. This hemoglobin comes from the destruction of red blood cells in the
reticuloendothelium of liver, spleen and bone marrow. The bilirubin itself is an
endogenously synthesized pigment that can be toxic specially in newborn children.
The remaining 20% of bilirubin comes from multiple sources like myoglobin,
cytochromes etc. 3.8 mg / kg or Approximately 250-300 mg of bilirubin is produced
daily in normal adults. The amount of bilirubin production in neonates is much higher
than adults. The bilirubin produced is then transported to the liver in the bound form
with plasma albumin. 8 mg / kg or Approximately 250-300 mg of bilirubin is
produced daily in normal adults. The amount of bilirubin production in neonates is
much higher than adults. The bilirubin produced is then transported to the liver in the
bound form with plasma albumin. 8 mg / kg or Approximately 250-300 mg of
bilirubin is produced daily in normal adults. The amount of bilirubin production in
neonates is much higher than adults. The bilirubin produced is then transported to the
liver in the bound form with plasma albumin.

The three main types of jaundice are hepatic, hepatocellular and obstructive types
 Hemolytic Jaundice: if the destruction (lysis) of red blood cells exceeds the
capacity of the liver to conjugate bilirubin (binding bilirubin to the polar group

8
 so that it makes it soluble in water and can be excreted through the kidneys),
hemolytic jaundice will occur. causes include transfusion reactions, sickle cell
anemia, thalassemia, and autoimmune diseases.
 Hepatocellular Jaundice : hepatocyte dysfunction will limit the uptake and
conjugation of bilirubin. liver dysfunction can occur in hepatitis, liver cancer,
cirrhosis or congenital liver disorders, and can also be caused by several
drugs.
 Obstructive Jaundice : if the outflow of bile from the liver (through the hepatic
duct) or the bile duct outside the liver (blocked ductus) is blocked, then the
liver can still conjugate bilirubin even though the bilirubin cannot reach the
small intestine. Blockage of hepatic ducts by stones or tumors is considered an
intrahepatic cause of obstructive jaundice.

Etiology of jaundice is caused by several factors:

- excessive production of bilirubin: for example in hemolysis increases in
incompetent, closed circulation, sepsis
- liver congjugation disorders: these disorders can be caused by liver immunity, lack
of bilirubin congestion substrate or the absence of the enzyme gluconin transferase
- bilirubin transport disruption: bilirubin in the blood bound to albumin is then
elevated to the liver
- interference in excretion: obstruction can occur in the liver or outside the liver

There are three main types of jaundice: pre-hepatic, hepatocellular, and post-hepatic.
1. Pre-Hepatic
In pre-hepatic jaundice, there is excessive red cell breakdown which
overwhelms the liver’s ability to conjugate bilirubin. This causes an
unconjugated hyperbilirubinaemia.Any bilirubin that manages to
become conjugated will be excreted normally, yet it is the
unconjugated bilirubin that remains in the blood stream to cause the
jaundice. Normal : 300mg a days
2. Hepatocellular
In hepatocellular (or intrahepatic) jaundice, there is dysfunction of
the hepatic cells. The liver loses the ability to conjugate bilirubin, but

9
Pre-Hepatic Hepatocellular Post-Hepatic
in cases where it also may become cirrhotic, it compresses the intra-
hepatic portions of the biliary tree to cause a degree of obstruction.This
leads to both unconjugated and conjugated bilirubin in the blood,
termed a ‘mixed picture’.
3. Post-Hepatic
Post-hepatic jaundice refers to obstruction of biliary drainage. The
bilirubin that is not excreted will have been conjugated by the liver,
hence the result is a conjugated hyperbilirubinaemia

Table 1 - difference between jaundice classification

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 Haemolytic anaemia 1. Alcoholic liver disease  Intra-luminal causes, such as gallstones
 Gilbert’s syndrome 2. Viral hepatitis  Mural causes, such as
 Criggler-Najjar 3. Iatrogenic, e.g. medication cholangiocarcinoma, strictures, or drug-
syndrome 4. Hereditary haemochromatosis induced cholestasis
5. Autoimmune hepatitis  Extra-mural causes, such as pancreatic
6. Primary biliary cirrhosis or cancer or abdominal masses (e.g.
primary sclerosing cholangitis lymphomas)
7. Hepatocellular carcinoma

Table 2 – Potential Causes for Jaundice, divided into pre-hepatic, hepatocellular,

and post-hepati

hepatobiliary mechanism
mechanism haematological

Intrahepatic Extra obstructive hemolytic jaundice

obstructive jaundice jaundice hepatic

Lysis of erythrocytes >>

Hepatocellular damage Obstruction of the bile duct

obstruction in bile (kolestasis)
canaliculi Inadequate capacity -
terganggu- conjugation of
Accumulation of conjugated bilirubin into the
Excretion of bilirubin bilirubin into the bloodstream bloodstream
<<

Conjugated and unconjugated conjugated hyperbilirubinemia Unconjugated

hyperbilirubinemia hyperbilirubinemia

Deposit bilirubin in the network

jaundice
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4. Explain the patomechanism of symptoms based on the scenario!

Pathomechanism of Nausea and Vomiting

The natural path of throwing has also not been approved. Some
pathophysiology is known to cause nausea and gag have been had. The main
coordinator is the vomiting center, a collection of nerves that are placed in the
medulla oblongata. These nerves receive input from:
A. Trigger Zone (CTZ) in the postrema area
B. Vestibular system (which is associated with ground drinks and nausea due
to middle ear disease)
C. The vagus nerve (which carries signals from the gastrointestinal tract)
D. Spinoreticular system (which triggers nausea related to physical damage)
E. Nucleus tract solitarius (which completes the reflex of the gag reflex)

The main stimulus is centered on CTZ.Emetic stimulus from the intestine

from afferent nerve fibers
a. Mechanoreceptors: placed in the intestinal wall and activated by intestinal
contractions and distension, physical damage and manipulation during
surgery.
b. Chemoreceptors: placed in the upper intestinal mucosa and sensitive to
chemical stimuli.

The center of vomiting, the lateral side of the reticular in the medulla
oblongata, mediates the gag reflex. This section is very close to the nucleus
tractus solitarius and the postrema area. Chemoreseptor Trigger Zone (CTZ)
is located in the postrema area. Peripheral and central stimulation can
stimulate both the vomiting center and CTZ. Afferent from pharynx, GI tract,
mediastinum, kidney, peritoneum and genital can stimulate the vomiting
center. Central stimulation of the cerebral cortex, upper cortical and central
brain stem, nucleus tractus solitarius, CTZ, and vestibular system in the ear

12
and center of vision can also stimulate the vomiting center. Because the
postrema area is not effective against the blood-brain barrier, drugs or
chemicals in the blood or in brain fluid can immediately stimulate CTZ.
The upper cortical and limbic systems can cause nausea and vomiting
associated with discomfort, vision, aroma, memory and feeling of fear.
Nucleus tract solitaries can also cause nausea and vomiting by sympathetic
and parasympathetic stimulation through stimulation of the heart, billiary
tract, gastrointestinal tract and urinary tract.35 The vestibular system can be
stimulated through sudden movements that cause interference with the
vestibular middle ear.14 Receptors such as 5-HT3 , dopamine type 2 (D2),
opioids and neurokinin-1 (NK-1) can be found at CTZ.
Nucleus tractus solitarius has a high concentration in enkepalin,
histaminergic, and cholinergic muscarinic receptors. These receptors send
messages to the vomiting center when stimulated. Actually NK-1 receptors
can also be found at the vomiting center. The vomiting center coordinates
impulses into the vagus, phrenic, and spinal nerves, breathing and abdominal
muscles to reflex vomiting.

Pathomechanism of urine colored like tea

Bilirubin Formation About 85% of bilirubin is formed from the breakdown
of old erythrocytes (average age 120 days) in the macrophage monocyte
system. Every day 50 ml of blood is destroyed, producing 250-350 mg
bilirubin or 4 mg / kgBB / day. Whereas 15% of bilirubin comes from the
destruction of mature erythrocytes in the bone marrow (ineffective
hematopoiesis) and from other hemoproteins, especially from the liver. In
bilirubin catabolism (especially in the spleen, as the reticuloendothelial
system), hemoglobin is broken down into heme and globulin, after which
heme is converted to biliverdin. With the biliverdin reductase enzyme,
biliverdin is converted to unconjugated biirubin (B₁).
Excessive formation of bilirubin is due to increased breakdown of
erythrocytes, so that excess bilirubin is formed. Often called hemolytic
jaundice. Conjugation and transfer of bile pigment takes place normally, but
the supply of B₁ exceeds the ability of the liver so that the level of B₁ in the
blood increases. Because B₁ does not dissolve in water, it cannot be
channeled in the urine. But urobilinogen formation is increased (due to an
increase in the burden of bilirubin on the liver and increased conjugation and
excretion), which subsequently increases excretion in feces and urine (dark in
color). The color of urine such as tea water (brownish red) may be due to an
increase in bilirubin and urobilinogen. The presence of bilirubin shows
damage (blockage) in the biliary canalicular channel so that bilirubin cannot

13
get out, which eventually flows into the blood vessels to the kidneys. The
presence of urobilinogen in the urine shows normal urine but due to increased
levels resulting in excess oxidation which eventually turns brown reddish.

Patomechanism of Fever
Fever occurs when various infectious and non-infectious processes interact
with host defense mechanisms. In most children fever is caused by
microbiological agents that can be recognized and disappear after a short
period.In response to exogenous pyrogens (various kinds of infectious,
immunological, or toxin-related agents) certain white blood cells secrete
chemicals that have many effects against infections known as endogenous
pyrogens. This endogenous pyrogen will also work at the center of the
hypothalamus regulation which will cause prostaglandin secretion to increase
the hypothalamic thermostat benchmark which regulates body
temperatureThese endogenous pyrogens are cytokines, for example
interleukin (IL-1, β IL-1, α IL-6), tumor necrosis factor (TNF, α TNF -β) and
interferon-α (INF) produced by inflammatory host cells . In response to these
cytokines, prostaglandin synthesis occurs, especially prostaglandin E2
through the arachidonic acid metabolism of the cyclooxygenase-2 (COX-2)
pathway and causes an increase in body temperature.
The hypothalamus feels that the normal temperature before the fever is
too cold, and this organ triggers cold response mechanisms to increase the
new temperature set by the hypothalamus. Shivering is caused to rapidly
increase heat production, while skin vasoconstriction also takes place to
quickly reduce heat loss. Both of these mechanisms push the temperature up.
At the beginning of a fever these mechanisms cause a sudden feeling of
chills.

14
5. What is the corelation of high cholesterol with the jaundice?
The formation of cholestrol
1. Cholesterol is transported by micelles (aggregates / lumps containing
phospholipids, bile salts and cholesterol). If cholesterol saturation is
higher, it will be transported by vesicles.
2. VesiclesVesicles can be described as a two-layer circle. If the
concentration of cholesterol is so large that in order for cholesterol to be
transported, vesicles multiply their circular layers, so they are referred to
as multi-layered vesicles (multimellar vesicles)
3. Eventually, in the gallbladder, the gallbladder, cholesterol transporter, both
micelles and vesicles combine to become a multi-layer vesicle. These
vesicles in the presence of mucin protein will form cholesterol crystals.
Fragmented cholesterol crystals will eventually glue (put together).

Cholesterol stones occur because the concentration of cholesterol in

the bile is high. This is a result of cholesterol in the blood is quite high. If
cholesterol in the gallbladder is high, precipitation will occur and
eventually it will turn into stone. Cholesterol, which is a normal
constituent of bile, is insoluble in water. Its solubility depends on the bile
acids and lecithin (phospholipids) in the bile. In patients who tend to suffer
from gallstones there will be a decrease in bile acid synthesis and an
increase in cholesterol synthesis in the liver; this condition results in
supersaturation of bile sap by cholesterol which then comes out of bile
sap, settles and forms stones. Symptoms are jaundice which usually occurs
in ductal obstruction. One of the typical symptoms of obstruction of bile
flow into the duodenum is the absorption of bile by the blood which makes
the skin and mucous membranes turn yellow.

6. Explain the early management based on the scenario!

1. Fasting or low-fat diet so that the workload of gall bladder is reduced.
Start with eating a well-balanced, healthy diet as well as getting enough
sleep and exercise. Consumption of foods that are rich in fiber and low in
fat, for example fruits and vegetables.
2. Antibiotics such as piperacillin, ampicillin, meropenem. In severe, life-
threatening cases, imipenem / cilastatin is recommended.
3. Alternative regimens include third generation cephalosporins
supplemented with metronidazole.
4. Vomiting patients can be given antiemetics, such as prometazine or
prochlorperazine, to control nausea and prevent fluid and electrolyte
disturbances and it can be nasogastric suction.

15
7. What is the diagnostic steps?
A. Anamnesis
1. Patient Identity : Name, age, gender, patient’s job, address
2. The main complaint and explore the current medical history:
- the onset and duration of complaints: since when and how they arise
- things that aggravate and alleviate complaints
- other symptoms related to the main complaint
3. Asking complaints about other systems.
4. Exploring previous diseases
5. History of habits
6. Treatment history
7. history of internal medicine
8. Cross check
B. Physical examination
- Breathing: Cholecystitis will cause dyspea and sound abnormal breath
sounds.
- Cardiovascular: The patient will experience tachycardia and the risk of
bleeding due to vitamin K deficiency.
- Innervation: The patient has an increase in body temperature.
- Musculoskeletal: Cholecystitis will cause weakness.
- Skin / integument: The skin and mucous membrane will feel itchy and
yellow.
- Nutrition Pattern: The patient has nutritional deficiencies caused by nausea,
vomiting. Patients will also be intolerant of fat foods and 'gas makers'
foods.
- Elimination Pattern: Color changes in the urine and feces.
- Activity and Break Patterns: Patients will find it difficult to move and rest
due to pain.

IPPA (Inspection, Palpation, Percussion, and Auscultation)

Cholecystitis causes biliary colic pain in the right quadrant abdomen that
spreads to the back. In patients with cholecystitis found positive for Murphy's
sign (sharp local pain that occurs when the gallbladder is palpated and the
patient is instructed to breathe deeply). The patient's body will turn yellow
caused by bile sap in the blood.

16
C. Supporting examination:
Heart Function Test
1. Liver Enzymatic Test:
•Alkali Phosphatase (ALP)
ALP is secreted by tissue cell of hepatobiliary, bone, intestinal and
placenta. Also in the kidneys, lactating mamma gland, granulocytes and
cancer cells.
the purpose of the test is to detect:
- hepatobiliary disease: cholestasis / obstruction, tumor, stone or abscess
- bone disease with osteoblastic activity or vitamin D therapeutic response
to rickets
- the process of malignancy (metastasis to the liver)
- to detect malignancy processes (metastasis to heart).
•SGOT / AST
Glutamate Oxaloacetate Transaminase (GOT) = Amino Transferase
Aspartate / Aspartate Transaminase (AST / ASAT)
in liver and myocardial cells, musculoskeletal, kidney, pancreas, brain and
erythrocytes
Test Purpose:
- diagnose and evaluation of liver disease and heart disease
- monitor the effects of hepatotoxic and nephrotoxic drugs
•SGPT / ALT
Glutamate Pyruvate Transaminase (GPT) = Alanine Amino Transferase /
Alanin Transaminase (ALT / ALAT)
In liver cells, body fluids, heart, kidney and musculoskeletal.
Test Purpose:
- diagnose and evaluation of liver disease: this enzyme is an indicator of
damage liver cell
- monitoring the effects of hepatotoxic drugs
- to differentiate hemolytic jaundice with jaundice due to liver disease.

2.Bilirubin Serum Test

Bilirubin: the main product of Hb catabolism in the form of conjugated
bilirubin (indirect, prehepatic), in the liver becomes conjugated bilirubin
(direct, post hepatic)
Test Purpose:
- evaluation of hepatobiliary & erythropoetic function (g3 hemolytic blood
transfusion)
- diagnose jaundice and monitor progression
- diagnose differential biliary obstruction (direct bilirubin) and hemolytic

17
Radiology:
•Ultrasound (Ultrasonography)
This examination is recommended as a preliminary examination.
Examination results that indicate the possibility of cholecystitis include the
presence of fluid in the pericolelistic area and thickening of the gallbladder
wall up to> 4mm. Ultrasound examination can also detect calculi in the gall
bladder or dilated coledocated duct. This examination should be done after 8
hours of fasting because the gallstones are well visualized in the gallbladder
which is detected by bile.

Figure 2.2 Ultrasound examination in cholecystitis

A. CT Scan (Computerized Tomography Scan) and MRI (Magnetic

Resonance Imaging)
Examination results that can be used to predict the presence of
cholecystitis are thickening of the gallbladder wall> 4mm, pericolesystic
fluid, subserous edema, intramural gas, and mucosal peeling. This
examination is also useful to see the structure around if the diagnosis is
inconclusive.

B. ERCP (Endoscopic Retrograde Cholangiopancreatography)

This examination allows direct visualization of the structure that
can only be seen while doing a laparotomy. This examination involves

18
 insertion of a flexible optical fiber endoscope into the esophagus until it
reaches the descending duodenum pars. A cannula is inserted into the
koledokus duct and pancreatic duct, then contrast material is injected into
the duct to allow visualization and evaluation of biliary branching. ERCP
also facilitates access into the distal collections of the ducts to extract
gallstones. ERCP examination requires patient collaboration to allow
endoscope insertion without damaging the structure of the
gastrointestinal tract which includes biliary branching. Before the
examination is carried out, the patient explains the examination
procedure and the patient's role in the examination. Sedative preparations
are given just prior to the inspection. During an ERCP examination, the
nurse must monitor the intravenous fluids given, administer medication,
and adjust the patient's position. After the examination is done, the nurse
monitors the patient's condition again, observing vital signs and signs of
perforation / infection. Nurses also need to monitor the side effects of
each drug given during the examination process, and to recover gag
reflex after the use of local anesthesia.

8. What is the differential diagnosis based on the scenario ?

A. CHOLECYSTITIS

1. Definition of Cholecystitis
Cholecystitis is inflammation of the gallbladder that occurs most
commonly because of an obstruction of the cystic duct by gallstones
arising from the gallbladder (cholelithiasis). Uncomplicated cholecystitis
has an excellent prognosis; the development of complications such as
perforation or gangrene renders the prognosis less favorable.

2. Etiology
At least 90% of patients have gallstones. Helminthic infection is
one of the major causes of biliary disease in Asia, southern Africa, and
Latin America, but not the US. Infection with Salmonella organisms has
been described as a primary event in cholecystitis secondary to typhoid
fever. AIDS-related cholecystitis and cholangiopathy may be secondary to
CMV and Cryptosporidium organisms. Various microorganisms can be
identified early in the onset of disease. These include Escherichia
coli, Klebsiella, enterococci, Pseudomonas, and Bacteroides fragilis. It has
been suggested that this bacterial invasion is not a primary perpetrator of
injury, because in >40% of patients no bacterial growth is obtained from
surgical specimens. Generally, bacterial infection is a secondary feature
and not an initiating event.

19
 Occasionally, acute cholecystitis occurs in the absence of
gallstones (in 5% to 14% of cases). Starvation, total parenteral nutrition,
narcotic analgesics, and immobility are predisposing factors for acute
acalculous cholecystitis. It has also been described as a rare occurrence
during the course of acute Epstein-Barr virus (EBV) infection and can be
an atypical clinical presentation of primary EBV infection. Secondary
infection with gram-negative flora occurs in most cases of acute
acalculous cholecystitis.

3. Causes
The gallbladder is a small, pear-shaped organ connected to the
liver, on the right side of the abdomen. It stores bile and releases it into the
small intestine to help in the digestion of fat. The gallbladder holds bile, a
fluid that is released after we eat, especially after a meal that is high in fat,
and this bile aids digestion. The bile travels out of the gallbladder through
the cystic duct, a small tube that leads to the common bile duct, and from
there into the small intestine. The main cause of cholecystitis is gallstones
or biliary sludge getting trapped at the gallbladder's opening. This is
sometimes called a pseudolith, or "fake stone."
Other causes include:
 injury to the abdomen from burns, sepsis or trauma, or because of
surgery
 shock
 immune deficiency
 prolonged fasting
 vasculitis

An infection in the bile can lead to inflammation of the gallbladder.

A tumor may stop the bile from draining out of the gallbladder properly,
resulting in an accumulation of bile. This can lead to cholecystitis.

4. Risk factor
The following factors may increase the risk of developing gallstones:
 a family history of gallstones on the mother's side of the family
 Crohn's disease
 diabetes
 coronary artery disease
 end-stage kidney disease
 hyperlipidemia
 losing weight rapidly
 obesity
 older age
 pregnancy

Long labor during childbirth can damage the gallbladder, raising the
risk of cholecystitis during the following weeks.

20
5. Symptom
The main symptom of acute cholecystitis is a sudden, sharp pain in
the upper right-hand side of your tummy (abdomen). This pain spreads
towards your right shoulder. The affected part of the tummy is usually
very tender, and breathing deeply can make the pain worse. Unlike other
types of abdominal pain, the pain of acute cholecystitis is usually
persistent and does not go away within a few hours.
Some people may have additional symptoms, such as:

 a high temperature (fever)

 feeling sick
 being sick
 sweating
 loss of appetite
 yellowing of the skin and the whites of the eyes (jaundice)
 a bulge in the tummy

6. Pathogenesis
Over 90% of cases of acute cholecystitis result from obstruction of
the cystic duct by gall stones or by biliary sludge that has become
impacted at the neck of the gall bladder. Obstruction of the cystic duct
causes the intraluminal pressure within the gall bladder to increase and,
together with cholesterol supersaturated bile, triggers an acute
inflammatory response. The trauma caused by the gall stones stimulates
the synthesis of prostaglandins I2 and E2, which mediate the inflammatory
response. Secondary bacterial infection with enteric organisms (most
commonly Escherichia coli, Klebsiella, and Streptococcus faecalis) occur
in about 20% of cases.
Biliary sludge is a mixture of particulate matter and bile, and it
may stimulate microlithiasis. If the sludge persists—for example, because
the patient has already had several pregnancies or is receiving total
parenteral nutrition—gall stones can form. Most patients with biliary
sludge have no symptoms, but the sludge itself can cause acute
cholecystitis.
7. Diagnosis
A doctor will normally ask if a patient has a history of cholecystitis
because it often recurs. A physical examination will reveal how tender the
gallbladder is.

The following tests may also be ordered:

21
  Ultrasound: This can highlight any gallstones and may show the
condition of the gallbladder.
 Blood test: A high white blood cell count may indicate an infection.
High levels of bilirubin, alkaline phosphatase, and serum
aminotransferase may also help the doctor make a diagnosis.
 Computerized tomography (CT) or ultrasound scans: Images of the
gallbladder may reveal signs of cholecystitis.
 Hepatobiliary iminodiacetic acid (HIDA) scan: Also known as a
cholescintigraphy, hepatobiliary scintigraphy or hepatobiliary scan,
this scan creates pictures of the liver, gallbladder, biliary tract and
small intestine.

This allows the doctor to track the production and flow of bile from the
liver to the small intestine and determine whether there is a blockage, and
where any blockage is.

8. Treatment
A patient with cholecystitis will be hospitalized, and they will
probably not be allowed to consume any solid or liquid foods for some
time. They will be given liquids intravenously while fasting. Pain
medications and antibiotics may also be given.
Surgery is recommended for acute cholecystitis because there is a
high rate of recurrence from inflammation related to gallstones. However,
if there is a low risk of complications, surgery can be done as an outpatient
procedure.
If there are complications, such as gangrene or perforation of the
gallbladder, the patient will need immediate surgery to remove the
gallbladder. If the patient has an infection, a tube may be inserted through
the skin into the gallbladder to drain the infection. Removal of the
gallbladder, or cholecystectomy, can be performed by open abdominal
excision or laparoscopically.
Laparoscopic cholecystectomy involves several small incisions in
the skin. A camera is inserted into one incision to help the surgeon see
inside the abdomen, and tools for removing the gallbladder and inserted
through the other incisions. The benefit of laparoscopy is that the incisions
are small, so patients usually have less pain after the procedure and less
scarring.
After surgically removing the gallbladder, the bile will flow
directly into the small intestine from the liver. This does not normally
affect the patient's overall health and digestive system. Some patients may
have more frequent episodes of diarrhea.

9. Preventive
Some measures can reduce the risk of developing gallstones, and
this can decrease the chance of developing cholecystitis:

22
  avoiding saturated fats
 keeping to a regular breakfast, lunch and dinner times and not
skipping meals
 exercising 5 days per week for at least 30 minutes each time
 losing weight, because obesity increases the risk of gallstones
 avoiding rapid weight loss as this increases the risk of developing
gallstones

A healthy weight loss is generally around 1 to 2 pounds, or 0.5 to 1

kilograms, of body weight per week. The nearer a person is to their ideal
body weight, the lower the risk will be of developing gallstones.
Gallstones are more prevalent in people with obesity, compared with those
who have an appropriate body weight for their age, height, and body
frame.

B. CIRRHOSIS OF THE LIVER

1. Definition of Cirrhosis of the Liver

The liver, the largest internal organ in the body, is essential in
keeping the body functioning properly. It removes or neutralizes poisons
from the blood, produces immune agents to control infection, and removes
germs and bacteria from the blood. It makes proteins that regulate blood
clotting and produces bile to help absorb fats and fat-soluble vitamins.
You cannot live without a functioning liver. In cirrhosis of the liver, scar
tissue replaces normal, healthy tissue, blocking the flow of blood through
the organ and preventing it from working as it should. Cirrhosis is the
twelfth leading cause of death by disease, killing about 26,000 people each
year. Also, the cost of cirrhosis in terms of human suffering, hospital costs,
and lost productivity is high. Cirrhosis is a form of damage to the liver.
The liver is about the size of a football. It’s on the right side of the body
and it’s protected by the rib cage. It has over 500 functions and is very
important. You cannot live without your liver. When the liver is damaged,
it develops scars as it tries to fix the damage. Early stages of scarring are
called fibrosis. Someone has cirrhosis when serious and extensive injury
or scarring has developed in the liver. The scarring can stop the liver from
working properly. Cirrhosis Basics 5 Cirrhosis is a very slow-acting
disease. It can take up to 30 years to develop. The amount of time it takes
for cirrhosis to develop depends on a few factors, including the cause of
the cirrhosis, a person’s general health, lifestyle and genetics. Cirrhosis is
a serious condition. If left untreated, it can lead to liver failure, liver cancer
or death. Only a small number of people with cirrhosis will develop these

23
 serious problems. The good news is that there are things you can do to
manage cirrhosis and improve your health..
2. Etiology
Cirrhosis is caused by long-term injury to the liver. Many things
can cause it. This booklet has been written for people who have cirrhosis
caused by viral hepatitis. Viral hepatitis is a disease in which the liver
becomes damaged after getting infected by a really small germ called a
virus. Viruses that infect the liver are known as hepatitis viruses. You may
have heard of hepatitis A, hepatitis B and hepatitis C. (Hepatitis D and E
also exist.) Each hepatitis virus has its own characteristics and passes
between people in different ways. These viruses are also treated in
different ways and some are easier to eliminate than others Cirrhosis has
many causes. In the United States, chronic alcoholism and hepatitis C are
the most common ones.
• Alcoholic liver disease. To many people, cirrhosis of the liver is
synonymous with chronic alcoholism, but in fact, alcoholism is only one
of the causes. Alcoholic cirrhosis usually develops after more than a
decade of heavy drinking. The amount of alcohol that can injure the liver
varies greatly from person to person. In women, as few as two to three
drinks per day have been linked with cirrhosis and in men, as few as
three to four drinks per day. Alcohol seems to injure the liver by blocking
the normal metabolism of protein, fats, and carbohydrates.
• Chronic hepatitis C. The hepatitis C virus ranks with alcohol as a major
cause of chronic liver disease and cirrhosis in the United States. Infection
with this virus causes Cirrhosis of the Liver Information Sheet
(continued) inflammation of and low grade damage to the liver that over
several decades can lead to cirrhosis.
• Chronic hepatitis B and D. The hepatitis B virus is probably the most
common cause of cirrhosis worldwide, but it is less common in the
United States and the Western world. Hepatitis B, like hepatitis C, causes
liver inflammation and injury that over several decades can lead to
cirrhosis. Hepatitis D is another virus that infects the liver, but only in
people who already have hepatitis B.
• Autoimmune hepatitis. This disease appears to be caused by the
immune system attacking the liver and causing inflammation, damage,
and eventually scarring and cirrhosis.
• Inherited diseases. Alpha-1 antitrypsin deficiency, hemochromatosis,
Wilson disease, galactosemia, and glycogen storage diseases are among
the inherited diseases that interfere with the way the liver produces,

24
 processes, and stores enzymes, proteins, metals, and other substances the
body needs to function properly.
• Nonalcoholic steatohepatitis (NASH). In NASH, fat builds up in the
liver and eventually causes scar tissue. This type of hepatitis appears to
be associated with diabetes, protein malnutrition, obesity, coronary artery
disease, and treatment with corticosteroid medications.
• Blocked bile ducts. When the ducts that carry bile out of the liver are
blocked, bile backs up and damages liver tissue. In babies, blocked bile
ducts are most commonly caused by biliary atresia, a disease in which the
bile ducts are absent or injured. In adults, the most common cause is
primary biliary cirrhosis, a disease in which the ducts become inflamed,
blocked, and scarred. Secondary biliary cirrhosis can happen after
gallbladder surgery if the ducts are inadvertently tied off or injured.
• Drugs, toxins, and infections. Severe reactions to prescription drugs,
prolonged exposure to environmental toxins, the parasitic infection
schistosomiasis, and repeated bouts of heart failure with liver congestion
can all lead to cirrhosis.

3. Symptoms
Blood from the stomach and intestines passes through your liver,
where it is filtered and processed before heading to other parts of your
body. When scar tissue begins to replace healthy tissue in the liver, it is
harder for blood to flow normally through the liver and for the liver to
work in its usual way. Cirrhosis is a silent disease, and people who have it
sometimes don’t have symptoms until there’s been a lot of injury to the
liver. Injury may be occurring even if a person has few or no symptoms.
The symptoms of early liver cirrhosis (sometimes called compensated
cirrhosis) include:
• fatigue and loss of energy
• unexplained loss of appetite and weight loss
• nausea
• abdominal pain
• pinhead-sized spots on the skin from which tiny blood vessels
spread out in a circle (spider angiomas)
• redness of the palms of the hand (palmar erythema)
In some people, cirrhosis progresses over time and the liver’s ability to
work normally decreases. How quickly this happens varies from person to
person and depends on a few things, including the person’s general health,
their gender, the cause of the cirrhosis, the stage of the disease when they
were diagnosed, their diet and their alcohol intake. In a small number of

25
people with cirrhosis, the liver gets so damaged it can no longer work
properly. (This serious type of damage is called decompensated cirrhosis.)

Symptoms of more serious cirrhosis include:

• continuous weight loss
• extreme fatigue
• yellowing of the skin (jaundice) or eyes that doesn’t go away
• itchy skin
• dark, tea-coloured urine
• difficulty falling asleep and/or staying asleep; sleep patterns are reversed
for some people: they stay awake through the night and sleep during the
day
• frequent bacterial infections in fluid that can accumulate in the belly
(spontaneous bacterial peritonitis)
• bleeding gums or gums that get bruised easily
• swelling or ruptured veins (varices) in the esophagus (food pipe) and
stomach. (Some symptoms of this are black or bloody stools and dark
vomit that looks like coffee grounds. If you notice this, you need to get
medical attention right away. Bleeding varices are a very serious and
potentially life-threatening medical problem.)
• painful swelling of the legs (edema) and abdomen (ascites) due to an
imbalance of fluid
• shortness of breath, although this is not a common symptom
• confusion, forgetfulness, personality changes, changed sleep habits or
other changes in mental function (hepatic encephalopathy)

4. Pathology
Cirrhosis causes the liver to become lumpy and stiff. This prevents
blood from flowing through the liver easily and causes the build-up of
pressure in the portal vein, the vein that brings blood to the liver. High
pressure in the portal vein is called portal hypertension. To relieve this
pressure, the blood goes around the portal vein, through other veins. Some
of these veins, called varices, can be found in the pipe that carries food
from your mouth to your stomach (the esophagus) or in your stomach
itself. Portal hypertension also causes blood to back up into another organ
called the spleen. This causes the spleen to get bigger and destroy more
platelets than usual. Platelets are blood cells that help in blood clotting.
With cirrhosis, blood is blocked from entering the liver and toxic
substances that the liver normally filters escapes into general blood
circulation. Aside from the problems with liver blood flow, when cirrhosis

26
 is advanced, there aren’t enough healthy liver cells to make good
substances, such as albumin (a protein) and clotting factors that the liver
normally makes. Another complication is Liver cancer, called
hepatocellular carcinoma (HCC). This cancer can occur if some of the sick
liver cells start to multiply out of control. Liver cancer, may occur in any
stage of cirrhosis. There may be no signs of liver cancer until the cancer
has grown very large and causes pain.

5. Complications
Loss of liver function affects the body in many ways. Following
are the common problems, or complications, caused by cirrhosis.
• Edema and ascites. When the liver loses its ability to make the protein
albumin, water accumulates in the legs (edema) and abdomen (ascites).
• Bruising and bleeding. When the liver slows or stops production of the
proteins needed for blood clotting, a person will bruise or bleed easily.
The palms of the hands may be reddish and blotchy with palmar
erythema.
• Jaundice. Jaundice is a yellowing of the skin and eyes that occurs when
the diseased liver does not absorb enough bilirubin.
• Itching. Bile products deposited in the skin may cause intense itching.
• Gallstones. If cirrhosis prevents bile from reaching the gallbladder,
gallstones may develop.
• Toxins in the blood or brain. A damaged liver cannot remove toxins from
the blood, causing them to accumulate in the blood and eventually the
brain. There, toxins can dull mental functioning and cause personality
changes, coma, and even death. Signs of the buildup of toxins in the
brain include neglect of personal appearance, unresponsiveness,
forgetfulness, trouble concentrating, or changes in sleep habits.
• Sensitivity to medication. Cirrhosis slows the liver's ability to filter
medications from the blood. Because the liver does not remove drugs
from the blood at the usual rate, they act longer than expected and build
up in the body. This causes a person to be more sensitive to medications
and their side effects.
• Portal hypertension. Normally, blood from the intestines and spleen is
carried to the liver through the portal vein. But cirrhosis slows the normal
flow of blood through the portal vein, which increases the pressure inside
it. This condition is called portal hypertension.
• Varices. When blood flow through the portal vein slows, blood from the
intestines and spleen backs up into blood vessels in the stomach and
esophagus. These blood vessels may become enlarged because they are

27
 not meant to carry this much blood. The enlarged blood vessels, called
varices, have thin walls and carry high pressure, and thus are more likely
to burst. If they do burst, the result is a serious bleeding problem in the
upper stomach or esophagus that requires immediate medical attention.
• Insulin resistance and type 2 diabetes. Cirrhosis causes resistance to
insulin. This hormone, produced by the pancreas, enables blood glucose
to be used as energy by the cells of the body. If you have insulin
resistance, your muscle, fat, and liver cells do not use insulin properly.
The pancreas tries to keep up with the demand for insulin by producing
more. Eventually, the pancreas cannot keep up with the body's need for
insulin, and type 2 diabetes develops as excess glucose builds up in the
bloodstream.
• Liver cancer. Hepatocellular carcinoma, a type of liver cancer commonly
caused by cirrhosis, starts in the liver tissue itself. It has a high mortality
rate.
• Problems in other organs. Cirrhosis can cause immune system
dysfunction, leading to infection. Fluid in the abdomen (ascites) may
become infected with bacteria normally present in the intestines.
Cirrhosis can also lead to impotence, kidney dysfunction and failure, and
osteoporosis.

6. Diagnostical Test
Several different tests monitor your liver and help you and your
healthcare provider understand how cirrhosis is affecting it. You may have
some of the following types of tests:
• Blood tests assess injury or inflammation in the liver and how well your
liver is working. These tests have names like AST, ALT, GGT, INR,
albumin and bilirubin.
• Imaging tests determine whether the liver is an abnormal shape or size
and also measure how well blood is flowing through it. Ultrasounds
look at the shape and size of your liver, as well as checking for fluid in
the liver and monitoring for cancer. If anything out of the ordinary is
found, other tests like MRIs and CT scans can be used for further
testing.

You may also have tests to monitor the scarring (fibrosis) on your liver.
There are two common tests:
• FibroScan measures liver stiffness using sound waves—a scarred liver
is stiffer than a healthy one. This is a quick, painless procedure.

28
 • Liver biopsy involves inserting a needle into the body to take a small
piece of the liver. The piece is then studied under a microscope to look
for damage. Talk to your healthcare provider about the tests you’ll
need, how often you’ll need them, what to expect during each test and
how to prepare for each one.

7. Treatment
Liver damage from cirrhosis cannot be reversed, but treatment can
stop or delay further progression and reduce complications. Treatment
depends on the cause of cirrhosis and any complications a person is
experiencing. For example, cirrhosis caused by alcohol abuse is treated by
abstaining from alcohol. Treatment for hepatitis-related cirrhosis involves
medications used to treat the different types of hepatitis, such as interferon
for viral hepatitis and corticosteroids for autoimmune hepatitis. Cirrhosis
caused by Wilson disease, in which copper builds up in organs, is treated
with medications to remove the copper. These are just a few examples—
treatment for cirrhosis resulting from other diseases depends on the
underlying cause. In all cases, regardless of the cause, following a healthy
diet and avoiding alcohol are essential because the body needs all the
nutrients it can get, and alcohol will only lead to more liver damage. Light
physical activity can help stop or delay cirrhosis as well. Treatment will
also include remedies for complications. For example, for ascites and
edema, the doctor may recommend a low-sodium diet or the use of
diuretics, which are drugs that remove fluid from the body. Antibiotics
will be prescribed for infections, and various medications can help with
itching. Protein causes toxins to form in the digestive tract, so eating less
protein will help decrease the buildup of toxins in the blood and brain. The
doctor may also prescribe laxatives to help absorb the toxins and remove
them from the intestines. For portal hypertension, the doctor may prescribe
a blood pressure medication such as a beta-blocker. If varices bleed, the
doctor may either inject them with a clotting agent or perform a so-called
rubber-band ligation, which uses a special device to compress the varices
and stop the bleeding. When complications cannot be controlled or when
the liver becomes so damaged from scarring that it completely stops
functioning, a liver transplant is necessary. In liver transplantation surgery,
a diseased liver is removed and replaced with a healthy one from an organ
donor. About 80 to 90 percent of patients survive liver transplantation.
Survival rates have improved over the past several years because of drugs
such as cyclosporine and tacrolimus, which suppress the immune system
and keep it from attacking and damaging the new liver.

29
 One goal of treatment is to target the cause of the cirrhosis. For
example, if your cirrhosis is caused by viral hepatitis, treatment of the
infection will be an important part of your care. Treatments for hepatitis C
can cure the infection in many people. Treatments for hepatitis B do not
cure the infection, but they can help to keep the virus under control.
Another goal of treatment is to manage the symptoms and
complications of cirrhosis. Medications taken by people with cirrhosis
include the following:
• Blood-pressure medications, such as beta-blockers, are used to lower
pressure in blood vessels that carry blood through the liver.
• Diuretics (water pills), such as hydrochlorothiazide or furosemide, are
used to reduce the swelling from ascites and edema.
• The laxative lactulose helps to clear the toxin ammonia from your
system. This keeps your mind clear and prevents confusion or brain fog.
Talk to your healthcare provider about figuring out a way of taking it
that works for you and doesn’t disrupt your day-to-day activities.

Varices in the food pipe (esophagus) and stomach, which are a serious
complication of cirrhosis, can usually be treated. Doctors can use various
procedures to repair them and can prescribe medicines afterwards to
maintain treatment. Surgery, including liver transplant, may be an option
in serious cases of cirrhosis.

C. Hepatitis A
1. Definition of Hepatitis A
Hepatitis A is a liver disease caused by the hepatitis A virus. This
virus is spread mainly through ingests of food or water that is
contaminated with the feces of an infected person. This disease is closely
related to the lack of use of clean water, inadequate sanitation and poor
personal hygiene. Unlike hepatitis B and C, hepatitis A infection does not
cause chronic liver disease and is rarely fatal, but can cause symptoms that
weaken the body and can become fulminant hepatitis (acute liver failure),
which is associated with high mortality (WHO 2012).
Hepatitis A occurs sporadically and in epidemics throughout the
world, with a tendency to cyclic recurrence. Every year there are an
estimated 1.4 million cases of hepatitis A worldwide (WHO 2012).
The hepatitis A virus is one of the most frequent causes of
foodborne infections. Outbreaks related to contaminated food or water can
erupt explosively, such as the epidemic in Shanghai in 1988 which
affected about 300 000 people. In Indonesia, based on data from the

30
 Ministry of Health, hepatitis A still accounts for the largest proportion of
acute hepatitis cases treated, ranging from 39.8 - 68.3% .1 in several
regions such as Jakarta, Bandung and Makassar, ranging from 35% -45%
at the age of 5 years (Puspa R, 2011).
This disease can cause significant economic and social
consequences in society, because, it takes several weeks or months for
people to recover from the disease to return to work, school or daily life.
(WHO 2012).

2. Causes
Hepatitis A is caused by Hepatitis-A Virus (HAV). Generally not
to cause damage to liver tissue. Those who are infected by this virus, 99%
can recover fully. This HAV virus is transmitted by fecal-oral (fecal:
faeces, / feces, oral: mouth). It means spread and transmission of this virus
occurs through contamination of food or water by the HAV virus
contained in feces / feces of patients with Hepatitis A. Some risk factors
that can increase the spread of this virus include:
•Poor sanitation .
•Direct contact with sufferers.
•Share syringes.
•Having sex with a person, especially anal sex .
•Men who have sex with men.
•Work in areas related to dirt, such as gutters. (Sari, 2008)

3. Risk Factors for Hepatitis A

Transmission of hepatitis A often occurs from person to person ,.
This virus spreads through food or water that is contaminated with feces of
an infected person. In addition, hepatitis A can occur in people who:
1. Hygine and Environmental sanitation
Low quality of environmental sanitation and pollution of water
sources or food consumed by many people facilitate transmission and
outbreaks of extraordinary hepatitis A. Habits of people who pay less
attention to environmental cleanliness such as bowel movements in rivers
can increase transmission of hepatitis A. Feces contaminated with
hepatitis A will pollute another environment. Like water, soil and so on.
2. Economy
The socioeconomic level of the community will affect the
availability of clean water and healthy living behavior as well as the
ability to provide or provide hepatitis A vaccination . People with a low
social economy in general rarely pay attention to the quality of water

31
 used in meeting their daily needs. Poor quality water can be
contaminated with hepatitis A virus . In addition, families with a low
social economy generally have a low level of knowledge, so they don't
really think about how important the hepatitis vaccination is A. So
hepatitis A can spread quickly from one person to another.
3. Clean and Healthy Lifestyle
Clean and healthy lifestyle is a society that is very influential in
transmitting hepatitis A. Low clean and healthy life patterns will increase
the occurrence of hepatitis A virus transmission. Hepatitis A can be
transmitted quickly in day care centers, this virus will spread quickly
when the babysitter does not wash his hands after changing the baby's
diaper. Awareness of washing hands is also very important in dealing
with the transmission of the hepatitis virus. Bad habits such as sharing
food and utensils with hepatitis A as well as one of the medium of
transmission of hepatitis A 's.
4. Lifestyle
Lifestyle in society is also one of the risk factors for hepatitis. The
habit of eating raw vegetables, such as vegetables will increase the
likelihood of transmission of hepatitis A. Food ingredients such as
vegetables that are contaminated with hepatitis A virus if consumed by
the virus will move to humans. The virus will infect humans, causing
hepatitis. (Aryana, 2015)

4. Etiology
Acute viral hepatitis A is a viral infection that is transmitted
through the enteral transmission of RNA viruses that have a diameter of 27
nm. This virus is self-limiting and usually heals on its own, more often
attacking individuals who do not have hepatitis A virus antibodies as in
children, but infection can also occur in adults. Fulminant (0.01%) rarely
occurs and transmission to chronic hepatitis is not to be feared, there is no
correlation between the occurrence of primary liver cell carcinoma. Career
Healthy HAV is unknown. This infection causes the patient to have
lifelong immunity.
HAV consists of nucleic acids surrounded by one or more proteins,
some viruses also have outer-membrane envelopes. This virus is an
intracellular obligate parasite, it can only replicate within cells because its
nucleic acids do not encode many enzymes needed to metabolize proteins,
carbohydrates or lipids to produce high-energy phosphates. Normally viral
nucleic acids encode proteins needed for replication and wrap their nucleic
acids in host cell chemicals. HAV replication is limited in the liver, but

32
 this virus is present in the bile, liver, feces and blood during the incubation
period and the final phase of the disease. HAV is classified as
picornavirus, subclassified as hepatovirus, diameter 27-28 nm in
symmetric cube shape, single stranded, linear RNA molecule 7.5 kb, in
humans consisting of one serotype, three or more genotypes, containing
immunodominant neutralization sites single, containing three or four
virion polypeptides in capsomeres, replication in cytoplasm of infected
hepatocytes, no evidence of replication in the intestine, spread in non-
human primate strains and human cell strains (IPD UI, 2009).

5. Symptoms of Hepatitis A
The incubation period for hepatitis A varies between 14-28 days
with clinical symptoms that also vary from asymptomatic to symptomatic,
depending on age. In children aged <6 years, about 70% of cases show no
specific symptoms, while in adult cases about 85% show symptoms and
require hospitalization. Symptoms that can occur include fever, no
appetite, diarrhea, nausea, discomfort in the stomach, dark urine, and
yellow in the skin and eyes. In general, symptoms last around 2 months,
but in certain cases can continue for up to 6 months.

6. Clinical Manifestations
Clinical features of viral hepatitis vary greatly from asymptomatic
infections without jaundice to the very severe ones, namely fulminant
hepatitis which can cause death in just a few days. Symptoms of acute
hepatitis are divided into 4 stages: the incubation phase, the prodromal
phase (pre-jaundice), the jaundice phase, and the convalescent phase
(healing)

33
1. Incubation Phase. Is the time between the entry of the virus and the
onset of symptoms or jaundice. This phase varies in duration for each
hepatitis virus. The length of this phase depends on the dose of
inoculum transmitted and the transmission pathway, the greater the dose
of the inoculum, the shorter the incubation phase. In hepatitis A the
incubation phase can last for 14-50 days, with an average of 28-30 days.
2. Prodromal (pre-icteric) phase. The phase between the onset of first
complaints and the onset of jaundice. The onset can be brief or
insidious characterized by general malaise , muscle aches, joint pain,
fatigue, upper respiratory symptoms and anorexia . Nausea, vomiting
and anorexia are associated with changes in smell and taste. Low-grade
fever generally occurs in acute hepatitis A. Abdominal pain is usually
mild and persists in the right upper quadrant or epigastrium, sometimes
exacerbated by activity but rarely causes cholecystitis. These symptoms
are like "febrile influenza infection". In children and adolescents
symptoms of digestive disorders are more dominant, whereas in adults
more often show symptoms of jaundice accompanied by myalgia
3. The Jaundice Phase . Jaundice occurs after 5-10 days, but can also
occur together with the appearance of symptoms. In many cases this
phase is not detected. The end of the prodromal and the beginning of
the clinical phase is characterized by brown urine, persistent
urobilinogenuria, mild proteinuria and microhaematuria can develop.
Stool is usually acholic, with jaundice (60-70% in children, 80-90% in
adults). Some symptoms subside, but fever can still occur.
Hepatomegaly, splenomegaly liver tenderness, can be found. The end of
the LDL incubation period may increase as expression of virocyte
duplication, increase in SGOP, SGPT, GDH. Niali Transaminase is
usually not necessary to determine the severity. Increased serum iron is
always an expression of liver cell damage. AP and LAP increased
slightly. HAV RNA was detected about 17 days before the SHPT
increased and several days before HAV IgM appeared. Viremia lasts for
an average of 79 days after an increase in GPT , its duration is around
95 days (IPD UI, 2009).
4. The convalescent (healing) phase. It begins with the disappearance
of jaundice and other complaints, but hepatomegaly and abnormal liver
function persists. There is a feeling of being healthier and the return of
appetite. The acute situation will usually improve within 2-3 weeks. In
hepatitis A complete clinical and laboratory improvement occurs in 9
weeks. In 50-10 % of the clinical course cases it may be more difficult
to handle, only <1% become fulminant. (Wicaksono, 2014)

34
 Normalization of bile acid serum is also considered as a parameter of
healing kilnis symptoms:
 Hepatitis A Classical: occur suddenly preceded prodromal
symptoms approximately one week prior to jaundice
 Hepatitis A relapse: Arises 6-10 weeks after being declared
clinically cured. Most occur at the age of 20-40 years. Symptoms
of relapse are milder than the first form .
 Hepatitis A cholestatic: Occurs in 10% of symptomatic patients .
Characterized by prolongation of hepatitis symptoms within a few
months accompanied by heat, itching and jaundice.
 Hepatitis A protracted: In the liver biopsy found portal
inflammation with piecemeal necrosis, periportal fibrosis, and
lobular hepatitis
 Hepatitis A fulminant: The most severe and can cause death,
memberatnya characterized by jaundice, encephalopathy, and
lengthening the time prothrombin.

7. Pathogenesis
Starting with the entry of the virus into the digestive tract, then into
the flow of blood into the liver (portal vein), then invade the liver
parenchymal cells. In liver parenchyma cells replicate which causes liver
parenchyma cells to become damaged. After that the virus will come out
and invade other parenchyma cells or enter the bile duct which will be
excreted with feces. Damaged parenchyma cells will stimulate an
inflammatory reaction that is characterized by macrophage aggregation,
enlargement of kupfer cells that will suppress the biliary duct so that the
flow of direct bilirubin is blocked, then there is a decrease in the excretion
of bilirubin to the intestine. This situation causes an imbalance between
uptake and excretion of bilirubin from liver cells so that bilirubin that has
undergone a process of conjugation (direct) will continue to accumulate in
liver cells which will cause reflux (back flow up) to the blood vessels so
that it will manifest yellow in the skin tissue, especially in the sclera
sometimes accompanied by intense itching and dark urine, such as tea due
to small sized particles direct bilirubin so it can fit into the kidneys and
in eksresikan through urine.
Due to the lack of direct bilirubin in the intestine resulting in a
disruption in the production of bile acids (low production) so that the
process of digestion of fat is disrupted (the fat stays in the stomach for a
long time) which causes strain in the stomach thereby stimulating the

35
 sympathetic nerves and parasympathetic nerves resulting in its activation
of the vomiting center which is in the medulla oblongata which causes
symptoms of nausea, vomiting and decreased appetite. (Kumar, 2007).
According to IPD (2009), the pathogenesis of hepatitis A is that
HAV enters the liver from the digestive tract through the bloodstream, into
hepatocytes, and replicates in hepatocytes that involve RNA-dependent
polymerase. From the liver, HAV is eliminated through sinusoids,
canaliculi, into the intestine before the onset of clinical or laboratory
symptoms .
8. Diagnosis
The diagnosis can be made from anamnesis, physical examination
and supporting examination in the form of serological examination:
IgM anti- HAV can be detected during the acute phase and 3-6 months
later. Anti-HAV positive without anti-HAV IgM indicates past infection
Prevention Measures
To prevent transmission of the HAV virus, the thing that can be done is to
maintain the cleanliness of the food intake that we eat. Some good habits
that can be done for this purpose include making it a habit to wash hands
with soap before eating, maintain food sanitation, and avoid eating food
that is not yet known for its processing hygiene (food sold alongside roads,
etc.). In addition, prevention of Hepatitis A can also be done by
administering the Hepatitis A vaccine (Sari, 2008)
According to WHO, the best way to prevent transmission of
Hepatitis A is by improving environmental sanitation and vaccination. The
aspect of environmental sanitation is important so that transmission does
not occur quickly while vaccination is intended as protection. In Indonesia,
there is a law that reinforces the importance of vaccination to prevent the
outbreak of Hepatitis A. According to the Regulation of the Minister of
Health of the Republic of Indonesia Number 42 Year 2013 Regarding the
Implementation of Immunization, there are 3 types of immunization given
to the community, especially in infants (to form antibodies), namely
compulsory immunization , additional immunizations and choice
immunizations .
As stated in Article 11 paragraph 1, it is stated that "the type of
pillihan immunization can be in the form of Haemophillus influenza type b
(Hib), Pneumococcal, Rotavirus, Varicella Influenza, Measles Ruble
Mumps, Typhoid Fever, Hepatitis A, Human Papilloma Virus (HPV) and
Japanese Encephalitis ". Although the position of Hepatitis A in the
implementation of vaccination is only as an additional immunization, but
Hepatitis A is one of the diseases that are included in the list of diseases

36
that can be prevented through immunization by administering vaccines. As
stated in the Decree of the Minister of Health of the Republic of Indonesia
Number 1611 / Menkes / SK / XI / 2006 on Implementation Guidelines
Immunization is " type of diseases that can be prevented through
immunization include diseases communicable particular .
Hepatitis A vaccination should be given to several types of
conditions such as:
a. All children who are two years or older
b. Children and adolescents aged 2-18 years who live in areas where
routine vaccination programs are carried out because of the high
incidence of the disease
c. Patients with chronic liver disease : Vaccine for Hepatitis A is expected
to reduce the incidence of Hepatitis A, because Hepatitis A is a type of
disease that is very fast transmission. In addition, improvement of
environmental sanitation is very necessary in order to minimize the
incidence of Hepatitis A.

Hepatitis can affect anyone regardless of age or economic factors.

Hepatitis can attack ranging from toddlers, children children to adults. For
hepatitis A when attacking children ranging from 1-18 years can be
vaccinated by administering a vaccine dose of 2 or 3 drops of the vaccine
dose in accordance with treatment standards. Whereas for adults with
greater vaccination with a vaccine period of 6-12 months after the first
dose of vaccine. With this vaccination an effective preventive measure can
last 15-20 years or more. Vaccine aims to prevent before the infection of
the hepatitis A virus and provide protection against the virus as early as
possible 2-4 weeks after vaccination. (Price, 2005)
Vaccination for hepatitis A is given to:
1. Those who use illegal drugs (psychotropic drugs) using syringes
2. Those who work as waitresses, especially those who have food that are
not getting enough attention to the safety and cleanliness of the food
itself.
3. People who live in a cottage or dormitory that every day come in direct
contact. Maybe among the boarding school dwellers have a history of
hepatitis A.
4. Toddlers and children who may live in environments that have a higher
risk of hepatitis.
5. Someone who likes to have oral sex / anal.
6. Someone who is identified as having chronic liver disease.

37
 Maintaining personal hygiene and the environment around the
residence is a very important initial effort as an early prevention process
before contracting or experiencing a higher risk of hepatitis. Always
maintain cleanliness by starting an easy step one of them by getting used
to washing hands before and after touching something.
But for those who like to travel abroad in the country who may have
poor sanitation as a precaution it could not hurt to vaccinate at least 2
months before traveling to abroad. However, for those who have been
identified as having hepatitis A virus (HAV), immune globulin (IG)
should be given as soon as possible by giving a vaccine at least 2 weeks
after the hepatitis A virus is identified .

10. Supporting Investigation

a. Serologic Examination

The presence of anti-HAV IgM in a patient's serum is considered the gold

standard for diagnosis of acute hepatitis A.7 infection. Viruses and
antibodies can be detected by commercial methods of RIA, EIA, or
ELISA. The above examination is used to detect anti-HAV IgM and total
anti-HAV (IgM and IgG). Anti-HAV IgM can be detected during the acute
phase and 3-6 months thereafter. Because anti-HAV IgG lasts a lifetime
after acute infection, if someone is detected as positive anti-HAV IgG
without being accompanied by anti-HAV IgM, it indicates an infection in
the past. Immunity testing of HAV is not affected by passive
administration of immunoglobulin / vaccination, because the prophylactic
dose is below the level of detection dose.

b. Rapid Test

Detection of antibodies can be done through rapid tests using the

immunochromatographic assay method, with commercial diagnostic tools
available.22 This diagnostic tool has 3 lines that have been coated by
antibodies, namely "G" (HAV IgG Test Line), "M" (HAV IgM Test Line),
and "C" (Control Line) located on the membrane surface. Purple "G" and
"M" lines will appear in the results window if sufficient anti-HAV IgG and
/ or IgM levels are present in the sample. By using a rapid test with the
immunochromatographic assay method, it was found specificity in
detecting anti-HAV IgM up to an accuracy level of 98.0% with a
sensitivity level of up to 97.6%.

38
 c. Other Supporting Examinations

Diagnosis of hepatitis can be made based on biochemical tests of liver

function (laboratory tests of: urine bilirubin and urobilinogen, total and
direct serum bilirubin, alanine transaminase (ALT) and aspartate
transaminase (AST), alkaline phosphatase (ALP), prothrombin time (PT) ,
total protein, serum albumin, IgG, IgA, IgM, and complete blood cell
count). If laboratory tests are not possible, epidemiologic evidence can
help to make the diagnosis.

11. Treatment
There is no specific treatment for hepatitis A virus (HAV).
Treatment is given supportively rather than directly curative. Medications
that may be given include analgesics, antiemetics, vaccines, and
immunoglobulins. Prevention either before or after exposure to HAV
becomes more important. There is no specific treatment for Hepatitis A,
because the infection itself will usually heal itself. The administration of
pharmacotherapy is to reduce morbidity and prevent complications.
Pharmacotherapy or drugs commonly used are antipyretic analgesics or
fever and pain relievers, antiemetics or anti-vomiting, vaccines, and
immunoglobulins. There is no specific therapy available. The
antienteroviral studied pleconaril drugs (Disoxaril; ViroPharma) had no
activity against the hepatitis A virus (HAV).
Hospitalization is indicated for patients with significant
dehydration due to vomiting or those with fulminant hepatitis. But in other
severe cases where complications of fluid deficiency due to excessive and
continuous vomiting resulting in complications of fluid and electrolyte
deficiency are recommended for treatment at the hospital. Consultation
with subspecialists is generally not required.
Fulminant hepatitis sufferers may need to be consulted by a
pediatrician or intensive care specialist. Although the acetaminophen fever
drug can safely be used to treat some symptoms associated with hepatitis
A virus (HAV) infection, the dosage should be no more than 4 grams a
day or 8 tablets a day. In children aged 12 years do not exceed 2 grams or
4 tablets a day. To reduce the impact of damage to the liver while speeding
up the healing process, adequate rest is taken so that it provides strength to
the immune system to fight infection. Anti-nausea medication can be
given to prevent excessive nausea and vomiting. Impaired sense of nausea
and vomiting that can reduce appetite eat. it is must be overcome because
nutrient intake is very important in the healing process.

39
 In hepatitis A, the most disturbed organ is the liver or liver. The
function of the liver is to metabolize drugs that have been used in the
body. Because the heart is experiencing sore, then drug- drugs that do not
need as well as alcohol and the like should be avoided during illness.
Some researchers believe that the use of corticosteroids can influence
patients to develop hepatitis A recurrence. Although very rare,
complications can often occur with hepatitis A infections such as acute
kidney failure, interstitial nephritis, pancreatitis, red blood cell aplasia,
agranulocytosis, bone marrow aplasia, block temporary heart disease,
Guillain-Barré syndrome, acute arthritis, Still's disease, lupuslike
syndrome, autoimmune hepatitis and Sjögren's syndrome, recurrence of
Hepatiotic A infection occur in about 3-20% of sufferers. After passing
through the acute infection phase, the remission phase lasts 3-6 weeks.
Recurrence occurs after a short period of time usually more than 3 weeks
and the symptoms are like the initial symptoms even though the symptoms
are milder. There is a case report of a patient being transplanted today due
to recurrence and accompanied by other diseases that do not improve with
treatment (Children, 2012)

D. Pankreatitis
1. Definition of Pankreatitis
Pankreatitis is a chronic inflammatory reaction. Clinically, acute
sepsis is characterized by acute abdominal pain accompanied by an
increase in the respiratory enzymes in the blood and urine. The pathology
of the disease is very variable from the very limited self-limited, severe
accompanying shock with renal and lung disorders that can be cronic.
In severe pancreatitis, pancreatic enzymes, vasoactive materials
and other toxin substances emerge from the pancreatic ducts and mausk
into the posterior pararenal space, the lesser sac and the peritoneal cavity.

2. Etiology
The factors that determine the extent of acute west creatitis are
largely unknown. In nearly 80% of cases of acute creatitis, the tissue of the
pancreas becomes inflamed, still alive; this condition is called
intertisreatreatitis, and the rest develops pancreatic or peripankreas
necrosis. Peripankreas necroetiologysis is thought to occur as a result of
activation of the pancreatic lipase in the peripankreas fat tissue; whereas
the causes of multi-factor pancreatic necrosis include damage to
microsiculation and the direct effects of pancreatic enzymes. When the
pancreas experiences necrosis, especially if the necrosis is extensive, the

40
 systemic state of the toxin will remain. The cause is not clear, but what is
certain is the release of enzymes in the pancreas and toxins and secondary
infections in necrotic tissue.

3. Epidemiology
Causes and frequency
Incidents vary greatly from one country to another and also in one
place with another place in the same country. This is caused in addition to
due to actual environmental factors (alcoholic, gallstones, etc.). In western
countries the main causes are the use of alcohol (80-90% in men) and
gallstones (75% in women). In the west when gallstones are the main
cause of acute creatitis, most age is around 60 years and there are more in
women (75%) when associated with the causes of excessive alcohol use
then more men (80-90%).

4. Pathogenesis
Partly in contrast to the various etiological factors accompanying
acute pancreatitis, there is a uniform set of pathophysiological events that
occur in the onset of this disease. This incident is based on enzyme activity
in the pancreas which then results in organ autodigestion.
Under normal circumstances the pancreas is protected from the
enzymatic effects of its own digestive enzymes. This enzyme is
synthesized in part by an active zimogen and is activated by enzymatic
breakdown of the peptide chain. Proteolytic enzymes (trypsin,
chymotrypsin, carboxypeptidase, elastase) and phospholipase A belong to
this group. Other digestive enzymes, such as amylase and lipase, are
inactivated and are stored in zimogen grains so that they are isolated by the
phospholipid membrane in these original cells. In addition, there are
inhibitors in the tissues of the pancreas, the liquid of the pancreas and
serum so that they can activate activated proteases too early. In the process
of activating enzymes in the pancreas, an important role lies in trypsin
which activates all the scavenger zimogens seen in the autodigestion
process (jimotripsinogen, proelastease, phospholipase A). Only active
lipases are not disturbed in trypsin. Activation of zimogen normally starts
by enterokinase in the duodenum. This results in another zimogen
activation beginning. So it is suspected that the early activation of
trypsinogen to trypsin is a trigger for the enzyme cascade and pancreatic
autodigestion.
The mechanisms that initiate the activation of enzymes include
reflux of duodenal contents and reflux of bile fluids, activation of the

41
 complement system, stimulus, excessive enzyme secretion. The contents
of the duodenum are a mixture of active pancreatic enzymes, bile acids,
lysolestin and fat that have undergone emulsification all of which are able
to induce acute creatitis. Bile acids have a detergent effect on the cells of
the pancreas, increase the activation of lipases and phospholipase A, break
down lestin into lysolestin and fatty acids and induce spontaneous small
amounts of tripcinogen so that later it activates other pancreatic prozymes.
Continuing the perfusion of bile acids into the creator's ductus increases
the permeability and thereby induces spontaneous small amounts of
tripcinogen so that the next activates another pancreatic prozim. clear
structural changes.
The main histologic abnormalities found in acute creatitis are
necrotic parenchymal coagulation and necrotic asin nuclei picnosis and
arising debris. The presence of edema, bleeding and thrombosis factors
indicate vascular damage that occurs together.

5. Clinical picture
It is stated that acute creatoritis can be so mild that it can only be
found by examining serum enzyme levels in the serum or can be found by
examining pancreatic enzymes in the serum or can be severe and fatal
stings in a short time. press on the right upper abdomen due to peritoneal
stimulation, sometimes peritonitis is common. Reducing or eliminating
bowel sounds indicate paralytic ileus. With deep palpation, most can be
felt like there is a mass in the epigastrium that corresponds to a swollen
pancreas and inflammation of the infiltrate around the pancreas. High
temperatures indicate the possibility of cholecystysis or pancreatic abscess.
Jaundice is found in some cases, sometimes ascites that are colored like
flesh extract and pleural effusion especially the left side.

6. Diagnosis
The diagnosis of acute pancreatitis can generally be made if the
patient presents with abdominal pain that arises suddenly found:
1. Increase in serum or urine amylase or lipase value in serum at least three
times the highest normal price.
2. Or ultrasonographic findings that are appropriate for acute creatitis.
3. Or the discovery of surgery / autopsy that is appropriate for acute
creatitis.

Laboratory tests aim not only to establish a diagnosis, but also to

determine the severity of the disease and monitor the course of the disease,

42
 to follow the therapy to track complications and evaluate the remaining
function of the pancreas.
Increased amylase or serum lipase is still the key for diagnosis. Serum
amylase shows only a significant increase in 75%, reaches a maximum
within 24-36 hours and then decreases within 24-36 hours. Examination of
iso amylase is more specific for acute pancreatitis. Serum lipase increases
at 50% and lasts longer ie 5-10 days. Rapid return numbers of this enzyme
increase to normal usually show signs of a good prognosis, a persistent
increase leading to a suspicion of complications such as progressing
creator obstruction and arise pancreatic pseudocyst abscess or pancreatic
necrosis or a persistent inflammatory process.

7. Therapy
Pharmacology
The goal of treatment in acute pneumonia is to stop the process of
inflammation and autodigestion or stabilize at least the clinical situation so
as to provide a chance for resolution of the disease.
Conservative measures are still considered basic therapy of only acute
stage creatitis and consists of:
1. Provision of strong analgesics such as petidine and pentazokin several
times a day. Morphine is not recommended because it causes sphincter
oddi spasm.
2. The pengreas is rested by the way the patient is satisfied
3. Provided parenteral nutrition with total in the form of electrolyte fluid,
nutrition, plasma protein fluid.
4. Suction of gastric fluid in severe cases to reduce the release of gastrin
from lambunng to reduce stimulation to the pancreas. Installation of
pipes for decompression if paralytic ileus is present, controlling
vomiting, preventing aspiration.

Antibiotics are not routinely given and given if the patient has a high
fever for more than 3 days or if the patient is suffering from pancreatitis
due to gallstones or to a severe creator.

Surgical procedure
Immediate action for surgical exploration is generally not done,
except in severe cases where there are:
1. Worsen circulation and pulmonary function after several days of
intensive therapy.

43
 2. In the case of necrotizing hemorrhagic creators accompanied by shock
that is difficult to overcome.
3. The emergence of sepsi
4. Progressive kidney dysfunction
5. Signs of peritonitis
6. Severe intestinal bleeding.

Surgery can also be done after the disease progresses for some time
(mostly after 2-3 weeks of intensive care) when complications arise such
as pseudocyst formation, or abscess, formation, fistula, ileus due to
obstruction in the duodenum or colon, in obstructive jaundice and in
severe retroperitoneal bleeding. or intestinal.

8.supporting investigation

1.Examination of creactive protein (CRP)

Examination of C reactive protein (CRP) is widely known as an indicator of

the severity of panyakit. The value of serum peak levels 48 hours after disease
onset is an accurate prognostic factor, values more than 150 mg / L have 80%
sensitivity, 76% specificity, PPV / positive predictive value 76% and NPV?
negative predictive value of 86% as an indicator of acute pangkreatitis and also
to assess leukocytosis, hemoconsetrate, and inflammatory markers.

2. Electrolyte serum, and Blodd urea nitrogen, creatinine, and glucose

Blodd urea nitrogen (BUN) increases at time of entry (> 20 mg / dl) or

increases 24 hours afterwards, identifying deterioration.

3. Amylase & lipase

Serum lipase usually increases more specifically in pangkreatitis than

amylase and the levels persist for up to 12 days. While serum amylase will
usually increase after 6-12 hours of onset for 3-5 days (up to 3 times the
normal value).

4. Lipid profile

An examination of total cholesterol, LDH, HDL, and triglycerides to

evaluate the possibility of the underlying etiology.

5. Alkaline phosphatase, total bilirubin, serum glutamic-oxalocetic transaminase

(SGOT) and serum glutamic-pyruvic transaminase (SGPT)

44
9. Explain the islamic perspective according to the scenario !

۟ ُ‫وا ِزينَت َ ُك ْم ِعن َد ُك ِل َم ْس ِج ٍد َو ُكل‬

‫وا‬ ۟ ُ‫۞ َٰيَبَنِى َءا َد َم ُخذ‬
ٓ
ُّ ‫وا َو ََل ت ُ ْس ِرفُ ٓو ۟ا ۚ ِإنَّهُۥ ََل يُ ِح‬
َ‫ب ْٱل ُم ْس ِرفِين‬ ۟ ُ‫َوٱ ْش َرب‬
Artinya: ‘’ Hai anak Adam, pakailah pakaianmu yang indah di setiap
(memasuki) mesjid, makan dan minumlah, dan janganlah berlebih-lebihan.
Sesungguhnya Allah tidak menyukai orang-orang yang berlebih-lebihan.’’
(Al-A’raf 7:31)

From Karimah Al-Miqdad ibn Ma'di Kariba radhiyallahu 'anhu, he said, "I
heard the Messenger of Allah sallallaahu' alaihi wasallam said, "It was not
Adam's children and grandchildren filling containers that were worse than his
stomach, in fact just a few bribes were enough to strengthen his ribs. Even if
he had to fill them, then 1/3 for food, 1/3 for drinks, and 1/3 for breathing. "

45
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