11 topics with brief reviews: definitions, key facts, and class questions.
This chapter is dedicated to the morphological features of diseases developing during the prenatal period, labor, and childhood. A child's body is not a miniature copy of an adult, which is why pathological processes take a different course here. We will examine perinatal pathology (asphyxia, birth trauma, hemolytic disease of the newborn), intrauterine and classic childhood infections, as well as the specific characteristics of pneumonia and digestive system diseases in children.
A separate section covers developmental and metabolic disorders. You will study the classification of congenital malformations, the pathomorphology of rickets, and the histological distinctiveness of pediatric tumors, which most frequently originate from dysontogenesis.
What is most frequently asked in class: Instructors will definitely ask about the morphological markers of intrauterine infections, gross specimens of birth trauma (cephalohematomas, intraventricular hemorrhages), and types of congenital heart defects. Favorite exam questions include the pathogenesis of hemolytic disease of the newborn, bone changes in rickets, and the differences between nephroblastoma and "adult" renal tumors. Learn the details; they make all the difference.
Can a diagnosis of prematurity be made based on weight alone?
No, a weight of less than 2,500 g is not the sole criterion. Approximately one-third of full-term infants are born with such low birth weight.
Why is jaundice more severe in premature infants?
This is due to the marked immaturity of the liver's enzyme systems, specifically the insufficient activity of glucuronyl transferase.
Which infections cause IUGR in the fetus?
The main pathogens leading to growth restriction include cytomegalovirus (CMV), rubella virus, herpes simplex virus, and Toxoplasma.
What is caput succedaneum and is it dangerous?
This is edema and subcutaneous hemorrhage in the presenting part of the fetus. As a rule, it is clinically insignificant and resolves quickly without sequelae.
Why are premature infants at maximum risk for cerebral hemorrhage?
In infants born before 34 weeks of gestation, the germinal matrix zone persists. Its blood vessels lack stroma and have a weak basement membrane, making them prone to rupture with the slightest blood pressure fluctuations.
What is genomic imprinting and how does it manifest?
This is the dependence of the phenotype on which parent the mutation was inherited from. A striking example is the 15q11-12 deletion: if the segment is inherited from the father, Prader-Willi syndrome develops (obesity, hypogonadism); if from the mother, Angelman syndrome (atonia, bouts of laughter, epilepsy).
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