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					Intrauterine growth. Critical
 periods in developement.
    Parturition. Multiple
        pregnancies
     81402 – Histology and Embryology
       Summer semester, Lecture – 15
               Zuzana Jirsová
INTRAUTERINE GROWTH
Fetal period: from the beginning of the 9th week to birth. Maturation of tissues and organs.
Rapid growth of the body (between the 3rd and 5th months). Length of the fetus is indicated:
CRL (crown-rump length) or CHL (crown-heel length).
Incerase in weight is most striking during the last two months of gestation

                                                             (Langman´s Medical Embryology, Sadler, 2004)




Intrauterine growth restriction (IUGR) – infants are at or bellow 10% weight at a given
gestational age. Causes: chromosomal abnormalities, teratogens, congenital infections;
poor maternal health, the mother´s nutritional status and her use of cigarettes, alcohol, and
other drugs; placental insufficiency; and multiple birth (e.g. twins, triplets)
Growth in lenght of the
fetus is rapid during the
the third, fourth and fifth
Months

Size of the head in the
relation to the rest of
the body




Photo: Hamilton, Boyd, Mossman, Human
Embryology, 1972
In general, length of pregnancy for full-term fetus is considered to
be 280 days (or 40 weeks) after onset of the last menstruation
(LNMP) or more accurately 266 days (or 38 weeks) after fertilization

For the first 34 to 38 weeks of gestation, myometrium does not correspond to
signals for parturition (birth) During the last 2 to 4 weeks of pregnancy uterus
undergoes a transitional phase in preparation for the onset of LABOR (thickening
of the myometrium in the upper region of the uterus and softening and thinning of
the lower region and cervix)

PRETERM BIRTH
Delivery before 34 weeks
Factors iniciating labor are not known and may involve “retreat from maintenance
of pregnancy“, in which pregnancy-supporting factors (e.g. hormones) are
withdrawn, or active induction caused by stimulatory factors targeting the uterus.
Pregnancy complication reguiring premature delivery (e.g. maternal hypertension
and diabets as well as abruption of placenta).
Preterm birth of premature infants is the second leading cause of infant mortality
and contributes significantly to morbidity
PARTURITION (BIRTH)
Labor itself is divided into three stages:

(1) EFFACEMENT (thinning and shortening) and DILATATION OF THE CERVIX
    stage is produced by uterine contractions that force the amniotic sac against the
    cervical canal as a wedge and, if the membranes (amniochorionic membrane fused
    with decidua capsularis) have ruptured then pressure will be exerted by the
    presenting part of the fetus, usually the head this stage ends when the cervix is fully
    dilated

(2) DELIVERY OF THE FETUS
    stage is also assisted by uterine contractions, but the most important force is
    provided by increased intra-abdominal pressure from contraction of abdominal
    muscles

(3) DELIVERY OF THE PLACENTA AND FETAL MEMBRANES
    stage requires uterine contraction and is aided by increasing intra-abdominal
    pressure

Uterine contractions usually begin about 10 minutes apart; then, during the second
stage of labor, they may occur less than 1 minute apart and last from 30 to 90 seconds.
Their occurrence in pulses is essential to fetal survival, since they are sufficient force to
compromise uteroplacental blood flow to the fetus.
SIGNS OF FULL TERM BABY

The weight: 3000 – 3400 g, length (CHL): 50 cm

Skin is pink and smooth; remnants of the lanugo are only on the back
and shoulders.
Subcutaneous fat is developed, baby has well-rounded contours.
Hairs are several cm long; eyebrows and eyelashes are formed.
The nails extend beyond the tips of fingers/toes.

Bones of the skull are hard, fontanelles are separated.

Sexual characteristics are pronounced - developed external genitalia,
testes are in the scrotum, labia majora cover labia minora.
BIRTH DEFECTS
- congenital malformation, congenital anomaly
are synonymous terms used to describe
structural, behavioral, functional and metabolic disorders

These disorders are studied by TERATOLOGY (Gr. teratos = monster)

Genetic factors – chromosome abnormalities (numerical and structural
                                               mutant genes)
Environmental factors

Teratogenic effect depends on:
Genotype of fetus and maternal genome
Developmental stage at the time of exposure
The most sensitive period for inducing birth defects is
the third to eighth week of gestation (period of embryogenesis)
Dose and duration of exposure

PRENATAL DIAGNOSIS
Ultrasonography, amniocentesis, chorionic villus sampling,
Maternal serum screening
CAUSES OF THE HUMAN BIRTH DEFECTS
 A = unknown causes: 50 60 %, B = multifactorial inheritance: 20 – 25 %,
 C = chromosome abnormalities: 6 - 7 %, D = mutant genes: 7 – 8 %,
 E = environmental factors: 7 – 10 %




                                                                                 A


  A
                                                                                 B

                                                            E
 B                                                                               C

                                         D
                               C                                                 D



                                                                                 E

                                             Diagram: The Developing Human, Moore, Persaud, 1998
 TERATOGENES ASSOCIATED WITH HUMAN MALFORMATIONS

INFECTIOUS AGENTS
Rubella virus, Cytomegalovirus, Herpes simplex virus, Varicella virus, HIV
Toxoplasmosis, Syphilis

PHYSICAL AGENTS
X-rays, Hypothermia

CHEMICAL AGENTS
Thalidomide, anticonvulsants (phenytoin, valproic acid), antipsychotic and antianxiety
agents (phenothiazine, lithium), anticoagulant warfarin, alcohol
Vitamin A embryopathy
Industrial solvents, organic mercury, lead
Hormones – diethylstilbestrol


MATERNAL DIABETES

Nutritional deficiencies (endemic cretinism is related to iodine deficiency)
                    Numerical abnormalities
Normal somatic cell: 46 chromosomes, diploid; the normal gamete: 23 chromosomes, haploid.
                                                             Abnormalities of chromosome number
                                                             may originate during meiotic divisions.


                                                                NONDISJUNCTION

                                                                In the anaphase of the first meiotic
                                                                division, the two members of a pair
                                                                of homologous chromosomes
                                                                separate so that each daughter cell
                                                                recieves one member of each pair.
                                                                In the case that separation of the
                                                                homologous chromosomes does not
                                                                occur (nondisjunction), both
                                                                chromosomes move into one cell.
                                                                As a resultof nondisjunction of the
                                                                chromosomes, one cell recieves
                                                                24 chromosomes, and the other
                                                                recieves 22.




                                    Trisomy 21 – Down syndrome

                                                               Scheme: Langman´s Medical Embryology, Sadler, 2004
     46                                                    47




                                                                                    DOWN SYNDROME


  Photo: The Developing Human, Moore, Persaud, 1998


Prenatal screening test – FISH technique: orange probe is locus is
specific for chromosome 21 and the green probe is locus-specific for
chromoseme 13              Photomicrography: Human Histology, Ross, Pawlina, 2006
                                                    Maternal alcohol abuse is considered to
                                                      be most common cause of mental
                                                                  retardation


                                                    Characteristic triad of abnormalities includes
                                                    growth deficiency, mental retardation, and
                                                    abnormal facial features

                                                    The central nervous system is particularly
                                                    sensitive to alcohol

                                                    Even moderate alcohol consumption may
                                                    produce fetal alcohol effects (i.e., behavioral
                                                    and learning difficulties).


                                                    Characteristic features of a child with FAS
                                                    (fetal alcohol syndrome) – abnormal facial
                                                    features: widely spaced eyes, epicanthus,
                                                    long philtrum, thin upper lip, depressed
Photo: The Developing Human, Moore, Persaud, 1998
                                                    nasal bridge, short nose, , micrognathia,
                                                    and flat midface
           Neural crest cells and craniofacial defects
SYNDROMES INVOLVING THE FIRST PHARYNGEAL ARCH

Pierre Robin syndrome involves extreme micrognathia (small mandible), cleft palate,
and associated defects of the ear

Treacher Collins syndrome (mandibulofacial dysostosis) is typically inherited as an
autosomal dominant condition, including hypoplasia of the mandible and facial bones,
malformations of the external and middle ears, high or cleft palate, faulty dentition,
and coloboma-type defects of the lower eyelid.

The most extreme form of the first arch hypoplasia is agnathia, in which lower jaw
basically fails to form.

BIRTH DEFECTS INVOLVING PHARYNGEAL REGION

Lateral cysts, sinuses, and fistulas
Ectopic thymic and parathyroid tissue

FACIAL CLEFTS

Cleft lip and palate are common defects that result in abnormal facial appearance and
defective speech. Anterior and posterior cleft deformities – incisive foramen
Oblique facial clefts, median cleft lip
TWIN PREGNANCIES
Incidence - monozygotic: 3 – 4 per 1,000 birth
             dizygotic: 7 – 11 per 1,000 birth
Twins have a higher incidence of perinatal mortality and morbidity
and a tendency toward preterm delivery.
Twins are usually small at birth and birth defects are also more common
than in singletons


TRIPLETS
Triplets are rare (about 1 per 7,600)
May be derived from:
(1) one zygote and be identical
(2) two zygotes and consist of identical twins and single infant
(3) three zygotes and be of the same sex or different sexes


MULTIPLE BIRTH
Higher than triplets are uncommon, but they have occurred more often in
recent years following the administration of gonadotropins to women with
ovulatory failure
Dizygotic (nonidentical, fraternal) twins - may be of the same sex or different sexes, they have
different genetic constitutions. Twins have no more resemblance then any other brothers or sisters




     blastocysts implant separately

     blastocysts implant close together




                                                                         Scheme: Before We Are Born, Moore, Persaud, 1993
MONOZYGOTIC TWINS develop from a single fertilized ovum (identical twins – are genetically identical, they
have the same sex and they are very similar in physical appearance (blood groups, fingerprint, eye and hair color).

MZ twins result from splitting of the zygote
at various stages of development


A: about 35 % of MZ twins begin to develop early
in the first week and result from the separation of
the blastomeres (at two-, four- or eight-cell stages.
Each blastomere (or group of blastomeres) gives
rise to blastocyst that implants separately and
develops its own placenta



B: about 65 % of MZ twins begins to develop around
the end of the first week and result from early
division of the embryoblast (inner cell mass) into
two embryonic primordia. Embryos have its own
amniotic sac, develop within one chorionic sac and
have a common placenta



C: in rare cases, the separation occurs at the
bilaminar ebmryonic disc stage, just before the
appaerance of the primitive streak. Embryos
have common amniotic and chorionic sacs, and
common placenta


The rate for MZ twins is 3 to 4 per 1,000
         Scheme: Langman´s Medical Embryology, Sadler, 2004

				
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