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{{DiseaseDisorder infobox |
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Name = Jaundice, NOS |
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Image =Jaundice_eye.jpg|
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Caption = Yellowing of the [[skin]] and [[sclera]] (actually, the [[conjunctiva]] overlying the sclera) caused by [[Hepatitis|Hepatitis A]].|
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ICD10 = {{ICD10|R|17||r|10}} |
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ICD9 = {{ICD9|782.4}} |
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OMIM = |
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MedlinePlus = 003243 |
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eMedicineSubj = |
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eMedicineTopic = |
  +
DiseasesDB = 7038 |
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MeshID = D007565 |
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}}
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'''Jaundice''', also known as '''icterus''' (attributive adjective: "icteric"), is a yellowish discoloration of the [[skin]], the [[conjunctiva]]l membranes over the [[sclera|sclerae]] (whites of the eyes), and other [[mucous membrane]]s caused by hyperbilirubinemia (increased levels of [[bilirubin]] in the blood). This hyperbilirubinemia subsequently causes increased levels of [[bilirubin]] in the extracellular fluids. Typically, the concentration of bilirubin in the [[Blood plasma|plasma]] must exceed 1.5 [[milligram|mg]]/[[decilitre|dL]]<ref name="MedPhy">{{cite book
  +
| last = Guyton
  +
| first = Arthur
  +
| coauthors = Hall, John
  +
| title = Textbook of Medical Physiology
  +
| publisher = Saunders
  +
| date = September 2005
  +
| isbn = 978-0721602400}}</ref>, three times the usual value of approximately 0.5[[milligram|mg]]/[[decilitre|dL]]<ref name="MedPhy" />, for the coloration to be easily visible. ''Jaundice'' comes from the [[French language|French]] word ''jaune'', meaning yellow.
  +
  +
One of the first tissues to change color as [[bilirubin]] levels rise in jaundice is the [[conjunctiva]] of the eye, a condition sometimes referred to as [[scleral icterus]]. However, the [[sclera]] themselves are not "icteric" (stained with bile pigment) but rather the conjunctival membranes that overlie them. The yellowing of the "white of the eye" is thus more properly [[conjunctival icterus]].<ref>http://findarticles.com/p/articles/mi_m3225/is_1_71/ai_n8702953 accessed Nov. 22, 2008</ref> See photographic illustration at right.
  +
  +
==Normal physiology==
  +
[[Image:Jaundice2008.jpg|right|thumb|200px|Jaundice in a man with hepatic failure ]]
  +
In order to understand how jaundice results, the pathological processes that cause jaundice to take their effect must be understood. Jaundice itself is not a disease, but rather a sign of one of many possible underlying pathological processes that occurs at some point along the normal physiological pathway of the metabolism of bilirubin.
  +
  +
===Pre-hepatic events===
  +
When red blood cells have completed their life span of approximately 120 days, or when they are damaged, their membranes become fragile and prone to rupture. As each red blood cell traverses through the [[reticuloendothelial system]], its cell membrane ruptures when its membrane is fragile enough to allow this. Cellular contents, including [[hemoglobin]], are subsequently released into the blood. The hemoglobin is phagocytosed by [[macrophages]], and split into its [[heme]] and [[globin]] portions. The globin portion, being [[protein]], is degraded into [[amino acids]] and plays no further role in jaundice. Two reactions then take place with the heme molecule. The first [[oxidation]] reaction is catalyzed by the microsomal enzyme heme oxygenase and results in biliverdin (green color pigment), iron and carbon monoxide. The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment called [[bilirubin]] by cytosolic enzyme biliverdin reductase. This bilirubin is "unconjugated", "free" or "indirect" bilirubin. Approximately 4 mg per kg of bilirubin is produced each day.<ref name="PedRev">{{cite journal
  +
| last = Pashankar
  +
| first = D
  +
| coauthors = Schreiber, RA
  +
| title = Jaundice in older children and adolescents
  +
| journal = Pediatrics in Review
  +
| volume = 22
  +
| issue = 7
  +
| pages = 219–226
  +
| date = July 2001
  +
| doi = 10.1542/pir.22-7-219
  +
| pmid = 11435623}}</ref> The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. However approximately 20 per cent comes from other heme sources, including ineffective [[erythropoiesis]], breakdown of other heme-containing proteins, such as muscle [[myoglobin]] and [[cytochrome]]s.<ref name="PedRev" />
  +
  +
===Hepatic events===
  +
The unconjugated bilirubin then travels to the [[liver]] through the bloodstream. Because this bilirubin is not soluble, however, it is transported through the blood bound to [[serum albumin]]. Once it arrives at the liver, it is conjugated with [[glucuronic acid]] (to form bilirubin diglucuronide, or just "conjugated bilirubin") to become more water soluble. The reaction is catalyzed by the enzyme UDP-glucuronide transferase.
  +
  +
This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of [[bile]]. Intestinal bacteria convert the bilirubin into [[urobilinogen]]. From here the urobilinogen can take two pathways. It can either be further converted into [[stercobilinogen]], which is then [[oxidized]] to [[stercobilin]] and passed out in the [[faeces]], or it can be reabsorbed by the intestinal cells, transported in the blood to the [[kidneys]], and passed out in the [[urine]] as the oxidised product [[urobilin]]. Stercobilin and urobilin are the products responsible for the coloration of faeces and urine, respectively.
  +
  +
==Causes==
  +
When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result. Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:
  +
* '''Pre-hepatic''': The pathology is occurring prior the liver
  +
* '''Hepatic''': The pathology is located within the liver
  +
* '''Post-Hepatic''': The pathology is located after the conjugation of bilirubin in the liver
  +
  +
===Pre-hepatic===
  +
'''Pre-hepatic''' jaundice is caused by anything which causes an increased rate of [[hemolysis]] (breakdown of [[red blood cell]]s). In tropical countries, [[malaria]] can cause jaundice in this manner. Certain [[Genetic disorder|genetic diseases]], such as [[sickle cell anemia]], [[spherocytosis]] and [[glucose 6-phosphate dehydrogenase deficiency]] can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such as [[hemolytic uremic syndrome]], can also lead to coloration. Defects in [[bilirubin metabolism]] also present as jaundice. Jaundice usually comes with high fevers. Rat fever (leptospirosis) can also cause jaundice.
  +
  +
'''Laboratory findings''' include:
  +
* Urine: no bilirubin present, urobilirubin > 2 units (except in infants where [[gut flora]] has not developed).
  +
* Serum: increased unconjugated bilirubin.
  +
  +
===Hepatic===
  +
'''Hepatic''' jaundice causes include acute [[hepatitis]], [[hepatotoxicity]] and [[alcoholic liver disease]], whereby cell necrosis reduces the liver's ability to metabolise and excrete [[bilirubin]] leading to a buildup in the blood. Less common causes include [[primary biliary cirrhosis]], [[Gilbert's syndrome]] (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population), [[Crigler-Najjar syndrome]], [[metastasis|metastatic]] [[carcinoma]] and [[Niemann-Pick disease, type C]]. Jaundice seen in the newborn, known as neonatal jaundice, is common, occurring in almost every newborn as [[hepatic]] machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age.
  +
  +
'''Laboratory Findings''' include:
  +
* Urine: Conjugated bilirubin present, Urobilirubin > 2 units but variable (Except in children)
  +
  +
===Post-hepatic===
  +
'''Post-hepatic''' jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of [[bile]] in the biliary system. The most common causes are [[gallstone]]s in the [[common bile duct]], and [[pancreatic cancer]] in the head of the [[pancreas]]. Also, a group of parasites known as "[[liver fluke]]s" live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, [[biliary atresia]], [[ductal carcinoma]], [[pancreatitis]] and [[pancreatic pseudocyst]]s. A rare cause of obstructive jaundice is [[Mirizzi's syndrome]].
  +
  +
The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from [[bile pigment]]s.
  +
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Patients also can present with elevated serum cholesterol, and often complain of severe itching or "pruritus".
  +
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===Laboratory tests===
  +
No one test can differentiate between various classifications of jaundice. A combinations of liver function tests is essential to arrive at a diagnosis.
  +
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{| class="wikitable"
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|-
  +
!
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! Pre-hepatic Jaundice
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! Hepatic Jaundice
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! Post-hepatic Jaundice
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|-
  +
! Total bilirubin
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| Normal / Increased
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| Increased
  +
| Increased
  +
|-
  +
! Conjugated bilirubin
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| Normal
  +
| Normal / Decreased
  +
| Increased
  +
|-
  +
! Unconjugated bilirubin
  +
| Increased
  +
| Normal / Increased
  +
| Normal
  +
|-
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! Urobilinogen
  +
| Increased
  +
| Normal / Increased
  +
| Decreased / Negative
  +
|-
  +
! Urine Color
  +
| Normal
  +
| Dark
  +
| Dark
  +
|-
  +
! Stool Color
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| Normal
  +
| Normal
  +
| Pale
  +
|-
  +
! Alkaline phosphatase levels
  +
| normal
  +
| normal
  +
| increased
  +
|-
  +
! Alanine transferase and Aspartate transferase levels
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| normal
  +
| increased
  +
| normal
  +
|}
  +
  +
==Neonatal jaundice==
  +
{{main|Neonatal jaundice}}
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'''Neonatal jaundice''' is usually harmless: this condition is often seen in [[infants]] around the second day after birth, lasting until day 8 in normal births, or to around day 14 in [[premature birth]]s. Serum [[bilirubin]] normally drops to a low level without any intervention required: the jaundice is presumably a consequence of metabolic and physiological adjustments after birth. In extreme cases, a brain-damaging condition known as [[kernicterus]] can occur; there are concerns that this condition has been rising in recent years due to inadequate detection and treatment of neonatal hyperbilirubinemia. Neonatal jaundice is a risk factor for hearing loss.<ref>{{cite journal
  +
| last = O'Keefe
  +
| first = Lori
  +
| title = Increased vigilance needed to prevent kernicterus in newborns
  +
| journal = American Academy of Pediatrics
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| volume = 18
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| issue = 5
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| pages = 231
  +
| publisher =
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| location =
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| date = 2001-05-05
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| url = http://aapnews.aappublications.org/cgi/content/full/18/5/231
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| doi =
  +
| id =
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| accessdate = 2007-06-27}}</ref>
  +
  +
==Jaundiced eye==
  +
It was once believed persons suffering from the medical condition jaundice saw everything as yellow. By extension, the jaundiced eye came to mean a prejudiced view, usually rather negative or critical. [[Alexander Pope]], in 'An Essay on Criticism' (1711), wrote: "All seems infected that the infected spy, As all looks yellow to the jaundiced eye."<ref name=eye>From "The Dictionary of Cliches" by James Rogers (Ballantine Books, New York, 1985).</ref> Similarly in the mid 19th century the English poet Lord [[Alfred Tennyson]] wrote in the poem 'Locksley Hall': "So I triumphe'd ere my passion sweeping thro' me left me dry, left me with the palsied heart, and left me with a jaundiced eye."
  +
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==See also==
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* [[Cirrhosis (liver)]]
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* [[Hepatitis]]
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* [[Infectious disoders]]
  +
  +
==External links==
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*[http://www.childliverdisease.org/education/yellowalert Children's Liver Disease Foundation: information on jaundice in infants]
  +
*[http://www.nnpdf.org/npdisease_01.html National Niemann Pick Disease Foundation: jaundice at birth combined with enlarged spleen and/or enlarged liver can indicate Niemann Pick disease]
  +
{{wiktionary|jaundice}}
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==See also==
  +
*[[Cholestasis]]
  +
*[[Neonatal jaundice]]
  +
  +
==References==
  +
{{reflist|2}}
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  +
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{{Digestive system and abdomen symptoms and signs}}
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[[Category:Diseases and disorders]]
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[[Category:Digestive system disorders]]
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[[Category:Gastroenterology]]
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[[Category:Hepatology]]
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[[category:Liver disordes]]
  +
  +
<!--
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[[ar:يرقان]]
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[[bs:Žutica]]
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[[bg:Жълтеница]]
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[[ca:Icterícia]]
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[[cs:Žloutenka]]
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[[da:Gulsot]]
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[[de:Ikterus]]
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[[es:Ictericia]]
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[[eo:Iktero]]
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[[eu:Ikterizia]]
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[[fr:Ictère]]
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[[hr:Žutica]]
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[[it:Ittero]]
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[[he:צהבת]]
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[[la:Icterus]]
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[[lt:Gelta]]
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[[ml:മഞ്ഞപ്പിത്തം]]
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[[ms:Demam kuning jaundis]]
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[[nl:Geelzucht]]
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[[ja:黄疸]]
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[[no:Gulsott]]
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[[nn:Gulsot]]
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[[pl:Żółtaczka (medycyna)]]
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[[pt:Icterícia]]
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[[ru:Желтуха]]
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[[sco:Gulsoch]]
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[[sq:Verdhëza]]
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[[si:සෙංගමාලය]]
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[[simple:Jaundice]]
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[[sk:Žltačka]]
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[[sl:Zlatenica]]
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[[sh:Žutica]]
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[[fi:Keltaisuus]]
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[[sv:Gulsot]]
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[[te:పచ్చకామెర్లు]]
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[[vi:Hoàng đản]]
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[[tr:Sarılık]]
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[[zh:黄疸]]
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-->
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{{enWP|Jaundice}}

Latest revision as of 01:14, February 6, 2009

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Jaundice_eye.jpg|
Jaundice, NOS
ICD-10 R17
ICD-9 782.4
OMIM [1]
DiseasesDB 7038
MedlinePlus 003243
eMedicine /
MeSH {{{MeshNumber}}}


Jaundice, also known as icterus (attributive adjective: "icteric"), is a yellowish discoloration of the skin, the conjunctival membranes over the sclerae (whites of the eyes), and other mucous membranes caused by hyperbilirubinemia (increased levels of bilirubin in the blood). This hyperbilirubinemia subsequently causes increased levels of bilirubin in the extracellular fluids. Typically, the concentration of bilirubin in the plasma must exceed 1.5 mg/dL[1], three times the usual value of approximately 0.5mg/dL[1], for the coloration to be easily visible. Jaundice comes from the French word jaune, meaning yellow.

One of the first tissues to change color as bilirubin levels rise in jaundice is the conjunctiva of the eye, a condition sometimes referred to as scleral icterus. However, the sclera themselves are not "icteric" (stained with bile pigment) but rather the conjunctival membranes that overlie them. The yellowing of the "white of the eye" is thus more properly conjunctival icterus.[2] See photographic illustration at right.

Normal physiologyEdit

File:Jaundice2008.jpg

In order to understand how jaundice results, the pathological processes that cause jaundice to take their effect must be understood. Jaundice itself is not a disease, but rather a sign of one of many possible underlying pathological processes that occurs at some point along the normal physiological pathway of the metabolism of bilirubin.

Pre-hepatic eventsEdit

When red blood cells have completed their life span of approximately 120 days, or when they are damaged, their membranes become fragile and prone to rupture. As each red blood cell traverses through the reticuloendothelial system, its cell membrane ruptures when its membrane is fragile enough to allow this. Cellular contents, including hemoglobin, are subsequently released into the blood. The hemoglobin is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, being protein, is degraded into amino acids and plays no further role in jaundice. Two reactions then take place with the heme molecule. The first oxidation reaction is catalyzed by the microsomal enzyme heme oxygenase and results in biliverdin (green color pigment), iron and carbon monoxide. The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment called bilirubin by cytosolic enzyme biliverdin reductase. This bilirubin is "unconjugated", "free" or "indirect" bilirubin. Approximately 4 mg per kg of bilirubin is produced each day.[3] The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. However approximately 20 per cent comes from other heme sources, including ineffective erythropoiesis, breakdown of other heme-containing proteins, such as muscle myoglobin and cytochromes.[3]

Hepatic eventsEdit

The unconjugated bilirubin then travels to the liver through the bloodstream. Because this bilirubin is not soluble, however, it is transported through the blood bound to serum albumin. Once it arrives at the liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just "conjugated bilirubin") to become more water soluble. The reaction is catalyzed by the enzyme UDP-glucuronide transferase.

This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen. From here the urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the faeces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin. Stercobilin and urobilin are the products responsible for the coloration of faeces and urine, respectively.

CausesEdit

When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result. Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:

  • Pre-hepatic: The pathology is occurring prior the liver
  • Hepatic: The pathology is located within the liver
  • Post-Hepatic: The pathology is located after the conjugation of bilirubin in the liver

Pre-hepaticEdit

Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells). In tropical countries, malaria can cause jaundice in this manner. Certain genetic diseases, such as sickle cell anemia, spherocytosis and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also present as jaundice. Jaundice usually comes with high fevers. Rat fever (leptospirosis) can also cause jaundice.

Laboratory findings include:

  • Urine: no bilirubin present, urobilirubin > 2 units (except in infants where gut flora has not developed).
  • Serum: increased unconjugated bilirubin.

HepaticEdit

Hepatic jaundice causes include acute hepatitis, hepatotoxicity and alcoholic liver disease, whereby cell necrosis reduces the liver's ability to metabolise and excrete bilirubin leading to a buildup in the blood. Less common causes include primary biliary cirrhosis, Gilbert's syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population), Crigler-Najjar syndrome, metastatic carcinoma and Niemann-Pick disease, type C. Jaundice seen in the newborn, known as neonatal jaundice, is common, occurring in almost every newborn as hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age.

Laboratory Findings include:

  • Urine: Conjugated bilirubin present, Urobilirubin > 2 units but variable (Except in children)

Post-hepaticEdit

Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, ductal carcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.

The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments.

Patients also can present with elevated serum cholesterol, and often complain of severe itching or "pruritus".

Laboratory testsEdit

No one test can differentiate between various classifications of jaundice. A combinations of liver function tests is essential to arrive at a diagnosis.

Pre-hepatic Jaundice Hepatic Jaundice Post-hepatic Jaundice
Total bilirubin Normal / Increased Increased Increased
Conjugated bilirubin Normal Normal / Decreased Increased
Unconjugated bilirubin Increased Normal / Increased Normal
Urobilinogen Increased Normal / Increased Decreased / Negative
Urine Color Normal Dark Dark
Stool Color Normal Normal Pale
Alkaline phosphatase levels normal normal increased
Alanine transferase and Aspartate transferase levels normal increased normal

Neonatal jaundiceEdit

Main article: Neonatal jaundice

Neonatal jaundice is usually harmless: this condition is often seen in infants around the second day after birth, lasting until day 8 in normal births, or to around day 14 in premature births. Serum bilirubin normally drops to a low level without any intervention required: the jaundice is presumably a consequence of metabolic and physiological adjustments after birth. In extreme cases, a brain-damaging condition known as kernicterus can occur; there are concerns that this condition has been rising in recent years due to inadequate detection and treatment of neonatal hyperbilirubinemia. Neonatal jaundice is a risk factor for hearing loss.[4]

Jaundiced eyeEdit

It was once believed persons suffering from the medical condition jaundice saw everything as yellow. By extension, the jaundiced eye came to mean a prejudiced view, usually rather negative or critical. Alexander Pope, in 'An Essay on Criticism' (1711), wrote: "All seems infected that the infected spy, As all looks yellow to the jaundiced eye."[5] Similarly in the mid 19th century the English poet Lord Alfred Tennyson wrote in the poem 'Locksley Hall': "So I triumphe'd ere my passion sweeping thro' me left me dry, left me with the palsied heart, and left me with a jaundiced eye."

See alsoEdit

External linksEdit

Look up this page on
Wiktionary: jaundice

See alsoEdit

ReferencesEdit

  1. 1.0 1.1 Guyton, Arthur; Hall, John (September 2005). Textbook of Medical Physiology, Saunders.
  2. http://findarticles.com/p/articles/mi_m3225/is_1_71/ai_n8702953 accessed Nov. 22, 2008
  3. 3.0 3.1 Pashankar, D, Schreiber, RA (July 2001). Jaundice in older children and adolescents. Pediatrics in Review 22 (7): 219–226.
  4. O'Keefe, Lori (2001-05-05). Increased vigilance needed to prevent kernicterus in newborns. American Academy of Pediatrics 18 (5): 231.
  5. From "The Dictionary of Cliches" by James Rogers (Ballantine Books, New York, 1985).


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