Week 3-8 - Teratology of Embryonic week pptx

During embryonic week 3-8, the developing embryo is most susceptible to teratogenic agents, which can cause birth defects or congenital anomalies. Teratology is the study of abnormalities in development.

Here are some key points about teratology during embryonic week:

Week 3:

- The embryo's major organs and body systems begin to form.
- The neural tube, which will become the brain and spinal cord, closes.
- The heart begins to beat.

Teratogens can cause:

- Neural tube defects (NTDs)
- Cardiac anomalies

Week 4:

- The embryo's limbs, digits, and organs continue to develop.
- The neural crest cells migrate to form the peripheral nervous system.

Teratogens can cause:

- Limb abnormalities
- Neural crest-related defects (e.g., cleft palate)

Week 5:

- The embryo's major organs and body systems continue to develop.
- The lungs, liver, and kidneys start to function.

Teratogens can cause:

- Organ-specific defects (e.g., heart, lung, liver)
- Growth restriction

Week 6-8:

- The embryo's development accelerates.
- The brain, spinal cord, and nervous system mature.
- The limbs and digits develop further.

Teratogens can cause:

- Brain and nervous system abnormalities
- Skeletal defects

Exposure to teratogenic agents during this critical period can result in various congenital anomalies, depending on the timing and severity of exposure. It's essential for pregnant women to avoid potential teratogens, such as certain medications, chemicals, and viruses, to ensure a healthy pregnancy.
During embryonic week 3-8, the developing embryo is most susceptible to teratogenic agents, which can cause birth defects or congenital anomalies. Teratology is the study of abnormalities in development.

Here are some key points about teratology during embryonic week:

Week 3:

- The embryo's major organs and body systems begin to form.
- The neural tube, which will become the brain and spinal cord, closes.
- The heart begins to beat.

Teratogens can cause:

- Neural tube defects (NTDs)
- Cardiac anomalies

Week 4:

- The embryo's limbs, digits, and organs continue to develop.
- The neural crest cells migrate to form the peripheral nervous system.

Teratogens can cause:

- Limb abnormalities
- Neural crest-related defects (e.g., cleft palate)

Week 5:

- The embryo's major organs and body systems continue to develop.
- The lungs, liver, and kidneys start to function.

Teratogens can cause:

- Organ-specific defects (e.g., heart, lung, liver)
- Growth restriction

Week 6-8:

- The embryo's development accelerates.
- The brain, spinal cord, and nervous system mature.
- The limbs and digits develop further.

Teratogens can cause:

- Brain and nervous system abnormalities
- Skeletal defects

Exposure to teratogenic agents during this critical period can result in various congenital anomalies, depending on the timing and severity of exposure. It's essential for pregnant women to avoid potential teratogens, such as certain medications, chemicals, and viruses to ensure it

1. TERATOLOGY OF EMBRYONIC WEEK BY: W.O. QUADRI AND ALFRED SLOH Submitted To: DR MRS KOMOLAFE MAY, 2023.

2. INTRODUCTION During embryonic period major external and internal structures are established during the third to eighth weeks. By the end of this period, the main organ systems have started to develop As the tissues and organs form, the shape of the embryo changes and by the eighth week, it has a distinctly human appearance.

3. INTRODUCTION CONT. Human development may be divided into three phases, which to some extent are interrelated: The first phase is growth , which involves cell division and the elaboration of cell products. The second phase is morphogenesis (development of shape, size, and other features of a particular organ or part or the whole body).

4. INTRODUCTION CONT. Morphogenesis is a complex molecular process controlled by the expression and regulation of specific genes in an orderly sequence. The third phase is differentiation . Completion of differentiation results in the organization of cells in a precise pattern of tissues and organs.

5. INTRODUCTION CONT. Because the tissues and organs are differentiating rapidly, exposure of embryos to teratogens during this period may cause major birth defects. Teratogens are agents such as alcohol, drugs and viruses that produce or increase the incidence of birth defects

6. HIGHLIGHT OF EMBRYONIC WEEK Third of week of development include the process of gastrulation i.e the development of the trilaminar germ disc ( ectoderm, intermediate mesoderm and endoderm). With the appearance of primitive streek, groove, node and pit. Development of notochord, intraembryonic coelom, development of somite and formation of neural tube ( neurolation).

7. Diagram showing Neurulation

8. HIGHLIGHT CONTINUE The fourth week of development include the closure of the neuropores, appearance of the pharygeal arches, appearance of upper limb bud, lower limb bud otic pit, and many rudiment organ system (e.g cadiovascular system). The fifh week of development include rapid development of brain and facial prominence and development of urogenital ridge

9. HIGHLIGHT CONTINUE Sixth week of development include formation of retinal pigment ( prominent eyeball), and umblical hernia. It has been reported that embryos in the sixth week show spontanous movements, such as twitching of the trunk and limbs. Embryo at this stage show refles response to touch.

10. HIGHLIGHT CONTINUE In the seventh week notches appear in the hand plates seperating the future digits. Communication between the primordal gut and the umbilical vessicle is now reduced to a slender duct called omphaloenteric duct. In week eight appearance of scalp vascular plexus, noticeble webbed digit of the hand.

11. And at the end of the embryonic week the embryo has visually distinct human characteristics During embryonic period / weeks the embryo undergoe embryonic folding (i.e head and tail fold, and lateral folding)

12. Anomalies of embryonic week CNS Anomalies Holoprosencephaly (HPE): This refers to an anomaly which result in the failure of the prosencephalon (embryonic forebrain) to sufficiently differentiate into double lobes (right and left cerebral hemispheres); HPE can be classified into three categories, depending on the degree of defect in the development of prosencephalon: alobar HPE, semi lobar HPE, and lobar HPE.

13. ANOMALIES CONTINUE Alobar HPE is when the embryo brain hasn’t divided into two hemispheres thus leading to Cyclopia. Cylopia a condition which is characterized by a single eye centered in the middle of the face. Semilobar HPE is when the baby’s brain partially divides into two hemispheres Lobar HPE is when most of your baby’s brain has not separated into two hemispheres, but there is an incomplete division of the two halves.

14. DIAGRAM SHOWING THE HOLOPROSCENPHALY

15. EMBRYONIC ANOMALIES CONT. Exencephaly: The morphological characteristics of exencephaly are exposed brain and absence of the skull and scalp . This condition arises due to the failure to close the cephalic part of the neural tube. Although the understanding remains unclear, folic acid deficiency is a suggested factor for anencephaly

16. DIAGRAM SHOWING THE EXENCEPHALY AND ANENCEPHALY

17. EMBRYONIC ANOMALIES CONT. Spina bifida: It is the most common congenital anomaly of the CNS, resulting from the incomplete fusion of the vertebrae and hence exposure of the spinal cord Although Spina bifida can be recognized as early as week 4, when the closure of the neural tube is supposed to be completed.

18. EMBRYONIC ANOMALIES CONT. Facial anomalies Cleft lip , often accompanied by cleft palate, is the most common congenital facial anomaly that causes dental defects, yielding defective speech and feeding disorders. Cleft lip can be recognized as early as week 7, and is considered a multifactorial defect, involving genetic & environmental factors, teratogens, and maternal conditions.

19. EMBRYONIC ANOMALIES CONT. Micrognathia: It is a facial malformation characterized by an underdeveloped and receded mandible, It is often a part of chromosomal disorder; it is commonly seen in people of Pierre Robin syndrome, and is associated with trisomy 13, trisomy 18 etc. It can be detected in week 7 of development. It leads to dental anomalies, breathing problems, and tongue growth defect. There is no need for surgical treatment, since it can be naturally corrected through growth.

20. DIAGRAM SHOWING THE CLEFT LIP AND PALATE

21. EMBRYONIC ANOMALIES CONT. Anomalis of cardiac region Clinically, heart malformations are typically classified as malformations that are associated with cyanosis ( cyanotic defects ) in postnatal life and those that are not ( acyanotic defects ). Cyanosis results when the blood contains more than 5 g/dL of reduced Hemoglobin.

22. EMBRYONIC ANOMALIES CONT. Polycythemia; an increased concentration of erythrocytes in the blood resulting from the overall decreased oxygen saturation of the blood. Interatrial Septal Defects; anatomical defects in the interatrial septum can result in a persisting shunt between the two atria. The most common varieties are caused by excessive resorption of tissue around the foramen secundum

23. EMBRYONIC ANOMALIES CONT. Persistent Atrioventricular Canal; The usual basis for persistent atrioventricular canal is underdevelopment of the endocardial cushions that results in a lack of division of the early atrioventricular canal into right and left channels. Tricuspid Atresia; the etiology of which is poorly understood, the normal valvular opening between the right atrium and the right ventricle is completely occluded. Such a defect alone causes death because the blood cannot gain access to the lungs for oxygenation.

24. DIAGRAM SHOWING ATRIOVENTRICULAR CANAL

25. DIAGRAM SHOWING THE TRICUSPID ATRESIA

26. EMBRYONIC ANOMALIES CONT. Persistent truncus arteriosus is caused by the lack of partitioning of the outflow tract by the truncoconal ridges If the septation of the outflow tract by the truncoconal ridges is asymmetrical either the aorta or the pulmonary artery is abnormally narrowed, resulting in aortic and pulmonary stenosis

27. DIAGRAM SHOWING PERSISTENT TRUNCUS ARTERIOSUS

28. EMBRYONIC ANOMALIES CONT. Esophageal atresia and tracheoesophageal fistula esophageal atresia (EA) is a congenital malformation characterized by an interruption of the continuity of the esophagus with or without a persistent communication with the trachea (tracheo-esophageal fistula – TEF). The etiology of EA, with or without TEF, is still not completely understood and is likely to be multifactorial.

29. DIAGRAM SHOWING ESOPHAGEAL ATRESIA ND ESOPHGEAL FISTULA

30. EMBRYONIC ANOMALIES CONT. ESOPHAGEAL STENOSIS Congenital esophageal stenosis (CES), defined by Nihoul-Fekete as “an intrinsic stenosis of the esophagus present although not necessarily symptomatic at birth which is caused by congenital malformation of the esophageal wall architecture CES can be associated with other malformations, such as cardiac anomalies, intestinal atresia, duodenal duplication, anorectal malformations, and chromosomal anomalies

31. DIAGRAM SHOWING ESOPHAGEAL STENOSIS

32. EMBRYONIC ANOMALIES CONT. ESOPHAGEAL DUPLICATION CYSTS Esophageal duplications are rare lesions that are predominantly congenital in nature and represent the second most common duplication of the alimentary tract, after the ileum. Most alimentary tract duplications are cystic. Duplication cysts are usually small and round, but they may also be long tubular structures adjacent to the esophagus

33. EMBRYONIC ANOMALIES CONT. GUT TUBE ANOMALIES INFANTILE HYPERTOPHIC PYLORIC STENOSIS ;  (IHPS) is a complex disorder characterized by gastric outlet obstruction due to an abnormal thickening of the pyloric muscle. The precise etiology of IHPS in unknown, although an association with genetic and environmental factors, such as exposure to erythromycin in the first weeks of life, maternal smoking and young age,

34. EMBRYONIC ANOMALIES CONT. CONGENITAL STENOSIS AND ATRESIA; Atresia is a loss of continuity of the bowel lumen, either by complete absence of a variably long segment, or occlusion of the lumen. stenosis is a localized luminal narrowing that may produce a partial obstruction to passage of intestinal contents.

35. EMBRYONIC ANOMALIES CONT. All parts of the intestinal tract can be affected. Based on anatomical characteristics four types of intestinal atresia have been described Duodenal Atresia; Unlike most of the other intestinal atresias, duodenal atresia is frequently associated with other congenital anomalies.  The majority of cases are associated with Down’s syndrome, while less frequently related anomalies are malrotation, cardiac malformations and the VATER association

36. EMBRYONIC ANOMALIES CONT. Jejunal and Ileal Atresia  Jejunoileal atresia (JIA) is the commonest type of intestinal atresia births. A localized intrauterine vascular event with necrosis of the bowel and subsequent reabsorption of the affected segment is the best accepted etiologic theory.    JIA associated with in-utero intussusception, or others may confirm the occurrence of the vascular accident. Over one-third of affected children are born prematurely

37. EMBRYONIC ANOMALIES CONT. Colonic Atresia  As isolated entity, without imperforated anus or cloacal extrophy, colonic atresia and stenosis are very rare, occurring in 4/10,000 live births . They are mainly localized in the ascending and transverse colon

38. DIAGRAM SHOWING CONGENITAL ATRESIA AND STENOSIS DIAGRAM SHOWING THE HOLOPROSCENPHALY

39. EMBRYONIC ANOMALIES CONT. OMPHALOMESENTERIC DUCT REMNANTS OMD is an embryonic structure, which connects the yolk sac to the midgut, and it is the last point to close after the separation of the intestine from the yolk sac. The failure of its closure or resorption results in various anomalies including  Meckel’s diverticulum, the most common congenital anomaly of the gastrointestinal tract

40. DIAGRAM SHOWIMG OMPHACELOMESENTRY DUCT REMANANT

41. EMBRYONIC ANOMALIES CONT. MALROTATION; refers to a group of congenital abnormalities of the intestinal position, resulting from non-rotation, incomplete rotation of the embryonic gut. HIRSCHSPRUNG DISEASE (HSCR), also known as congenital aganglionic megacolon is a complex multigenetic congenital anomaly characterized by the absence of ganglion cells in a portion of the intestinal tract, usually the distal colon, due to a disruption of the normal neural crest cell migration, and differentiation,

42. DIAGRAM OF MALROTATION OF INTESTINE

43. EMBRYONIC ANOMALIES CONT. Anomalies of extremities Polydactyly: it is a limb malformation, characterized by additional digit(s) in the limbs. There can be preaxial, postaxial, or median polydactyly, corresponding to extra digits on the radial This malformation is more likely to occur in the hands than in the feet, and can be estimated at CS 16

44. DIAGRAM SHOWING POLYDACTYL

45. EMBRYONIC ANOMALIES CONT. Cleft hand/foot, also known as split-hand/split-foot malformation (SHFM), is a limb malformation that imparts an appearance resembling a lobster claw due to the absence of the middle finger and hence an abnormal gap between the second and fourth metacarpal bones and soft tissues It can be observed as early as week 7, at the stage when the finger rays develop.

46. Urogenital abnormalities Ectopic kidney: A birth defect given by an abnormal (unilateral or bilateral) kidney position. The ectopic kidney is more often located on the left side. There are several ectopic kidney types: the caudal (lumbar, iliac, sacral) kidney, the cranial kidney and the crossed kidney. Renal dystopia: Initially, in embryonic life, the hill and pelvis are located in the anterior part, and then they undergo a rotation around the longitudinal axis, until they reach the median side

47. Bladder anomalies Megacystis is a neurodysplastic disease, due to the anomaly of innervation. This leads to bladder dilatation (over 7 cm in diameter). Urethral malformations The most common obstructive cause of the lower urinary tract is the posterior urethral valve (PUV). PUV is due to the existence of membranes in the posterior urethra. Urethral malformations Urethral agenesis (absence of urethra) is a rare malformation, incompatible with life unless an alternative communication between the bladder and amniotic sac exists.

48. Rear urethral valves: mucosal lining located in the posterior urethra originating from the seminal colonic and insertion on the anterior wall of the urethra Epispadias : abnormality characterized by opening the urethra on the dorsal face of the penis at variable distance of the gland, dorsal curvature of the penis and foreskin abnormalities. Hypospadias: the anomaly is characterized by opening the urethra on the ventral side of the penis, at any level between the gland and the perineum, causing a ventral penis (chord).

49. Uropathies Uropathies are the most common reno -urinary abnormalities diagnosed during the prenatal period and may be caused by obstructive or nonobstructive factors. The most common urinary malformations encountered in children are vesicoureteral relux (VUR), obstructive megaureter , posterior urethral valve and megacystis . Fetal hydronephrosis may result in a number of conditions, like pelvic or vesicoureteral junction obstruction, posterior urethral valves, vesicoureteral relux , pelvic-ureteric junction obstruction and other rare congenital anomalies Ureteral abnormalities Ureteral agenesis is accompanied by the absence of the ipsilateral kidney. It may be uni - or bilateral, the later being incompatible with life. Incomplete ureteral duplication (ureter issus or ureter biid )—a double-sided pyeloureteral system: the ureters bend before opening into the bladder through a single orifice. Complete ureteral duplication (duplex ureter)—a double-sided pyeloureteral collection system: the ureters open through separate boreholes in the bladder, one in orthoposition and the other in the ectopic position

50. Reference OpenStax College, Anatomy & Physiology. OpenStax College. 19 June 2013. Nakano, S., Makishima, H., and Yamada, S., (2018). “Congenital Anomalies in Human Embryos”. O'Rahilly R, & Gardner E., (1975). “The timing and sequence of events in the development of the limbs Sharma D, Yadav J, & Garg E., (2014). “ Cyclopia syndrome. BMJ Case Reports” Ianakiev P, Kilpatrick MW, et al., (2000). “Split-hand/split-foot malformation is caused by mutations in the p63 gene on 3q27”.

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