PANELMODUL “MATA KUNING”

BLOCK BASIC MECHANISM DISEASEMEDICAL FACULTY

MUSLIM UNIVERSITY OF INDONESIA2016

GROUP 15th BY:

GROUP

15

Muh. Asy Shidiq 110 2015 0003A. Muh. Yasser Mukti 110 2015 0022Andira Ratu Nurrasyid 110 2015 0030Andi Aisya Zealand 110 2015 0051Nur Zamzam Azizah 110 2015 0059Amaliah Hakim 110 2015 0070Rifqy Aditya 110 2015 0078Rindang Cahyani Putri H Abas110 2015 0101Elsa Shafira Prasetyati 110 2015 0117Cindy Purnamasari 110 2015 0136Atika Rahmah Mustapa 110 2015 0147

S C E N A R I O 3

A 45 years old woman had developed abdominal pain and jaundice over 5

weeks. On physical examination, there was right upper quadrant pain,

but no abdominal distention. Abdominal CT scan showed a

markedly thickened gallbladder wall. Souce : http://m.patient.media/images/om831a.jpg

DIFFICULT WORDS

Jaundice Abdominal distention Gallbladder CT Scan

• Jaundice or icterus is yellow skin and sclerae, the color becoming apparent when circulating bilirubin concentration exceed 2.5-3.0 mg/dl

• CT Scan : a cross sectional, three dimentional image of an internal body part produced by computed tomography for diagnostic purposes

• Gallbladder : is a place for stored a bile in posteroinferior of liver

Editor David S. Strayer, MD, PhD. 2012.Robin’s Pathology seventh edition: Clinicopathologic Foundation of Medicine. Philadelphia: Wolters Kluwer Health. Page 829www.merriam-webster.com. Medical Dictionary: Definition of CT scan. Access on April 29th 2016Kamus Saku Kedokteran Dorland Edisi 29. Singapura:Elsevier

KEY WORDS

Jaundice No abdominal distention

Abdominal pain in right upper

quadranThickened gallbladder

QUESTIONS

How is the structures of anatomy that involved?

How is the structures of histology that involved?

Explain the pshsiology and biomecanic struktures that invoved?

What is the causes of jaundice?

QUESTIONS

What is the relation of the thickened gallbladder wall to jaundice?

Who can get this disease?

What is the complication if there are abdominal distention in the symptomps?

How to treat this disease?

Is there any additional examination to detect the disease?

What is the prevention?

1. How is the structures of anatomy that involved?

Location of the liver

The liver occupies the whole of the right hypo-chondrium, the greater part of the epigastrium, and extends into the left hypochondrium reaching up to the left lateral line.

From the above it will be obvious that most of the liver is covered by ribs and costal cartilages, except in the upper part of the epigastrium where it is in contact with the anterior abdominal wall.

Chaurasia, Late Dr BD. 2005.HUMAN ANATOMY Regional and Applied : Dissection and Clinical Volume 24th edition. New Delhi: CBS publisher and distribution

Chaurasia, Late Dr BD. 2005.HUMAN ANATOMY Regional and Applied : Dissection and Clinical Volume 24th edition. New Delhi: CBS publisher and distribution

Region Location Internal OrgansRight hypochondriac

 Right, upper one-third of

abdomenGallbladder; portions of liver and

right kidneyEpigastric Upper, central one-third of

abdomenPortions of liver, stomach, pancreas, and duodenum

Left hypochondriac  

Left, upper one-third of abdomen

Spleen; splenic flexure of colon; portions of left kidney and small

intestine

Right lateral  

Right, lateral one-third of abdomen

Cecum; ascending colon; hepatic flexure; portions of right kidney

and smallintestine

Umbilical Center of abdomenJejunum; ileum; portions of

duodenum, colon, kidneys, and major abdominal

vesselsLeft lateral Left, lateral one-third of

abdomenDescending colon; portions of left kidney and small intestine

Right inguinal Right, lower one-third of abdomen

Appendix; portions of cecum and small intestine

Pubic (hypogastric) Lower, center one-third of abdomen

Urinary bladder; portions of small intestine and sigmoid colon

Left inguinal Left, lower one-third of abdomen

Portions of small intestine, descending colon, and sigmoid

colonChaurasia, Late Dr BD. 2005.HUMAN ANATOMY Regional and Applied : Dissection and Clinical Volume 24th edition. New Delhi: CBS publisher and distribution

Lobes of the liver is divided into right and left lobes.Anteriorly and superiorly : by the attachment of the falciform ligament Interiorly : by the fissure for the ligamentum teres and posteriorly : by the fissure for the ligamentum venosum The right lobe is much larger than the left lobe.

Graf, Van De. 2001. Human Anatomy 6th Edition. New York: Mc Graw-Hill

Paulsen, F. Waschke, J. 2010. Sobotta Atlas Anatomi Manusia, Edisi 23. Jakarta:EGC

The caudate lobe is situated on the posterior surface.The quadrate lobe is situated on the inferior surface, and is rectangular in shape.

Graf, Van De. 2001. Human Anatomy 6th Edition. New York: Mc Graw-Hill

Paulsen, F. Waschke, J. 2010. Sobotta Atlas Anatomi Manusia, Edisi 23. Jakarta:EGC

2. How is the structures of histology that

involved?

The main functional cell in the liver is a form of epithelial cell called the hepatocyte. These cells are arranged as thin plates separated by fine vascular sinusoids through which blood flows. The close association of liver cells and the circulation allows absorption of nutrients from digestion as well as secretion of products into the blood. Blood flow into the liver sinusoids comes from terminal branches of both the hepatic portal vein and hepatic artery.

Hepatocytes

Hepatocytes are large polyhedral cells with round nuclei with peripherally dispersed chromatin and prominent nucleoli. The nuclei vary greatly in size, reflecting an unusual cellular feature; more than half the hepatocytes contain twice the normal (diploid) complement of chromosomes within a single nucleus (i.e. they are tetraploid) and some contain four or even eight times this amount (polyploid).

Sinusoid lining cells

The sinusoid lining cells include at least three cell types. The majority of cells lining the hepatic sinusoids are endothelial cells En with flat darkly stained nuclei and thin fenestrated cytoplasm.

Scattered among the endothelial cells are large plump phagocytic cells with ovoid nuclei. Known as Kupffer cells K, these form part of the monocyte-macrophage defence system and, with the spleen, participate in the removal of spent erythrocytes and other particulate debris from the circulation.

The third cell type, known variously as stellate cells, Ito cells or hepatic lipocytes, cannot be easily distinguished by light microscopy. This cell type has lipid droplets containing vitamin A in their cytoplasm. These cells have the dual functions of vitamin A storage and production of extracellular matrix and collagen.

3. Explain the pshsiology and biomecanic struktures that invoved?

Source : Ilmu Penyakit Dalam. Jilid II. Ed.4.Jakarta:Interna Publishing. Pg. 1931-1932.

Physiology of liver

Formation and excretion of bileCarbohydate, protein and fat

metabolism

Physiology of Gall Bladder

• Gall bladder store bile that secreted from liver cells.• Inside the gall bladder, consist of lymphatic vessels and

blood vessels which absorb water and inorganic salts -> condense bile.

• .

Price, Sylvia A. Wilson, Lorraine M. Patofisiologi. Ed4. 1992. Jakarta: EGC. Pg. 431

Bilirubin metabolism

• Pre-hepatic• Formation of bilirubin• Plasma transport

• Enterohepatic• Liver uptake• Conjugation

• Post-Hepatic• Billiary excretion

23Ilmu Penyakit Dalam. Jilid II. Ed.4.Jakarta:Interna Publishing. Pg. 1937-1938.

Bilirubin Metabolism

Erytrocytes hemolisis by reticuloendotelial cells

Eritroid hemolysis in lymph and bone marrow

HemoglobinGlobin

Hem

Biliverdin

Hem Oksigenase

Unconjugated Bilirubin ~ Albumin

Biliverdin Reduktase

PREHEPATIK

Enter the liver

Unconjugated Bilirubin released from Albumin

Bilirubin Diglucuronide(conjugated bilirubin,soluble

in water)

Excrete into gall bladder

To intestine

Urobilinogen

Glukuronosil Transferase

Intestinal bacteria

ENTEROHEPATIK

POSTHEPATIC

Urobilinogen

Small quantity absorbed by

intestine

Vena Porta

Excrete into bile Kidney

Excrete by urine

POSTHEPATIK

Excrete into faeces

Strekobilin

4. What is the causes of jaundice?

Marfan syndromeMarfan syndrome is a genetic disease that usually attacked the baby. Marfan syndrome that abnormalities in glukoronosil transferase enzyme resulting unconjugate bilirubin can not be converted into bilirubin conjuugate.

Hemolytic anemiaHemolytic anemia namely the destruction of red blood cells which is very much prematurely resulting in bilirubin unconjugate many forms.

Obstruction of the bileObstruction of the bile duct caused by the usual fat or clog the bile duct carcinomas. so that, bilirubin conjugate can not flow out of the bladder bile. eventually causing jaundice and causes acholic feces

Reference : www.rightdiagnosis.com

5. What is the relation of the thickened gallbladder wall to jaundice?

Abdominal distension is the swelling or enlarging of the abdomen in the area between the ribs and the groin. Complication of abdominal distention are :1. Infection2. Malignancy3. Inflammation4. Trauma5. Fluid retention6. Obstruction

Reference : www.rightdiagnosis.com

6. What is the epidemiology of jaundice?

80%

20%

Neonatus

Approximately 20 percent term newborns develop jaundice in the first week of life, primarily because of immaturity of the hepatic conjugation process. Physiologic jaundice in premature neonates is more severe then in term neonates.

Gender & Age

In the 352 cases of jaundice, male to female ratio is 1.88:1. The proportion of men and women of all age groups are consistent with the total sex ratio, and male to female ratio in the middle-aged group is especially statistically significant, indicating that from the gender distribution, the incidence of jaundice in men is more than that in women.

The youth group of patients with viral hepatitis is the most common, accounting for 31.94%, much higher than the middle age group of 9.23% and 4.26% of the elderly group.

If a person consumes more alcohol or drugs than their body is able to process the liver will be come damaged and be unable to function properly. People who are alcoholics or who abuse drugs often have a damaged liver as a result of their lifestyle. So alcoholics or who abuse drugs have higher chance to get jaundice than who are not.

7. What is complication of abdominal distention ?

Abdominal distension is the swelling or enlarging of the abdomen in the area between the ribs and the groin. Complication of abdominal distention are :1. Infection2. Malignancy3. Inflammation4. Trauma5. Fluid retention6. Obstruction

Reference : www.rightdiagnosis.com

8. How to treat this disease?

SERUM TESTING

First-line serum testing in a patient presenting with jaundice should include a complete blood count (CBC) and determination of bilirubin (total and direct fractions), aspartate transaminase (AST), alanine transaminase (ALT), -glutamyl transpeptidase, and alka-line phosphatase levels.

Blood tests (bilirubin,

aminotransferase, alkaline

phosphatase)

Blood tests include measurement of total and direct bilirubin, aminotransferase, and alkaline phosphatase levels in all patients. Results help differentiate cholestasis from hepatocellular dysfunction (important because patients with cholestasis usually require imaging tests):• Hepatocellular dysfunction: Marked aminotransferase elevation (> 500 U/L) and moderate alkaline phosphatase elevation (< 3 times normal)• Cholestasis: Moderate aminotransferase elevation (< 200 U/L) and marked alkaline phosphatase elevation (> 3 times normal)• Hyperbilirubinemia without hepatobiliary dysfunction: Mild hyperbilirubinemia (eg, < 3.5 mg/dL [< 59 μmol/L]) with normal aminotransferase and alkaline phosphatase levels

Interpretation result• Hepatocellular dysfunction: Marked aminotransferase elevation (> 500 U/L) and moderate alkaline phosphatase elevation (< 3 times normal)• Cholestasis: Moderate aminotransferase elevation (< 200 U/L) and marked alkaline phosphatase elevation (> 3 times normal)• Hyperbilirubinemia without hepatobiliary dysfunction: Mild hyperbilirubinemia (eg, < 3.5 mg/dL [< 59 μmol/L]) with normal aminotransferase and alkaline phosphatase levels

Physical examinati

on

Vital signs are reviewed for fever and signs of systemic toxicity (eg, hypotension, tachycardia).Head and neck examination includes inspection of the sclerae and tongue for icterus and the eyes for Kayser-Fleischer rings. Mild jaundice is best seen by examining the sclerae in natural light; it is usually detectable when serum bilirubin reaches 2 to 2.5 mg/dL (34 to 43 μmol/L). Breath odor should be noted (eg, for fetor hepaticus).

Cont..

The abdomen is inspected for collateral vasculature, ascites, and surgical scars. The liver is palpated for hepatomegaly, masses, nodularity, and tenderness. The spleen is palpated for splenomegaly.

The abdomen is examined for umbilical hernia, shifting dullness, fluid wave, masses, and tenderness. The rectum is examined for gross or occult blood.

TreatmentThe cause and any complications are

treated. Jaundice itself requires no treatment in adults (unlike in neonates. Itching, if bothersome, may be relieved with cholestyramine 2 to 8 g po bid. However, cholestyramine is ineffective in patients with complete biliary obstruction

9. Is there any additional examination to detect the disease?

• HematologyIncluding examination of reticulocyte counting and Coombs test, which can show signs of hemolytic anemia. The reticulocyte counting is normal apparently got rid of hemolytic jaundice. Leukocytosis can be a sign of infection (cholangitis) or carcinoma. Mononuclear cells showed abnormal infectious mononucleosis (Paul-Bunnell) or perhaps, viral hepatitis. Complete blood count-macrocytosis, thrombocytopenia or urea low by diuretics) is a poor prognostic sign.

Reference : www.rightdiagnosis.com

• UrinalysisHemolytic jaundice is akolurik (no bilirubin in urine), but urine contains excessive urobilinogen because the amount of bilirubin to excessive intestine and is excreted again as urobilinogen. Obstructive jaundice gives the dark color in the urine due to excess bilirubin and urobilinogen reduced levels of urine, because little or nothing at all of bilirubin reach the intestine obstruction that can not be absorbed and is excreted again.

• Liver function testsLiver function tests can measure the ability of the liver to perform its normal functions. Low albumin levels may be nonspecific. Transaminases could give clues to whether jaundice is especially true since the cause of hepatocellular (SGOT and SGPT> alkaline phosphatase) or cholestatic (alkaline phosphatase or γGT [gamma-glutamyl transferase]> SGOT), although it can also be a mixture. Normal transaminases showed abnormalities are more rare hemolysis or Gilbert's syndrome.

• Abdominal imagingX-rays and ultrasonography can show gallstones and will record the size of the liver and spleen. Isotopic liver scanning can show a 'hole' secondary result carcinomatous (or enlarged bile duct obstruction). Heart ultrasound can help the clinical diagnosis, because it can show abnormalities such as focal liver metastases, liver abscess, vascular atau disorder. You can find signs of biliary obstruction (dilated common bile duct) and cause jaundice (gallstones, cancer of the pancreas). It could also not visible abnormalities.

• Needle biopsy of the liverLiver histology remains the definitive examination of jaundice hepatocellular and some cases of cholestatic jaundice (primary biliary cirrhosis, intrahepatic cholestasis by drugs [drug-induced]). There are a variety of absolute indications for this examination. Biliary obstruction is relatively contraindicated because of the potential danger of causing biliary peritonitis. Biopsy with ultrasound and CT guidance can help with the diagnosis of focal histological lesions.

• ERCP (Endoscopic Retrograde Cholangiopancreatography)If there are signs of biliary obstruction, ERCP remains the definitive test to determine whether the obstruction intraluminal (gallstones in the common bile duct [CBD]) or extraluminal (malignant structure of carcinoma of the pancreas).

• SerologyAlways perform serologic antibody viral hepatitis, especially in patients with unclear causes. Antimitochondrial antibodies are found in 90% of cases of primary biliary cirrhosis. Antinuclear factor and smooth muscle antibodies are detected in more than 50% of cases of chronic active hepatitis

10. What are

the Preventions

?

• Reducing fat consumption – If an infection were to occur, it can change the

absorptive behavior of the bile’s mucus, potential water absorption, bile salts, and other substances to keep cholesterol in solution.

– Cholesterol precipitation on the bile duct• Reducing drugs consumption

– Some drugs such as analgesic and antipiuretic can cause liver necrosis if used excessively.

• Reducing Alcohol consumption– Can cause alcohol hepatitis which leads to

jaundice. – Can be tested by determining the gamma-

glutamyltransferase (GGT) enzyme which is released from a damaged tissue

CONCLUSION• Jaundice or icterus is yellow skin and sclerae, the color becoming apparent when

circulating bilirubin concentration exceed 2.5-3.0 mg/dl• The usual cause of jaundice is large quantities of bilirubin in the extracell fluid• The common cause of jaundice are heolytic jaundice and obstructive jaundice• Epidemiology of jaundice is : varies with age and sex.. Incidence varies with etnicity and

geography.• Alcohol is the one can cause jaundice• To treat the jaundice : laparoscopic cholecystectomy for symptomatic, and expectant for

asymptomatic• The additional examination for the disease : hematology, urinalysis, liver function tesr.

Serology, abdominal imaging, needle biopsy of the liver• To prevent : determined by fat consumption, taking precautions on drug

consumption,and reducing alcohol.

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