Jaundice , also known as jaundice , is a yellowish and greenish pigmentation of the skin and white of the eyes due to high bilirubin levels. Usually associated with itching. The dirt may be pale and urine dark. Jaundice in infants occurs in more than half in the first week after birth and is mostly not a problem. If the levels of bilirubin in infants are very high for a long time, a type of brain damage, known as kernicterus, may occur.
The cause of jaundice varies from non-serious to potentially fatal. The level of bilirubin in the blood is usually below 1.0 mg/dL (17 Ã,Âμmol/L) and levels above 2-3Ã, mg/dL (34-51 Ã,Âμmol/L) usually produce jaundice. High bilirubin is divided into two types: unconjugated (indirect) and conjugated (direct). Bilirubin conjugation can be confirmed by finding bilirubin in the urine. Other conditions that can cause yellowish skin but not jaundice include carotenemia due to eating large amounts of food and certain drugs such as rifampicin.
High unconjugated bilirubin may be caused by excessive red blood cell damage, large bruises, genetic conditions such as Gilbert's syndrome, no long-term eating, newborn jaundice, or thyroid problems. High conjugated bilirubin may be caused by liver disease such as cirrhosis or hepatitis, infection, medication, or blockage of the bile ducts. In developed countries, the cause is more frequent clogging of bile ducts or temporary drugs in developing countries, more frequent infections such as viral hepatitis, leptospirosis, schistosomiasis, or malaria. Blockage of bile ducts can occur due to gallstones, cancer, or pancreatitis. Medical imaging such as ultrasound is useful for detecting blockage of the bile ducts.
Treatment of jaundice is usually determined by the underlying cause. If there is a blockage of the bile ducts, surgery is usually necessary; if not, management is medical. Medical management may involve treating infectious causes and stopping medications that may contribute. Among newborns, depending on age and prematurity, bilirubin greater than 4-21 mg/dL (68-360 Ã,Âμmol/L) may be treated with phototherapy or transfusion in exchange. Itching can be helped by draining the gallbladder or ursodeoxycholic acid. The word jaundice comes from the French jaunisse , which means "jaundice".
Video Jaundice
Signs and symptoms
The main sign of jaundice is a yellowish discoloration of the white areas of the eyes and skin. The urine is dark. A slight increase in serum bilirubin is best detected by examining sclerae, which has a special affinity for bilirubin because of its high elastin content. The presence of scleral jaundice shows serum bilirubin at least 3 mg/dL. The eye conjunctiva is one of the first tissues to change color when bilirubin levels increase in jaundice. This is sometimes referred to as scleral icterus . Sklera itself is not "jaundiced" (stained with bile pigment), however, but a conjunctival membrane that transcends it. The yellowing of the "white eye" is thus more accurately called the conjunctival jaundice . The term "icterus" itself is sometimes incorrectly used to refer to jaundice recorded in the eye sclera; a more general and more precise meaning is entirely synonymous with jaundice, however.
Complications
Hyperbilirubinemia, more precisely hyperbilirubinemia due to unconjugated fraction, can cause bilirubin to accumulate in the central gray matter of the central nervous system, potentially causing irreversible neurological damage leading to a condition known as kernicterus. Depending on the level of exposure, the effect varies from clinical not seen to severe brain damage and even death. Newborns are particularly susceptible to hyperbilirubinemia-induced neurological damage and should therefore be carefully monitored for changes in their serum bilirubin levels.
Maps Jaundice
Differential diagnosis
When pathological processes interfere with the normal functioning of the metabolism and excretion of bilirubin just described, the possibility of jaundice is the result. Jaundice is classified into three categories, depending on which physiological pathology is affected by pathology. The three categories are:
Pre-care
Pre-hepaticular jaundice is caused by anything that causes an increase in the rate of haemolysis (breakdown of red blood cells). Unconjugated bilirubin is derived from the breakdown of the heme pigment found in red blood cell hemoglobin. Increased red blood cell damage leads to an increase in the number of unconjugated bilirubin present in the blood and deposition of unconjugated bilirubin to various tissues can lead to the appearance of jaundice. In tropical countries, severe malaria can cause jaundice in this way. Certain genetic diseases, such as sickle cell anemia, spherocytosis, thalassemia, pyruvate kinase deficiency, and 6-phosphate dehydrogenase glucose deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Generally, kidney disease, such as haemolytic uremic syndrome, can also cause staining.
In jaundice secondary to haemolysis, increased production of bilirubin causes increased urobilinogen production of urine. Bilirubin is not usually found in the urine because unconjugated bilirubin is insoluble in water, so, a combination of urinary urobilogen elevation without bilirubin (because, unconjugated) in urine is a suggestion of hemolytic jaundice.
Laboratory findings include:
- Urine: no bilirubin, urobilinogen & gt; 2 units (ie, hemolytic anemia causes an increase in heme metabolism: exceptions: infants in which the intestinal flora has not developed).
- Serum: increases unconjugated bilirubin.
- Kernicterus is associated with an increase in unconjugated bilirubin not carried by albumin. Newborns are particularly vulnerable to this because of the increased permeability of the brain's blood barrier.
Hepatocellular
Laboratory findings depend on the cause of jaundice.
- Urine: conjugate bilirubin, urobilirubin & gt; 2 units but variables (except in children). Kernicterus is a condition not associated with an increase in conjugated bilirubin.
- Plasma proteins show characteristic changes.
- The plasma albumin level is low but plasma globulin is increased due to increased antibody formation.
Transport of bilirubin across the hepatocytes can be impaired at any point between the unconjugated bilirubin taking into cells and conjugated bilirubin transport to the biliary canalule. In addition, cell swelling and edema due to inflammation lead to intrahepatic bile mechanical obstruction. Therefore in hepatocellular jaundice, the concentration of unconjugated and conjugated bilirubin increases in the blood. In hepatocellular disease, there is usually a disruption to all major steps of bilirubin metabolism - taking, conjugation and excretion. Excretion is a step that limits the rate, however, and is usually distracted for the most part. Consequently, conjugated hyperbilirubinemia predominates.
Unconjugated bilirubin still enters the liver cells and becomes conjugated in the normal way. This conjugated bilirubin is then returned to the blood, possibly due to the rupture of the dense bile canaliculi and instantly emptying the bile into the lymph that leaves the liver. Thus, most of the bilirubin in plasma becomes a conjugate type rather than an unconjugated type, and this conjugated bilirubin, which does not enter the intestine into urobilinogen, gives the urine a dark color.
Post-heart
Post-liver jaundice, also called obstructive jaundice, is caused by disorders of bile drainage containing conjugated bilirubin in the biliary system. The most common causes are gallstones in the bile ducts, and pancreatic cancer in the pancreas head. Also, a group of parasites known as "heartworms" can live in the bile ducts, causing obstructive jaundice. Other causes include biliary bile duct stricture, biliary atresia, cholangiocarcinoma, pancreatitis, chest colestasis, and pancreatic pseudocyst. The rare cause of obstructive jaundice is Mirizzi syndrome (gallstone impaction in the cystic duct or gallbladder neck, with enlarged gallbladder squeezing in the common hepatic ducts).
In the complete obstruction of the bile ducts, no urobilinogen is found in the urine, because bilirubin has no access to the intestine and in the intestine bilirubin will be converted to urobilinogen by microorganisms, with urobilinogen which is then reabsorbed from the gut into the general circulation, and then excreted into urine. In this case, the presence of bilirubin (conjugated) in urine without urobilinogen suggests obstructive jaundice, either intra-hepatic or post-liver.
The presence of pale stools and dark urine suggests an obstructive or post-liver cause as normal impurities get their color from the bile pigment. They can, however, occur in many intra-liver diseases and therefore are not a reliable clinical feature to distinguish obstruction from the cause of jaundice in the liver.
Patients may also present with elevated serum cholesterol, and often complain of severe itching or "pruritus" due to the direct and indirect effects of pruritogens in bile such as bile salts.
There is no single test that can differentiate between various classifications of jaundice. The combination of liver function tests is very important to achieve the diagnosis.
Neonatal jaundice
Neonatal jaundice is usually harmless: this condition is often seen in infants around the second day after birth, lasting until day 8 at normal birth, or around day 14 at premature birth. Common causes for neonatal jaundice include normal physiological jaundice, jaundice due to formula supplementation, and haemolytic abnormalities including hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, pyruvate kinase deficiency, ABO/Rh blood autoantibody group, or infantile pyknocytosis. Bilirubin serum usually drops to low levels without any necessary intervention. In the case of elevated higher bilirubin, a brain damaging condition known as kernicterus may occur, leading to significant defects. This condition has increased in recent years due to less time spent outdoors. Bili Light is often a tool used for early treatment, which often consists of exposing the baby to intensive phototherapy. Sunburn is an effective treatment, and has the advantage of ultra-violet-B, which promotes the production of Vitamin D. The count of bilirubin is reduced by defecation and urination, so frequent and effective feeding is essential.
Differential diagnosis
The yellow coloration of the skin, especially on the palms of the hands and soles of the feet, but not on the sclera or in the mouth is due to carotenemia - a harmless condition.
Pathophysiology
Jaundice itself is not a disease, but a sign of one of the many underlying pathological processes that occur at some point along the normal physiological pathway of bilirubin metabolism in the blood.
When red blood cells have completed their life span of about 120 days, or when they are damaged, their membranes become fragile and susceptible to rupture. When each red blood cell passes through the reticuloendothelial system, its cell membrane ruptures when its membrane is fragile enough to allow it. Cell contents, including hemoglobin, are released into the blood. Hemoglobin is phagocytosed by macrophages, and is divided into parts of heme and globin. The globin part, protein, is degraded to amino acids and does not play a role in jaundice. Two reactions then occur with the heme molecule. The first oxidation reaction is catalyzed by the microsomal enzyme heme oxygenase and produces biliverdin (green pigment), iron and carbon monoxide. The next step is reducing biliverdin to a yellow tetrapyrol pigment called bilirubin by the cytosolic enzyme biliverdin reductase. These bilirubin are "unconjugated", "free" or "indirect" bilirubin. About 4 mg of bilirubin per kg of blood is produced daily. The majority of these bilirubin come from the breakdown of heme from expired red blood cells in the process just described. About twenty percent come from other heme sources, however, including ineffective erythropoiesis, and the breakdown of other heme-containing proteins, such as muscle myoglobin and cytochrome.
Hepatic events
Unconjugated bilirubin then moves to the liver through the bloodstream. Because this bilirubin is insoluble, however, it is transported through the blood attached to the albumin serum. Upon arriving at the liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or simply "conjugated bilirubin") to become more soluble in water. The reaction is catalyzed by UDP-glucuronyl transferase enzyme.
This conjugated bilirubin is excreted from the liver into the bile ducts and cysts as part of the bile. Intestinal bacteria convert bilirubin into urobilinogen. From here urobilinogen can take two paths. It can be converted further into stercobilinogen, which is then oxidized to stercobilin and fainting in the stool, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and out in the urine as oxidized products. urobilin. Stercobilin and urobilin are the products responsible for stool and urine staining, respectively.
Epidemiology
It is unclear how common it is among adults.
Diagnostic approach
Most patients with jaundice will have a variety of predictable patterns of liver panel abnormalities, although there are significant variations. Typical liver panels will include blood enzyme levels found primarily from the liver, such as aminotransferase (ALT, AST), and alkaline phosphatase (ALP); bilirubin (which causes jaundice); and protein levels, in particular, total protein and albumin. Other major laboratory tests for liver function include gamma glutamyl transpeptidase (GGT) and prothrombin time (PT).
Some bone and heart disorders can cause increased ALP and aminotransferase, so the first step in distinguishing this from liver problems is to compare GGT levels, which will only increase in special liver conditions. The second step is to distinguish from biliary (cholestatic) or liver (heart) causes of jaundice and laboratory results are changed. The first usually shows a surgical response, while the latter usually tends toward a medical response. ALP and GGT levels will usually increase with one pattern while aspartate aminotransferase (AST) and alanine aminotransferase (ALT) increase in a separate pattern. If levels of ALP (10-45 IU/L) and GGT (18-85) increase proportionally as high as AST levels (12-38 IU/L) and ALT (10-45 IU/L), this indicates a cholestasis problem. On the other hand, if AST and ALT increase significantly higher than ALP and GGT increase, this indicates liver problems. Finally, distinguishing between the causes of jaundice, comparing AST and ALT levels can prove useful. AST level will usually be higher than ALT. This remains the case in most liver disorders except for hepatitis (viral or hepatotoxic). Alcoholic liver damage can see a fairly normal ALT level, with AST 10x higher than ALT. On the other hand, if ALT is higher than AST, it indicates hepatitis. ALT and AST levels do not correlate well with liver damage levels, although a rapid decline in these levels from very high levels may indicate severe necrosis. Low albumin levels tend to show chronic conditions, while normal in hepatitis and cholestasis.
Lab results for the liver panel are often compared to their magnitude of difference, not the pure amount, as well as by their ratio. AST: ALT ratio can be a good indicator of whether the disorder is alcoholic liver damage (above 10), some other forms of liver damage (above 1), or hepatitis (less than 1). A bilirubin level of more than 10 times normal may indicate neoplastic or intrahepatic cholestasis. Lower levels of this tend to indicate a hepatocellular cause. AST levels over 15x tend to show acute hepatocellular damage. Less of this tends to indicate an obstructive cause. ALP levels greater than 5x normal tend to indicate obstruction, whereas levels greater than 10x can indicate a drug (toxic) caused by cholestatic hepatitis or Cytomegalovirus. Both of these conditions can also have ALT and AST greater than normal 20â € ". GGT levels greater than 10x usually indicate cholestasis. Levels 5-10ÃÆ'â € "tend to indicate viral hepatitis. Levels of less than 5ÃÆ'â € "normal tend to indicate drug toxicity. Acute hepatitis typically has ALT and AST levels rising from 20 to 30â € "normal (above 1000), and may continue to increase significantly over several weeks. The toxicity of acetaminophen can produce ALT and AST levels over 50 × normal.
Etymology
Jaundice comes from the French jaune , which means yellow. The medical term for jaundice is jaundice. Icterus comes from the Greek word ??????? ; form of adjective, jaundice.
References
External links
- Definition of dictionaries from ikterus in Wiktionary
- Media related to Jaundice in Wikimedia Commons
Source of the article : Wikipedia
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