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  #1  
Old 06-17-2012
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Pediatrics Neonatal Jaundice; What will happen?

An 18-year-old woman gives birth to a term infant after an uncomplicated pregnancy and delivery. Over the first few days of life, the infant becomes mildly icteric. On physical examination, there are no morphologic abnormalities. Laboratory studies show a neonatal bilirubin concentration of 4.9 mg/dL. The direct Coombs test of the infant's RBCs yields a positive result. The infant's blood type is A negative, and the mother's blood type is O positive. Based on these findings, which of the following events is most likely to occur?
(A) Kernicterus
(B) Complete recovery
(C) Respiratory distress syndrome
(D) Failure to thrive
(E) Hemolytic anemia throughout infancy
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  #2  
Old 06-17-2012
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No clue .. A) Kernicterus ?
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Old 06-17-2012
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Quote:
Originally Posted by anomali View Post
An 18-year-old woman gives birth to a term infant after an uncomplicated pregnancy and delivery. Over the first few days of life, the infant becomes mildly icteric. On physical examination, there are no morphologic abnormalities. Laboratory studies show a neonatal bilirubin concentration of 4.9 mg/dL. The direct Coombs test of the infant's RBCs yields a positive result. The infant's blood type is A negative, and the mother's blood type is O positive. Based on these findings, which of the following events is most likely to occur?
(A) Kernicterus
(B) Complete recovery
(C) Respiratory distress syndrome
(D) Failure to thrive
(E) Hemolytic anemia throughout infancy
Bbbb..complete recovery(physiologic jaundice)
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  #4  
Old 06-17-2012
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Default my answer

I read this question twice bc I couldn't find find anything abnormal here..
B) complete recovery
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Old 06-17-2012
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answer is complete recovery\\\\


but this explanation just for readers who wonder why, or the idea of the question

--> the direct Coombs test is positive, a visual indication that antibodies (and/or complement proteins) are bound to the surface of red blood cells--->
->> people normally form IgM [dont cross placenta to infant] antibodies against other ABO subtypes, except when they are of the O type [like the mother here].... she forms IgG antibodies against the B,AB, or A[like her infant]... this IgG crosses the placenta,,, and as soon as her antibodies ware-off and disappear, then the infant can become normal and recover completely... if a question like this comes in the test,,, they might ask when do these symptoms disappear, and it'd be 3-6 months,,,, same time when children with aggamaglobinemia[immune disorder] start to develop infections [when mommy's antibodies go away]
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Old 06-17-2012
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B.complete recovery
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  #7  
Old 06-18-2012
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I go for B...
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Old 06-18-2012
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ABO HDN
MOTHERS-BLOOD GROUP O
FETUS-BLOOD GROUP A OR B
BLOOD GROUP O INDIVIDUALS HAVE ANTI-A AND B -IgG ANTIBODIES
IgG CROSS PLACENTA AND ATTACH TO FETAL A OR B RBCs
FETAL SPLENIC MACROPHAGES PHAGOCYTOSE RBCs-MILD ANEMIA
UNCONJUGATED BILIRUBIN FROM EXTRAVASCULAR HEMOLYSIS IS DISPOSED OF IN THE MOTHER'S LIVER
JAUNDICE DEVELOPS WITHIN THE FIRST 24 HOURS AFTER BIRTH
NEWBORN LIVER CANNOT HANDLE THE EXCESS BILIRUBIN LOAD
RISK FOR KERNICTERUS IS VERY SMALL
ANEMIA-MILD NORMOCYTIC OR NO ANEMIA AT ALL
POSITIVE DIRECT COOMBS' TEST ON FETAL CORD BLOOD RBCs
DUE TO ANTI-A OR B IgG ANTIBODIES COATING FETAL A OR B RBCs
SPHEROCYTES ARE PRESENT ,DUE TO MACROPHAGE REMOVAL OF A PORTION OF THE RBC MEMBRANE
TRANSFUSIONS ARE RARELY INDICATED
RH HDN
MOTHER-RH NEGATIVE
FETUS-RH POSITIVE
MOTHER DEVELOPS ANTI-D-IgG ANTIBODIES WHEN EXPOSED TO FETAL RH POSITIVE CELLS
FIRST RH INCOMPATIBLE PREGNANCY DOES NOT AFFECT THE FIRSTBORN
ANTI-D-IgG ANTIBODIES CROSS THE PLACENTA AND ATTACH TO FETAL RH POSITIVE RBCs,FETAL SPLENIC MACROPHAGES PHAGOCYTOSE RBCs-SEVERE ANEMIA,MAY DEVELOP HIGH-OUTPUT CARDIAC FAILURE LEADING TO HYDROPS FETALIS WHICH IS A COMBINED LEFT-AND -RIGHT HEART FAILURE WITH ASCITES AND EDEMA
JAUNDICE DEVELOPS SHORTLY AFTER BIRTH
MOST OF THE UNCONJUGATED BILIRUBIN IS NOT BOUND BY ALBUMIN AND CIRCULATES FREE IN THE BLOOD
INCREASED RISK FOR KERNICTERUS(IN THE BASAL GANGLIA)
POSITIVE DIRECT AN INDIRECT COOMBS' TEST
NO SPHEROCYTES -MACROPHAGES PHAGOCYTOSE THE ENTIRE RBC
TRANSFUSIONS ARE REQUIRED -CORRECTS ANEMIA,REMOVES ANTIBODIES AND UNCONJUGATED BILIRUBIN
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  #9  
Old 06-18-2012
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Quote:
Originally Posted by irakly View Post
ABO HDN
MOTHERS-BLOOD GROUP O
FETUS-BLOOD GROUP A OR B
BLOOD GROUP O INDIVIDUALS HAVE ANTI-A AND B -IgG ANTIBODIES
IgG CROSS PLACENTA AND ATTACH TO FETAL A OR B RBCs
FETAL SPLENIC MACROPHAGES PHAGOCYTOSE RBCs-MILD ANEMIA
UNCONJUGATED BILIRUBIN FROM EXTRAVASCULAR HEMOLYSIS IS DISPOSED OF IN THE MOTHER'S LIVER
JAUNDICE DEVELOPS WITHIN THE FIRST 24 HOURS AFTER BIRTH
NEWBORN LIVER CANNOT HANDLE THE EXCESS BILIRUBIN LOAD
RISK FOR KERNICTERUS IS VERY SMALL
ANEMIA-MILD NORMOCYTIC OR NO ANEMIA AT ALL
POSITIVE DIRECT COOMBS' TEST ON FETAL CORD BLOOD RBCs
DUE TO ANTI-A OR B IgG ANTIBODIES COATING FETAL A OR B RBCs
SPHEROCYTES ARE PRESENT ,DUE TO MACROPHAGE REMOVAL OF A PORTION OF THE RBC MEMBRANE
TRANSFUSIONS ARE RARELY INDICATED
RH HDN
MOTHER-RH NEGATIVE
FETUS-RH POSITIVE
MOTHER DEVELOPS ANTI-D-IgG ANTIBODIES WHEN EXPOSED TO FETAL RH POSITIVE CELLS
FIRST RH INCOMPATIBLE PREGNANCY DOES NOT AFFECT THE FIRSTBORN
ANTI-D-IgG ANTIBODIES CROSS THE PLACENTA AND ATTACH TO FETAL RH POSITIVE RBCs,FETAL SPLENIC MACROPHAGES PHAGOCYTOSE RBCs-SEVERE ANEMIA,MAY DEVELOP HIGH-OUTPUT CARDIAC FAILURE LEADING TO HYDROPS FETALIS WHICH IS A COMBINED LEFT-AND -RIGHT HEART FAILURE WITH ASCITES AND EDEMA
JAUNDICE DEVELOPS SHORTLY AFTER BIRTH
MOST OF THE UNCONJUGATED BILIRUBIN IS NOT BOUND BY ALBUMIN AND CIRCULATES FREE IN THE BLOOD
INCREASED RISK FOR KERNICTERUS(IN THE BASAL GANGLIA)
POSITIVE DIRECT AN INDIRECT COOMBS' TEST
NO SPHEROCYTES -MACROPHAGES PHAGOCYTOSE THE ENTIRE RBC
TRANSFUSIONS ARE REQUIRED -CORRECTS ANEMIA,REMOVES ANTIBODIES AND UNCONJUGATED BILIRUBIN

gr8 explanation....thanku

and the right option is B....COMPLETE RECOVERY
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  #10  
Old 06-19-2012
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Complete Recovery..
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  #11  
Old 06-19-2012
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Quote:
Originally Posted by jonrick21 View Post
i will go with "c' respiratory distress syndrome
rds in newborn
pathogenesis
a. Prematurity
b. Maternal diabetes
surfactant synthesized by type ii pneumocytes
stored in lamellar bodies
synthesis begins in 28th week of gestation
lecithin is the major component
synthesis is increased by cortisol and thyroxine and decreased by insulin
fetal hyperglycemia(maternal diabetes) increases insulin release
cesarean section-lack of stress-induced increase in cortisol from a vaginal delivery
women who have to delivery prematurely receive glucocorticoids in order to increase fetal surfactant synthesis ,good maternal glycemic control decreases the risk for rds
widespread atelectasis results in massive intrapulmonary shunting-perfusion without ventilation
collapsed alveoli are lined by hyaline membranes
clinical findings
respiratory difficulty begins within a few hours after birth
grunting
tachypnea
inercostal retractions
hypoxemia,respiratory acidosis
chest radiograph-,,ground glass'' appearance
complications
superoxide free radical damage from o2 therapy may result in blindness and bronchopulmonary dysplasia
intraventricular hemorrhage
patent ductus arteriosus
necrotizing enterocolitis -intestinal ischemia allows entry of gut bacteria into the intestinal wall
hypoglycemia in newborn-due to excess insulin in response to fetal hyperglycemia -seizures and damage to neurons.must give newborns glucose
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Old 07-29-2012
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for a case like this , it has to be the second child for IgG to cross to the fetus, otherwise it's clinically irrelevant. plus jaundice should be in the first 24 hours of birth.

Am I right?
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Old 07-29-2012
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Actually, I couldn't find any prove that In such case , the mother would develop IgG antibodies against the fetus RBC, all what I know is IgM and it won't cross and that includes all blood groups,but may be it stays there for the next pregnancy and will eventually produce IgG? I don't know. If someone has an explanation please provide us .

Thanks in advance.
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