Hyperbilirubinemia
Hyperbilirubinemia, Neonatal
Jaundice, Neonatal
Kernicterus
Gilbert Disease
Phototherapy
Hyperbilirubinemia, Hereditary
Exchange Transfusion, Whole Blood
Jaundice
Glucuronosyltransferase
Crigler-Najjar Syndrome
Jaundice, Chronic Idiopathic
Term Birth
Neonatal Screening
Glucosephosphate Dehydrogenase Deficiency
Organic Anion Transport Polypeptide C
Blood Group Incompatibility
Erythroblastosis, Fetal
Metalloporphyrins
Nomograms
Histocompatibility, Maternal-Fetal
Heme Oxygenase (Decyclizing)
Hearing Loss, Central
Protoporphyrins
Indinavir
ABO Blood-Group System
Hemolysis
Porphyrins
Pyridines
Coombs Test
Liver
Ultraviolet Therapy
Cholestasis
Organic Anion Transporters
Imino Acids
Anemia, Hemolytic
Infant, Premature, Diseases
Plasma Exchange
Technetium Tc 99m Disofenin
Mandatory Reporting
Bile Canaliculi
Glucosephosphate Dehydrogenase
Patient Readmission
Gestational Age
Role of bilirubin overproduction in revealing Gilbert's syndrome: is dyserythropoiesis an important factor? (1/56)
Gilbert's syndrome was diagnosed in 37 patients with unconjugated hyperbilirubinaemia without overt haemolysis or structural liver abnormality, who had a marked reduction in hepatic bilirubin UDP-glucuronosyltransferase activity (B-GTA) (as compared with that of 23 normal subjects). No significant correlation existed in these patients between serum bilirubin level and the values of B-GTA, thus suggesting that factors other than a low B-GTA must influence the degree of hyperbilirubinaemia in Gilbert's syndrome. Studies of 51Cr erythrocyte survival and 59Fe kinetics in 10 unselected patients demonstrated slight haemolysis in eight, whereas mild ineffective erythropoiesis was suggested in all from a low 24-hour incorporation of radioactive iron into circulating red cells. This overproduction of bilirubin resulting from mild haemolysis and perhaps dyserythropoiesis might reflect only an extreme degree of the normal situation. It certainly contributes to the hyperbilirubinaemia of Gilbert's syndrome and may play a major role in the manifestation of this condition. (+info)Involvement of an organic anion transporter (canalicular multispecific organic anion transporter/multidrug resistance-associated protein 2) in gastrointestinal secretion of glutathione conjugates in rats. (2/56)
We investigated the role of cMOAT/MRP2 (canalicular multispecific organic anion transporter/multidrug resistance-associated protein 2) in the intestinal secretion of organic anions by comparing the behavior in Sprague-Dawley (SD) rats and Eisai hyperbilirubinemic rat (EHBR) whose cMOAT/MRP2 is hereditarily defective. After i.v. administration of 1-chloro-2,4-dinitrobenzene (30 micromol/kg), the biliary and intestinal excretion of its glutathione conjugate 2, 4-dinitrophenyl-S-glutathione (DNP-SG), a substrate for cMOAT/MRP2, was significantly reduced in EHBR compared with SD rats. This result also was confirmed by Ussing chamber studies; DNP-SG showed 1.5-fold greater serosal-to-mucosal flux compared with the mucosal-to-serosal flux in SD rats, whereas a similar flux was observed in both directions in EHBR. In addition, metabolic inhibitors reduced the preferential serosal-to-mucosal flux of DNP-SG in SD rats. In everted sac studies, intestinal secretion clearance, defined as the efflux rate of DNP-SG into the mucosal side divided by the area under the curve on the serosal side, was significantly lower in the jejunum of EHBR than that in SD rats. Northern blot analyses demonstrated the highest mRNA level of cMOAT/MRP2 in the jejunum, which is in good agreement with the results of the everted sac studies. These results suggest that cMOAT/MRP2 is involved in the secretion of organic anions in the small intestine. (+info)Stimulation of defective Gunn-rat liver uridine diphosphate glucuronyltransferase activity in vitro by alkyl ketones. (3/56)
Addition of alkyl ketone (10mM) to Gunn-rat liver homogenates increased UDP-glucuronyltransferase activity towards 2-aminophenol by 10--20 fold, up to enhanced values of enzyme activity observed with similarly treated Wistar-rat liver homogenates. Alkyl ketones also activate the defective enzyme purified from Gunn-rat liver. This genetic deficiency of UDP-glucuronyltransferase activity is no longer apparent when assayed in the presence of alkyl ketones. (+info)Liver ultrastructure in Gilbert's syndrome. (4/56)
Electron microscopy of hepatic tissue obtained by percutaneous needle biopsy from nine patients with Gilbert's syndrome has revealed in every case gross hypertrophy of hepatocyte agranular endoplasmic reticulum but no other important abnormality. While this may have relevance to impairment of microsomal enzyme activity controlling bilirubin conjugation within liver cells, the serum bilirubin levels in all nine patients were below that normally associated with demonstrable UDP-glucuronyl transferase deficiency. Gross hypertrophy of agranular endoplasmic reticulum may be, therefore, a constant feature of this form of Gilbert's syndrome and may have some diagnostic value in the investigation of unconjugated hyperbilirubinaemia. (+info)The urinary concentrating defect in the Gunn strain of rat. Role of bilirubin. (5/56)
The role of high serum and tissue levels of unconjegated bilirubin in the pathogenesis of the impaired urinary concentrating ability was investigated in homozygous (jj) Gunn rats with the congenital absence of hepatic glucuronyl transferase. Continuous phototherapy with blue fluorescent lights at a wave length of 460 nm or oral cholestyramine feeding or both reduced serum levels of unconjugated hilirubin to levels consistently below 3.0 mg/100 ml for several weeks in both weanling and adult jj Gunn rats. The renal concentrating defect was already present in weanling jj Gunn rats by 21 days of age. In treated weanling jj animals, maximum concentrating ability and the concentration of urea and nonurea solutes in the papilla and medulla, determined after 24 h of fluid deprivation, were normal when compared to unaffected heterozygous (Jj) littermates. Solute-free water reabsorption which is reduced in jaundiced jj Gunn rats was restored to normal in treated weanling jj rats. The tissue concentration of unconjugated bilirubin was reduced throughout the papilla and inner and outer medulla in the treated jj rats in comparison with untreated jj littermates. The defect in urinary concentrating ability was only partially reversible and sometimes irreversible in adult jj rats, probably because of permanent renal parenchymal damage occurring secondary to massive crystalline deposits in the papilla and medulla. It is concluded that unconjugated bilirubin is directly involved in the pathogenesis of the concentrating defect in jaundiced jj Gunn rats. (+info)Population studies on Gilbert's syndrome. (6/56)
Total serum bilirubin concentration was measured by an Autoanalyzer technique in 197 normal males and 102 normal females. The mean bilirubin concentration was significantly lower in the females than in the males. Total bilirubin concentration in the males showed a bimodal distribution with an antimode at 24 mumol/1 (1.4 mg/100ml). Individuals with bilirubin concentration above this value had unconjugated hyperbilirubinaemia and probable Gilbert's syndrome. Total bilirubin concentration in the females again showed a bimodal distribution with an antimode at 12 mumol/1 (0.7 mg/100ml). It is conceivable that females with bilirubin levels above this also have Gilbert's syndrome. This suggests that the population incidence of Gilbert's syndrome could be as high as 6% and that the sex incidence is approximately equal. (+info)Comparison of treatments for congenital nonobstructive nonhaemolytic hyperbilirubinaemia. (7/56)
A patient with Crigler-Najjar disease has survived with the help of phototherapy to the age of 2 years without neurological damage. Because long periods of phototherapy are a threat to normal development, a search was made for supplementary treatments. Cholestyramine and a high fat diet were effective, and possibly also aspartic acid. Maintenance therapy with cholestyramine allowed the amount of phototherapy given to be reduced. (+info)Effect of dietary composition on the unconjugated hyperbilirubinaemia of Gilbert's syndrome. (8/56)
The influence of dietary composition on the unconjugated hyperbilirubinaemia of Gilbert's syndrome was studied in 29 patients. After a period on a normal diet (10 MJ) an intravenous infusion of 40% glucose (8-4 MJ) together with a 1-6 MJ oral diet for two days resulted in an increment in plasma bilirubin concentration of 127 +/- 18% (mean +/- SEM) above the basal level. Both the administration of intravenous Intralipid 20% and the return to a normal diet caused a prompt reversal of this glucose effect. An increment of 135 +/- 10% in plasma bilirubin concentration was obtained when a standard "fasting" diet (1-6 MJ) was given for two days. When the lipid content of this "fasting" diet was increased from 33% to 85%, the rise in plasma bilirubin was only 49 +/- 19%. A 10 MJ oral diet for three days, which contained most of its energy content as carbohydrate and only 0-6% as lipid, produced a 76 +/- 12% increase in plasma bilirubin concentration. When the lipid content of the diet was increased to 9% of the energy intake no significant change from the basal level was observed. These findings support the hypothesis that the hyperbilirubinaemia associated with both carbohydrate feeding and fasting is attributable, at least in part, to lipid withdrawal. Although a restricted dietary intake or the parenteral administration of lipid-free solutions has a marked effect on the hyperbilirubinaemia of patients with Gilbert's syndrome, normal daily variation in dietary composition is unlikely to cause a significant change. The influence of different feeding regimes on neonatal hyperbilirubinaemia requires investigation. (+info)Hyperbilirubinemia is a medical condition characterized by an excessively high level of bilirubin in the bloodstream. Bilirubin is a yellowish pigment produced by the liver when it breaks down old red blood cells. Normally, bilirubin is conjugated (made water-soluble) in the liver and then excreted through the bile into the digestive system. However, if there is a problem with the liver's ability to process or excrete bilirubin, it can build up in the blood, leading to hyperbilirubinemia.
Hyperbilirubinemia can be classified as either unconjugated or conjugated, depending on whether the bilirubin is in its direct (conjugated) or indirect (unconjugated) form. Unconjugated hyperbilirubinemia can occur due to increased production of bilirubin (such as in hemolytic anemia), decreased uptake of bilirubin by the liver, or impaired conjugation of bilirubin in the liver. Conjugated hyperbilirubinemia, on the other hand, is usually caused by a problem with the excretion of conjugated bilirubin into the bile, such as in cholestatic liver diseases like hepatitis or cirrhosis.
Symptoms of hyperbilirubinemia can include jaundice (yellowing of the skin and eyes), dark urine, light-colored stools, itching, and fatigue. Treatment depends on the underlying cause of the condition and may involve medications, dietary changes, or surgery.
Neonatal hyperbilirubinemia is a condition characterized by an excessively high level of bilirubin in the blood of newborn infants. Bilirubin is a yellowish pigment produced by the normal breakdown of red blood cells. Normally, bilirubin is processed by the liver and excreted through the bile into the digestive system. However, in neonatal hyperbilirubinemia, the liver may be unable to process bilirubin quickly enough, leading to its accumulation in the bloodstream. This can cause the skin and eyes of the newborn to appear yellow, a condition known as jaundice.
Neonatal hyperbilirubinemia is relatively common and usually resolves on its own within a few days or weeks. However, if bilirubin levels become too high, they can cause brain damage (kernicterus) in severe cases. Treatment may include phototherapy to help break down bilirubin, exchange transfusions, or other interventions to support liver function and reduce bilirubin levels.
Bilirubin is a yellowish pigment that is produced by the liver when it breaks down old red blood cells. It is a normal byproduct of hemoglobin metabolism and is usually conjugated (made water-soluble) in the liver before being excreted through the bile into the digestive system. Elevated levels of bilirubin can cause jaundice, a yellowing of the skin and eyes. Increased bilirubin levels may indicate liver disease or other medical conditions such as gallstones or hemolysis. It is also measured to assess liver function and to help diagnose various liver disorders.
Neonatal jaundice is a medical condition characterized by the yellowing of a newborn baby's skin and eyes due to an excess of bilirubin in the blood. Bilirubin is a yellowish substance produced by the normal breakdown of red blood cells, which are then processed by the liver and excreted through the bile. In neonatal jaundice, the liver is not yet fully developed and cannot process bilirubin quickly enough, leading to its accumulation in the body.
Neonatal jaundice typically appears within the first 2-4 days of life and can range from mild to severe. Mild cases may resolve on their own without treatment, while more severe cases may require medical intervention such as phototherapy or a blood transfusion. Risk factors for neonatal jaundice include prematurity, bruising during birth, blood type incompatibility between mother and baby, and certain genetic disorders.
It is important to monitor newborns closely for signs of jaundice and seek medical attention if concerned, as untreated neonatal jaundice can lead to serious complications such as brain damage or hearing loss.
Kernicterus is a severe form of brain damage caused by high levels of bilirubin, a yellow pigment that forms when red blood cells break down. It's most commonly seen in newborns, particularly those with a condition called ABO or Rh incompatibility, where the baby's blood type is different from the mother's. This can lead to an increased breakdown of the baby's red blood cells and a buildup of bilirubin.
In kernicterus, the bilirubin reaches such high levels that it becomes toxic and can damage the brain, particularly areas like the basal ganglia and brainstem. This can result in symptoms such as severe jaundice (a yellowing of the skin and eyes), lethargy, high-pitched crying, poor feeding, and eventually seizures, hearing loss, and developmental delays.
Kernicterus is preventable with timely treatment, which may include phototherapy (using light to break down bilirubin) or exchange transfusion (replacing the baby's blood with fresh donor blood). If you suspect your newborn has jaundice or if their skin appears yellow, it's important to seek medical attention immediately.
Gilbert's disease, also known as Gilbert's syndrome, is a common and mild condition characterized by **intermittent** elevations in bilirubin levels in the bloodstream without any evidence of liver damage or disease. Bilirubin is a yellowish pigment that forms when hemoglobin breaks down. Normally, it gets processed in the liver and excreted through bile.
In Gilbert's disease, there is an impaired ability to conjugate bilirubin due to a deficiency or dysfunction of the enzyme UDP-glucuronosyltransferase 1A1 (UGT1A1), which is responsible for the glucuronidation process. This results in mild unconjugated hyperbilirubinemia, where bilirubin levels may rise and cause mild jaundice, particularly during times of fasting, illness, stress, or dehydration.
Gilbert's disease is typically an incidental finding, as it usually does not cause any significant symptoms or complications. It is often discovered during routine blood tests when bilirubin levels are found to be slightly elevated. The condition is usually harmless and does not require specific treatment, but avoiding triggers like fasting or dehydration may help minimize the occurrence of jaundice.
Phototherapy is a medical treatment that involves the use of light to manage or improve certain conditions. It can be delivered in various forms, such as natural light exposure or artificial light sources, including lasers, light-emitting diodes (LEDs), or fluorescent lamps. The wavelength and intensity of light are carefully controlled to achieve specific therapeutic effects.
Phototherapy is most commonly used for newborns with jaundice to help break down bilirubin in the skin, reducing its levels in the bloodstream. This type of phototherapy is called bilirubin lights or bili lights.
In dermatology, phototherapy can be applied to treat various skin conditions like psoriasis, eczema, vitiligo, and acne. Narrowband ultraviolet B (UVB) therapy, PUVA (psoralen plus UVA), and blue or red light therapies are some examples of dermatological phototherapies.
Phototherapy can also be used to alleviate symptoms of seasonal affective disorder (SAD) and other mood disorders by exposing patients to bright artificial light, which helps regulate their circadian rhythms and improve their mood. This form of phototherapy is called light therapy or bright light therapy.
It's essential to consult a healthcare professional before starting any phototherapy treatment, as inappropriate use can lead to adverse effects.
Hyperbilirubinemia is a condition characterized by an excess of bilirubin in the blood. Bilirubin is a yellowish substance produced by the liver when it breaks down old red blood cells. Normally, bilirubin is processed by the liver and excreted through the bile ducts and into the digestive system. However, if there is a problem with the liver or the bile ducts, bilirubin can build up in the blood, causing hyperbilirubinemia.
Hereditary hyperbilirubinemia refers to forms of the condition that are caused by genetic mutations. There are several types of hereditary hyperbilirubinemia, including:
1. Dubin-Johnson syndrome: This is a rare autosomal recessive disorder characterized by chronic conjugated hyperbilirubinemia and a dark brownish-black pigmentation of the liver. It is caused by mutations in the MRP2 gene, which provides instructions for making a protein that helps to remove bilirubin from the liver cells into the bile ducts.
2. Rotor syndrome: This is another rare autosomal recessive disorder characterized by chronic conjugated hyperbilirubinemia. It is caused by mutations in the SLCO1B1 and SLCO1B3 genes, which provide instructions for making proteins that help to transport bilirubin into the liver cells.
3. Crigler-Najjar syndrome: This is a rare autosomal recessive disorder characterized by severe unconjugated hyperbilirubinemia. It is caused by mutations in the UGT1A1 gene, which provides instructions for making an enzyme that helps to conjugate bilirubin in the liver.
4. Gilbert syndrome: This is a common autosomal recessive disorder characterized by mild unconjugated hyperbilirubinemia. It is caused by mutations in the UGT1A1 gene, but to a lesser degree than Crigler-Najjar syndrome.
In general, hereditary hyperbilirubinemias are managed with close monitoring of bilirubin levels and may require treatment with phototherapy or exchange transfusion in severe cases. In some cases, liver transplantation may be necessary.
An exchange transfusion of whole blood is a medical procedure in which a patient's blood is gradually replaced with donor whole blood. This procedure is typically performed in newborns or infants who have severe jaundice caused by excessive levels of bilirubin, a yellowish pigment that forms when hemoglobin from red blood cells breaks down.
During an exchange transfusion, the baby's blood is removed through a vein or artery and replaced with donor whole blood through another vein or artery. The process is repeated several times until a significant portion of the baby's blood has been exchanged with donor blood. This helps to reduce the levels of bilirubin in the baby's blood, which can help prevent or treat brain damage caused by excessive bilirubin.
Exchange transfusions are typically performed in a neonatal intensive care unit (NICU) and require close monitoring by a team of healthcare professionals. The procedure carries some risks, including infection, bleeding, and changes in blood pressure or heart rate. However, it can be a lifesaving treatment for newborns with severe jaundice who are at risk of developing serious complications.
I'm sorry for any confusion, but "Rats, Gunn" is not a recognized medical term or phrase. It appears to be a nonsensical expression without specific meaning in the context of medicine or healthcare. If you have any questions about medical terminology or concepts, I would be happy to try and help answer those for you!
Jaundice is a medical condition characterized by the yellowing of the skin, sclera (whites of the eyes), and mucous membranes due to an excess of bilirubin in the bloodstream. Bilirubin is a yellow-orange pigment produced when hemoglobin from red blood cells is broken down. Normally, bilirubin is processed by the liver and excreted through bile into the digestive system. However, if there's an issue with bilirubin metabolism or elimination, it can accumulate in the body, leading to jaundice.
Jaundice can be a symptom of various underlying conditions, such as liver diseases (hepatitis, cirrhosis), gallbladder issues (gallstones, tumors), or blood disorders (hemolysis). It is essential to consult a healthcare professional if jaundice is observed, as it may indicate a severe health problem requiring prompt medical attention.
Glucuronosyltransferase (UDP-glucuronosyltransferase) is an enzyme belonging to the family of glycosyltransferases. It plays a crucial role in the process of biotransformation and detoxification of various endogenous and exogenous substances, including drugs, hormones, and environmental toxins, in the liver and other organs.
The enzyme functions by transferring a glucuronic acid moiety from a donor molecule, uridine diphosphate glucuronic acid (UDP-GlcUA), to an acceptor molecule, which can be a variety of hydrophobic compounds. This reaction results in the formation of a more water-soluble glucuronide conjugate, facilitating the excretion of the substrate through urine or bile.
There are multiple isoforms of glucuronosyltransferase, classified into two main families: UGT1 and UGT2. These isoforms exhibit different substrate specificities and tissue distributions, allowing for a wide range of compounds to be metabolized through the glucuronidation pathway.
In summary, Glucuronosyltransferase is an essential enzyme in the detoxification process, facilitating the elimination of various substances from the body by conjugating them with a glucuronic acid moiety.
Crigler-Najjar Syndrome is a rare inherited genetic disorder that affects the metabolism of bilirubin, a yellow pigment produced when hemoglobin breaks down. This condition is characterized by high levels of unconjugated bilirubin in the blood, which can lead to jaundice, kernicterus, and neurological damage if left untreated.
There are two types of Crigler-Najjar Syndrome: Type I and Type II.
Type I is the more severe form, and it is caused by a mutation in the UGT1A1 gene, which encodes for an enzyme responsible for conjugating bilirubin. People with this type of Crigler-Najjar Syndrome have little to no functional enzyme activity, leading to very high levels of unconjugated bilirubin in the blood. This form is usually diagnosed in infancy and requires regular phototherapy or a liver transplant to prevent neurological damage.
Type II is a milder form of the disorder, caused by a mutation that results in reduced enzyme activity but not complete loss of function. People with this type of Crigler-Najjar Syndrome usually have milder symptoms and may not require regular phototherapy or a liver transplant, although they may still be at risk for neurological damage if their bilirubin levels become too high.
Both types of Crigler-Najjar Syndrome are inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to develop the condition.
Chronic Idiopathic Jaundice is not a widely accepted medical diagnosis and the term "idiopathic" is used to denote that the cause of the jaundice is unknown. However, it is generally used to describe a condition where a person has persistent jaundice without any identifiable underlying cause.
Jaundice itself refers to the yellowing of the skin, sclera (whites of the eyes), and mucous membranes due to an accumulation of bilirubin in the body. Bilirubin is a yellowish substance that is produced when hemoglobin, the protein in red blood cells that carries oxygen, breaks down. Normally, bilirubin is processed by the liver and excreted through the bile ducts into the digestive system.
In Chronic Idiopathic Jaundice, the bilirubin level remains elevated over an extended period of time without any apparent explanation. The condition may be asymptomatic or associated with symptoms such as fatigue, itching, and abdominal discomfort. It is important to note that while "idiopathic" implies an unknown cause, further investigation and monitoring are often necessary to rule out any underlying liver disease or other conditions that may contribute to the jaundice.
A newborn infant is a baby who is within the first 28 days of life. This period is also referred to as the neonatal period. Newborns require specialized care and attention due to their immature bodily systems and increased vulnerability to various health issues. They are closely monitored for signs of well-being, growth, and development during this critical time.
A "term birth" is a medical term that refers to a delivery or pregnancy that has reached 37 weeks or more. It is the normal length of a full-term pregnancy and is considered a healthy and low-risk period for childbirth. Babies born at term have the best chance of being healthy and not experiencing any significant medical issues, compared to those born preterm (before 37 weeks) or postterm (after 42 weeks). The different types of term births are:
* Early Term: Between 37 weeks and 38 weeks, 6 days.
* Full Term: Between 39 weeks and 40 weeks, 6 days.
* Late Term: Between 41 weeks and 41 weeks, 6 days.
* Postterm: 42 weeks or later.
It is important to note that while a term birth is generally considered low-risk, there can still be variations in the health of babies born at different points within this range. For example, research has shown that babies born at 39 weeks have better outcomes than those born at 37 or 38 weeks. Therefore, it is always best to consult with a healthcare provider for individualized guidance and recommendations regarding pregnancy and childbirth.
Neonatal screening is a medical procedure in which specific tests are performed on newborn babies within the first few days of life to detect certain congenital or inherited disorders that are not otherwise clinically apparent at birth. These conditions, if left untreated, can lead to serious health problems, developmental delays, or even death.
The primary goal of neonatal screening is to identify affected infants early so that appropriate treatment and management can be initiated as soon as possible, thereby improving their overall prognosis and quality of life. Commonly screened conditions include phenylketonuria (PKU), congenital hypothyroidism, galactosemia, maple syrup urine disease, sickle cell disease, cystic fibrosis, and hearing loss, among others.
Neonatal screening typically involves collecting a small blood sample from the infant's heel (heel stick) or through a dried blood spot card, which is then analyzed using various biochemical, enzymatic, or genetic tests. In some cases, additional tests such as hearing screenings and pulse oximetry for critical congenital heart disease may also be performed.
It's important to note that neonatal screening is not a diagnostic tool but rather an initial step in identifying infants who may be at risk of certain conditions. Positive screening results should always be confirmed with additional diagnostic tests before any treatment decisions are made.
Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is a genetic disorder that affects the normal functioning of an enzyme called G6PD. This enzyme is found in red blood cells and plays a crucial role in protecting them from damage.
In people with G6PD deficiency, the enzyme's activity is reduced or absent, making their red blood cells more susceptible to damage and destruction, particularly when they are exposed to certain triggers such as certain medications, infections, or foods. This can lead to a condition called hemolysis, where the red blood cells break down prematurely, leading to anemia, jaundice, and in severe cases, kidney failure.
G6PD deficiency is typically inherited from one's parents in an X-linked recessive pattern, meaning that males are more likely to be affected than females. While there is no cure for G6PD deficiency, avoiding triggers and managing symptoms can help prevent complications.
Organic anion transport polypeptide C (OATPc or OATPC) is not a widely recognized or established term in the medical field. It seems that this terminology might be referring to one or more members of the organic anion transporting polypeptides (OATPs) family, specifically those localized to the canalicular membrane of hepatocytes.
OATPs are a group of membrane transporters primarily responsible for the uptake of various amphipathic organic molecules, including bile salts, steroid conjugates, thyroid hormones, and various drugs. They play a crucial role in the hepatic clearance and disposition of many endogenous and exogenous substances.
The term "OATPc" might be referring to OATP1B1 (SLCO1B1) and/or OATP1B3 (SLCO1B3), which are the two major isoforms found in the human liver's canalicular membrane. However, it is essential to note that there isn't a universally accepted or standardized definition for "OATPc."
To obtain accurate and reliable information, consult scientific literature, textbooks, or databases specializing in medical definitions and terminology.
Blood group incompatibility refers to a situation where the blood type of a donor and a recipient are not compatible, leading to an immune response and destruction of the donated red blood cells. This is because the recipient's immune system recognizes the donor's red blood cells as foreign due to the presence of incompatible antigens on their surface.
The most common type of blood group incompatibility occurs between individuals with different ABO blood types, such as when a person with type O blood receives type A, B, or AB blood. This can lead to agglutination and hemolysis of the donated red blood cells, causing potentially life-threatening complications such as hemolytic transfusion reaction.
Another type of blood group incompatibility occurs between Rh-negative mothers and their Rh-positive fetuses. If a mother's immune system is exposed to her fetus's Rh-positive red blood cells during pregnancy or childbirth, she may develop antibodies against them. This can lead to hemolytic disease of the newborn if the mother becomes pregnant with another Rh-positive fetus in the future.
To prevent these complications, it is essential to ensure that donated blood is compatible with the recipient's blood type before transfusion and that appropriate measures are taken during pregnancy and childbirth to prevent sensitization of Rh-negative mothers to Rh-positive red blood cells.
Erythroblastosis, fetal is a medical condition that occurs in the fetus or newborn when there is an incompatibility between the fetal and maternal blood types, specifically related to the Rh factor or ABO blood group system. This incompatibility leads to the destruction of the fetal red blood cells by the mother's immune system, resulting in the release of bilirubin, which can cause jaundice, anemia, and other complications.
In cases where the mother is Rh negative and the fetus is Rh positive, the mother may develop antibodies against the Rh factor during pregnancy or after delivery, leading to hemolysis (breakdown) of the fetal red blood cells in subsequent pregnancies if preventive measures are not taken. This is known as hemolytic disease of the newborn (HDN).
Similarly, incompatibility between the ABO blood groups can also lead to HDN, although it is generally less severe than Rh incompatibility. In this case, the mother's immune system produces antibodies against the fetal red blood cells, leading to their destruction and subsequent complications.
Fetal erythroblastosis is a serious condition that can lead to significant morbidity and mortality if left untreated. Treatment options include intrauterine transfusions, phototherapy, and exchange transfusions in severe cases. Preventive measures such as Rh immune globulin (RhIG) injections can help prevent the development of antibodies in Rh-negative mothers, reducing the risk of HDN in subsequent pregnancies.
Metalloporphyrins are a type of porphyrin molecule that contain a metal ion at their center. Porphyrins are complex organic compounds containing four modified pyrrole rings connected to form a planar, aromatic ring known as a porphine. When a metal ion is incorporated into the center of the porphyrin ring, it forms a metalloporphyrin.
These molecules have great biological significance, as they are involved in various essential processes within living organisms. For instance, heme, a type of iron-containing porphyrin, plays a crucial role in oxygen transport and storage in the body by forming part of hemoglobin and myoglobin molecules. Chlorophyll, another metalloporphyrin with magnesium at its center, is essential for photosynthesis in plants, algae, and some bacteria.
Metalloporphyrins have also found applications in several industrial and medical fields, including catalysis, sensors, and pharmaceuticals. Their unique structure and properties make them valuable tools for researchers and scientists to study and utilize in various ways.
A nomogram is a graphical representation of a mathematical formula or equation that allows the user to quickly solve a problem by simply drawing a line between different values on the chart. In the field of medicine, nomograms are often used as a tool for predicting patient outcomes, assessing risk, or making diagnostic decisions based on specific clinical data.
For example, a nomogram may be used to estimate the probability of survival in patients with a particular type of cancer, based on factors such as age, tumor size, and stage of disease. The user would locate the appropriate values for each factor on the nomogram, draw a line connecting them, and read off the estimated probability at the intersection point.
Nomograms can be a useful and intuitive way to communicate complex medical information and help clinicians make informed decisions in a timely manner. However, it is important to note that nomograms are only as accurate as the data they are based on, and should always be used in conjunction with clinical judgment and other relevant factors.
Histocompatibility, maternal-fetal, refers to the compatibility between the human leukocyte antigens (HLAs) and other antigenic proteins expressed on the fetal tissues and those present in the mother's immune system. The HLAs are a group of proteins encoded by the major histocompatibility complex (MHC) and play a crucial role in the recognition and presentation of foreign peptides to the immune cells.
During pregnancy, the fetal tissues express paternal HLA antigens that can be recognized as non-self by the mother's immune system. However, the maternal-fetal interface, which includes the placenta and decidua, has several mechanisms to prevent the activation of the maternal immune response against the fetus. These mechanisms include the expression of unique HLA molecules (HLA-G, -C, and -E) by the trophoblast cells, which have immunomodulatory functions, as well as the production of anti-inflammatory cytokines and the suppression of pro-inflammatory responses.
Despite these immune tolerance mechanisms, in some cases, the maternal immune system may still recognize the fetal tissues as foreign and mount an immune response, leading to pregnancy complications such as preeclampsia, recurrent miscarriage, or intrauterine growth restriction. The degree of histocompatibility between the mother and fetus can influence the risk of these complications, with a higher degree of mismatch increasing the risk.
In transplantation medicine, the concept of histocompatibility is critical in matching donors and recipients to minimize the risk of rejection. However, in pregnancy, the unique immune environment at the maternal-fetal interface allows for the coexistence of two genetically distinct individuals without the need for full histocompatibility.
Central hearing loss is a type of hearing disorder that occurs due to damage or dysfunction in the central auditory pathways of the brain, rather than in the ear itself. This condition can result from various causes, such as stroke, tumors, trauma, infection, or degenerative diseases affecting the brain.
In central hearing loss, the person may have difficulty understanding and processing speech, even when they can hear sounds at normal levels. They might experience problems with sound localization, discriminating between similar sounds, and comprehending complex auditory signals. This type of hearing loss is different from sensorineural or conductive hearing loss, which are related to issues in the outer, middle, or inner ear.
Protoporphyrins are organic compounds that are the immediate precursors to heme in the porphyrin synthesis pathway. They are composed of a porphyrin ring, which is a large, complex ring made up of four pyrrole rings joined together, with an acetate and a propionate side chain at each pyrrole. Protoporphyrins are commonly found in nature and are important components of many biological systems, including hemoglobin, the protein in red blood cells that carries oxygen throughout the body.
There are several different types of protoporphyrins, including protoporphyrin IX, which is the most common form found in humans and other animals. Protoporphyrins can be measured in the blood or other tissues as a way to diagnose or monitor certain medical conditions, such as lead poisoning or porphyrias, which are rare genetic disorders that affect the production of heme. Elevated levels of protoporphyrins in the blood or tissues can indicate the presence of these conditions and may require further evaluation and treatment.
Indinavir is an antiretroviral medication used in the treatment and management of HIV (Human Immunodeficiency Virus) infection. It belongs to a class of drugs known as protease inhibitors, which work by blocking the action of protease enzymes that are necessary for the HIV virus to replicate. By inhibiting this process, indinavir helps prevent the spread of HIV in the body and reduces the risk of developing AIDS (Acquired Immunodeficiency Syndrome).
Indinavir is often prescribed as part of a combination therapy regimen with other antiretroviral drugs. It is available in capsule form and is typically taken several times a day, usually on an empty stomach. As with all medications, indinavir can have side effects, which may include nausea, diarrhea, headache, and changes in liver function. Regular monitoring of blood tests is necessary to ensure that the drug is working effectively and not causing any harmful side effects.
It's important to note that while antiretroviral therapy can help manage HIV infection and improve quality of life, it does not cure the disease. Therefore, it is essential for individuals with HIV to continue taking their medications as prescribed and to follow up regularly with their healthcare provider.
The ABO blood-group system is a classification system used in blood transfusion medicine to determine the compatibility of donated blood with a recipient's blood. It is based on the presence or absence of two antigens, A and B, on the surface of red blood cells (RBCs), as well as the corresponding antibodies present in the plasma.
There are four main blood types in the ABO system:
1. Type A: These individuals have A antigens on their RBCs and anti-B antibodies in their plasma.
2. Type B: They have B antigens on their RBCs and anti-A antibodies in their plasma.
3. Type AB: They have both A and B antigens on their RBCs but no natural antibodies against either A or B antigens.
4. Type O: They do not have any A or B antigens on their RBCs, but they have both anti-A and anti-B antibodies in their plasma.
Transfusing blood from a donor with incompatible ABO antigens can lead to an immune response, causing the destruction of donated RBCs and potentially life-threatening complications such as acute hemolytic transfusion reaction. Therefore, it is crucial to match the ABO blood type between donors and recipients before performing a blood transfusion.
Hemolysis is the destruction or breakdown of red blood cells, resulting in the release of hemoglobin into the surrounding fluid (plasma). This process can occur due to various reasons such as chemical agents, infections, autoimmune disorders, mechanical trauma, or genetic abnormalities. Hemolysis may lead to anemia and jaundice, among other complications. It is essential to monitor hemolysis levels in patients undergoing medical treatments that might cause this condition.
A premature infant is a baby born before 37 weeks of gestation. They may face various health challenges because their organs are not fully developed. The earlier a baby is born, the higher the risk of complications. Prematurity can lead to short-term and long-term health issues, such as respiratory distress syndrome, jaundice, anemia, infections, hearing problems, vision problems, developmental delays, and cerebral palsy. Intensive medical care and support are often necessary for premature infants to ensure their survival and optimal growth and development.
Porphyrins are complex organic compounds that contain four pyrrole rings joined together by methine bridges (=CH-). They play a crucial role in the biochemistry of many organisms, as they form the core structure of various heme proteins and other metalloproteins. Some examples of these proteins include hemoglobin, myoglobin, cytochromes, and catalases, which are involved in essential processes such as oxygen transport, electron transfer, and oxidative metabolism.
In the human body, porphyrins are synthesized through a series of enzymatic reactions known as the heme biosynthesis pathway. Disruptions in this pathway can lead to an accumulation of porphyrins or their precursors, resulting in various medical conditions called porphyrias. These disorders can manifest as neurological symptoms, skin lesions, and gastrointestinal issues, depending on the specific type of porphyria and the site of enzyme deficiency.
It is important to note that while porphyrins are essential for life, their accumulation in excessive amounts or at inappropriate locations can result in pathological conditions. Therefore, understanding the regulation and function of porphyrin metabolism is crucial for diagnosing and managing porphyrias and other related disorders.
I'm sorry for any confusion, but "Pyridines" is not a medical term. It is a chemical term that refers to a class of organic compounds with the chemical structure of a six-membered ring containing one nitrogen atom and five carbon atoms (heterocyclic aromatic compound).
In a biological or medical context, pyridine derivatives can be found in various natural and synthetic substances. For example, some medications contain pyridine rings as part of their chemical structure. However, "Pyridines" itself is not a medical term or condition.
The Coombs test is a laboratory procedure used to detect the presence of antibodies on the surface of red blood cells (RBCs). It is named after the scientist, Robin Coombs, who developed the test. There are two types of Coombs tests: direct and indirect.
1. Direct Coombs Test (DCT): This test is used to detect the presence of antibodies directly attached to the surface of RBCs. It is often used to diagnose hemolytic anemia, a condition in which RBCs are destroyed prematurely, leading to anemia. A positive DCT indicates that the patient's RBCs have been coated with antibodies, which can occur due to various reasons such as autoimmune disorders, blood transfusion reactions, or drug-induced immune hemolysis.
2. Indirect Coombs Test (ICT): This test is used to detect the presence of antibodies in the patient's serum that can agglutinate (clump) foreign RBCs. It is commonly used before blood transfusions or during pregnancy to determine if the patient has antibodies against the RBCs of a potential donor or fetus, respectively. A positive ICT indicates that the patient's serum contains antibodies capable of binding to and agglutinating foreign RBCs.
In summary, the Coombs test is a crucial diagnostic tool in identifying various hemolytic disorders and ensuring safe blood transfusions by detecting the presence of harmful antibodies against RBCs.
The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:
1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.
Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.
Ultraviolet (UV) therapy, also known as phototherapy, is a medical treatment that uses ultraviolet light to treat various skin conditions. The UV light can be delivered through natural sunlight or artificial sources, such as specialized lamps or lasers.
In medical settings, controlled doses of UV light are used to target specific areas of the skin. The most common type of UV therapy is narrowband UVB (NB-UVB) phototherapy, which uses a specific wavelength of UVB light to treat conditions such as psoriasis, eczema, vitiligo, and dermatitis.
The goal of UV therapy is to reduce inflammation, slow skin cell growth, and improve the overall appearance of the skin. It is important to note that while UV therapy can be effective in treating certain skin conditions, it also carries risks such as skin aging and an increased risk of skin cancer. Therefore, it should only be administered under the supervision of a qualified healthcare professional.
Cholestasis is a medical condition characterized by the interruption or reduction of bile flow from the liver to the small intestine. Bile is a digestive fluid produced by the liver that helps in the breakdown and absorption of fats. When the flow of bile is blocked or reduced, it can lead to an accumulation of bile components, such as bilirubin, in the blood, which can cause jaundice, itching, and other symptoms.
Cholestasis can be caused by various factors, including liver diseases (such as hepatitis, cirrhosis, or cancer), gallstones, alcohol abuse, certain medications, pregnancy, and genetic disorders. Depending on the underlying cause, cholestasis may be acute or chronic, and it can range from mild to severe in its symptoms and consequences. Treatment for cholestasis typically involves addressing the underlying cause and managing the symptoms with supportive care.
Organic anion transporters (OATs) are membrane transport proteins that are responsible for the cellular uptake and excretion of various organic anions, such as drugs, toxins, and endogenous metabolites. They are found in various tissues, including the kidney, liver, and brain, where they play important roles in the elimination and detoxification of xenobiotics and endogenous compounds.
In the kidney, OATs are located in the basolateral membrane of renal tubular epithelial cells and mediate the uptake of organic anions from the blood into the cells. From there, the anions can be further transported into the urine by other transporters located in the apical membrane. In the liver, OATs are expressed in the sinusoidal membrane of hepatocytes and facilitate the uptake of organic anions from the blood into the liver cells for metabolism and excretion.
There are several isoforms of OATs that have been identified, each with distinct substrate specificities and tissue distributions. Mutations in OAT genes can lead to various diseases, including renal tubular acidosis, hypercalciuria, and drug toxicity. Therefore, understanding the function and regulation of OATs is important for developing strategies to improve drug delivery and reduce adverse drug reactions.
Imino acids are organic compounds that contain a nitrogen atom as part of an amide-like structure. They are structurally similar to amino acids, which contain a carboxyl group and an amino group, but instead of the amino group, imino acids have a structural unit known as an imine or Schiff base, which is a carbon-nitrogen double bond with a hydrogen atom attached to the nitrogen atom.
One example of an imino acid is proline, which is a cyclic imino acid that plays important roles in protein structure and function. Proline is unique among the 20 standard amino acids because its side chain is linked to the nitrogen atom of the backbone, forming a ring-like structure. This structural feature gives proline unique properties, such as restricted rotation around the bond between the nitrogen and alpha carbon atoms, which can affect protein folding and stability.
Other imino acids may be formed through chemical reactions or enzymatic processes, and they can play important roles in various biological pathways, including the biosynthesis of amino acids, nucleotides, and other biomolecules. However, imino acids are not typically considered to be part of the standard set of 20 amino acids that make up proteins.
Hemolytic anemia is a type of anemia that occurs when red blood cells are destroyed (hemolysis) faster than they can be produced. Red blood cells are essential for carrying oxygen throughout the body. When they are destroyed, hemoglobin and other cellular components are released into the bloodstream, which can lead to complications such as kidney damage and gallstones.
Hemolytic anemia can be inherited or acquired. Inherited forms of the condition may result from genetic defects that affect the structure or function of red blood cells. Acquired forms of hemolytic anemia can be caused by various factors, including infections, medications, autoimmune disorders, and certain medical conditions such as cancer or blood disorders.
Symptoms of hemolytic anemia may include fatigue, weakness, shortness of breath, pale skin, jaundice (yellowing of the skin and eyes), dark urine, and a rapid heartbeat. Treatment for hemolytic anemia depends on the underlying cause and may include medications, blood transfusions, or surgery.
A "premature infant" is a newborn delivered before 37 weeks of gestation. They are at greater risk for various health complications and medical conditions compared to full-term infants, due to their immature organ systems and lower birth weight. Some common diseases and health issues that premature infants may face include:
1. Respiratory Distress Syndrome (RDS): A lung disorder caused by the lack of surfactant, a substance that helps keep the lungs inflated. Premature infants, especially those born before 34 weeks, are at higher risk for RDS.
2. Intraventricular Hemorrhage (IVH): Bleeding in the brain's ventricles, which can lead to developmental delays or neurological issues. The risk of IVH is inversely proportional to gestational age, meaning that the earlier the infant is born, the higher the risk.
3. Necrotizing Enterocolitis (NEC): A gastrointestinal disease where the intestinal tissue becomes inflamed and can die. Premature infants are at greater risk for NEC due to their immature digestive systems.
4. Jaundice: A yellowing of the skin and eyes caused by an accumulation of bilirubin, a waste product from broken-down red blood cells. Premature infants may have higher rates of jaundice due to their liver's immaturity.
5. Infections: Premature infants are more susceptible to infections because of their underdeveloped immune systems. Common sources of infection include the mother's genital tract, bloodstream, or hospital environment.
6. Anemia: A condition characterized by a low red blood cell count or insufficient hemoglobin. Premature infants may develop anemia due to frequent blood sampling, rapid growth, or inadequate erythropoietin production.
7. Retinopathy of Prematurity (ROP): An eye disorder affecting premature infants, where abnormal blood vessel growth occurs in the retina. Severe ROP can lead to vision loss or blindness if not treated promptly.
8. Developmental Delays: Premature infants are at risk for developmental delays due to their immature nervous systems and environmental factors such as sensory deprivation or separation from parents.
9. Patent Ductus Arteriosus (PDA): A congenital heart defect where the ductus arteriosus, a blood vessel that connects two major arteries in the fetal heart, fails to close after birth. Premature infants are at higher risk for PDA due to their immature cardiovascular systems.
10. Hypothermia: Premature infants have difficulty maintaining body temperature and are at risk for hypothermia, which can lead to increased metabolic demands, poor feeding, and infection.
Plasma exchange, also known as plasmapheresis, is a medical procedure where the liquid portion of the blood (plasma) is separated from the blood cells. The plasma, which may contain harmful substances such as antibodies, clotting factors, or toxins, is then removed and replaced with fresh plasma or a plasma substitute. This process helps to remove the harmful substances from the blood and allows the body to replenish its own plasma with normal components. Plasma exchange is used in the treatment of various medical conditions including autoimmune diseases, poisonings, and certain types of kidney diseases.
Technetium Tc 99m Disofenin is not a medical condition, but rather a radiopharmaceutical used in diagnostic imaging. It is a radioactive tracer used in nuclear medicine scans, specifically for liver and biliary system imaging. The compound consists of the radioisotope Technetium-99m (Tc-99m) bonded to the pharmaceutical Disofenin.
The Tc-99m is a gamma emitter with a half-life of 6 hours, making it ideal for diagnostic imaging. When administered to the patient, the compound is taken up by the liver and excreted into the bile ducts and gallbladder, allowing medical professionals to visualize these structures using a gamma camera. This can help detect various conditions such as tumors, gallstones, or obstructions in the biliary system.
It's important to note that Technetium Tc 99m Disofenin is used diagnostically and not for therapeutic purposes. The radiation exposure from this compound is generally low and considered safe for diagnostic use. However, as with any medical procedure involving radiation, the benefits and risks should be carefully weighed and discussed with a healthcare professional.
Mandatory reporting is a legal requirement that healthcare professionals, as well as other designated individuals or organizations, must report suspected or confirmed cases of abuse, neglect, or exploitation of vulnerable populations to the appropriate authorities. These vulnerable populations often include children, elderly persons, and individuals with disabilities. The purpose of mandatory reporting is to ensure the protection and safety of these at-risk individuals and to facilitate interventions that can address and prevent further harm.
Healthcare professionals who are mandated reporters typically include doctors, nurses, mental health professionals, social workers, and teachers, among others. Mandatory reporting requirements vary by jurisdiction but generally involve immediate notification upon suspicion or knowledge of maltreatment. Failing to report as required can result in legal consequences for the mandated reporter, including potential penalties such as fines, license suspension, or even criminal charges.
The specifics of mandatory reporting laws and regulations differ between countries, states, and provinces; therefore, it is essential for healthcare professionals to be familiar with the requirements applicable to their particular practice settings.
Oligopeptides are defined in medicine and biochemistry as short chains of amino acids, typically containing fewer than 20 amino acid residues. These small peptides are important components in various biological processes, such as serving as signaling molecules, enzyme inhibitors, or structural elements in some proteins. They can be found naturally in foods and may also be synthesized for use in medical research and therapeutic applications.
Bile canaliculi are the smallest bile-transporting structures in the liver. They are formed by the close apposition of hepatocyte (liver cell) plasma membranes, and they are responsible for the majority of bile production. The bile canaliculi merge to form bile ductules, which then merge to form larger bile ducts that transport bile to the gallbladder and small intestine. Bile is a fluid that contains water, electrolytes, bile salts, cholesterol, phospholipids, and bilirubin, which are produced by the liver and play important roles in digestion and elimination of waste products.
Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), also known as Glucosephosphate Dehydrogenase, is an enzyme that plays a crucial role in cellular metabolism, particularly in the glycolytic pathway. It catalyzes the conversion of glyceraldehyde 3-phosphate (G3P) to 1,3-bisphosphoglycerate (1,3-BPG), while also converting nicotinamide adenine dinucleotide (NAD+) to its reduced form NADH. This reaction is essential for the production of energy in the form of adenosine triphosphate (ATP) during cellular respiration. GAPDH has been widely used as a housekeeping gene in molecular biology research due to its consistent expression across various tissues and cells, although recent studies have shown that its expression can vary under certain conditions.
Patient readmission refers to the event when a patient who was previously discharged from a hospital or healthcare facility returns for further treatment, often within a specified period. It is measured as a percentage of patients who are readmitted within a certain time frame, such as 30, 60, or 90 days after discharge. Readmissions may be planned or unplanned and can occur due to various reasons, including complications from the initial illness or treatment, inadequate post-discharge follow-up care, or the patient's inability to manage their health conditions effectively at home. High readmission rates are often considered an indicator of the quality of care provided during the initial hospitalization and may also signify potential issues with care coordination and transitions between healthcare settings.
Gestational age is the length of time that has passed since the first day of the last menstrual period (LMP) in pregnant women. It is the standard unit used to estimate the age of a pregnancy and is typically expressed in weeks. This measure is used because the exact date of conception is often not known, but the start of the last menstrual period is usually easier to recall.
It's important to note that since ovulation typically occurs around two weeks after the start of the LMP, gestational age is approximately two weeks longer than fetal age, which is the actual time elapsed since conception. Medical professionals use both gestational and fetal age to track the development and growth of the fetus during pregnancy.
Extracorporeal circulation (ECC) is a term used in medicine to describe the process of temporarily taking over the functions of the heart and lungs by using a machine. This allows the surgeon to perform certain types of surgery, such as open-heart surgery, on a still and bloodless operating field.
During ECC, the patient's blood is circulated outside the body through a pump and oxygenator. The pump helps to maintain blood flow and pressure, while the oxygenator adds oxygen to the blood and removes carbon dioxide. This allows the surgeon to stop the heart and arrest its motion, making it easier to perform delicate procedures on the heart and surrounding structures.
Extracorporeal circulation is a complex and high-risk procedure that requires careful monitoring and management by a team of healthcare professionals. It carries risks such as bleeding, infection, and injury to blood vessels or organs. However, when performed correctly, it can be a life-saving measure for patients undergoing certain types of surgery.
Hereditary hyperbilirubinemia
Jaundice
Hyperbilirubinemia in adults
Hemoglobin O
Blueberry muffin baby
List of syndromes
List of MeSH codes (C18)
List of MeSH codes (C16)
Spherocytosis
Hereditary coproporphyria
List of ICD-9 codes 240-279: endocrine, nutritional and metabolic diseases, and immunity disorders
List of diseases (H)
Mean corpuscular hemoglobin concentration
Hemolytic jaundice
Bilirubin glucuronide
Neonatal jaundice
Breast milk
Harrison's Principles of Internal Medicine
Beta thalassemia
Hemolysis
Gilbert's syndrome
Hemolytic anemia
Crigler-Najjar syndrome
Causes of hearing loss
Aldolase A deficiency
Athetoid cerebral palsy
Audiology and hearing health professionals in developed and developing countries
List of OMIM disorder codes
Sensorineural hearing loss
Causes of autism
Hereditary hyperbilirubinemia - Wikipedia
Hereditary Spherocytosis: Practice Essentials, Pathophysiology, Etiology
Congenital nonhemolytic hyperbilirubinemias
Effect of splenectomy of hepatic bilirubin clearance in patients with hereditary spherocytosis. Implications for the diagnosis...
Hemolytic Disease of the Newborn Treatment & Management: Approach Considerations, Medical Care, Complications
UDP-Glucuronosyltransferase-mediated Protection Against In Vitro DNA Oxidation and Micronucleus Formation Initiated by...
Pomalidomide in Combination With Low-dose Dexamethasone or Pomalidomide in Combination With Low-dose Dexamethasone and...
International Classification of Diseases - Endocrine, Nutritional and Metabolic Diseases, and Immunity Disorders
Inborn Metabolic Disorders Causing Hyperbilirubinemia - Hepatic and Biliary Disorders - Merck Manuals Professional Edition
Dubin-Johnson Syndrome: Practice Essentials, Background, Pathophysiology and Etiology
Shop Національне Питання В Норвегії
Hereditary Spherocytosis: Background, Pathophysiology, Etiology
PPT - CHAPTER 18 PowerPoint Presentation, free download - ID:150949
Multiple Myeloma Clinical Trial: Study of ACY-241 Alone and in Combination With Pomalidomide and Dexamethasone in Multiple...
Crigler-Najjar Syndrome Type 1 - Metabolic Support UK
MedlinePlus: Genetic Conditions: F
Tooth Discoloration: Practice Essentials, Background, Pathophysiology
Pancreas disorders-Pancreatitis-acute, chronic, hereditary - Cancer Therapy Advisor
Free Cheats, Game Hacks, Spoofer & Bots | Executor, Game Hacks, Spinbot | // Conor Toumarkine | Producer | Photographer |...
Classification-Schedules
Buy Regulon pills online
Precision Health Database|Search|PHGKB
...
Nitric Oxide Enhancer | GreenMedInfo | Pharmacological Action
Dynowski
amino acid metabolic disorder - Ontology Browser - Rat Genome Database
Citrin Deficiency - GeneReviews® - NCBI Bookshelf
Dubin-Johnson Syndrome: Practice Essentials, Background, Pathophysiology and Etiology
Vol 5 Issue 5 - Український журнал медицини, біології та спорту.
Jaundice
Bilirubin8
- Hereditary hyperbilirubinemia refers to the condition where levels of bilirubin are elevated, for reasons that can be attributed to a metabolic disorder. (wikipedia.org)
- A common feature of congenital nonhemolytic hyperbilirubinemias is an abnormal serum bilirubin level without other abnormalities in routine liver functional tests. (nih.gov)
- Hereditary genetics defect of enzymes taking part in metabolism of bilirubin is the cause of CNH. (nih.gov)
- Effect of splenectomy of hepatic bilirubin clearance in patients with hereditary spherocytosis. (nih.gov)
- Laboratory studies reveal conjugated hyperbilirubinemia, with total bilirubin serum levels usually in the 2- to 5-mg/dL range (but potentially as high as 25 mg/dL). (medscape.com)
- Hyperbilirubinemia or jaundice is a pathological condition that occurs with an increase in the content of bilirubin in the blood plasma. (californiansforastrongeramerica.com)
- Violation of this sequence at any stage leads to an increase in the concentration of blood bilirubin or hyperbilirubinemia. (californiansforastrongeramerica.com)
- Rotor syndrome (OMIM #237450) is the simultaneous and complete deficiency of OATP1B1 and 1B3 which disrupts the hepatic reuptake of conjugated bilirubin and clinically presents as mild hyperbilirubinemia [7, 8]. (solvobiotech.com)
Congenital3
- Congenital nonhemolytic hyperbilirubinemias (CNH) are quite rare pathology of liver. (nih.gov)
- Once the diagnosis of congenital nonhemolytic hyperbilirubinemia is confirmed, patients should be informed of the disease process and its benign nature to prevent needless work-up in the future. (nih.gov)
- Patient Experience with Congenital (Hereditary) Thrombotic Thrombocytopenic Purpura: A Conceptual Framework of Symptoms and Impacts. (cdc.gov)
Dubin-Johnson syndrome a2
- They are divided into two groups: with unconjugated hyperbilirubinemia (Crigler-Najjar syndrome, Gilbert syndrome) and conjugated hyperbilirubinemia (Dubin-Johnson syndrome and Rotor syndrome). (nih.gov)
- Dubin-Johnson syndrome and Rotor syndrome cause conjugated hyperbilirubinemia, but without cholestasis, causing no symptoms or sequelae other than jaundice. (merckmanuals.com)
Jaundice4
- Eventually it causes unconjugated hyperbilirubinemia and jaundice as substance accumulates in the body due to the reduced ability of the enzyme. (wikipedia.org)
- As result, it causes unconjugated hyperbilirubinemia and jaundice. (metabolicsupportuk.org)
- According to this mechanism, jaundice occurs in severe malaria, hereditary diseases of the blood system. (californiansforastrongeramerica.com)
- Decreased expression of OATP1B1 and 1B3 in cholestatic diseases correlates with jaundice [9], and chronic treatment with fusidic acid, a widely used bacteriostatic that besides OATP1B1 also inhibits NTCP and BSEP, is often accompanied by cholestasis and conjugated hyperbilirubinemia [10]. (solvobiotech.com)
Hemolytic anemia7
- Five Years' Experience with Gene Panel Sequencing in Hereditary Hemolytic Anemia Screened by Routine Peripheral Blood Smear Examination. (cdc.gov)
- Clinical Utility of Targeted Next-Generation Sequencing Panel in Routine Diagnosis of Hereditary Hemolytic Anemia: A national reference laboratory experience. (cdc.gov)
- Hereditary hemolytic anemia in newborns: clinical significance of genetic diagnosis]. (cdc.gov)
- Iron overload in patients with rare hereditary hemolytic anemia: Evidence-based suggestion on whom and how to screen. (cdc.gov)
- Molecular diagnostic update in hereditary hemolytic anemia and neonatal hyperbilirubinemia. (cdc.gov)
- Glucose phosphate isomerase (GPI) deficiency is a rare autosomal recessive disorder that causes hereditary nonspherocytic hemolytic anemia (HNSHA). (biomedcentral.com)
- He suffered from moderate hemolytic anemia (hemoglobin levels ranging from 62 to 91 g/L) associated with macrocytosis, reticulocytosis, neutropenia, and hyperbilirubinemia. (biomedcentral.com)
Spherocytosis4
- Hereditary spherocytosis (HS) is a familial hemolytic disorder associated with a variety of mutations that lead to defects in red blood cell (RBC) membrane proteins. (medscape.com)
- BRT and CBR were determined from studies of radiobilirubin kinetics in 14 patients undergoing splenectomy for hereditary spherocytosis. (nih.gov)
- Effects of SPTA1 Gene Variants on the Hematological Phenotype of Mexican Patients with Hereditary Spherocytosis. (cdc.gov)
- Influence of diabetes and hypercholesterolemia on laboratory methods for hereditary spherocytosis diagnosis. (cdc.gov)
Deficiency2
- Glucose-6-phosphate isomerase (GPI) deficiency (MIM 613470), one of hereditary nonspherocytic hemolytic anemias (HNSHA), is a rare autosomal recessive hereditary disease caused by homozygous or compound heterozygous mutations of GPI gene on chromosome 19q13 [ 1 ]. (biomedcentral.com)
- Clinical Manifestations Nursing Management Clinical Manifestations Acute Pharyngitis Decreasing Fatigue COLORECTAL NEOPLASMS Endometrial Hyperplasia Human Immune Deficiency Virus Infection and Acquired Immune Deficiency Syndrome Medical Management Health Promotion Calcitonin Pacemaker Surveillance Acne Vulgaris Emergency Management Pathophysiology Pathophysiology Angiomas Hereditary Hyperbilirubinemia Assessment and Diagnostic Findings Medical Management Crohn's Disease (Regional Enteritis) Medical Management Unit 12: Kidney and Urinary Tract Function Complications Assessment and Diagnostic Findings Pathophysiology Otoscopic Examination Enfermería Medicoquirúrgica. (britzerdamm.de)
Liver1
- [ 1 ] This rare autosomal recessive condition is characterized by conjugated hyperbilirubinemia with normal liver transaminases, a unique pattern of urinary excretion of heme metabolites (coproporphyrins), and the deposition of a pigment that gives the liver a characteristic black color (see the image below). (medscape.com)
Autosomal2
- Patients with autosomal recessive type I (complete) disease have severe unconjugated hyperbilirubinemia typically beginning shortly after birth. (merckmanuals.com)
- Patients with autosomal recessive type II (partial) disease (which has variable penetrance) often have less severe unconjugated hyperbilirubinemia ( 20 mg/dL [ 342 micromol/L]) and usually live into adulthood without neurologic damage. (merckmanuals.com)
Mild1
- Hereditary hemochromatosis and mild unconjugated hyperbilirubinemia in patient with ulcerative colitis. (krakow.pl)
Diagnostic1
- After that diagnostic workups, such as for example determined tomography, magnetized resonance imaging, chromosomal evaluation, or any other hereditary analysis, was indeed performed because of the neonatologists as needed. (comfortdentalbd.com)
Disorders1
- hereditary or acquired), and rare hereditary disorders of vitamin B12 metabolism or factors involved in hemostasis. (medilib.ir)
Patients1
- 3.0 × ULN for patients with hereditary benign hyperbilirubinaemia. (survivornet.com)
Result1
- As a result of hyperbilirubinemia, yellowness of the skin and mucous membranes is noted. (californiansforastrongeramerica.com)
Neonatal3
- In addition, elevated serum AFP concentrations have been measured in patients with other noncancerous diseases, including ataxia telangiectasia, hereditary tyrosinemia, neonatal hyperbilirubinemia, acute viral hepatitis, chronic active hepatitis, and cirrhosis. (rapidtest.com)
- If your child is suffering from neonatal hypoglycemia, hip displasia, kernicterus or hyperbilirubinemia or the after effects of these conditions, caused as a result of medical negligence by a health care provider, a UK specialist medical negligence solicitor can ensure that they get a fair deal by taking the guesswork out of selecting a lawyer. (dailyhealthscience.us)
- Infants who required a stay in the neonatal intensive care unit are at increased risk for developing hearing loss due to hypoxia, hyperbilirubinemia, very low birth weight, and ototoxic medications. (redrosehearing.com)
Fructose intolerance4
- Hereditary fructose intolerance is a metabolic disorder in which the small intestine cannot process fructose (fruit sugar) into a source of energy because of an enzyme deficiency that prevents fructose absorption. (healthofchildren.com)
- Hereditary fructose intolerance is estimated to affect one in about 20,000 people. (healthofchildren.com)
- Several gene mutations causing hereditary fructose intolerance have been identified. (healthofchildren.com)
- Avoid use of PHEBURANE in patients with rare hereditary problems of fructose intolerance, glucose-galactose malabsorption or sucrase-isomaltase insufficiency. (nih.gov)
Hemolytic6
- Hereditary hemolytic anemia (HHA) is a group of genetically and phenotypically heterogeneous disorders characterized by premature destruction of red blood cells (RBCs) with clinical manifestations ranging from asymptomatic to marked hemolytic anemia. (nih.gov)
- [ 17 ] This technique does not differentiate between HS and autoimmune hemolytic anemia (AIHA), but it distinguishes HS from other hereditary membrane disorders. (medscape.com)
- Osmotic gradient ektacytometry distinguishes HS from other hereditary membrane pathologies but does not differentiate HS from autoimmune hemolytic anemia. (medscape.com)
- Hereditary stomatocytosis (HSt) is a type of congenital hemolytic anemia caused by abnormally increased cation permeability of erythrocyte membranes. (nature.com)
- Several inherited disorders can also produce unconjugated hyperbilirubinemia, including Gilbert syndrome, Crigler-Najjar syndromes type I and II, and inherited disorders causing hemolytic anemia. (statpearls.com)
- Aldolase A deficiency is an autosomal recessive disorder associated with hereditary hemolytic anemia (Kishi et al. (beds.ac.uk)
Forms of hereditary1
- Scientists have identified more than 400 different forms of hereditary hearing loss. (redrosehearing.com)
Diseases1
- This because of the peculiarity of the condition itself, Gilbert's disease is hereditary in nature yet unlike other hereditary diseases it does not have any major effects on the body. (in.my)
Syndromes1
- The cation-leaky hereditary stomatocytosis syndromes: A tale of six proteins. (amedeo.com)
Genetics1
- Hereditary Genetics 1:114. (rochester.edu)
Diagnosis1
- For this purpose, we developed a target capture sequencing (TCS) system for precise and comprehensive diagnosis of suspected hereditary red cell membrane disorders in patients 10 . (nature.com)
Stomatocytosis2
- Dehydrated hereditary stomatocytosis 1 with or without pseudohyperkalemia and/or perinatal edema (DHS1: OMIM#194380) is a dominantly inherited red cell membrane disorder caused by gain-of-function mutations of PIEZO1 in most cases. (nature.com)
- Dehydrated hereditary stomatocytosis-2 (DHS2, OMIM#616689) is caused by a heterozygous mutation in KCNN4 . (nature.com)
Disorders2
- We participated in clinical research on patients with hereditary red cell membrane disorders. (nature.com)
- Neurodegeneration with brain iron accumulation (NBIA) is a term used for a group of hereditary neurological disorders with abnormal accumulation of iron in basal ganglia. (bvsalud.org)
Mutations1
- The mildest and usual Gilbert syndrome is characterized by mild hyperbilirubinemia caused by mutations that lead to reduced levels of gene expression. (ivami.com)
Pathophysiology1
- This activity describes the pathophysiology and management of unconjugated hyperbilirubinemia. (statpearls.com)
Differentiate1
- Explain how to differentiate unconjugated hyperbilirubinemia from conjugated hyperbilirubinemia. (statpearls.com)
Disease2
- Over 70 years ago, a disease characterized by CPH was first described in Southdown sheep flocks in New Zealand.1 Results of subsequent breeding trials revealed that the disease was caused by an inherited recessive trait.2 In the 1960s, the disease was observed in Southdown sheep in California.3 Affected sheep had hyperbilirubinemia but no discoloration of the liver and also had delayed clearance of various organic anions. (hmto-hnas.com)
- A hepatopathy screening including viral hepatitis (hepatitis B, C, D, and E), auto-immune and hereditary liver disease was negative, except a document of remote hepatitis A infection. (biomedcentral.com)
Gilbert1
- Gilbert syndrome is frequently an autonomic recessive disorder and is a familiar origin of unconjugated hyperbilirubinaemia. (in.my)
Spherocytes1
- for spherocytes and, thus, eliminates anemia and hyperbilirubinemia and lowers the high reticulocyte number to nearly normal levels. (shadowebike.com)
Conjugation1
- Therefore, unconjugated hyperbilirubinemia can result from dysfunction of any of these conjugation steps. (statpearls.com)
Condition1
- Such as syringe is usually idiopathic and does not increase restenosis rate remains high enough quality to allow prognostic evaluation, despite the lack of a hereditary condition. (lowerbricktown.com)
Terms1
- Among the numerous clinical phenotypes observed are Leigh syndrome, Leber hereditary optic neuropathy and MELAS syndrome (see these terms). (nih.gov)
Medical1
- The patient has been handled for about six weeks with antibiotics along with percutaneous drain pipes put into learn more the greatest abscesses and was discharged after specialized medical improvement and resolution from the hyperbilirubinemia. (tauroursodeoxycholic.com)