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==Pathophysiology==
==Pathophysiology==


==== For more information about viral hepatitis pathophysiology [[Viral hepatitis|click here]] ====
====  Bilirubin formation and metabolism ====
 
==== For more information about cirrhosis pathophysiology [[Cirrhosis pathophysiology|click here]] ====
 
==== For more information about neonatal jaundice pathophysiology [[Neonatal jaundice pathophysiology|click here]] ====
 
=== Bilirubin formation and metabolism===
*[[Bilirubin]] is the final [[catabolic]] product of the [[heme]]. The heme is a component of various biological molecules and [[enzymes]] but, it is mainly incorporated in the [[hemoglobin]] which is the primary component of the [[red blood cells]].<ref name="pmid5824077">{{cite journal| author=Berk PD, Howe RB, Bloomer JR, Berlin NI| title=Studies of bilirubin kinetics in normal adults. | journal=J Clin Invest | year= 1969 | volume= 48 | issue= 11 | pages= 2176-90 | pmid=5824077 | doi=10.1172/JCI106184 | pmc=297471 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5824077  }}</ref><ref name="pmid15422003">{{cite journal| author=LONDON IM, WEST R, SHEMIN D, RITTENBERG D| title=On the origin of bile pigment in normal man. | journal=J Biol Chem | year= 1950 | volume= 184 | issue= 1 | pages= 351-8 | pmid=15422003 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15422003  }}</ref>
*[[Bilirubin]] is the final [[catabolic]] product of the [[heme]]. The heme is a component of various biological molecules and [[enzymes]] but, it is mainly incorporated in the [[hemoglobin]] which is the primary component of the [[red blood cells]].<ref name="pmid5824077">{{cite journal| author=Berk PD, Howe RB, Bloomer JR, Berlin NI| title=Studies of bilirubin kinetics in normal adults. | journal=J Clin Invest | year= 1969 | volume= 48 | issue= 11 | pages= 2176-90 | pmid=5824077 | doi=10.1172/JCI106184 | pmc=297471 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5824077  }}</ref><ref name="pmid15422003">{{cite journal| author=LONDON IM, WEST R, SHEMIN D, RITTENBERG D| title=On the origin of bile pigment in normal man. | journal=J Biol Chem | year= 1950 | volume= 184 | issue= 1 | pages= 351-8 | pmid=15422003 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15422003  }}</ref>
*[[Bilirubin]] is formed mainly in [[Liver|the liver]] and [[spleen]] through two steps which include:<ref name="pmid3700551">{{cite journal| author=Knobloch E, Hodr R, Herzmann J, Houdková V| title=Kinetics of the formation of biliverdin during the photochemical oxidation of bilirubin monitored by column liquid chromatography. | journal=J Chromatogr | year= 1986 | volume= 375 | issue= 2 | pages= 245-53 | pmid=3700551 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3700551  }}</ref><ref name="pmid5038868">{{cite journal| author=Bissell DM, Hammaker L, Schmid R| title=Liver sinusoidal cells. Identification of a subpopulation for erythrocyte catabolism. | journal=J Cell Biol | year= 1972 | volume= 54 | issue= 1 | pages= 107-19 | pmid=5038868 | doi= | pmc=2108858 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5038868  }}</ref>
*[[Bilirubin]] is formed mainly in [[Liver|the liver]] and [[spleen]] through two steps which include:<ref name="pmid3700551">{{cite journal| author=Knobloch E, Hodr R, Herzmann J, Houdková V| title=Kinetics of the formation of biliverdin during the photochemical oxidation of bilirubin monitored by column liquid chromatography. | journal=J Chromatogr | year= 1986 | volume= 375 | issue= 2 | pages= 245-53 | pmid=3700551 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3700551  }}</ref><ref name="pmid5038868">{{cite journal| author=Bissell DM, Hammaker L, Schmid R| title=Liver sinusoidal cells. Identification of a subpopulation for erythrocyte catabolism. | journal=J Cell Biol | year= 1972 | volume= 54 | issue= 1 | pages= 107-19 | pmid=5038868 | doi= | pmc=2108858 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5038868  }}</ref>
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***The [[unconjugated bilirubin]] is reabsorbed back into [[Blood|the blood]] and to the liver through the [[enterohepatic circulation]] of [[bilirubin]].
***The [[unconjugated bilirubin]] is reabsorbed back into [[Blood|the blood]] and to the liver through the [[enterohepatic circulation]] of [[bilirubin]].
***A small amount of [[bilirubin]] is cleared into the [[urine]] as [[urobilinogen]].
***A small amount of [[bilirubin]] is cleared into the [[urine]] as [[urobilinogen]].
==== For more information about viral hepatitis pathophysiology [[Viral hepatitis|click here]] ====
==== For more information about cirrhosis pathophysiology [[Cirrhosis pathophysiology|click here]] ====
==== For more information about neonatal jaundice pathophysiology [[Neonatal jaundice pathophysiology|click here]] ====
===Pathogenesis of Adult jaundice===
===Pathogenesis of Adult jaundice===
* Jaundice in adult patients classified into two major types:
* Jaundice in adult patients classified into two major types:
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** [[Conjugated bilirubin|Conjugated]] [[hyperbilirubinemia]]
** [[Conjugated bilirubin|Conjugated]] [[hyperbilirubinemia]]
=== Unconjugated hyperbilirubinemia ===
=== Unconjugated hyperbilirubinemia ===
The main [[pathophysiology]] of unconjugated hyperbilirubinemia includes:
The primary [[pathophysiology]] of unconjugated hyperbilirubinemia include:<ref name="pmid16512459">{{cite journal |vauthors=Duseja A, Das A, Das R, Dhiman RK, Chawla Y, Bhansali A |title=Unconjugated hyperbilirubinemia in nonalcoholic steatohepatitis--is it Gilbert's syndrome? |journal=Trop Gastroenterol |volume=26 |issue=3 |pages=123–5 |date= 2005 |pmid=16512459 |doi= |url=}}</ref>
* Overproduction of [[bilirubin]]
* Overproduction of [[bilirubin]]
* Reduced [[bilirubin]] uptake
* Reduced [[bilirubin]] uptake
* Impaired [[bilirubin]] [[conjugation]]
* Impaired [[bilirubin]] [[conjugation]]
** The combination of progestational and estrogenic steroids results in increased [[UDP glucuronosyltransferase 1 family, polypeptide A1|UDP-glucuronyl transferase]] activity
** The combination of progestational and estrogenic steroids may result in increased [[UDP glucuronosyltransferase 1 family, polypeptide A1|UDP-glucuronyl transferase]] activity


==== Conjugated hyperbilirubinemia ====
=== Conjugated hyperbilirubinemia ===
* [[Biliary obstruction|Biliary tract obstruction]]<ref name="pmid18345288">{{cite journal| author=Abdallah AA, Krige JE, Bornman PC| title=Biliary tract obstruction in chronic pancreatitis. | journal=HPB (Oxford) | year= 2007 | volume= 9 | issue= 6 | pages= 421-8 | pmid=18345288 | doi=10.1080/13651820701774883 | pmc=2215354 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18345288  }}</ref>
 
** [[Biliary obstruction|Biliary tract obstruction]] leads to both conjugated and unconjugated bilirubinemia
==== Biliary tract obstruction<ref name="pmid18345288">{{cite journal| author=Abdallah AA, Krige JE, Bornman PC| title=Biliary tract obstruction in chronic pancreatitis. | journal=HPB (Oxford) | year= 2007 | volume= 9 | issue= 6 | pages= 421-8 | pmid=18345288 | doi=10.1080/13651820701774883 | pmc=2215354 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18345288  }}</ref> ====
** [[Bilirubin]] is transported back to the plasma by ATP-consuming pumps
* [[Biliary obstruction|Biliary tract obstruction]] leads to both conjugated and unconjugated bilirubinemia.
** The markers are serum concentrations of [[bilirubin]] and [[alkaline phosphatase]]  
* [[Bilirubin]] is transported back to the plasma by ATP-consuming pumps.
** Biliary retention secondary to obstruction may reverse the glucuronidation
* The markers are serum concentrations of [[bilirubin]] and [[alkaline phosphatase]].
** Produced unconjugated [[bilirubin]] will diffuse or be transported back into the [[plasma]]
* Biliary retention secondary to obstruction may reverse the glucuronidation.
*** [[Mirizzi syndrome]]<ref name="pmid23002333">{{cite journal| author=Beltrán MA| title=Mirizzi syndrome: history, current knowledge and proposal of a simplified classification. | journal=World J Gastroenterol | year= 2012 | volume= 18 | issue= 34 | pages= 4639-50 | pmid=23002333 | doi=10.3748/wjg.v18.i34.4639 | pmc=3442202 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23002333  }}</ref>
* Produced unconjugated [[bilirubin]] will diffuse or be transported back into the [[plasma]].
**** [[Extrahepatic bile ducts]] compression by a distended [[gallbladder]] due to [[cholelithiasis]]
* [[Mirizzi syndrome]]<ref name="pmid23002333">{{cite journal| author=Beltrán MA| title=Mirizzi syndrome: history, current knowledge and proposal of a simplified classification. | journal=World J Gastroenterol | year= 2012 | volume= 18 | issue= 34 | pages= 4639-50 | pmid=23002333 | doi=10.3748/wjg.v18.i34.4639 | pmc=3442202 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23002333  }}</ref>
*** Primary sclerosing cholangitis and cholangiocarcinoma
** [[Extrahepatic bile ducts]] compression by a distended [[gallbladder]] due to [[cholelithiasis]].
**** [[Intrahepatic bile ducts|Intrahepatic]] and [[Extrahepatic bile ducts|extrahepatic]] portions of the bile ducts are affected  
* [[Primary sclerosing cholangitis]] and cholangiocarcinoma
** [[Parasites]]  
** [[Intrahepatic bile ducts|Intrahepatic]] and [[Extrahepatic bile ducts|extrahepatic]] portions of the bile ducts are affected.
*** Adult ''[[Ascaris lumbricoides]]''
* [[Parasites]]  
*** Eggs of certain [[liver flukes]] (e.g., ''[[Clonorchis sinensis]]'', ''[[Fasciola hepatica]]'')
** Adult ''[[Ascaris lumbricoides]]''
** [[AIDS]] cholangiopathy<ref name="pmid15010025">{{cite journal |vauthors=Yusuf TE, Baron TH |title=AIDS Cholangiopathy |journal=Curr Treat Options Gastroenterol |volume=7 |issue=2 |pages=111–117 |date=April 2004 |pmid=15010025 |doi= |url=}}</ref>
** Eggs of certain [[liver flukes]] (e.g., ''[[Clonorchis sinensis]]'', ''[[Fasciola hepatica]]'')
*** ''[[Cryptosporidium]]'' species
* [[AIDS]] cholangiopathy<ref name="pmid15010025">{{cite journal |vauthors=Yusuf TE, Baron TH |title=AIDS Cholangiopathy |journal=Curr Treat Options Gastroenterol |volume=7 |issue=2 |pages=111–117 |date=April 2004 |pmid=15010025 |doi= |url=}}</ref>
*** [[Cytomegalovirus]]
** ''[[Cryptosporidium]]'' species
*** [[HIV]]  
** [[Cytomegalovirus]]
**** [[Viral hepatitis]] ([[Hepatitis|hepatitis viruses]], [[herpes simplex virus]], [[Epstein-Barr virus]])
** [[HIV]]  
**** [[Mycobacterium tuberculosis|''Mycobacterium'' tuberculosis]] and [[atypical mycobacteria]] (especially [[Mycobacterium avium intracellulare|''Mycobacterium avium'' intracellulare]])
*** [[Viral hepatitis]] ([[Hepatitis|hepatitis viruses]], [[herpes simplex virus]], [[Epstein-Barr virus]])
**** [[Fungal infections]] (''[[Cryptococcus neoformans]]'', ''[[Histoplasma capsulatum]]'', ''[[Candida albicans]]'', ''[[Coccidioides immitis]]'')
*** [[Mycobacterium tuberculosis|''Mycobacterium'' tuberculosis]] and [[atypical mycobacteria]] (especially [[Mycobacterium avium intracellulare|''Mycobacterium avium'' intracellulare]])
**** [[Parasites]] (''[[Pneumocystis carinii]]'')
*** [[Fungal infections]] (''[[Cryptococcus neoformans]]'', ''[[Histoplasma capsulatum]]'', ''[[Candida albicans]]'', ''[[Coccidioides immitis]]'')
**** Tumor infiltration ([[lymphoma]], [[Kaposi sarcoma]])
*** [[Parasites]] (''[[Pneumocystis carinii]]'')
**** Drug-induced liver disease
*** Tumor infiltration ([[lymphoma]], [[Kaposi sarcoma]])
* [[Intrahepatic cholestasis|Intrahepatic causes]]
*** Drug-induced liver disease
** [[Viral hepatitis]]: For more information about viral hepatitis [[Viral hepatitis X (non-A,-B,-C,-D,-E)|click here]]
 
** [[Alcoholic hepatitis]]: For more information about viral hepatitis [[Alcoholic hepatitis pathophysiology|click here]]
==== Liver infrastructure damage ====
** [[Nonalcoholic steatohepatitis]]: For more information about viral hepatitis [[Non-alcoholic fatty liver disease|click here]]
* [[Viral hepatitis]]: For more information about viral hepatitis [[Viral hepatitis X (non-A,-B,-C,-D,-E)|click here]]
** [[Primary biliary cholangitis]]: For more information about viral hepatitis [[Primary biliary cirrhosis pathophysiology|click here]]
* [[Alcoholic hepatitis]]: For more information about viral hepatitis [[Alcoholic hepatitis pathophysiology|click here]]
** [[Toxicity]]<ref name="pmid171822">{{cite journal |vauthors=Schaffner F |title=Hepatic drug metabolism and adverse hepatic drug reactions |journal=Vet. Pathol. |volume=12 |issue=2 |pages=145–56 |date= 1975 |pmid=171822 |doi=10.1177/030098587501200206 |url=}}</ref>
* [[Nonalcoholic steatohepatitis]]: For more information about viral hepatitis [[Non-alcoholic fatty liver disease|click here]]
*** Dose-related fashion (e.g., alkylated steroids such as [[methyltestosterone]] and [[ethinyl estradiol]])  
* [[Primary biliary cholangitis]]: For more information about viral hepatitis [[Primary biliary cirrhosis pathophysiology|click here]]
*** [[Idiosyncratic reaction|Idiosyncratic]] or [[allergic reaction]] (e.g., [[chlorpromazine]], [[halothane]]).
* [[Toxicity]]<ref name="pmid171822">{{cite journal |vauthors=Schaffner F |title=Hepatic drug metabolism and adverse hepatic drug reactions |journal=Vet. Pathol. |volume=12 |issue=2 |pages=145–56 |date= 1975 |pmid=171822 |doi=10.1177/030098587501200206 |url=}}</ref>
*** [[Pyrrolizidine alkaloid|Pyrrolizidine alkaloids]] which may cause [[veno-occlusive disease]] of the [[liver]] (e.g., Jamaican bush tea)
** Dose-related fashion (e.g., alkylated steroids such as [[methyltestosterone]] and [[ethinyl estradiol]])  
** [[Sepsis]] and low perfusion states<ref name="pmid12919846">{{cite journal |vauthors=Famularo G, De Simone C, Nicotra GC |title=Jaundice and the sepsis syndrome: a neglected link |journal=Eur. J. Intern. Med. |volume=14 |issue=4 |pages=269–271 |date=July 2003 |pmid=12919846 |doi= |url=}}</ref>
** [[Idiosyncratic reaction|Idiosyncratic]] or [[allergic reaction]] (e.g., [[chlorpromazine]], [[halothane]]).
*** [[Hypotension]]
** [[Pyrrolizidine alkaloid|Pyrrolizidine alkaloids]] which may cause [[veno-occlusive disease]] of the [[liver]] (e.g., Jamaican bush tea)
*** [[Drugs]]
* [[Sepsis]] and low perfusion states<ref name="pmid12919846">{{cite journal |vauthors=Famularo G, De Simone C, Nicotra GC |title=Jaundice and the sepsis syndrome: a neglected link |journal=Eur. J. Intern. Med. |volume=14 |issue=4 |pages=269–271 |date=July 2003 |pmid=12919846 |doi= |url=}}</ref>
*** [[Bacterial endotoxins]]
** [[Hypotension]]
** [[Paraneoplastic syndromes]]  
** [[Drugs]]
*** [[Renal cell carcinoma]]  
** [[Bacterial endotoxins]]
*** [[Lymphoproliferative disease|Malignant lymphoproliferative diseases]]
* [[Paraneoplastic syndromes]]  
*** [[Gynecologic cancer|Gynecologic malignancies]]
** [[Renal cell carcinoma]]  
*** [[Prostate cancer]]
** [[Lymphoproliferative disease|Malignant lymphoproliferative diseases]]
**  [[Infiltrative and Metabolic Diseases Affecting the Liver|Infiltrative diseases of the liver]]
** [[Gynecologic cancer|Gynecologic malignancies]]
*** [[Amyloidosis]]
** [[Prostate cancer]]
*** [[Lymphoma]]
* [[Infiltrative and Metabolic Diseases Affecting the Liver|Infiltrative diseases of the liver]]
*** [[Sarcoidosis]]
** [[Amyloidosis]]
*** [[Tuberculosis]]
** [[Lymphoma]]
** [[Total parenteral nutrition|Total parenteral nutrition (TPN)]]<ref name="pmid8468653">{{cite journal |vauthors=Moss RL, Das JB, Ansari G, Raffensperger JG |title=Hepatobiliary dysfunction during total parenteral nutrition is caused by infusate, not the route of administration |journal=J. Pediatr. Surg. |volume=28 |issue=3 |pages=391–6; discussion 396–7 |date=March 1993 |pmid=8468653 |doi= |url=}}</ref>
** [[Sarcoidosis]]
*** At least two to three weeks of [[Total parenteral nutrition|TPN]] may lead to development of [[cholestasis]]
** [[Tuberculosis]]
**** Intestinal [[endotoxins]] transfer into the [[portal system]]
* [[Total parenteral nutrition|Total parenteral nutrition (TPN)]]<ref name="pmid8468653">{{cite journal |vauthors=Moss RL, Das JB, Ansari G, Raffensperger JG |title=Hepatobiliary dysfunction during total parenteral nutrition is caused by infusate, not the route of administration |journal=J. Pediatr. Surg. |volume=28 |issue=3 |pages=391–6; discussion 396–7 |date=March 1993 |pmid=8468653 |doi= |url=}}</ref>
**** Bacterial [[sepsis]]
** At least two to three weeks of [[Total parenteral nutrition|TPN]] may lead to development of [[cholestasis]].
**** Formation of secondary [[Bile acid|bile acids]] (e.g., lithocholic acid)
*** Intestinal [[endotoxins]] transfer into the [[portal system]]
**** Biliary sludge after six weeks of [[Total parenteral nutrition|TPN]]
*** Bacterial [[sepsis]]
**** Hepatotoxic factors, such as [[tryptophan]] degradation metabolites and [[Aluminium|aluminum]] contaminants
*** Formation of secondary [[Bile acid|bile acids]] (e.g., lithocholic acid)
**** [[Small bowel bacterial overgrowth syndrome|Bacterial overgrowth in the small intestine]]
*** Biliary sludge after six weeks of [[Total parenteral nutrition|TPN]]
** [[Sickle cell disease]]<ref name="pmid3186339">{{cite journal |vauthors=Mallouh AA, Asha MI |title=Acute cholestatic jaundice in children with sickle cell disease: hepatic crises or hepatitis? |journal=Pediatr. Infect. Dis. J. |volume=7 |issue=10 |pages=689–92 |date=October 1988 |pmid=3186339 |doi= |url=}}</ref>
*** Hepatotoxic factors, such as [[tryptophan]] degradation metabolites and [[Aluminium|aluminum]] contaminants
*** [[Hemolysis]]  
*** [[Small bowel bacterial overgrowth syndrome|Bacterial overgrowth in the small intestine]]
*** Mild [[hepatic dysfunction]]  
* [[Sickle cell disease]]<ref name="pmid3186339">{{cite journal |vauthors=Mallouh AA, Asha MI |title=Acute cholestatic jaundice in children with sickle cell disease: hepatic crises or hepatitis? |journal=Pediatr. Infect. Dis. J. |volume=7 |issue=10 |pages=689–92 |date=October 1988 |pmid=3186339 |doi= |url=}}</ref>
*** Both [[Unconjugated bilirubin|unconjugated]] and [[conjugated bilirubin]] accumulate in the [[plasma]]
** [[Hemolysis]]  
** [[Intrahepatic cholestasis of pregnancy]]<ref name="pmid19418576">{{cite journal| author=Geenes V, Williamson C| title=Intrahepatic cholestasis of pregnancy. | journal=World J Gastroenterol | year= 2009 | volume= 15 | issue= 17 | pages= 2049-66 | pmid=19418576 | doi= | pmc=2678574 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19418576  }}</ref>
** Mild [[hepatic dysfunction]]  
*** Usually in the third trimester but sometimes earlier  
** Both [[Unconjugated bilirubin|unconjugated]] and [[conjugated bilirubin]] accumulate in the [[plasma]]
*** Heralds [[cholestasis]] and then frank jaundice  
* [[Intrahepatic cholestasis of pregnancy]]<ref name="pmid19418576">{{cite journal| author=Geenes V, Williamson C| title=Intrahepatic cholestasis of pregnancy. | journal=World J Gastroenterol | year= 2009 | volume= 15 | issue= 17 | pages= 2049-66 | pmid=19418576 | doi= | pmc=2678574 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19418576  }}</ref>
*** May be associated with increased [[stillbirths]] and [[prematurity]]  
** Usually in the third trimester but sometimes earlier  
*** All the pathologic changes would disappear after [[delivery]]
** Heralds [[cholestasis]] and then frank jaundice  
* [[Hepatocellular Disease|Hepatocellular injury]]<ref name="pmid21532726">{{cite journal| author=Gowda S, Desai PB, Hull VV, Math AA, Vernekar SN, Kulkarni SS| title=A review on laboratory liver function tests. | journal=Pan Afr Med J | year= 2009 | volume= 3 | issue=  | pages= 17 | pmid=21532726 | doi= | pmc=2984286 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21532726  }}</ref>
** May be associated with increased [[stillbirths]] and [[prematurity]]  
** Different presentations simulate [[Cholestatic liver diseases|cholestatic syndromes]]  
** All the pathologic changes would disappear after [[delivery]]
** Intracellular [[proteins]] and small molecules are released into the [[plasma]]
 
** Increased [[transaminases]], such as [[Aspartate aminotransferase|aspartate aminotransferase (AST)]] and [[Alanine aminotransferase|alanine aminotransferase (ALT)]]
==== [[Hepatocellular Disease|Hepatocellular injury]]<ref name="pmid21532726">{{cite journal| author=Gowda S, Desai PB, Hull VV, Math AA, Vernekar SN, Kulkarni SS| title=A review on laboratory liver function tests. | journal=Pan Afr Med J | year= 2009 | volume= 3 | issue=  | pages= 17 | pmid=21532726 | doi= | pmc=2984286 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21532726  }}</ref> ====
* Different presentations simulate [[Cholestatic liver diseases|cholestatic syndromes]].
* Intracellular [[proteins]] and small molecules are released into the [[plasma]].
* Increased [[transaminases]], such as [[Aspartate aminotransferase|aspartate aminotransferase (AST)]] and [[Alanine aminotransferase|alanine aminotransferase (ALT)]].
<br>
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==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
{{WH}}
{{WS}}


[[Category:Needs content]]
[[Category:Needs content]]
[[Category:Primary care]]
[[Category:Disease]]
[[Category:Disease]]
[[Category:Gastroenterology]]
[[Category:Gastroenterology]]
[[Category:Hepatology]]
[[Category:Hepatology]]
{{WH}}
{{WS}}

Latest revision as of 22:27, 29 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2], Ahmed Elsaiey, MBBCH [3]

Overview

Bilirubin is the catabolic product of the heme which is the main component of the red blood cells. Bilirubin is formed in the liver and spleen then it passes through several process in order to be metabolized. Metabolism processes include hepatic uptake, conjugation, clearance and excretion of the bilirubin in the bile. Jaundice develops due to increase the level of bilirubin and deposition under the skin and cause the yellow discoloration of the skin. Pathogenesis of neonatal jaundice includes physiologic process of bilirubin accumulation or pathological mechanism. The pathological jaundice may be acquired or inherited. Acquired neonatal jaundice include Rh hemolytic disease, ABO incompatibility disease, and hemolytic disease due to G6PD enzyme deficiency. Inherited neonatal jaundice is due to defect of one of the processes of bilirubin metabolism and it concludes some inherited syndromes. Inherited neonatal jaundice include Gilbert's syndrome, Crigler-Najjar syndrome type I and II, Lucey-Driscoll syndrome, Dubin-Johnson syndrome, and Rotor syndrome.

Pathophysiology

 Bilirubin formation and metabolism

For more information about viral hepatitis pathophysiology click here

For more information about cirrhosis pathophysiology click here

For more information about neonatal jaundice pathophysiology click here

Pathogenesis of Adult jaundice

Unconjugated hyperbilirubinemia

The primary pathophysiology of unconjugated hyperbilirubinemia include:[10]

Conjugated hyperbilirubinemia

Biliary tract obstruction[11]

Liver infrastructure damage

Hepatocellular injury[19]


 
Sepsis
 
Paraneoplastic syndrome
 
Infiltrative hepatic diseases
 
Total parenteral nutrition
 
Sickle cell disease
 
Pregnancy
 
Extravascular hemolysis
 
Intravascular hemolysis
 
Extravasation
 
Dyserythropoiesis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Cholelithiasis
Tumor
Primary biliary cholangitis
Parasites
Pancreatitis
Stricture
 
Choledochal cyst
Cholelithiasis
Tumor
 
Biliary atresia
Choledochal cyst
 
 
 
 
• Decreased hepatic blood flow
• Decreased delivery of bilirubin
 
• Capillarization of the sinusoidal endothelial cells (loss of fenestrae)
 
• Impaired bilirubin uptake at the sinusoidal surface of hepatocytes
 
Rifamycin antibiotics
Probenecid
• Flavaspidic acid
• Bunamiodyl (a cholecystographic agent)
 
 
Type I and II Crigler Najjar syndrome
 
Hyperthyroidism
Ethinyl estradiol
 
Novobiocin
Gentamicin
 
Chronic persistent hepatitis
• Advanced cirrhosis
Wilson's disease
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Adult
 
Children
 
Neonates and infants
 
 
 
 
Heart failure
Portosystemic shunt
 
Cirrhosis
 
Gilbert's Syndrome
 
Drug-induced defect
 
 
↓ or NoUGT activity
 
 
 
 
 
Inhibit UGT
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hepatocellular Disease
 
Biliary obstruction
 
 
 
 
Intrahepatic cholestasis
 
 
 
 
 
 
Reduced bilirubin uptake
 
 
 
 
 
Overproduction of bilirubin
 
 
 
 
 
Impaired bilirubin conjugation
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Conjugated hyperbilirubinemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Unconjugated hyperbilirubinemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Jaundice
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

References

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