Jaundice pathophysiology

Jump to: navigation, search

Jaundice Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Jaundice from other Conditions

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Chest X Ray

Electrocardiogram

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Jaundice pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Jaundice pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Jaundice pathophysiology

CDC on Jaundice pathophysiology

Jaundice pathophysiology in the news

Blogs on Jaundice pathophysiology

Directions to Hospitals Treating Jaundice

Risk calculators and risk factors for Jaundice pathophysiology

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

  1. Berk PD, Howe RB, Bloomer JR, Berlin NI (1969). "Studies of bilirubin kinetics in normal adults.". J Clin Invest. 48 (11): 2176–90. PMC 297471Freely accessible. PMID 5824077. doi:10.1172/JCI106184. 
  2. LONDON IM, WEST R, SHEMIN D, RITTENBERG D (1950). "On the origin of bile pigment in normal man.". J Biol Chem. 184 (1): 351–8. PMID 15422003. 
  3. Knobloch E, Hodr R, Herzmann J, Houdková V (1986). "Kinetics of the formation of biliverdin during the photochemical oxidation of bilirubin monitored by column liquid chromatography.". J Chromatogr. 375 (2): 245–53. PMID 3700551. 
  4. Bissell DM, Hammaker L, Schmid R (1972). "Liver sinusoidal cells. Identification of a subpopulation for erythrocyte catabolism.". J Cell Biol. 54 (1): 107–19. PMC 2108858Freely accessible. PMID 5038868. 
  5. Paludetto R, Mansi G, Raimondi F, Romano A, Crivaro V, Bussi M; et al. (2002). "Moderate hyperbilirubinemia induces a transient alteration of neonatal behavior.". Pediatrics. 110 (4): e50. PMID 12359823. 
  6. Weiss JS, Gautam A, Lauff JJ, Sundberg MW, Jatlow P, Boyer JL; et al. (1983). "The clinical importance of a protein-bound fraction of serum bilirubin in patients with hyperbilirubinemia.". N Engl J Med. 309 (3): 147–50. PMID 6866015. doi:10.1056/NEJM198307213090305. 
  7. Chowdhury JR, Chowdhury NR, Wu G, Shouval R, Arias IM (1981). "Bilirubin mono- and diglucuronide formation by human liver in vitro: assay by high-pressure liquid chromatography.". Hepatology. 1 (6): 622–7. PMID 6796486. 
  8. Bosma PJ, Seppen J, Goldhoorn B, Bakker C, Oude Elferink RP, Chowdhury JR; et al. (1994). "Bilirubin UDP-glucuronosyltransferase 1 is the only relevant bilirubin glucuronidating isoform in man.". J Biol Chem. 269 (27): 17960–4. PMID 8027054. 
  9. Vítek L, Zelenka J, Zadinová M, Malina J (2005). "The impact of intestinal microflora on serum bilirubin levels.". J Hepatol. 42 (2): 238–43. PMID 15664250. doi:10.1016/j.jhep.2004.10.012. 
  10. Duseja A, Das A, Das R, Dhiman RK, Chawla Y, Bhansali A (2005). "Unconjugated hyperbilirubinemia in nonalcoholic steatohepatitis--is it Gilbert's syndrome?". Trop Gastroenterol. 26 (3): 123–5. PMID 16512459. 
  11. Abdallah AA, Krige JE, Bornman PC (2007). "Biliary tract obstruction in chronic pancreatitis.". HPB (Oxford). 9 (6): 421–8. PMC 2215354Freely accessible. PMID 18345288. doi:10.1080/13651820701774883. 
  12. Beltrán MA (2012). "Mirizzi syndrome: history, current knowledge and proposal of a simplified classification.". World J Gastroenterol. 18 (34): 4639–50. PMC 3442202Freely accessible. PMID 23002333. doi:10.3748/wjg.v18.i34.4639. 
  13. Yusuf TE, Baron TH (April 2004). "AIDS Cholangiopathy". Curr Treat Options Gastroenterol. 7 (2): 111–117. PMID 15010025. 
  14. Schaffner F (1975). "Hepatic drug metabolism and adverse hepatic drug reactions". Vet. Pathol. 12 (2): 145–56. PMID 171822. doi:10.1177/030098587501200206. 
  15. Famularo G, De Simone C, Nicotra GC (July 2003). "Jaundice and the sepsis syndrome: a neglected link". Eur. J. Intern. Med. 14 (4): 269–271. PMID 12919846. 
  16. Moss RL, Das JB, Ansari G, Raffensperger JG (March 1993). "Hepatobiliary dysfunction during total parenteral nutrition is caused by infusate, not the route of administration". J. Pediatr. Surg. 28 (3): 391–6; discussion 396–7. PMID 8468653. 
  17. Mallouh AA, Asha MI (October 1988). "Acute cholestatic jaundice in children with sickle cell disease: hepatic crises or hepatitis?". Pediatr. Infect. Dis. J. 7 (10): 689–92. PMID 3186339. 
  18. Geenes V, Williamson C (2009). "Intrahepatic cholestasis of pregnancy.". World J Gastroenterol. 15 (17): 2049–66. PMC 2678574Freely accessible. PMID 19418576. 
  19. Gowda S, Desai PB, Hull VV, Math AA, Vernekar SN, Kulkarni SS (2009). "A review on laboratory liver function tests.". Pan Afr Med J. 3: 17. PMC 2984286Freely accessible. PMID 21532726. 




Linked-in.jpg