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HEPATITIS VIRUS AKUT

Merupakan keradangan akut parenchym hati karena infeksi virus
hepatitis (tipe A/B/C/D/E,dsb).
Keluhan utama yang timbul berupa sclera mata kuning (ikterus).
Keluhan lain yang mungkin timbul adalah
anoreksia/nausea(mual)/vomiting (muntah)/panas
badan/kelemahan tubuh/kencing kuning-coklat/"transient"
pruritus. Gejala lain berupa ascites (cairan bebas dalam rongga
perut), hipoglikemia, edema, terjadi bila keadaannya sudah berat.
Biasanya gejala klinis tersebut terjadi dalam 3 fase, yaitu :
1. fase preikterik : gangguan pencernaan (mual/muntah), lemah
badan, gejala seperti flu, air seni mulai lebih kuning coklat,
sedang tinja mulai lebih pucat. Berlangsung 3-10 hari sampai
2 minggu.
2. fase ikterik : gejala saluran pencernaan dan "flu like
syndrome" berkurang sampai hilang, kecuali lemah badan
disertai adanya mata kuning, sebah, nyeri tekan pada daerah
hypochondrium kanan (perut kanan atas). Air seni juga mulai
bertambah kecoklatan (seperti air teh). Berlangsung 1-2
minggu.
3. fase penyembuhan : mulai timbul nafsu makan, lemah badan
mulai berkurang, sebah berkurang sampai hilang, warna
kuning mulai berkurang sampai hilang, warna air seni mulai
lebih muda lagi. Ikterus umumnya hilang dalam 2-6 minggu.
Penyembuhan sempurna terjadi dalam 3-4 bulan (12-16
minggu)
Pada pemeriksaan didapatkan : ikterus, hepar (hati) sedikit
membesar/lunak/nyeri tekan (+ 70 % kasus), lien (limpa) membesar
(+ 20 % kasus), panas (umumnya hilang setelah ada
ikterus/"transient" pruritus). Pada pemeriksaan laboratorium,
yaitu terdapat peningkatan SGOT/SGPT, LED meninggi,
bilirubinemia, hipoalbuminemia, dan peningkatan waktu protrombin
(menunjukkan nekrosis hepatoseluler yang luas). Pemeriksaan urine
didapatkan bilirubin (+), yang akan bertambah pada fase ikterik
dan mulai menghilang pada fase penyembuhan. Pemeriksaan
serologis akan positif (tergantung jenis dan perjalanan

penyakitnya), antara lain HBsAg, IgM antiHAV, IgM antiHBc, anti
HCV. Untuk lebih jelasnya lihat tabel berikut :

HBs Ag
+
+
+
+
-

IgM anti IgM anti
Anti HCV
HAV
HBc
+
+
+
+
+
+
+
+
+

Interpretasi Diagnostik (Dienstag & Isselbacher,
1994)
Hepatitis akut B
Hepatitis kronis B
Hepatitis akut A superimposed on hepatitis
kronis B
Hepatitis akut A dan B
Hepatitis akut A
Hepatitis akut A dan B (HBs Ag dibawah ambang
deteksi)
Hepatitis akut B (HBs Ag dibawah ambang
deteksi)
Hepatitis akut C

Masa inkubasi Hepatitis virus, terbanyak terjadi pada usia :
@ hepatitis A (HAV) : 15-45 hari, terbanyak usia : anak/dewasa
muda
@ hepatitis B (HBV) : 30-180 hari, terbanyak usia : dewasa
muda/bayi/balita
@ hepatitis C (HCV) : 15-160 hari, terbanyak usia : setiap umur,
utamanya orang dewasa
@ hepatitis D (HDV) : 30-180 hari, terbanyak usia : setiap umur
@ hepatitis E (HEV) : 14-60 hari, terbanyak usia : dewasa muda
(20-40 tahun)
Cara penularan Hepatitis virus :
@ hepatitis A (HAV) : fecal & oral (+++)/perkutan (+)/perinatal
(-)/seksual (+)
@ hepatitis B (HBV) : fecal & oral (-)/perkutan (+++)/perinatal (++
+)/seksual (++)
@ hepatitis C (HCV) : fecal & oral (-)/perkutan (+++)/perinatal
(+)/seksual (+)

@ hepatitis D (HDV) : fecal & oral (-)/perkutan (+++)/perinatal
(+)/seksual (++)
@ hepatitis E (HEV) : fecal & oral (+++)/perkutan (-)/perinatal
(-)/seksual (-)
Keterangan : fecal & oral ~ via saluran pencernaan; perkutan ~ via
darah/suntikan, dsb; perinatal ~ ibu ke bayinya, sewaktu lahir;
seksual ~ hubungan seksual.
Terapi pada hepatitis virus akut tidak ada pengobatan spesifik,
antara lain : interferon (untuk HBV: 40% efektif; untuk HCV: 50%
efektif); tirah baring total; diet tinggi kalori (termasuk parenteral
nutrisi bila diperlukan) dan pembatasan intake protein;
cholesteramine (untuk gatalnya); kemudian tindakan-tindakan lain
utnuk mempertahankan keseimbangan cairan dan menjaga jalan
nafas, menjaga sirkulasi, mengendalikan perdarahan, mengatasi
hipoglikemi, dan menangani komplikasi yang mungkin timbul pada
pendertia koma.
Perjalanan penyakit : umumnya baik. Hepatitis virus A dikatakan
tidak pernah memberikan bentuk kronis dan memberi kesembuhan
sempurna tanpa cacat. Hepatitis virus B akut : 90% penderita
mengalami kesembuhan sempurna. Perjalanan penyakit hepatitis
virus B ini jelek bila timbul ascites, edema, gejala encefalohepatik,
disertai tanda laboratorium berupa waktu protrombin yang
memanjang, kadar albumin rendah, kadar gula darah rendah, dan
bilirubin darah lebih dari 20 %. Pada hepatitis virus C 50% akan
menjadi kronis dan terus memberat. Pada Hepatitis D bila akut
perjalanan penyakitnya baik, tetapi bila kronis menjadi jelek.
Untuk Hepatitis virus D perjalanan penyakitnya baik.

Fakta-fakta tentang Iris Mata

Pola iris mata mulai terbentuk sejak bulan ke-7 kehamilan melalui proses yang
dikenal dengan kekacauan morfogenesis (chaotic morphogenesis) yakni
perkembangan dan reaksi jaringan secara random terhadap kondisi-kondisi
lingkungan yang berubah.

bilirubin diikat oleh 2 protein intraseluler utama dalam sitoplasma. bahkan iris mata kanan dan kiri dari orang yang sama pun berbeda dan bersifat unik. tetapi sangat larut dalam lemak (konfigurasi bilirubin IXa [Z. akan mengalami perubahan lagi menjadi biliverdin. Struktur bilirubin yang dihasilkan dari perubahan tersebut bersifat tidak larut dalam air. Pada permukaan sinusoid hati. lalu bilirubin. Tidak ada dua iris mata yang persis sama. bilirubin harus diangkut dengan bantuan suatu pembawa (karier). dan masuk melalui membran sel hati dengan cara difusi (facilitated diffusion). maka di dalam plasma darah. yang merupakan bagian nonprotein dari hemoglobin. Ambilan bilirubin Di dalam sel hati (hepatosit). . bilirubin tidak terkonjugasi akan melepaskan diri dari ikatannya dengan albumin. Ini terjadi karena rantai hidrogen intramolekuler melindungi bagian hidrofilik dari molekul bilirubin. Hem. Keseluruhan proses perubahan ini berlangsung di hati.Z]). untuk kemudian masuk ke dalam sel hati. Bilirubin dalam bentuk ikatan bilirubinalbumin (yang lemah) akan beredar di dalam sirkulasi darah. ligandin atau glutathione S-transferase B) dan protein sitosolik z (dikenal juga sebagai fatty acid–binding protein [FABP]). Ikatan bilirubin-albumin Karena sifat tidak larut dalam air ini. dan karier fisiologis tersebut adalah albumin serum.  Anak kembar yang identik memiliki pola DNA yang sama tetapi mempunyai pola iris mata yang berbeda dan benar-benar unik. protein sitosolik Y (misalnya. << Fitur-fitur unik iris mata Metabolisme bilirubin Hemoglobin akan mengalami proses pemecahan menjadi hem dan globin.

Proses esterifikasi tersebut dikatalisasi oleh suatu enzim yang disebut bilirubin uridin-difosfat glukuronil transferase (lazimnya disebut enzim glukuronil transferase saja). sebagian besar berada dalam bentuk diglukuronida (80%). sekaligus meningkatkan ambilan bilirubin. dan sebagian kecil dalam bentuk monoglukuronida. Hasil konjugasi (yang kita sebut sebagai bilirubin terkonjugasi) ini. Sifat yang sebaliknya terdapat pada bilirubin terkonjugasi. Karena kelarutannya yang tinggi pada lemak. Peningkatan dari bilirubin tidak terkonjugasi dapat menimbulkan efek yang sangat tidak kita . sebagian besar bilirubin akan dikonjugasikan dengan asam glukuronat. terlebih dulu ia harus dibuat dapat larut dalam air. Bilirubin terkonjugasi Agar bilirubin dapat diekskresikan ke dalam empedu (untuk kemudian dikeluarkan ke usus). Untuk mencapai maksud tersebut. terjadi perubahan sifat bilirubin. yang berlokasi di retikulum endoplasmik sel hati. Akibat konjugasi tersebut. sehingga proses yang terjadi disebut proses esterifikasi. tapi mempunyai afinitas tinggi terhadap lemak. mekanisme yang terjadi adalah melekatnya asam glukuronat (secara enzimatik) kepada salah satu atau kedua gugus asam propionat dari bilirubin IXa (Z. bilirubin tidak terkonjugasi dapat larut di dalam lapisan lemak dari membran sel. Perbedaan yang paling mencolok antara bilirubin terkonjugasi dan tidak terkonjugasi adalah sifat kelarutannya dalam air dan lemak. bilirubin tak terkonjugasi tidak akan diekskresikan ke urin. Dalam proses konjugasi yang berlangsung di dalam retikulum endoplasma sel hati tersebut.Z).Ikatan bilirubin dengan protein-protein tersebut akan menurunkan kemungkinan kembalinya bilirubin ke dalam plasma. Penempelan gugus glukuronida pada gugus propionat terjadi melalui suatu ikatan ester. maka di dalam sel parenkim hati. Karena sifat inilah. Bilirubin tidak terkonjugasi bersifat tidak larut dalam air.

4. Urobilin memberi kontribusi terhadap warna dari urin kita. yang kita sebut lobulus hati. Ia akan sampai ke kandung empedu untuk disimpan. Sel-sel parenkim hati (hepatosit) Vena sentralis Sinusoid Cabang-cabang vena porta Cabang-cabang arteri hepatika Sel-sel retikuloendotelial stelata (sel Kupffer) . maka feses akan berwarna putih seperti dempul. 2. Sedemikian kecilnya lobulus ini sehingga kita baru dapat melihatnya bila menggunakan mikroskop. Bilirubin terkonjugasi yang dikeluarkan ke dalam usus halus akan dimetabolisme oleh bakteri usus dan mengalami proses reduksi menjadi sterkobilin dan urobilinogen. 3. Sterkobilin adalah senyawa yang membuat feses kita berwarna kecoklatan. berupa kerusakan jaringan otak. Sebagian urobilinogen (10-20%) akan diserap dari rongga usus dan masuk ke dalam vena porta untuk menjalani siklus enterohepatik. Sebagian lagi akan diserap untuk dikeluarkan melalui ginjal.inginkan. Inilah yang terjadi pada kasus Kern ikterus. yaitu: 1. Setiap lobulus hati terbangun dari berbagai komponen. Sterkobilin dan urobilin Bilirubin terkonjugasi akan dikeluarkan melalui membran sel hati ke dalam kanalikuli bilier. Bila karena suatu hal senyawa ini tidak terbentuk (misalnya pada ikterus obstruktif). 6. atau langsung dikeluarkan ke dalam usus halus. 5. Hal ini terjadi karena otak merupakan jaringan yang banyak mengandung lemak. Organ Hati Histologi Lobus hati sesungguhnya dibangun dari puluhan ribu unit struktural. Urobilinogen (yang tidak berwarna) mudah mengalami oksidasi dan berubah menjadi urobilin (yang merupakan pigmen coklat).

vitamin. dan mengeluarkan berbagai zat hasil metabolisme di hati. darah akan mengalir ke pembuluh yang lebih besar. darah yang berasal dari vena porta dan arteri hepatika bercampur. protein. Sel-sel hati akan 'dibanjiri' darah yang kaya oksigen dari arteri hepatika. Mengambil berbagai zat yang masuk dari vena porta dan arteri hepatika. Sinusoid Sinusoid terletak di antara jajaran sel-sel hati. yaitu vena hepatika. Triad portal terdiri atas cabang-cabang arteri hepatika. Pada bagian pinggir lobulus terdapat apa yang kita sebut 'triad portal'. Selain itu. Kanalikuli biliaris Lobulus hati berbentuk poligonal dengan vena sentralis sebagai pusatnya. sedangkan selsel hati tersusun sangat rapat. vena porta dan duktus biliaris. Untuk mudahnya. maka lobulus hati berbentuk banyak sisi (poligon). Bedanya. Cabang-cabang vena porta . dan darah yang kaya nutrisi dari vena porta. dengan pola radial yang berpusat pada vena sentralis. mari kita bayangkan bentuk roda pedati. Vena sentralis Vena sentralis merupakan tempat berkumpulnya darah yang telah diproses dalam lobulus hati. Dari vena hepatika. jari-jari roda tersusun dalam jarak yang berjauhan. Selain itu.7. bila roda pendati berbentuk bundar. di dalam sinusoid juga terdapat sel-sel pertahanan tubuh yang disebut sel Kupffer. Melalui sinusoid inilah. seperti glukosa. Dari vena sentralis. Darah yang masuk ke vena sentralis berasal dari sinusoid. Jari-jari roda pedati dapat kita asumsikan sebagai sel hati. darah akan menuju ke vena cava inferior. sel-sel hati melakukan berbagai fungsinya. Di dalam sinusoid. lemak. sedangkan sumbu rodanya merupakan vena sentralis. Hepatosit Sel-sel hati di dalam lobulus tersusun dalam bentuk lempengan.

Duktus hepatikus komunis akan bergabung dengan duktus sistikus (dari kandung empedu). Its levels are The structure of Bilirubin elevated in certain diseases and it is responsible for the yellow color of bruises and the brown color of feces. Bilirubin is a yellow breakdown product of normal heme catabolism. Merupakan sel pemangsa (fagosit) yang tugasnya menghancurkan sel-sel darah merah dan putih yang sudah tidak berguna lagi. Bilirubin is a yellow breakdown product of normal heme catabolism. vena interlobularis. untuk kemudian masuk ke saluran empedu yang lebih besar yaitu duktus hepatikus kanan dan kiri. empedu akan dialirkan ke duktus biliaris yang kecil.Vena porta masuk ke dalam hati dan bercabang-cabang. dan disebut duktus biliaris komunis. Its levels are elevated in certain diseases and it is responsible for the yellow color of bruises and the brown color of feces. Sel-sel retikuloendotelial stelata (sel Kupffer) Sel Kupffer terletak pada sinusoid. Tugasnya adalah mengumpulkan empedu yang dihasilkan oleh sel hati. bakteri pun turut dihancurkan olehnya. akan berjalan bersama cabang arteri hepatika dan duktus biliaris sepanjang tabung jaringan penyambung yang meliputi lobulus hati. Cabang yang lebih kecil. Kanalikuli biliaris Kanalikuli biliaris berjalan diantara dua sel hati. Saluran empedu tersebut kemudian bergabung menjadi duktus hepatikus komunis (common hepatic duct). . Dari sini. Selain itu.

etc. and the body does not control levels.. there is no "normal" level of bilirubin. Bilirubin is an excretion product. Test results may be listed as "BU" for unconjugated bilirubin and "BC" for conjugated bilirubin.The terms "direct" and "indirect" reflect the way the two types of bilirubin react to certain dyes. etc). Total bilirubin measures both BU and BC. Conjugated bilirubin is water-soluble and reacts directly when dyes are added to the blood specimen. delta E. in the liver. the measurement of this type of bilirubin is indirect. free bilirubin does not react to the reagents until alcohol is added to the solution. . and blood collection tubes (especially serum tubes) should therefore be protected from such exposure. The indirect form is insoluble and it is transformed into a soluble or direct form. Bilirubin levels reflect the balance between production and excretion. To further elucidate the causes of jaundice or increased bilirubin. Hepatitis A. Bilirubin is either in the insoluble form. or bound to glucuronic acid to form the so called conjugated bilirubin (also direct bilirubin). AST. Thus. Therefore. GGT.) or evidence of infective hepatitis (e.Contents [hide]  1 Bilirubin blood tests 2 Interpretation 3 Jaundice 4 Bilirubin toxicity 5 Bilirubin benefits 6 Chemistry 7 Trivia  8 See also       [edit] Bilirubin blood tests Bilirubin is broken down by light. it is usually simpler to look at other liver function tests (especially the enzymes ALT. Total and direct bilirubin levels can be measured from the blood. unconjugated bilirubin (also indirect bilirubin). but indirect bilirubin is calculated from the total and direct bilirubin.g. Alk Phos). B. blood film examination (hemolysis. The non-water soluble. C.

[edit] Jaundice Jaundice may be noticeable in the sclera (white) of the eyes at levels above about 30-50 μmol/l.a genetic disorder of bilirubin metabolism which can result in mild jaundice. Moderate rise in bilirubin may be caused by   Drugs (especially anti-psychotic. depending on exact features of the cirrhosis. found in about 5% of the population. Mild rises in bilirubin may be caused by   Hemolysis or increased breakdown of blood.3 mg/dL. where the newborn's liver is not able to properly conjugate the bilirubin (see jaundice).4 μmol/L or 0 . Crigler-Najjar syndrome Dubin-Johnson syndrome Cirrhosis may cause normal. Gilbert's syndrome .[edit] Interpretation The reference range for total bilirubin is 2 .14 μmol/L or 0.9 mg/dL. and in the skin at higher levels. For direct bilirubin.3 . tumour obstructing common bile duct etc. and a wide range of other drugs).1. Severe hepatitis. Jaundice is classified depending upon whether the bilirubin is free or conjugated to glucuronic acid into:   Conjugated jaundice Unconjugated jaundice . Severe liver failure with cirrhosis. Unusually large bile duct obstruction. it is 0 .0. eg stone in common bile duct. some sex hormones. Hepatitis (levels may be moderate or high). Very high levels of bilirubin may be caused by       Neonatal hyperbilirubinaemia. moderately high or high levels of bilirubin.

This is used in the phototherapy of jaundiced newborns: the illuminated version of bilirubin is more soluble than the unilluminated version. neonates in general are at increased risk since they lack the intestinal bacteria that facilitate the breakdown and excretion of conjugated billirubin in the feces (this is largely why the feces of a neonate are paler than those of an adult). Aside from specific chronic medical conditions that may lead to hyperbilirubinaemia. a phenomenon known as kernicterus. Statistical analysis of people with high normal or slightly elevated bilirubin levels in blood shows that they have a lower risk of developing cardiovascular diseases. Evidence is accumulating that suggests bilirubin can protect tissues against oxidative damage caused by free radicals and other reactive oxygen species. [edit] Chemistry Bilirubin consists of an open chain of four pyrroles (tetrapyrrole). Like these other pigments. abnormal reflexes and eye movements. Bilirubin is very similar to the pigment phycobilin used by certain algae to capture light energy. seizures. and to the pigment phytochrome used by plants to sense light. . bilirubin changes its conformation when exposed to light. All of these contain an open chain of four pyrroles. by contrast. [edit] Bilirubin benefits Reasonable levels of bilirubin can be beneficial to the organism. with consequent irreversible damage to these areas manifesting as various neurological deficits. the heme molecule is a ring of four pyrroles. called porphyrin. Instead the conjugated billirubin is converted back into the unconjugated form by the enzyme b-glucoronidase and a large proportion is reabsorbed through the enterohepatic circulation.Neonatal hyperbilirubinemia .other cause is increased destruction of blood cells (Foetal hemoglobin resorption) over liver's capacity to conjugate [edit] Bilirubin toxicity Unconjugated hyperbilirubinaemia in the neonate can lead to accumulation of bilirubin in certain brain regions.

Bacteria deconjugate some of the primary and secondary conjugated bile salts back to lipid soluble bile acids. Venous blood from the ileum goes straight into the portal vein and then into the sinusoids of the liver. bacteria dehydroxylate some of the primary bile salts to form secondary conjugated bile salts (which are still water soluble). These lipid soluble bile acids are conjugated mainly to glycine or taurine molecules to form water soluble primary conjugated bile acids. often multiple times during a single digestive phase. these conjugated primary bile salts are reabsorbed actively into hepatic portal circulation. which are passively absorbed into hepatic portal circulation. where it is produced. to the small intestine.” In the lower small intestine and colon. There. Finally. jaundice may be observed. Liver hepatocytes metabolize cholesterol to cholic acid and chenodeoxycholic acid. most of the bile acids are ionized and mostly occur as their sodium salts which are then called “primary conjugated bile salts. Enterohepatic circulation refers to the circulation of bile from the liver. If bile does escape. Enterohepatic circulation also means that some molecules which would not otherwise be very toxic can become extremely hepatotoxic as they reach unexpectedly high hepatic concentrations. back to the liver. The net effect of enterohepatic recirculation is that each bile salt molecule is reused about 20 times. Along the proximal and distal ileum.Several textbooks and research articles show incorrect chemical structures for the two isoforms of bilirubin. hepatocytes extract bile acids very efficiently. the conjugated bile acids which remained un-ionized conjugated bile acids are passively absorbed. and little escapes the healthy liver into systemic circulation. Drugs may remain in the . These bile acids travel to the gall bladder during the interdigestive phase for storage and to the second part of the duodenum via the common bile duct during digestion. 95% of the bile acids which are delivered to the duodenum will be recycled by the enterohepatic circulation. where it aids in digestion of fats and other substances. At the pH of the small intestine.

It performs and regulates a wide variety of high-volume biochemical reactions requiring specialized tissues.enterohepatic circulation for a prolonged period of time as a result of this recycling process The liver is an organ in living beings. Medical terms related to the liver often start in hepato. hepar. This organ also is the largest gland in the human body. including humans. . which is important in digestion. It plays a major role in metabolism and has a number of functions in the body including glycogen storage.or hepatic from the Greek word for liver. plasma protein synthesis. It produces bile. and drug detoxification.

The liver lies on the right .1 Fetal blood supply 6 Liver as food 7 Cultural allusions 8 References 9 See also 10 References 11 Support groups . It is the second largest organ (the largest organ being the skin) and the largest gland within the human body.Contents [hide]  1 Anatomy o 1.1 Surface anatomy o 1.3 .2 Functional anatomy 2 Physiology 3 Diseases of the liver 4 Liver transplantation 5 Development o 5.0 kilograms.pediatric  12 External links           [edit] Anatomy View from below The adult human liver normally weighs between 1. pinkish-brown "boomerang shaped" organ. and is a soft.3. Its anatomical position in the body is immediately under the diaphragm on the right side of the upper abdomen.

e. and small intestines. There is also some evidence of bipotential stem cells. a single hepatocyte can divide into two hepatocyte daughter cells). so that the liver can process the nutrients and byproducts of food digestion. The liver is among the few internal human organs capable of natural regeneration of lost tissue. which in turn merge to form the common hepatic duct. The branchings of the bile ducts resemble those of a tree. [edit] Surface anatomy . and indeed the term "biliary tree" is commonly used in this setting. This is predominantly due to the hepatocytes acting as unipotential stem cells (i. The hepatic veins drain directly into the inferior vena cava. called oval cells. as little as 25% of remaining liver can regenerate into a whole liver again. These eventually drain into the right and left hepatic ducts.of the stomach and makes a kind of bed for the gallbladder (which stores bile). The common bile duct and the pancreatic duct enter the duodenum together at the ampulla of Vater. The hepatic artery normally comes off the celiac trunk. The portal vein brings venous blood from the spleen. The liver is supplied by two main blood vessels on its right lobe: the hepatic artery and the portal vein. pancreas. which can differentiate into either hepatocytes or cholangiocytes (cells that line the bile ducts). Bile can either drain directly into the duodenum via the common bile duct or be temporarily stored in the gallbladder via the cystic duct. which merge to form bile ducts. The cystic duct (from the gallbladder) joins with the common hepatic duct to form the common bile duct. The bile produced in the liver is collected in bile canaliculi.

a thin. the liver is covered entirely by visceral peritoneum. the functional lobes are further divided into a total of eight segments based on secondary and tertiary branching of the blood supply. the transverse fissure (or porta hepatis) divides the caudate from the quadrate lobe. portal vein. vein. The falciform ligament is visible on the front (anterior side) of the liver. and the portions of the liver supplied by these branches constitute the functional left and right lobes. The peritoneum folds back on itself to form the falciform ligament and the right and left triangular ligaments. there are two additional lobes between the right and left. which the inferior vena cava runs over. the lobes are divided up by the ligamentum venosum and ligamentum teres (anything left of these is the left lobe). but they are easily recognizable surface landmarks. This divides the liver into a left anatomical lobe. it is crucial to understand the fundamental importance of the liver on the blood supply and biliary drainage system. From behind. to look at it from behind (the visceral surface). and a right anatomical lobe. separates these two lobes from the right lobe. These are the caudate lobe (the more superior). and artery divide into left and right branches. Apart from a patch where it connects to the diaphragm.The liver is the largest internal organ of the human body. The functional lobes are separated by a plane joining the gallbladder fossa to the inferior vena cava. The duct. and hepatic artery enter the liver is the hilum or "porta hepatis". double-layered membrane that reduces friction against other organs. The segments corresponding to the surface anatomical lobes are as follows: . [edit] Functional anatomy For purposes such as advanced liver surgery. and have essentially no functional importance. The central area where the common bile duct. and the right sagittal fossa. In the widely used Couinaud or "French" system. Traditional gross anatomy divided the liver into four lobes based on surface features. These "ligaments" are in no way related to the true anatomic ligaments in joints. and below this the quadrate lobe. If the liver is flipped over.

and some is stored in the gallbladder. This sometimes results in toxication. 8 [edit] Physiology The various functions of the liver are carried out by the liver cells or hepatocytes. VII.         The liver produces and excretes bile required for dissolving fats. X and XI. iron. lactate or glycerol) o Glycogenolysis (the formation of glucose from glycogen) (muscle tissues can also do this) o Glycogenesis (the formation of glycogen from glucose) o The breakdown of insulin and other hormones o The liver is responsible for the mainstay of protein metabolism.Lobe Couinaud segments Caudate 1 Left 2. The liver also performs several roles in lipid metabolism: o Cholesterol synthesis o The production of triglycerides (fats). II (prothrombin). 3 Quadrate Right 4 5. The liver breaks down hemoglobin. The liver produces coagulation factors I (fibrinogen). vitamin B12. protein S and antithrombin. and copper. The liver performs several roles in carbohydrate metabolism: o Gluconeogenesis (the formation of glucose from certain amino acids. The liver stores a multitude of substances. The liver breaks down toxic substances and most medicinal products in a process called drug metabolism. Some of the bile drains directly into the duodenum. including glucose in the form of glycogen. when the metabolite is more toxic than its precursor. 7. V. as well as protein C. 6. creating metabolites that are added to bile as pigment. The liver converts ammonia to urea. . IX.

autoimmunity or hereditary conditions. replacing dead liver cells. a hereditary disease which causes the body to retain copper. . a hereditary disease causing the accumulation of iron in the body. usually from other parts of the gastrointestinal tract). Some functions can be emulated by liver dialysis. autoimmune in nature. normally.the reticuloendothelial system of the liver contains many immunologically active cells. the liver is the main site of red blood cell production. The liver is responsible for immunological effects. By the 32nd week of gestation. caused mainly by various viruses but also by some poisons.          Hepatitis. Wilson's disease. there is no artificial organ or device capable of emulating all the functions of the liver. Currently. Primary sclerosing cholangitis. The bilirubin results from the breakup of the hemoglobin of dead red blood cells. eventually leading to liver damage. Cancer of the liver (primary hepatocellular carcinoma or cholangiocarcinoma and metastatic cancers. the liver removes bilirubin from the blood and excretes it through bile. Primary biliary cirrhosis.  In the first trimester fetus. The death of the liver cells can for example be caused by viral hepatitis. [edit] Diseases of the liver Many diseases of the liver are accompanied by jaundice caused by increased levels of bilirubin in the system. Hemochromatosis. found in about 5% of the population. alcoholism or contact with other liver-toxic chemicals. inflammation of the liver. an experimental treatment for liver failure. the bone marrow has almost completely taken over that task. Cirrhosis is the formation of fibrous tissue in the liver. a genetic disorder of bilirubin metabolism. autoimmune disease of small bile ducts Budd-Chiari syndrome. an inflammatory disease of the bile duct. obstruction of the hepatic vein. Gilbert's syndrome. acting as a 'sieve' for antigens carried to it via the portal system.

adult-to-adult liver transplantation has been done using the donor's right hepatic lobe which amounts to 60% of the liver. [edit] Liver transplantation Human liver transplant was first performed by Thomas Starzl in USA and Roy Calne in England in 1963 and 1965 respectively. and many others. Less commonly. These test for the presence of enzymes in blood that are normally most abundant in liver tissue. including biliary atresia. Due to the ability of the liver to regenerate. both the donor and recipient end up with normal liver function if all goes well. Living donor liver transplantation is a technique in which a portion of a living person's liver is removed and used to replace the entire liver of the recipient. A number of liver function tests are available to test the proper function of the liver. and indeed there have been at least 2 donor deaths out of the first several hundred cases. and at least 14 cases have been found. alpha-1 antitrypsin deficiency. This procedure is more controversial as it entails performing a much larger operation on the donor. and progressive familial intrahepatic cholestasis. such as chronic hepatitis C. Only 20% of an adult's liver (Couinaud segments 2 and 3) is needed to serve as a liver allograft for an infant or small child. metabolites or products. Its initial blood supply is primarily from the vitelline veins that drain blood from the yolk sac. alcoholism. liver transplantation is done for fulminant hepatic failure. in which liver failure occurs over days to weeks. Most transplants are done for chronic liver diseases leading to cirrhosis. The superior part of the hepatic . Liver allografts for transplant usually come from non-living donors who have died from fatal brain injury. A recent publication has addressed the problem of donor mortality. ([1]) The risk of postoperative complications (and death) is far greater in right sided hepatectomy than left sided operations [edit] Development The liver develops as an endodermal outpocketing of the foregut called the hepatic diverticulum.There are also many pediatric liver disease. to name but a few. Liver transplantation is the only option for those with irreversible liver failure. autoimmune hepatitis. More recently. alagille syndrome. This was first performed in 1989 for pediatric liver transplantation.

a major source of blood to the liver is the umbilical vein which supplies nutrients to the growing fetus.5 g Fat 3. and does not perform the normal filtration of the infant liver. After birth. the former becomes the ligamentum teres and the latter becomes the ligamentum venosum. The fetal liver releases some blood stem cells that migrate to the fetal thymus.7 g Protein 21 g Vitamin A 6500 μg 722% Riboflavin (Vit. In the fetus. and passes upward along the free margin of the falciform ligament of the liver to the inferior surface of the liver. The umbilical vein enters the abdomen at the umbilicus. allowing placental blood to bypass the liver. Once the fetus is delivered. the formation of blood stem cells in infants shifts to the red bone marrow. the umbilical vein and ductus venosus are completely obliterated two to five days postpartum. the umbilical vein can open up again.diverticulum gives rise to the hepatocytes and bile ducts. In the disease state of cirrhosis and portal hypertension. are created from fetal liver stem cells. There it joins with the left branch of the portal vein. while the inferior part becomes the gallbladder and its associated cystic duct. the liver is developing throughout normal gestation. [edit] Fetal blood supply In the growing fetus. [edit] Liver as food Pork liver Nutritional value per 100 g Energy 130 kcal 560 kJ Carbohydrates 2. called T-cells. but receives nourishment from the mother via the placenta. B2) 3 mg 200% . so initially the lymphocytes. The ductus venosus carries blood from the left portal vein to the left hepatic vein and thence to the inferior vena cava. The liver does not perform digestive processes because the fetus does not consume meals directly.

which would regenerate overnight. Source: USDA Nutrient database Mammal and bird livers are commonly eaten as food: products include liver paté. with the gallbladder counteracting this. B3) 15 mg 100% Vitamin B6 0. Braunschweiger. leverpostej and liver sashimi. . However. Ethon) would peck out his liver.[1]. Very high doses of Vitamin A can be toxic. Percentages are relative to US RDI values for adults. since it is present in a less toxic form than in many dietary supplements. the latter fatally. Liverwurst. chopped liver.7 mg 54% Folate (Vit. from eating husky liver.Niacin (Vit. Curiously. possibly due to survived injuries in battle. Antarctic explorers Douglas Mawson and Xavier Mertz were both poisoned. Both animal and fish livers are rich in iron and Vitamin A and cod liver oil is commonly used as a supplement. the USDA specifies 3000 μg per day as a tolerable upper limit. acute vitamin A poisoning is not likely to result from liver consumption. which amounts to about 50g of raw pork liver or 3g of polar-bear liver. foie gras.[2] [edit] Cultural allusions In Greek mythology. In the US. B9) 212 μg 53% Vitamin B12 26 μg 1083% Iron 23 mg 184% Sodium 87 mg 6% Beef and chicken liver are comparable. a characteristic which may have already been known to the Greeks. the liver is the only human internal organ that actually can regenerate itself to a significant extent. Prometheus was punished by the gods for revealing fire to humans by being chained to a rock where a vulture (or an eagle. The Talmud (tractate Berakhot 61b) refers to the liver as the seat of anger.

Treatment. eds. ISBN 0-7817-3007-4 Sheila Sherlock. Sorrell. Hind bint Utbah is implyed or portrayed eating the liver of Hamza ibn Abd-al-Muttalib during the Battle of Uhud." e. McGraw-Hill. Philadelphia : Lippincott. 2002. James Dooley. ISBN 1-58333-188-3. ISBN 0-7216-9051-3 These are for the lay reader or patient: Sanjiv Chopra. his Columbia University web site. In the motion picture The Message. and Recovery. ISBN 0-7434-0585-4 Melissa Palmer. Schiff's diseases of the liver.  Liver function tests . "Diseases of the liver" [edit] See also Look up liver in Wiktionary. 4th ed. UK . Atria. her webpage. the liver is used in figurative speech to refer to courage and strong feelings. The Liver Book: A Comprehensive Guide to Diagnosis. 2002. MA : Blackwell Science. 2003. Williams & Wilkins. Boyer. Michael F. Avery Publishing Group. "This Mecca has thrown to you the pieces of its liver!" [3] The legend of Liver-Eating Johnson says that he would cut out and eat the liver of each man killed. Willis C. 1999. or "their best. 2003. The Liver Disorders Sourcebook. ISBN 0-7373-0090-6. 11th ed. 9th ed.g. Maddrey. ISBN 0-632-05582-0 David Zakim. eds. It is well known that Inuit will not eat the liver of polar bears or seals [4] [edit] References       The following are standard medical textbooks: Eugene R. Dr. Philadelphia: Saunders. 2004. Melissa Palmer's Guide to Hepatitis and Liver Disease: What You Need to Know. Hepatology: a textbook of liver disease. Oxford. the free dictionary. Revised edition May 24. Schiff. Worman. Diseases of the liver and biliary system.In Arabic and Persian language. Thomas D. Howard J. Malden.

78.studentbmj. and solid forms of retinol supplements are more toxic than oil-based preparations".php Your continued donations keep Wikipedia running! Gallbladder From Wikipedia.php?id=94 4.com/issues/02/05/life/158. ^ http://www. ^ http://www. Hepatocyte [edit] References 1.org/m/faq_qanda. Clinical Nutrition. emulsified. J. search . ^ A. "Water-miscible. the free encyclopedia Jump to: navigation. 1152 (2003) 3. ^ Myhre et al. Aggrawal.shawuniversitymosque.. Am. Death by Vitamin A 2.

Gall bladder Histology Digestive system diagram showing the bile duct .

which is released when llllllloooopfood containing fat enters the digestive tract. which are pouches inside the lining.7 Gallbladder cancer o 3.4 Cholecystitis o 3. The bile emulsifies fats and neutralizes acids in partly digested food.The gallbladder (or cholecyst sometimes gall bladder) is a pear-shaped organ that stores about 50 mL of bile (or "gall") until the body needs it for digestion. followed by a muscular wall that contracts in response to cholecystokinin. Contents [hide]     1 Microscopic anatomy 2 Function 3 Role in disease o 3.8 Gallbladder Polyps and Primary Sclerosing Cholangitis 4 External links [edit] Microscopic anatomy The gallbladder has an epithelial lining characterized by recesses called Aschoff's recesses. stimulating the secretion of cholecystokinin (CCK).3 Cholelithiasis o 3. a peptide hormone secreted by the duodenum. [edit] Function The gallbladder stores bile. The gallbladder is about 7-10cm long in humans and is dark green in appearance due to its contents (bile).5 Choledocholithiasis o 3. Under the epithelium there is a layer of connective tissue. After being stored in the gallbladder. the bile becomes more concentrated .1 Cholestasis o 3. not its tissue.2 Biliary colic o 3. It is connected to the liver and the duodenum by the biliary tract.6 Gallstone ileus o 3.

lecithin and bile acids. Another more serious complication is total blockage of the bile duct which leads to jaundice. It can lead to jaundice. diarrhoea. composed of cholesterol.than when it left the liver. which if it is not corrected naturally or by a surgical procedure can be fatal as it causes liver damage. The only long term solution is the removal of the gall bladder. This condition causes severe pain in the right upper abdomen and sometimes through to the upper back. Other symptoms are nausea and vomiting. bleeding caused by continuous vomiting. and dehydration caused by the nausea and diarrhoea. increasing its potency and intensifying its effect on fats. [edit] Cholelithiasis Main article: Cholelithiasis Cholecystectomy seen through a laparoscope Up to 25% of all people have gallstones (cholelithiasis). [edit] Role in disease [edit] Cholestasis Cholestasis is the blockage in the supply of bile into the digestive tract. It can be "intrahepatic" (the obstruction is in the liver) or "extrahepatic" (outside the liver). These can cause colicky shooting . and is identified by the presence of elevated bilirubin level that is mainly conjugated. [edit] Biliary colic This is when a gallstone blocks either the common bile duct or the duct leading into it from the gallbladder.

in which the gallbladder forms a fistula with the digestive tract. the patient develops jaundice and liver cell damage. and it is in fact one of the most common procedures done through the lapae. The actual inflammation is due to secondary infection with bacteria of an obstructed gallbladder. It is a medical emergency. People traditionally considered at an increased risk of cholelithiasis are people who are 5 F's:      Female Fat (obesity) Fair (Caucasian. with the obstruction caused by the gallstone. [edit] Choledocholithiasis Main article: Choledocholithiasis When gallstones obstruct the common bile duct. Surgery (cholecystectomy. and generally block the gut at the level of Treitz' ligament or the ileocecal valve. removal of the gallbladder) is the most common treatment for gallstones. The treatment is surgical. or gallstone ileus. It can be performed laparoscopically.abdominal pain. [edit] Gallstone ileus A rare clinical entity is ileus (bowel obstruction) by a large gallstone. requiring endoscopic or surgical treatment. 90% of cases of acute cholecystitis are caused by the presence of gallstones. usually in relation with the meal. two narrow points in the digestive tract. This condition develops in patients with longstanding gallstone disease. but this is disputed by recent studies) Forty (middle-aged) Fertile (multiple children) [edit] Cholecystitis Main article: Cholecystitis Acute or chronic inflammation of the gall bladder causes abdominal pain. Large stones pass into the bowel. . as the gallbladder contracts and gallstones pass through the bile duct.

Patients with polyps 10 mm to 15 mm have a lower risk but they should still discuss removal of their gallbladder with their physician. jaundice. cigarette smoking. It is associated with a lifetime risk of 7% to 12% for gallbladder cancer. weight loss. Small gallbladder polyps (up to 10 mm) pose little or no risk. estrogens. the free encyclopedia Jump to: navigation. Despite aggressive modern surgical approaches. It has been associated with gallstone disease. and ascites. Of special note is a condition called primary sclerosing cholangitis. advanced imaging techniques. every year your gall bladder gets smaller so when you reach about age of 60 it dissapears completly. alcohol consumption and obesity. but large ones (greater than 15 mm) pose some risk for cancer. Polyps are often detected in this condition and have a very high likelihood of malignancy. although primary sclerosing cholangitis tends to strike younger men who have ulcerative colitis. [edit] Gallbladder Polyps and Primary Sclerosing Cholangitis Polyps (growths) are sometimes detected during diagnostic tests for gallbladder disease. search Vein: Hepatic vein . Hepatic vein From Wikipedia.[edit] Gallbladder cancer Cancer of the gallbladder is a rare but highly fatal disease. which causes inflammation and scarring in the bile duct. so the gallbladder should be removed. The cause is unknown. and endoscopy. nearly 90% of patients die from advanced stages of the disease and experience pain.

.The portal vein and its tributaries.

The hepatic veins are seen on the superior portion of the IVC. inferior vena cava (IVC). shortly before it flows into the right atrium. Latin Gray's Venæ hepaticæ subject #173 . azygos vein and their tributaries. which is not shown.Superior vena cava.

[edit] External links    Hepatic veins . None of the hepatic veins have valves.definition .medterms.com) Hepatic Histology: The Lobule . more specifically the central vein of the liver lobule.The Encyclopaedia of Medical Imaging Volume II (amershamhealth. They can be differentiated into two groups. They arise from the substance of the liver.com Hepatic Histology: The Lobule The liver is bounded by a connective tissue capsule which extends into .a detailed description . are three in number. Occlusion of the hepatic veins is known as Budd-Chiari syndrome. and are typically smaller than those in the upper group. The lower group arise from the right lobe and caudate lobe. are variable in number.   The upper group typically arises from the posterior aspect of the liver.680 Drains to inferior vena cava Artery Hepatic artery In human anatomy. small intestine and colon) into the inferior vena cava.Describes the liver lobule and central vein. Hepatic veins . the upper group and lower group. the hepatic veins are the blood vessels that drain deoxygenated blood from the liver and blood cleaned by the liver (from the stomach. pancreas. and drain the quadrate lobe and left lobe.

the capsule and septae are stained blue . Efferent vessels traverse a route separate from connective tissue scaffolding.its substance as highly branched septae. The connective tissue septae invaginating from the capsule delineate hepatic lobules. immediately below a large capsular blood vessel. In the section of equine liver below (Masson's trichrome stain). . the connective tissue surrounding lobules is particularly abundant and easy to identify in pig livers. while hepatocytes are magenta . the structural unit of the liver. The afferent blood vessels and lymphatics follow this connective tissue highway throughout the liver. Relative to other common species. Notice how the capsule extends as a septum into the liver about one-third of the way from left. as shown below in an H&Estained section (Pass your mouse pointer over the image to confirm lobule boundaries).

At the vertices of the lobule are regularly distributed portal triads (also known as portal tracts). a lobule is a roughly hexagonal arrangement of plates of hepatocytes radiating outward from a central vein (CV) in the center. but are tough to see in standard paraffin sections. Examination of a triad in cross section should reveal a bile duct and branches of the hepatic artery and hepatic portal vein. Due to plane of section. Central veins are quite prominent and provide an easy means of orientation in sections of liver. Lymphatic vessels are also present. which is probably why it is not called a portal tetrad. one can often observe more than one of each of these structures in a given portal tract or absence of one or more structures.As you can observe above. Portal tract in equine liver (trichrome stain) .

Portal tract in porcine liver (H&E stain) without visible bile duct Lobules are almost impossible to miss in porcine liver. The following image is from a section of equine liver (H&E stain). . orienting on central veins and portal tracts allow "easy" identification. It goes without saying. that the majority of lobules seen in a tissue section are not as "typical" as seen here and in other histology texts. See if you can picture the lobule. of course. then move your mouse pointer into the image to confirm it. Although the precise boundaries of lobules are sometimes difficult to discern. but one should also be able to recognize them in other species.