...reabsorbrion- urine (small part)+ liver and re-excretion. MEASUREMENT OF SERUM BILIRUBIN Conjugated measured by direct reaction and total efter addition of reagent, unconjugated by calculation. Delta bilirubin- conjugated+albumin (half life of bilirubin like albumin 20d)- not secreted in urine- prolonged hyperbilirubunemia- explains prolonged hyperbilirubinemia dispite of resolution and absence of bilirubin in urine. CAUSE MECHANISM Ineffective Erythropoiesis Overproduction of bilirubin Indirect Hyperbilirubinemia Cobalamin deficiency Hemolytic Disorders Overproduction of bilirubin Folate deficiency Inherited Profound iron deficiency Red cell enzyme defects (e.g., glucose-6-phosphate dehydrogenase deficiency) Thalassemia Sickle cell disease Drugs: Rifampin, Probenecid Impaired hepatocellular uptake Spherocytosis and elliptocytosis Inherited ConditionsCrigler-Najjar syndrome types I and II Impaired conjugation of bilirubin Acquired Gilbert's syndrome Drugs and toxins Other Hypersplenism Hematoma Overproduction of bilirubin Immune mediated Direct Hyperbilirubinemia Paroxysmal nocturnal hemoglobinuria Inherited Conditions Traumatic: macro- or microvascular injury Rotor's syndrome Dubin-Johnson syndrome Impaired excretion of conjugated bilirubin Gilbert- A mutation in UDP glucuronyl transferase - reduction in enzyme activity. Crigler-Najjar syndrome, types I (absence of enzyme activity) and II (significantly...
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...Treating Hyperbilirubinemia Enzyme inducers have the ability to conjugate bilirubin which leads to the decrease of bilirubin content in the serum, thus helps treat Hyperbilirubinemia and also treat Criggler Najjar Type II disease (inherited disorder affecting the metabolism of bilirubin). 2. Monitoring of drug compliance In chronic alcoholics, a very high concentration of y-glutamyltransferase activity occurs in their serum which is observed to reduce to normal levels upon withdrawal from consuming alcohol. Monitoring indicators of microsomal enzyme inducers can be helpful in deciding whether to increase/decrease or change a drug. 3. According to recent studies, inducers of liver microsomal enzymes enhance the hydroxylation of steroids in man. Phenobarbital, diphenylhydantoin, and phenylbutazonestimulate cortisol hydroxylase activity...
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...Erythroblastosis Fetalis by Jeanifer Aggarao Mrs. Carrig July 23, 2007 Table of Contents Definition 1 Pathophysiology 2 Signs and Symptoms 3 Risk Factors 5 Diagnosis 6 Treatment 8 Nursing Responsibilities 10 Psychosocial Implication 10 Bibliography 12 Definition Erythroblastosis fetalis is a fatal hemolytic disease of the newborn (HDN) caused by incompatibilities in the blood groups between the mother and her unborn child during pregnancy. Because of the incompatibility, the mother's immune system may launch an immune response against the red blood cells of the fetus through the placenta, resulting in the destruction of the red blood cells (hemolysis). In the destruction of the red blood cells, the fetus can develop anemia. The red blood cell destruction ranges from mild to very severe, and fetal death from heart failure can occur, as well as life-threatening problems for future pregnancies. The Rhesus system (Rh) blood group antigen is responsible for most of the fatal cases of erythroblastosis fetalis, hence, the term Rh incompatibility disease. However, other alloimmune antigens belonging to the Kell (K and k), Duffy (Fya), Kidd (Jka and Jkb), MNSs (M, N, S, and s), Diego, Xg, P, Ee, Cc antigen systems, as well as other antigens may also produce the disease. Incompatibilities of Landsteiner (A, B and O) blood group systems do not cause erythroblastosis fetalis. A French midwife reported the first case of HDN in a set of...
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...RNQuiz.com - NCLEX-RN Study Guide Neonatal Care 1 Cardiovascular system: o Closer of the foramen ovale secondary to: Expansion of the lungs, decreases pulmonary resistance Clamping of umbilical cord: Increases systemic vascular resistance Increases left atrial pressure Respiratory system: o First breath is a reflex to noise and light Renal system: o Not fully functional for the first year o Neonate’s ability to filter waste products improve over first year of life Gastrointestinal system: o No normal bacterial flora o Unable to digest fat Thermogenesis: o Rapid heat loss can occur in less than optimal environment Immunity: o Depends on immunity provided by mother o Neonate begins to development of own immune system within 3 months Hematopoietic system: o Prolonged coagulation time secondary to low vitamin K levels RNQUIZ.com Changes in the Neonate post delivery: RNQuiz.com - NCLEX-RN Study Guide Neurologic system: o Equal strength and symmetrical responses and reflexes Hepatic system: o Physiological jaundice is mild and last first few days after birth Apgar Assessment: 2 This is a way to evaluate the neonate’s cardiopulmonary and neurological status at 1 and 5 minutes after birth. A score of 8-10 indicates no immediate distress, less than 8; possible CPR. Sign Heart rate Respiratory Muscle tone Reflex irritability Color 0 Absent Absent Flaccid None Pale blue 1 Less than 100beats/min...
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...The Rh factor (ie, Rhesus factor) is a red blood cell surface antigen that was named after the monkeys in which it was first discovered. Rh incompatibility, also known as Rh disease, is a condition that occurs when a woman with Rh-negative blood type is exposed to Rh-positive blood cells, leading to the development of Rh antibodies. Rh incompatibility can occur by 2 main mechanisms. The most common type occurs when an Rh-negative pregnant mother is exposed to Rh-positive fetal red blood cells secondary to fetomaternal hemorrhage during the course of pregnancy from spontaneous or induced abortion, trauma,[1] invasive obstetric procedures, or normal delivery. Rh incompatibility can also occur when an Rh-negative female receives an Rh-positive blood transfusion. In part, this is the reason that blood banks prefer using blood type "O negative" or "type O, Rh negative," as the universal donor type in emergency situations when there is no time to type and crossmatch blood. The most common cause of Rh incompatibility is exposure from an Rh-negative mother by Rh-positive fetal blood during pregnancy or delivery. As a consequence, blood from the fetal circulation may leak into the maternal circulation, and, after a significant exposure, sensitization occurs leading to maternal antibody production against the foreign Rh antigen. Once produced, maternal Rh immunoglobulin G (IgG) antibodies may cross freely from the placenta to the fetal circulation, where they form antigen-antibody complexes...
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...disposal of bilirubin (the chemical that results from the normal breakdown of hemoglobin from red blood cells) is abnormal. The condition has also been referred to as constitutional hepatic dysfunction and familial nonhemolytic jaundice. The enzyme abnormality in Gilbert syndrome results in mild elevations of bilirubin in the blood, particularly after starvation or dehydration. Gilbert syndrome is the result of a genetic mutation in the promoter region of a gene for the enzyme UGT1A (one of the enzymes called UGT glucuronosyltransferases that are important for bilirubin metabolism). The gene is located on chromosome 2. Other types of mutations in the same gene cause the Crigler-Najjar syndrome, which is a more severe and dangerous form of hyperbilirubinemia (high bilirubin in the blood). People with two copies of the abnormal promoter region for the UGT1A gene (one inherited from each parent) have Gilbert's syndrome and elevated bilirubin levels, suggesting an autosomal recessive mode of inheritance. This means that both parents require the gene for expression of the abnormality in the offspring. Gilbert syndrome is a frequent finding in people in the United States and Europe. The condition is usually detected serendipitously (purely by accident) in the course of routine blood screening. The elevated bilirubin pigment can sometimes cause mild yellowing (jaundice) of the eyes. People with Gilbert syndrome are otherwise entirely normal with no other signs or symptoms. Their liver enzyme...
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...THE NEWBORN WITH SPECIAL CONSIDERATIONS A preterm infant is usually defined as a live-born infant born before the end of week 37 of gestation; another criterion is a weight of less than 2,500 grams (5lb 8oz) at birth I. INCIDENCE Occurs approximately 7% of live births of white infants, in Afro-American infants the rate is doubled 14% (Thilo & Rosenberg, 2003) CAUSES/FACTORS ASSOCIATED WITH PRETERM BIRTHS 1. Low socio-economic status 2. Poor nutritional status 3. Lack of prenatal care 4. Multiple pregnancy 5. Previous early birth 6. Race (non-whites have higher incidence than whites) 7. Cigarette smoking 8. Age of the mother (highest incidence is in mothers younger than age 20) 9. Order of birth (early termination is highest in first pregnancies and in those beyond 4th pregnancies) 10. Closed spaced pregnancies 11. Abnormalities of mother’s reproductive system, such as intrauterine septum 12. Infections (especially UTI) 13. Obstetric complications (PROM, premature separation of placenta 14. Early induction of labor 15. Elective cesarean birth ASSESSMENT A. History – detailed pregnancy history will reveal reason for the preterm birth; be careful not to convey disapproval of reported pregnancy behaviors such as smoking, etc. Being overburdened with guilt may be detrimental to her attempts to bond with her infant B. Appearance Criteria Posture Premature infant Resting posture – characterized by very little, if any, flexion in upper extremities and only partial flexion of...
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...delivery. The swelling extends beyond the sutures and can be associated with petechiae or ecchymosis. Most of the time, the problem is noticed after birth. No treatment is needed. The problem usually goes away on its own within a few days. Complications may include a yellow color to the skin. A cephalhematoma forms when blood vessels rupture during labor or delivery to produce bleeding into the area between the bone and its periosteum (Hockenberry & Wilson, 2011, p 281). Cephalohematomas are more common in first pregnancies, if the baby's head is larger than the birth canal. It gets better with no treatment within 3 months. The boundaries of the cephalhematoma are distinguishable and do not extend beyond the limits of the bone. Hyperbilirubinemia may result during resolution of the hematoma. A local infection can develop and is suspected when swelling suddenly increases (Hockenberry & Wilson, 2011, p...
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...ketoconazole itraconazole, clarithromycin, salicylates, and conivaptan; in renal impairment with felodipine, quiNIDine, telithromycin, pantoprazole, tamoxifen, azithromycin, amiodarone, saquinavir, darunavir, posaconazole, lapatinib, mifepristone, diltiazem, nelfinavir, verapamil, ranolazine, amiodarone, and dronedarone; and with grapefruit juice. Rivaroxaban’s effect is decreased with rifampin, carBAMazepine, phenytoin, and St. John’s wort. Half-life Elimination half-life is 5-11.7 hours, 11-13 hours in elderly, 10.1-10.4 hours for hepatic impairment, and 8.7-9.5 hours for renal impairment. 6. Adverse effects and drug interactions: Adverse effects a nurse must know include jaundice, cholestasis, increased hepatic enzymes, nausea, hyperbilirubinemia, pruritus, hypersensitivity, and blisters. Life-threatening side effects include cytolytic hepatitis; GI, adrenal, and intracranial bleeding; thrombocytopenia; epidural hematoma; hemiparesis; retinal hemorrhage; subdural hematoma; retroperitoneal hemorrhage; cerebral hemorrhage; anaphylactic reaction and shock; and Stevens-Johnson syndrome. Nurses must watch for signs of active bleeding, should educate the patient against abrupt discontinuation, and be aware that epidural or spinal hematomas may occur in patients who have taken anticoagulants and are receiving neuraxial anesthesia or undergoing spinal puncture. Nurses should also be aware that there is an increased effect in hepatic and renal disease, with grapefruit juice, and with...
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...hospitalized on six separate occasions over the years. He continues to drink and exhibits most of the common manifestations of alcoholic cirrhosis. He was recently hit by a car and was hospitalized for a broken leg. He appeared to be under the influence of alcohol at the time of the accident and had a blood alcohol level of 0.18. F.C.’s family reports that his mental functioning has deteriorated significantly over the past few months. Discussion Questions 1. What are the common manifestations of alcoholic cirrhosis? Which of these are secondary to hepatocellular failure? Which are secondary to portal hypertension? Common manifestations of alcoholic cirrhosis are as follows: * Jaundice: yellow pigmentation of the skin caused by hyperbilirubinemia. This condition is secondary to hepatocellular failure because the bilirubin metabolism becomes impaired due to malfunction of liver tissue. * Spontaneous Bacterial Peritonitis: acute bacterial infection of ascetic fluid caused by contamination of dialysate. This condition is considered secondary to portal hypertension because the normally, the fluid passes the portal vein into the liver to be killed off, but with a fluid back up, bacterial infection grows due to the increased fluid retention within the portal vein. * Hepatic Encephalopathy: accumulation of toxic substances in blood that are not removed because with a damage liver, the liver cannot kill of toxins leading to infection or constipation. This condition...
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...individual. However, there are some common characteristics that include: • Blindness or visual impairment which typically includes absent fixation, visual inattentiveness and strabismus. Symptoms may also include blindness in one or both eyes, pupil dilation in response to light, nystagmus (a rapid, involuntary to-and-fro movement of the eyes), inward and outward deviation of the eyes, hypotonia (low muscle tone), and hormonal problems. • Systematic and behavioral conditions like mental retardation, eplilepsy, cerebral palsy, attention deficit disorder and autism. • Seizures and prolonged skin and eye discoloration known as jaundice may also occur. • Developmental deficiencies such as underdeveloped midfacial structures, hypoglycemia, hyperbilirubinemia, disturbance in temperature regulation, muscular hypotonia and microgenitalism. • Developmental delays in the individual due to vision impairment or neurological problems. Presentation during pregnancy and infancy: • Concerns may be raised at a mid-trimester ultrasound scanning which is when the condition is usually diagnosed. However, it can also easily be missed. • The infant may also appear normal at birth but developmental problems may also set in at this stage such as poor growth of male genitalia. • Inexplicable hypoglycaemia is a sign of pituitary insufficiency in children. • Susceptibility to infection, sleep disturbances and seizures which occur mostly in patients with developmental delays. Treatment and Investigative...
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...Clinical Learning Packet – Newborn Assessment Newborn Client Initials: JS_____ Gender: M/F Date/Time of Delivery: 02/08/2013 1956_ Type of Delivery: SVD C/S IFD Vac Gestational Age by Dates:_40wks (as stated by primary nurse I could not find in chart)________ Age at Time of Assessments (hours): _13_______ APGARS: __8____ @ 1 min. ___9___ @5 min. Blood Type/Rh: Newborn (not taken per agency protocol)_______ Maternal _B+________ Blood Glucose: Reason___________________Frequency__________Last Results:______ Newborn Weight: @ birth 3.28kg__________ Current 3.26kg_________ % Weight loss:0.61%______ Length:_21in______ HC:_13.5in______ CC:_13in_____ Feeding: Breast: _x_____Formula (type): ________________ Feeding Frequency/Amount/Time:_On demand usually every two hours_ Vitamin K (date):_ 02/08/2013 ____________ Erythromycin eye ointment (date): 02/08/2013 ______________ Hepatitis B (date):_02/09/2013_____________________ Circumcision (date):_02/09/2013__________ Metabolic Screen Due:________ completed_________Hearing Screening: Pass /Fail /Reassess Comments: _Clients Bilirubin score was 3.2 at 3hrs after birth. The physician asked for it to be watched. We assessed the bilirubin score again at 14hrs after birth and received a 5.2. The bilirubin will be assessed again at 18 hours after birth and the physician will decide on a course of action at that time per agency protocol. The baby is in the High intermediate group right now although...
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...SPE-226 Date: January 11, 2016 Instructor: Brenda Combs What is intellectual disability? It is characterized by significant limitations in both intellectual functioning and in adaptive behavior, which covers many everyday social and practical skills (AAIDD, 2013). It affects 1-3% of the population, and there are many causes of intellectual disability, but doctors find a specific reason in only 25% of cases (May 2013). Some of the causes linked to intellectual disabilities are, infections that can be present at birth or occurring after birth. Chromosomal abnormalities such as Downs Syndrome, it could be environmental, and it can be due to trauma (May, 2013). Other factors related to intellectual disabilities are metabolic, such as hyperbilirubinemia, very high bilirubin levels in babies. Nutritional issues such as malnutrition, toxic (intrauterine expose to alcohol, cocaine, amphetamine, and other drugs), unexplained reasons is the largest category for unexplained occurrences of intellectual disability (May, 2013). Now we will look at Autism. Autism is a group of disabilities that can cause significant social, communication and behavioral challenges. (February,2015). Exact cause of autism is not known, but research has pointed to several possible factors, including genetics (hereditary), metabolic or neurological factors, certain types of infection, and problems occurring at birth. Both genetics and environment likely play a role in ASD (December 2015). Then we have multiple...
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...Infants with GER tend to spit up after feeding. “Severe GER can cause feeding difficulties, irritability, poor weight gain, and respiratory problems” (“short-andlong-termchallengesofprematurity”). Some infant formulas can aid in the digestion problems. When the infant’s gastrointestinal system matures, GER tends to resolve itself. Hyperbilirubinemia is another complication that premature infants face. This blood problem is when an infant has high levels of bilirubin, “which is produced by the normal breakdown of red blood cells” (“aprimeronpreemies”). High bilirubin blood counts lead to jaundice, which causes a yellowing of the skin. High levels are very dangerous and cause brain damage. Jaundice can be treated by placing the infant under special blue lights called bili lights which break down bilirubins. These levels are tested daily. In very rare cases, blood transfusions are needed for treatment. Anemia is also a very common blood problem in premature babies. Webster’s Dictionary defines Anemia as, “a condition in which a person has fewer red blood cells than normal...
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...Jaundice in the Newborn Jaundice and how it occurs Jaundice, or hyperbilirubinemia is a common condition found in newborn infants associated with high levels of bilirubin within the body. It is a common occurrence in infants 35-36 week gestation, with premature babies also having an increased risk for developing it. Most cases of jaundice within newborns occur as a result of increased erythrocyte breakdown and a decrease in the reuptake of bilirubin by the liver, called physiologic jaundice. Bilirubin is a normal product that results in the destruction of red blood cells. It also can take on two possible forms, unconjugated and conjugated. Unconjugated bilirubin is lipid-soluble, whereas conjugated bilirubin is water soluble. Jaundice occurs when there is an increased amount of...
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