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داء الغشاء الهياليني NRDS أشيع سبب لـ ؟


داء الغشاء الهياليني NRDS أشيع سبب لـ ؟

المعلومة

Neonatal Respiratory Distress Syndrome NRDS ( hyaline membrane disease )is the most common cause of respiratory failure in the newborn and is the most common cause of death in premature infants

متلازمة الضائقة التنفسية عند الوليد ( داء الغشاء الهياليني ) ؛ أشيع سبب لـ :
- القصور التنفسي عند الوليد
- الموت عند الخدج

المرجع

BRS Pathology -3rd edition P203

dr.msh's picture
by
بعد التخرج


سؤالي : هل نفكر بNRDS ( hyaline membrane disease عند full term neonates

إذا حدا بيعرف يا ريت يخبرنا

Al Durra's picture
Al Durra
بعد التخرج


شكرا شاكر.

qusei

Quote:
سؤالي : هل نفكر بNRDS ( hyaline membrane disease عند full term neonates

I have a theory

Now if the main problem in hyaline membrane disease is surfactant deficiency
and if surfactant synthesis stimulation requires cortisone and thyroxine
then probably any cause of decreased thyroxine ( hypothyrodisim ) or decreased cortisone ( familial addison disease ) can result in RDS in full term infants

so maybe results in the same C/P

BUT !

Now for ex. in meconium aspiration syndrome
Its well known that meconium aspiration during in utero life of an infant will result in surfactant dysfunction , airway obstruction , chemical pneumonitis

but here the difference is that the meconium's fatty acids will settle in the alveoli causing diffuse atelictiasis

so this weakens my theory that other factors in the process of the disease might give a different C\P than NRDS

but IN ALL CASES : THEY CAUSE respiratory distress , not syndrome , just distress of which NRDS is a 50 % of differntial Dx

am not sure if my theory is legal , am just suggesting

امرأة لا تتكرر's picture
امرأة لا تتكرر
السنة الخامسة


لمحة عن SURFACTANT للاطلاع

The known surfactant-associated apoproteins are surfactant proteins A, B, and C (Whitsett, 1992). The major one is surfactant A (SP-A), which is a glycoprotein with a molecular weight of about 28,000 to 35,000 d. It is synthesized in the type II cells, and increased synthesis is related temporally to increased surfactant formation in maturing fetal lungs. The amnionic fluid content of SP-A increases as a function of gestational age and fetal lung maturity. Synthesis of SP-A is increased by treatment of fetal lung tissue with cyclic adenosine monophosphate (AMP) analogues, epidermal growth factors, and triiodothyronine. Increases in surfactant apoprotein synthesis precede the increase in surfactant glycerophospholipid synthesis (Mendelson and associates, 1986).

SP-A gene expression is not detectable at 16 to 20 weeks, but it is demonstrable at 29 weeks (Snyder and colleagues, 1988). More recently, it has been demonstrated that there are two separate SP-A genes on chromosome 10 (SP-A1 and SP-A2). The regulation of synthesis of these two genes is distinctive and different. McCormick and Mendelson (1994) found that the two SP-A genes are differentially regulated. Cyclic AMP is more important in SP-A2 expression (11-fold), whereas dexamethasone caused a decrease in SP-A2 expression.

khalaf77


Corticosteroids and Fetal Lung Maturation

Liggins (1969) observed accelerated lung maturation in lambs that had been treated with glucocorticosteroids prior to preterm birth. Since that time, many investigators have suggested that fetal cortisol is the natural stimulus for lung maturation and augmented surfactant synthesis. Corticosteroids, however, may not be the only stimulus for augmented surfactant formation. For example, respiratory distress syndrome is not always observed in neonates in whom the capacity to secrete cortisol is limited. These situations include those with anencephaly, adrenal hypoplasia, or congenital adrenal hyperplasia. Nevertheless, there is now clinical evidence that glucocorticosteroids administered in large amounts to the woman at certain critical times during gestation effect an increase in the rate of fetal lung maturation. In addition, the advent of neonatal surfactant therapy, either alone or following prenatal corticosteroid treatment, has significantly reduced the incidence of respiratory disease. The use of betamethasone to accelerate fetal lung maturity as well as neonatal surfactant therapy is widely accepted

khalaf77


من الواضح ان تنظيم surfactant معقد اكثر مما نتخيل

Quote:
respiratory distress syndrome is not always observed in neonates in whom the capacity to secrete cortisol is limited. These situations include those with anencephaly, adrenal hypoplasia, or congenital adrenal hyperplasia
Quote:
Synthesis of SP-A is increased by treatment of fetal lung tissue with cyclic adenosine monophosphate (AMP) analogues, epidermal growth factors, and triiodothyronine. Increases in surfactant apoprotein synthesis precede the increase in surfactant glycerophospholipid synthesis
khalaf77

Quote:
The amnionic fluid content of SP-A increases as a function of gestational age and fetal lung maturity.

its also present in amnionic fluid
nice to know ..

Quote:
it has been demonstrated that there are two separate SP-A genes on chromosome 10

okay here's another thoery
wat if the surfactant gene is absent ?
cant we suggest the NRDS can b studied as a genetic disease ?
or it has nothing to do with genes ? just preterms ?

am just suggesting ..

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امرأة لا تتكرر
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