LBM 2 Urin was tea coloured

STEP 1

Transaminase enzyme test : transaminase enzyme is for katabolic pathway in amino acid
metabolid from amino acid be an other amin.such as
SGPT(serin,glutamin,pyruvic,transaminase):a test for a check the fungtional of serin glutamin
pyruvic and transaminase enzyme and specific for destructon of hepar

and SGOT (serin,glutamin,oksaloasetat,transaminase): a test for a check the fungtional of

serin glutamin oksaloasetat transaminase specific for spleen,bone,hepar

Ikterik : jaundice :change color become yellow caused by pigmen

bile,appereance in the plasma,skin and membrane mucous.

There is increase for bilirubrin in the sistemik circulation and this condition make yellow
appereance.

STEP 2

1. What make the urine become tea colored?

2. Why make the woman was complaining of having stomach discomfort ten days ago?
3. Why did she complain of having nausea?
4. Why does the sclera become icteric?
5. Why did the doctor suggest the transaminase enzyme test?
6. Why does the physical examination show right upper quadrat abdominal pain with
tenderness?
7. What is the function of the transaminase enzyme?
8. Why did the doctor prescribe for vitamin and recomend a proper diet?
9. Why did the doctor ask the patient history of consuming traditional medicine or
painkiller drugs
10. Why was the woman complaining of having vomiting?
11. Why was she complaining of having high fever?
12. What is the DD(definition,etiology,risk
factor,pathogenesis,classification,treatment,complication,prognosis,clinical
manifestation)?
13. Physical examination
14.

STEP 3
1. What make the urine become tea colored?
Important point :because increase of bilirubrin and urobilinogen.because the
obstructon from canaliculi duct,so the conjugated bilirubrin cannot exit for the
duct.and the condition reflux to vascularisasi system and will be go to duodenum and
ren.urine with urobilinogen is normal,but when the direct bilirubrin is increase make
the urine become abnormal because increase the oksidasi procces .and this is
condition make the color of the urine like tea

2. Why was the woman complaining of having stomach discomfort ten days ago?
From the location of stomach discomfort ,we find many organ(hepar,vesica fellea,).
And probably it is caused by the inflammation from the organ, and the inflammation
caused by bacteria or virus

3. Why did she complain of having nausea?

Stomach nausea vomiting,abnormal of liver  because metabolic disorder fatty
acid cannot change become asetyl coenzim AFatty acid activation nerves nausea
and vomiting in cranial that cause nutrition of brain is decrease  functional smell
sense is disorder

4. Why does the sclera become icteric?

Blocked of bile duct make the billirubrun stuck and refluxs to vascularitation .that
mean the blood wich flow to eyes is consist of bilirubrin.and make yellow appereance
in sclera
And because high amount of billirubrin can cause yellow appereance in her skin
because the bilirubin difuse in to the tissue

5. Why did the doctor suggest the transaminase enzyme test?

Because the test were conducted to determine is there any transaminase enzyme had
been produce in liver.that’’ll be release to blood if hepatosit cells injured
If the hepatosit cells injured can make catabolic pathway from aminoacid metabolic
increase.so enzyme increase too.

6. Why does the physical examination show right upper quadrat abdominal pain with
tenderness?
Sign from physical examination

7. What is the function of the transaminase enzyme?

for katabolic pathway in amino acid metabolic from amino acid be an other amin
8. Why did the doctor prescribe for vitamin and recomend a proper diet?
Vitamin A D E K :can catabolic the lipid.
Proper diet: for decrease the fatty consume

9. Why did the doctor ask the patient history of consuming traditional medicine or
painkiller drugs
There are traditional medicine or painkiller drugs can cause disorder metabolic in
liver.
The eliminate for ulkus gaster diagnosis(epigastrium upper left)

10. Why was the woman complaining of having vomiting?

It is a way of the git tract clear her self of its contains when almost of the upper git
track.iritation widely when inflated or even to impuls

11. Why was she complaining of having high fever?

Inflammationmediator inflammation (IL – 1, IL -6 Tnf)  Release prostaglandin
E2adenosin 5 monophospat(neurotransmitter hypothalamus anterion)increase
set point in hypothalamusfever
12. What is the DD(definition,etiology,risk
factor,pathogenesis,classification,treatment,complication,prognosis,clinical
manifestation)?
13. Physical examination
14. Penyebab infeksi pada hepar dan tandanya
15. Macam2 ikterik,tanda,
16. Kadar normal billirubrin
17. Pathogenesis ikterik
18. Apa yang membedakan inflamasi pada hepar dengan infeksi pada
hepar?(penyebab,gejala,tanda,)

STEP 4

STEP 5

STEP 6
STEP 7

1. What make the urine become tea colored?

jaundice occurs because of hyperbilirubinemia, the circumstances in which the concentration
of bilirubin in the blood is very high which can be caused by elevated levels of conjugated
bilirubin or conjugated bilirubin increased or both. Hyperbilirubinemia and jaundice may
arise as a result of increased bilirubin production, decreased rate of absorption of bilirubin by
the liver cells, impaired bilirubin conjugation and excretion of bilirubin conjugated disorders.

Over-production. Increasing the amount of hemoglobin released from red blood cells that are
old or who experience hemolysis will increase the production of bilirubin. Destruction of
erythrocytes most frequent cause of hyperbilirubinemia due to intravascular hemolysis
(autoimmune disorders, microangiopathic or hemoglobinopathy) or due to a large hematoma
resorbsi. Jaundice arising often called hemolytic jaundice. Bilirubin conjugation and transfer
take place normally, but the supply of unconjugated bilirubin exceeds the ability of liver
cells. In this situation the increase occurred in the conjugated bilirubin in the plasma. as the
body attempts to reduce the levels of conjugated bilirubin, the uptake into liver cells, as well
as the excretion of bilirubin by the liver cells increased. This resulted in the formation of
urobilinogen increased resulting in increased excretion in the urine is a dark color).
Sumber : repository.usu.ac.id
2. Why was the woman complaining of having stomach discomfort ten days ago?
3. Why did she complain of having nausea?
Nausea
It is a psychological sensation caused excitement in the visceral organs, and emosi.Selama
labirinth period nausea, decreased tonus greater curvature, corpus and fundus. Antral and
duodenal repetitive contraction, whereas relaxation duodeni bulbus causing reflux of
duodenal fluid into the stomach. In this phase has not yet occurred nausea active peristalsis.
4. Why does the sclera become icteric?
DEFINITION:
Jaundice, also called icterus, is marked by yellow discoloration of the skin, sclera (white) of
the eye, deeper tissues and body fluids. The yellow discoloration is caused due to increased
 level of bilirubin in the blood. Jaundice is not a disease but it is a symptom that signifies an
underlying disorder.

TYPE AND PATOPHYSIOLOGY:

Hemolytic Jaundice: Hemo means ‘blood’ and lytic means ‘breakdown of cells’; together
‘hemolytic’ means breakdown of red blood cells. In hemolytic jaundice or pre-hepatic
jaundice, the bilirubin level is raised due to excess breakdown of red blood cells.
Obstructive Jaundice: Also known as post-hepatic jaundice is caused by obstruction of bile
flow from the liver. This increases the level of bilirubin in the blood, thereby causing
obstructive jaundice. Obstructive Jaundice can cause extreme pruritus (itching) due to build
up of salt and other biles constituents.
Hepatocellular Jaundice: This type of jaundice is very common and occurs due to inability of
the liver to metabolize and remove bilirubin from the biliary system.
Neonatal Jaundice: This type of jaundice is usually harmless. Neontal jaundice is marked by
yellow discoloration of skin and other tissues of a newborn. The symptoms generally
become apparent on the second or fourth day after the baby is born and disappear on it
own within two to three weeks.

CAUSE:
Causes of Hemolytic Jaundice: Some of the common causes of hemolytic or prehepatic
jaundice are sickle cell anemia, malaria, thalassemia, autoimmune disorders, etc.
Causes of Obstructive Jaundice: Some of the common causes of obstructive jaundice or
post-hepatic jaundice are carcinoma in the bile duct or gall bladder, presence of gallstones
in the biliary system, infection by parasites, pancreatitis, etc.
Causes of Hepatocellular Jaundice: Some of the common causes are cirrhosis, cancer,
hepatitis, Gilbert’s syndrome, toxins or drugs, etc.
http://blog.ygoy.com/2009/06/03/types-of-jaundice-and-causes/

5. Why did the doctor suggest the transaminase enzyme test?

AST, or aspartate aminotransferase, is 1 of the 2 "liver enzymes." It is also known as serum
glutamic-oxaloacetic transaminase, or SGOT. AST is a protein made by liver cells. When liver
cells are damaged, AST leaks out into the bloodstream and the level of AST in the blood
becomes higher than normal. AST is different from ALT because AST is found in parts of the
body other than the liver--including the heart, kidneys, muscles, and brain. When cells in
any of those parts of the body are damaged, AST can be elevated.
http://www.hepatitis.va.gov/patient/diagnosis/labtests-AST.asp

6. Why does the physical examination show right upper quadrat abdominal pain with
tenderness?
In circumstances such as tea-colored urine (brownish red), indicating that there is disorder or
disturbance in the metabolism of bilirubin (bilirubinuria), where metabolism occurs in the liver.
According to the anatomical location, the position of the liver is the organ hipokondriaka dextra
 and epigastric region, sometimes even extends to regions hipokondriaka sinistra. Because of the
inflammatory process in the liver, it will cause tenderness in the right upper abdomen

Patofisiologi vol 1, Sylvia & Wilson, EGC

7. What is the function of the transaminase enzyme?

- Alanine transaminase (ALT) / serum glutamic pyruvic transaminase (SGPT)
- Apartate transaminase (AST) / serum glutamic Oxaloacetic transaminase (SGOT)
SGPT and SGOT is an enzyme produced by the liver. hepar using this enzyme for the metabolism
of amino acids and to make proteins. If there is damage to the liver SGPT and SGOT is released
into the blood stream so that the concentration in the blood will increase
Sumber : repository.usu.ac.id

Alanin Enzim yg dihasilkan di hati, yg

Luka pada sel hati
Transaminase dilepaskan ke dalam darah jika sel hati
(mis. hepatitis)
(ALT) / SGPT mengalami luka

Aspartat Enzim yg dilepaskan ke dalam darah jika Luka di hati,

Transaminase hati, jantung, otot atau otak mengalami jantung, otot atau
(AST) / SGOT luka otak

8. Why did the doctor prescribe for vitamin and recomend a proper diet?

9. Why did the doctor ask the patient history of consuming traditional medicine or
painkiller drugs

10. Why was the woman complaining of having vomiting

a. Nausea
It is a psychological sensation caused excitement in the visceral organs, and emosi.Selama
labirinth period nausea, decreased tonus greater curvature, corpus and fundus. Antral and
duodenal repetitive contraction, whereas relaxation duodeni bulbus causing reflux of
duodenal fluid into the stomach. In this phase has not yet occurred nausea active peristalsis.
b. Retching
In phase Retching, spasms and cessation of breathing occurs repeatedly, while the closed
glottis. Respiratory muscles and diaphragm contract intratorakal lead to negative pressure. At
the same time there was a contraction of the abdominal muscles and stomach, dilated fundus
and pyloric antrum while the contract. Lower esophageal sphincter to open, but the top is still
 closing lower esophageal sphincter causing chyme into the esophagus. At the end of the
relaxation phase occurs Retching abdominal wall and stomach so chyme that had been
entered into the esophagus back into the stomach.
c. expulsion
If Retching peaked and is supported by a contraction of the abdominal muscles and the
diaphragm, will continue to be a gag, if it can overcome the pressure of anti-reflux
mechanism of the LES (lower esophageal sphincter). In this expulsion phase pyloric antrum
and fundus and esophagus to contract while the relaxation and an open mouth. In this phase
also occurs intratorakal and intraabdominal pressure changes as well as the contraction of the
diaphragm.
In a single episode expulsion occurred intratorakal negative pressure and positive
intraabdominal pressure, and at the same time the rapid contraction of the diaphragm which
presses the fundus resulting in reflux of gastric contents into the esophagus. If expulsion has
occurred, pressure and diaphragm intratorakal positive return back to its normal position.
Sources: Despopoulos & Silbernagl. , 2003. Color Atlas Of Physiology Chapter 9. Elsevier:
Philadelphia

11. Why was she complaining of having high fever?

12. What is the DD(definition,etiology,risk

HEPATITIS

DEFINITION:
Hepatitis is inflammation of the liver. The inflammation happens when liver cells die and
the body's immune system sends in special cells that actually cause inflammation while
trying to help the body repair the liver. Such inflammation may clear up on its own, or
continue on as chronic inflammation.
http://hepatitis.about.com/od/ghi/g/hepatitis.htm

CLINICAL MANIFESTATIONS:
 Loss of appetite
 Fatigue
 Mild fever
 Muscle or joint aches
 Nausea and vomiting
 Abdominal pain
http://www.webmd.com/hepatitis/default.htm

Acute hepatitis
The symptoms of acute hepatitis vary considerably from person to person. Some
patients have no symptoms at all, and in most cases, children only show mild symptoms.
In the early stages:
 tiredness, general malaise, slight fever
 nausea, poor appetite, changes in taste perception
 pressure or pain below the right ribs caused by an enlarged liver
 aching muscles and joints, headache, skin rash.
The jaundiced phase:
 yellowing of sclerae (the whites of the eyes), skin and mucous membranes
 dark urine
 light-coloured stools
 around this time, the other symptoms subside.
The recovery phase:
 tiredness that can last for weeks.
Chronic hepatitis
 Many patients have no symptoms.
 Tiredness, an increased need for sleep, aching muscles and joints.
 Periodic light pressure or pain below the right ribs – enlarged liver.
 Jaundice is a very late symptom of chronic hepatitis. It is a sign that the disease
has become serious.
http://www.netdoctor.co.uk/diseases/facts/hepatitis.htm

How can hepatitis be prevented?

 By avoiding exposure to the infectious hepatitis viruses.
  By being vaccinated against hepatitis A and hepatitis B, if you have a high risk of
being infected.
 By refraining from drinking large amounts of alcohol.

Treatment & therapy:

 No medical treatment is generally required for acute viral hepatitis.
 Chronic hepatitis B can be treated with interferon alfa or other antiviral agents.
 Chronic hepatitis C can be treated with interferon alfa and ribavirin (tribavirin).
 Autoimmune hepatitis can by treated with corticosteroids.
http://www.netdoctor.co.uk/diseases/facts/hepatitis.htm

13. Physical examination

1. examination of the heart

hepar palpation may be performed on the upper right quadrant. Liver palpable yan will
show sharp edges, solid with a flat surface. Great care is estimated by performing
percussion upper limit and lower limit heart.
2. Other Diagnostic Examination

Ultrasound, CT and MRI are used fatherly mengidentuifikasi normal structures and
abnormalities of the liver and biliary branching.
Sumber : repository.usu.ac.id

14. Penyebab infeksi pada hepar dan tandanya

Liver abscess is a form of infection of the liver caused by a bacterial infection, parasites, fungi
and sterile necrosis resulting from gastrointestinal system
Sumber : repository.usu.ac.id

15. Macam2 ikterik,tanda,

gambaran Hemolitik Hepatoselular Obstruktif
Warna kulit Kuning pucat Oranye – kuning Kuning – hijau muda
muda atau tua atau tua
Warna urine Normal ( gelap dg Gelap Gelap
urobilin)
Warna feses Normal ( gelap dg Pucat ( sedikit Warna dempul (
sterkobilin ) sterkobilin ) tidak ada sterkobilin
Pruritus Tidak ada Tidak menetap Biasaya menetap
Bilirubin urin Tidak ada meningkat Meningkat
Urobilinogen urin meningkat Sedikit meningkat menurun
Patofisiologi vol 1, Sylvia & Wilson, EGC
16. Kadar normal billirubrin
Bilirubin total : 0.2 – 1 (mg %)
Bilirubin direk : 0 – 0.2 (mg %)
Bilirubin indirek : 0.2 – 0.8 (mg %)

17. Pathogenesis ikterik

aundice occurs because of hyperbilirubinemia, the circumstances in which the concentration of
bilirubin in the blood is very high which can be caused by elevated levels of conjugated bilirubin or
conjugated bilirubin increased or both. Hyperbilirubinemia and jaundice may arise as a result of
increased bilirubin production, decreased rate of absorption of bilirubin by the liver cells, impaired
bilirubin conjugation and excretion of bilirubin conjugated disorders.
1. Over-production. Increasing the amount of hemoglobin released from red blood cells that are old
or who experience hemolysis will increase the production of bilirubin. Destruction of erythrocytes
most frequent cause of hyperbilirubinemia due to intravascular hemolysis (autoimmune disorders,
microangiopathic or hemoglobinopathy) or due to a large hematoma resorbsi. Jaundice arising often
called hemolytic jaundice. Bilirubin conjugation and transfer take place normally, but the supply of
unconjugated bilirubin exceeds the ability of liver cells. In this situation the increase occurred in the
conjugated bilirubin in the plasma. as the body attempts to reduce the levels of conjugated bilirubin,
the uptake into liver cells, as well as the excretion of bilirubin by the liver cells increased. This
resulted in the formation of urobilinogen increased thus increasing fecal excretion in the urine (dark
color). Some of the causes of hemolytic jaundice: abnormal hemoglobin (hemoglobin cickle cell
anemia), erythrocyte disorders (spherocytosis heriditer), serum antibodies (Rh. incompatibility
transfusion), Medicines.
2. The decrease rate of absorption of bilirubin by the liver cells. Unconjugated bilirubin retrieval is
done by separating it from the albumin and protein binds to the recipient. In this situation no
conjugated bilirubin levels in plasma increased but no increase in the levels of urobilinogen in the
urine. Some genetic disorders such as Gilbert's syndrome, and various types of drugs such as acid
flavaspidat, novobiosin can affect this uptake.
3. Impaired bilirubin conjugation. Bilirubin conjugation disruption resulting in increased
unconjugated bilirubin. It is caused due to deficiency of the enzyme glukoronil transferase. If
glukoronil transferase enzymes are not at all, the concentration of conjugated bilirubin in the blood
will be very high. Furthermore, due to a conjugated bilirubin is not formed, there is no conjugated
bilirubin in the bile. Bile into colorless, pale stools, no urobilinogen in the urine.
18. Apa yang membedakan inflamasi pada hepar dengan infeksi pada
hepar?(penyebab,gejala,tanda,)
Inflamasi hepar
a diffuse inflammatory process in tissues that can be caused by viral infection and by the toxic
reactions to drugs and chemicals. (Sujono Hadi, 1999).
Infeksi hepar
Liver abscess is a form of infection of the liver caused by a bacterial infection, parasites, fungi
and sterile necrosis resulting from gastrointestinal system

SGOT: Serum glutamic oxaloacetic transaminase, an enzyme that is normally present in

liver and heart cells. SGOT is released into blood when the liver or heart is damaged. The
blood SGOT levels are thus elevated with liver damage (for example, from viral
hepatitis) or with an insult to the heart (for example, from a heart attack). Some
medications can also raise SGOT levels. SGOT is also called aspartate aminotransferase
(AST).
It facilitates the conversion of aspartate and alpha-ketoglutarate to oxaloacetate and
glutamate, and vice-versa.

SGPT: Serum glutamic pyruvic transaminase, an enzyme that is normally present in liver
and heart cells. SGPT is released into blood when the liver or heart are damaged. The
blood SGPT levels are thus elevated with liver damage (for example, from viral hepatitis)
or with an insult to the heart (for example, from a heart attack). Some medications can
also raise SGPT levels. Also called alanine aminotransferase (ALT).
It catalyzes the transfer of an amino group from alanine to a-ketoglutarate, the products
of this reversible transamination reaction being pyruvate and glutamate.
http://www.hepatitis.va.gov/patient/diagnosis/labtests-AST.asp