Hyperbilirubinemia in the Term Newborn - American Family
Hyperbilirubinemia in the Term Newborn - American Family
Conjugated & unconjugated bilirubin, causes & treatment of
Normal serum bilirubin levels in the newborn and the
High bilirubin levels: Meaning, symptoms, and tests
Bilirubin Chart For Newborn Babies
Bilirubin Levels In Newborns - What’s Normal? | BellyBelly
conjugated bilirubin - General Practice Notebook
Neonatal Bilirubin, Serum - Mayo Clinic Laboratories
What Is a Normal Range of Bilirubin in a Newborn?
Direct & Indirect Bilirubin Test: Normal Levels & Jaundice
conjugated bilirubin normal range newborn
conjugated bilirubin normal range newborn - win
The Science of Hepatotoxicity
Hello everyone, this will by my last big post for a little while. I wanted to address hepatotoxicity since it seems to be this big grey area for a lot of people. Drug metabolism is a very complicated processes, so I have tried to condense it into a readable format. I wanted to address how drugs are metabolized, how drug metabolism can affect the liver, how to determine liver damage, and how to prevent it. Please feel free to ask questions! Drug Metabolism When it comes to drug metabolism, the liver’s primary function is to metabolize the drug into a form that is suitable for elimination by the kidneys. The main goals of this metabolism is to reduce fat solubility, make the drug water soluble, and to decrease its biological activity so that it stops working. This occurs for not only foreign substances (known as xenobiotics, which drugs are considered), but also endogenous chemicals. Drug metabolism in the liver exists in two main phases, phase I and phase II.
Phase I: Phase I metabolism happens primarily in the smooth endoplasmic reticulum of hepatocytes. The main purpose of this phase is to make lipid soluble compounds water soluble. This typically renders the metabolites of the drug to be inactive, but not always.
Phase II: Phase II metabolism takes place in the cytosol of hepatocytes. In this phase, the products from phase I will undergo conjugation to increase their water solubility.
The efficacy of the enzymes used in drug metabolism are age-dependent. In newborns and the geriatric, the ability to metabolize drugs is greatly decreased. Smoking can increase the efficacy of drug metabolism through the inhalation of polycyclic aromatic hydrocarbons. This is most noticeably manifested in the increased metabolic activity of caffeine. Drug Induced Hepatotoxicity Drug induced hepatotoxicity can have many causes. Some medications cause direct damage to hepatocytes while others block certain metabolic processes. As an example, acetaminophen itself is not the source of hepatotoxicity, but rather one of its metabolites. When taken in extreme quantities, this metabolite accumulates because the enzymes required are unable to keep up in phase II metabolism and cell damage occurs. Likewise, mitochondrial damage can increase oxidative stress which can damage hepatocytes. These causes are categorized in seven general categories based on the mechanism of hepatotoxicity. The main categories where AAS and ancillaries are implicated are:
Steatosis: Steatosis is the accumulation of triglycerides in the liver. Liver function tests (LFTs) are unreliable when it comes to the diagnosis of hepatic steatosis. Often will have an AST/ALT ratio < 1. Imaging and possible biopsy is required to make an accurate diagnosis. AST and ALT both upwards of 4 times ULN. Tamoxifen and raloxifene have been shown to induce hepatic steatosis.
Zonal Necrosis: Zonal necrosis is essentially the death of cells in a specific zone of the liver. This is the most common manifestation of hepatotoxicity. This will cause an increase in ALT with normal ALP levels. This can be caused by C-17-alpha-alkylated (C17aa) steroids.
Cholestasis: Cholestasis is the impediment of biliary flow from the liver through the biliary tract. This is the cause of jaundice. The increase in bilirubin causes a yellowing of the skin and that is occurs with itching. C17aa steroids may cause hepatotoxic cholestasis. This can be seen on labs as normal levels of ALT and > 2 times ULN ALP. The mechanism of this is not well known. Testosterone and 19-nortestosterone compounds have been implicated in cases of hyperbilirubinemia, but rarely to the point of jaundice.
Hyperplasia and Neoplasia: C17aa compounds have been implicated in cases of hepatic hyperplasia and neoplasia, essentially cancer. However, non-C17aa steroids have also been noted as a cause of liver cancer in medical case reports.
Vascular Lesions: These vascular lesions are known as Peliosis Hepatis. These lesions are present on endothelial cells of hepatic vasculature and is typically asymptomatic. This can eventually lead to hepatomegaly (enlarged liver) and frequently death if untreated.
Effects of liver damage include jaundice, ankle edema, gynecomastia, increased bleeding due to decrease in clotting factor synthesis. Most of these effects come from deficiencies in synthesis of their respective plasma proteins. For example, damage to hepatocytes that are responsible for synthesis of SHBG will result in a decrease in SHBG. This will alter the free estrogen/free androgen ratio, potentially inducing gynecomasta. Likewise, a decrease in plasma proteins will change the blood colloid osmotic pressure, causing a change in capillary net filtration pressure leading to edema in the lower extremities. Liver Function Tests LFTs can be done to assess hepatic function. These are not exactly conclusive and require some sort of follow up to assess the degree of severity. Often this will be some sort of imaging or biopsy. Most of these biomarkers are assessed in a multiplication of the upper limit of normal (ULN), which is the top end of the normal range. Aminotransferases: Aminotransferases are enzymes that are used in the synthesis of amino acids. There are two aminotransferases that are checked as part of an LFT.
Aspartate Transaminase (AST): Reference range: 8 - 40 IU/L. While AST is found in the liver, this enzyme is also found in great quantities in cardiac and skeletal muscle. Because of these other sources, AST alone is not a good indicator of liver damage. Essentially, AST does not require the entire cell to be damaged for it to enter the plasma, where ALT does. This is due to its location within the cell. If AST is elevated then there is a good possibility that the source of the AST is from muscle damage. This can be caused by myocardial infarction (heart attack), rhadomyolysis, and even resistance training. This is why slightly elevated AST levels should not be of concern if you lift frequently.
Alanine Transaminase (ALT): Reference range: ≤ 52 IU/L. Much like AST, ALT is an enzyme used to catalyze the synthesis of amino acids. Unlike AST, ALT is found predominantly in the liver and requires significant damage to hepatocytes for it to be released in to the plasma.
AST to Platelet Ratio Index (APRI): This typically won’t be included in lab tests, but it is easy to figure out. An online calculator can be found here. APRI has been shown to be a predictor of liver cirrhosis. Alkaline Phosphatase (ALP): Reference rage: 30 - 120 IU/L. ALP is an enzyme that is located within hepatic biliary ducts. Elevations in plasma concentrations of this enzyme are indicative of either cholestasis or biliary obstruction. In these pathologies, ALT and AST may remain unaffected. Total Bilirubin: Reference range: 0.1-1.0 mg/dL. Bilirubin is a byproduct of hemoglobin catabolism. The heme group of hemoglobin is broken down into biliverdin, then bilirubin, which is transported to the liver for the production of bile salts along with urobilin (the pigment that makes urine yellow) and stercobilin (the pigment that makes feces brown). High hepatic sources of bilirubin are indicative of cirrhosis or hepatitis. 5'-nucleotidase (5'NTD): Another biomarker used int he diagnosis of cholestasis. Liver Protection
Cessation: Hepatotoxic drug withdrawal is the widely accepted treatment for drug induced liver damage.
Tauroursodeoxycholate (TUDCA): TUDCA is a bile acid that was found in bears. It is currently being researched in the treatment of ophthalmologic and neurologic conditions. TUDCA has been shown to reduce cholestasis, hepatic steatosis, cirrhosis, and transient liver enzyme levels. The extent of this efficacy still needs more research and clinical trials. No research exists to support its use in zonal necrosis, peliosis hepatis, or hyperplasia.
Milk Thistle: This is bullshit, don't waste your money
Why is the conjugated/direct bilirubin raised a little in a purely unconjugated icterus (i.e. hemolysis)?
I was talking about this with a resident today. The direct bilirubin is often raised by a small, clinically insignificant, amount (but enough to exceed the reference range) in hemolysis, jaundice of the newborn etc. We were discussing the pathofysiological mechanisms behind this phenomenon. At first, I thought it was simple: "More unconjugated bilirubin means the liver has a larger 'pool' of bilirubin it can conjugate, and conjugated bilirubin will rise as a bit as well". But a quick brush-up of bilirubin metabolism reminded me of the fact that conjugated bilirubin immediately gets excreted in the bile, and is not present in the blood in normal circumstances (modern testing has shown that there's virtually no conjugated bilirubin in the blood in normal circumstances. Any direct bilirubin under normal circumstances is actually a false positive for conjugated bilirubin). Does the raised unconjugated bilirubin create a kind of 'overflow' that forces some conjugated bilirubin back into the blood? I couldn't find any documentation on that. Can anyone point me to the correct mechanism? Or is it a measuring error? I've read that the older staining methods for direct/indirect bilirubin meant that direct bilirubin would get overestimated (because some unconjugated bilirubin will participate in the 'direct' reaction). Is this still a "problem" with more modern tests?
Direct (conjugated) bilirubin: less than 0.3 mg/dL; Indirect (unconjugated) bilirubin: about 0.2 to 1.2 mg/dL; Indirect bilirubin is calculated from direct and total figures, where indirect = total minus direct bilirubin. As such, the normal range given for indirect bilirubin is generally the same or very slightly lower than for total bilirubin. Normal bilirubin level for a newborn. It’s normal to have some bilirubin in your blood. Normal bilirubin levels for older children and adults should be at or below 1mg/dL (milligrams per deciliter). Almost all babies have increased bilirubin levels within 1-2 days of birth. Bilirubin can be described as the yellowish substance that is produced by the liver, when old cells are broken down. In case the levels of bilirubin in the body are within the normal range, it does not create a problem; however, at times it is possible for the amount of bilirubin in the body to rise to a very high level, which in turn can lead to serious health complications. Although the risk of bilirubin toxicity is probably negligible in a healthy term newborn without hemolysis,9 the physician should become concerned if the bilirubin level is above 25 mg per dL (428 Any range below these levels is considered healthy and normal. KidsHealth notes that high serum bilirubin levels indicate newborn jaundice, which has symptoms that include the yellowing of eyes and skin, difficulty feeding and excessive sleepiness. Thus, both conjugated and unconjugated bilirubin are retained and a wide range of abnormal serum concentrations of each form of bilirubin may be observed. Both conjugated and unconjugated bilirubins are increased in hepatitis and space-occupying lesions of the liver; and obstructive lesions such as carcinoma of the head of the pancreas, common The 95th percentile for bottle-fed infants is a serum bilirubin level of 11.4 mg/dL v 14.5 mg/dL for the breast-fed population, and the 97th percentiles are 12.4 and 14.8 mg/dL, respectively. Of the formula-fed infants, 2.24% had serum bilirubin levels greater than 12.9 mg/dL v 8.97% of breast-fed infants (P less than .000001). The approximate normal range of bilirubin in the blood serum There are several reasons for a rise in bilirubin levels outside the newborn period. but conjugated bilirubin is usually not Conjugated bilirubin (direct bilirubin) —formed in the liver when sugars are attached (conjugated) to bilirubin. It enters the bile and passes from the liver to the small intestines and is eventually eliminated in the stool. Normally, no conjugated bilirubin is present in the blood. Figure 1. Unconjugated bilirubin and conjugated bilirubin The proportion of conjugated bilirubin with respect to the total raised bilirubin can give a clue as to cause of jaundice. 20-40% of total: more suggestive of hepatic than posthepatic jaundice. 40-60% of total: occurs in either hepatic or posthepatic causes
SpACE and XpertCare Case Discussions January 16 2019. Bilirubin test in hindi/ bilirubin normal range/ bilirubin test/bilirubin test newborn/ bilirubin - Duration: 8:22. Dr. santosh medical awareness campaign 14,428 views 8:22 Bilirubin is the terminal product of heme metabolism. Heme is present in hemoglobin and in other oxidative compounds such as hepatic mitochondrial and microsomal cytochromes (P-450). Thus plasma ... Thanks for watching!You can Donate to us here: https://www.paypal.com/donate?hosted_button_id=HHUG6LHCMU8Z2Please like, comment subscribe and share :)To view... Grab our free cheatsheet covering the 63 Must Know Labs for nurses right here: http://www.NURSING.com/labsView this post on our blog: https://www.NURSING.com... https://www.facebook.com/ArmandoHasudunganSupport me: http://www.patreon.com/armandoInstagram:http://instagram.com/armandohasudunganTwitter:https://twitter.c... It is a highly toxic molecule and there is 0.2 - 0.3g of it produced every day in the body. Yet, a normal Bilirubin level is maintained at 0.2- 1.2mg/dl. http://www.handwrittentutorials.com - This tutorial is the first of the Bilirubin series. It explains the Bilirubin Pathway from the destruction of Red Blood... Find out how health professionals use short-hand for labs and the meaning of normal ranges. Rishi is a pediatric infectious disease physician and works at Kh... GET LECTURE HANDOUTS and other DOWNLOADABLE CONTENT FROM THIS VIDEOSUPPORT US ON PATREON OR JOIN HERE ON YOUTUBE.https://www.patreon.com/medsimplifiedBilirub...
