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30 Cards in this Set
- Front
- Back
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Definition...
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Yellow colouration of skin and sclera caused by raised bilirubin level (hyperbilirubinemia).
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Bilirubin Synthesis 1...
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Aging, immature and malformed RBC's broken down by reticuloendothelial system.
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Bilirubin Synthesis 2...
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Haemoglobin broken down into haem, globin and iron.
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Bilirubin Synthesis 3...
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Haem converted to biliverdin by enzyme bilirubin reductase to form unconjugated bilirubin (fat soluble).
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Bilirubin Synthesis 4...
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Unconjugated bilirubin transported in albumin (carrier plasma protein) to liver cells called hepatocytes.
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Bilirubin Synthesis 5...
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Unconjugated bilirubin detached from albumin and combined with glucose, oxygen and glucuronic acid and conjugation occurs using uridine diphosphate glucuronyl transferase (UDP-GT).
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Bilirubin Synthesis 6...
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Unconjugated bilirubin converts to bilirubin diglucuronide/conjugated bilirubin (water soluble).
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Bilirubin Synthesis 7...
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Conjugated bilirubin is water soluble and can be excreted via bilary system into small intestines where normal bacteria changes it into urobilinogen and oxidised into orange urobilin. Excreted in urine and meconium.
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Bilirubin Synthesis in Uterine Life...
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Fetal bilirubin excretion happens via the placenta and maternal liver due to immature fetal liver unable to conjugate and remove bilirubin. Neonate must take over this after birth (Stables and Rankin 2010).
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Causes of Hyperbilirubinemia...
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Some unconjugated bilirubin may escape to extra vascular tissue. Delay in passage of meconium. Conjugated becomes deconjugated and returns to circulation. Increase RBC's and bilirubin = liver can't cope and deposits bilirubin in subcut fat. Increased bilirubin/decreased albumin = Bilirubin free in blood cells. |
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Physiological Jaundice...
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Appears 3-4 days after birth in 60% of term and 80% of pre term babies. Increase in erythrocyte breakdown increases bilirubin. Immature liver cannot synthesis sufficient glucuronyl transferase for conjugation. Unconjugated fat soluble bilirubin cannot be excreted and therefore diffused into body tissue.
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Causes of Physiological Jaundice...
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Increased unconjugated bilirubin in the first few days due to transition. More efficient lungs increased oxygen = haemolysis. Prem = Greater liver immaturity. Birth trauma/bruising - erythrocyte breakdown = increased bilirubin. olythaemia = Excess RBC's to breakdown e.g. delayed cord clamping. Infection = Significant haemolysis. |
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Pathological Jaundice...
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Appears in the first 24 hrs of life and is assumed to be due to haemolysis until proven otherwise.
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Pathological Jaundice Causes: Blood Group Incompatability...
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Blood cells from rhesus positive baby enters rhesus negative mothers blood and her blood treats D antigen and babies blood as foreign and produces antibodies.
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Pathological Jaundice Causes: ABO Isoimmunisation... |
When mother's blood is O and baby's is A or B. Type O blood creates antibodies throughout life and may already have anti A/B antibodies which will cross the placenta and attack fetal blood cells. |
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Treatment: Phototherapy... |
Ultraviolet light catalyses the conversion of unconjugated bilirubin to conjugated bilirubin which is water soluble and an be excreted. Side effects can be blistering and retinal damage and treatment should stop when 50micromol/L below line. |
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Treatment: Immunoglobin... |
Infusion of set pooled immunoglobin used in isoimmune haemolysis. Helping to mop up antibodies and prevent a rise in bilirubin levels. |
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Treatment: Exchange Transfusion... |
Used if other treatments fail. Blood given which is double the baby's blood volume via an umbilical catheter; removing excess bilirubin and lowering the jaundice level. |
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Late Neonatal Jaundice... |
Bilirubin concentration remains raised beyond 14 days. Increased RBC destruction possible due to blood type incompatability, isoimmunisation, sepsis, hypothyroidism. Pale stools and dark urine present. |
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Direct/Conjugated Jaundice (Obstructive)... |
Increased direct bilirubin involves cholestasis and associated with alterations in hepatic function/interference with excretion of bilirubin into bile/obstructive bile flow (Blackburn 2013). |
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Unconjugated Breatfeeding Jaundice... |
Early onset at 3-4 days and can continue till day 14 with a gradual decline in bilirubin. Sometimes creates anxiety for parent who see it as an illness (Stables and Rankin 2010). |
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Caused of BF Jaundice... |
Inhabitation of glucuronyl transferase by substance found in breast milk such as hormone pregnanediol (problems with conjugation). Lipase releases fatty acids into intestines and alters their function. Enzyme β-glucuronidase splits conjugated bilirubin and increases shunting from bilirubin in intestines to liver. Delay in meconium in BF babies. |
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Two Forms of BF Jaundice... |
Early onset relating to process of feeding e.g. shunting, lower fluid/calorie intake and stooling patterns. Later onset prolonged jaundice is less common but is caused by the attributes of breastmilk interfering with normal conjugation and excretion. |
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Prevention of BF Jaundice... |
Early BF establishment and frequent feeds increasing gut and intestinal function for the removal of meconium (Less bilirubin for enzymes to convert back). Avoiding supplements. Parental support. |
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Trust (2013) & NICE (2010): Risk Factors for Jaundice... |
<38 weeks, family history, breastfeeding and visible jaundice <24 hours. |
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Trust (2013) & NICE (2010): Risk Factors for Kernicterus... |
High biliubin (>340microml/L), rising level (8.5micromol/L/Hr), clinical features of encephalopathy. |
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Trust (2013) & NICE (2010): Signs... |
Yellow skin in pale babies under natural light and yellow conjunctiae in dark skin babies. |
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Trust (2013) & NICE (2010): Assess... |
Pallor, poor feeding, drowsiness, blood group incompatibility. |
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Trust (2013) & NICE (2010): Investigations... |
Assessment of jaundice at every opportunity <72 hours. Suspected jaundice assessed <24 hours within 2 hors and >24 hours within 6 hours. If SBR >100micromol/L in first 24 hours repeat 6-12 hrs. Record on chart. In phototherapy repeat SBR 6-12 hourly when stable or falling and 12-18 hours after stopping treatment for rebound jaundice. |
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References... |
Stables and Rankin (2010) Marshall and Raynor (2014) Lumsden and Holmes (2010) Nurse (2009) Blackburn (2013) Trust (2013) & NICE (2010) |
