Gametogenesis

1. What is gametogensis ? (04J, 01J, 00M) Give the steps of spermatogenesis.(00M) Answer: See Main ‘Fetus’ page 22 and 23

2. Give the changes that occur during spermiogenesis. (01S) Answer: he series of changes resulting in the transformation of spermatid into spermatozoa is known as spermiogenesis. These changes include Formation of acrosome. Condensation of nucleus to form head. Formation of neck, middle piece and tail. Shedding of most of cytoplasm. (Langman)

Figure: Schematic drawings showing the important stages in transformation of the human spermatid into the Spermatozoon (Spermiogenesis).

3. Give the process of oogenesis. (04J, 01J, 00M, 06J) Answer: See Main ‘Fetus’ page 30

4. What are the results of meiotic cell division? (01M, 00S)Answer: Reduce the number of chromosomes to half that in normal somatic cell (46−›23) provide genetic variability

5. Differentiate between spermatogenesis & oogenesis. Answer: Following are the difference between Oogenesis and Spermatogenesis

Table: Difference between Oogenesis and Spermatogenesis0ogenesis spermatogenesis

1. It is the process of formation of mature ovum. .

2. Here primordial germ primordial germ cells are oogonia.3. One ovum is formed front, one oogonium 4. Polar bodies are formed.5. it begins in intra-uterine life

1. It is the process of formation of mature sperm.2. Here primordial germ cells are spermatogonium.3. Four sperm are formed from one

spermatogonium.4. Polar bodies are not formed.5. It begins shortly before puberty.

Reproductive cycles

1. What is ovulation? Describe the mechanism. (02M)Answer: Discharging of the secondary oocyte with it's cumulus oophorus cells from ovary is called ovulation. (Langman)MechanismOvulation occurs through the following sequence of events

1. Oocyte in the Graafian follicle completes 1st meiotic division.2. Then, bulging of the ovarian surface at the site of the follicle occurs.3. Later, stigma (an avascular spot) appears at the apex of this bulging.4. Then, weakening and degeneration of the surface of the stigma occurs.5. Then, follicular fluid oozes through it-> Released tension in the follicle-> Ovulation occurs under the

influence of L.H and also lesser extent by F S.H.

2. What is corpus luteum? (00M, 01J) The corpus luteum (Latin for "yellow body") (plural corpora lutea) is a temporary endocrine structure involved in production of progestogen, which is needed to maintain pregnancy.3. How corpus luteum is formed? (00M, 01J) Answer: See Main ‘Fetus’

page 434. What are the types of corpus luteum? Give their function. (00M, 01J) Answer: See Main ‘Fetus’

page 44

Type and functions

(i) Corpus Luteum of menstruation. Luteal cells undergo fatty degeneration and finally replaced by white connective tissue into corpus albicans.

(ii) Corpus luteum of pregnancy: secretes progesterone & other hormones to maintain early pregnancy5. Short Notes

a. Graffian follicleAnswer: See Main ‘Fetus’ page 37 and 39b. Ovulation (02M)Answer: See Main ‘Fetus’ page 41c. Corpus luteum (00M)Answer: See Main ‘Fetus’ page 43

6. Clinical correlatea. What is middle pain? Answer: In case of some women, ovulation is accompanied by slight pain which is known as the middle pain.

b. Give cause of middle pain.Answer: There is no known cause of ovulation pain, however, there are a number of theories as to why women

experience these mid-cycle cramps. During ovulation, egg is released from a follicle. When the follicle breaks, it releases fluid and blood. This fluid and

blood may actually irritate the lining of abdomen, causing pain. It may also be caused by the growth of the ovarian follicle, which can stretch the surface of ovary, causing pain.

Fertilization, cleavage and implantation

1. What is fertilization? Give the process of fertilization. (04M, 03J)Answer: See Main ‘Fetus’ page 53

2. What are the results of fertilization? (04M) Give the factors upon which fertilization depends.Answer: See Main ‘Fetus’ page 57

3. What do you mean by ectopic pregnancy? What is its fate? (01J, 03S) Name the sites of ectopic pregnancy.Answer: See Main ‘Fetus’ page 67

4. What is implantation at abnormal site? Give example. (02J)Answer: See Main ‘Fetus’ page 64

5. Give the mechanism of ovum transport through uterine tube and its fate.Answer: See Main ‘Fetus’ page 32

6. Give the fate of primary oocyte which does not mature into ovum.Answer: See Main ‘Fetus’ page 31

7. Give the features & fate of the polar body. (03J)Answer: See Main ‘Fetus’ page 31

8. What is acrosomal reaction? Give its process.Answer: See Main ‘Fetus’ page 57

9. Define capacitation. Give its process. Answer: See Main ‘Fetus’ page 57

10. Describe the process of implantation. (04M, 02J, 00S)11. What are the changes occur in the uterus after implantation?

Answer: See Main ‘Fetus’ page 6412. Give the stages of blastocyst formation.

Answer: See Main ‘Fetus’ page 62 to 6413. Describe the different phases of fertilization (03J, 04M)

Answer: See Main ‘Fetus’ page 57 14. Describe the changes taking place in endometrium during embedding. (02S)

Answer: See Main ‘Fetus’ page 6615. Discuss the changes in a fertilized ovum & uterine endometrium during implantation.

Answer: See Main ‘Fetus’ page 6616. Short note

a. ImplantationAnswer: See Main ‘Fetus’ page 64

b. Ectopic pregnancy (00M)Answer: See Main ‘Fetus’ page 67

c. Fertilization (05 Jan, 02S, 02J)

Answer: See Main ‘Fetus’ page 53d. Capacitation

Answer: See Main ‘Fetus’ page 57e. Acrosomal reaction

Answer: See Main ‘Fetus’ page 57f. Barr body

Mass of condensed sex chromatin in the nuclei of normal female somatic cells due to inactive X chromosome. According to the Lyon hypothesis, one of the two X xhromosomes in each somatic cell of the female is genetically inactivated. The Barr body represents the inactivated X chromosome. X inactivation occurs around the 16th day of embryonic development.

g. Decidual reaction?Answer: See Main ‘Fetus’ page 66

Clinical Correlates

1. Write about the clinical correlation of fertilization.Answer: See Main ‘Fetus’ page 58

2. What is azoospermia, oligospermia? (01S)Answer: See Main ‘Fetus’ page 27

3. What is in vitro fertilization? Give its process.Answer: See Main ‘Fetus’ page 59

4. Define ectopic pregnancy: Name the sites of ectopic pregnancy. What is its fate? (00M, 01J)Answer: See Main ‘Fetus’ page 67

Gastrulation5. What is gastrulation? (02M, 03M)

Answer: gastrulation is the process that establishes all three germ layers. (Langman, 10th edition)6. Mention the events that occur in 2nd wk. of human development.

Answer: See Main ‘Fetus’ page 76 to 777. Describe the formation of different germ layers.

Answer: See Main ‘Fetus’ page 82 to 848. State the importance of primitive streak.

Answer: See Main ‘Fetus’ page 829. 2nd week of development is known as week of two’s. (J-08)

Answer: See Main ‘Fetus’ page 8110. How secondary mesoderm is formed? (03M, 04J)

Answer: See Main ‘Fetus’ page 8211. What are the parts of secondary mesoderm? (03M, 02M)

Answer: See Main ‘Fetus’ page 8312. Describe formation & fate (J-08) importance (J-08) of notochord (05 ju, 03M, 04J, 02M, 00M)

Answer: See Main ‘Fetus’ page 9513. (i) Define somite. Give the number, parts & fate of somite.

Answer: See Main ‘Fetus’ page 87(ii) Short note: Somite. (06 JU)

Answer: See Main ‘Fetus’ page 8714. Notochord (00M, 02M, 03M, 04)

Answer: See Main ‘Fetus’ page 9315. Formation of trilaminer germ disc.

Derivatives

1. Name the structures develop from endoderm. (03J)Answer: See Main ‘Fetus’ page 104

2. Derivatives of surface actoderm. (J-08) Answer: See Main ‘Fetus’ page 100

3. Enumerate the derivatives of extra & intraembryonic mesoderm. (03M, 04J) Answer: See Main ‘Fetus’ page 103

Fetal membrane

1. Enumerate the extraembryonic foetal membrane. Answer: See Main ‘Fetus’ page 111

2. Short note on –‘amnion’.Answer: See Main ‘Fetus’ page 116

3. What is cloasa & cloacal membrane? What is the fate of cloasa in both sexes? (00J, 00S) Answer: See Main ‘Fetus’ page 252 to 253

4. Discuss different twinnings. Give the differences between monozygotic & dizygotic twins.Answer: See Main ‘Fetus’ page 135 and 137

5. Define vitello- intestinal duct. Give its fate. (04M)Answer: See Main ‘Fetus’ page 121

6. Define allantois. Give its fate & developmental anomalies.Answer: See Main ‘Fetus’ page 120

Placenta

1. Write down the functions of placenta. (05 Jan, 00M, 01S)Answer: See Main ‘Fetus’ page 128

2. Give the abnormalities of placenta.Answer: See Main ‘Fetus’ page 130

3. Name different types of anatomical placenta.Answer: See Main ‘Fetus’ page 130

4. Describe the formation of placenta. (00M, 00S)Answer: See Main ‘Fetus’ page 122

5. What are the hormone synthesized by placenta? Answer: See Main ‘Fetus’ page 134

6. (i) Give the structure of placental barrier. (05 jan)Answer: See Main ‘Fetus’ page 133(ii) Short note: Placental barrier. (06J)Answer: See Main ‘Fetus’ page 133

7. Give the contest and development of umbilical cord.8. Write in short about placental circulation. (04M)

Answer: See Main ‘Fetus’ page 133

Short Notes

1. Umbilical cord (01S, 01J)Answer: See Main ‘Fetus’ page 121

2. SomiteAnswer: See Main ‘Fetus’ page 87

3. Primitive streak (03S)Answer: See Main ‘Fetus’ page 82

4. PlacentaAnswer: See Main ‘Fetus’ page 128

5. ChorionAnswer: See Main ‘Fetus’ page 115

6. Yolk sac (03S)Answer: See Main ‘Fetus’ page 118

7. AmnionAnswer: See Main ‘Fetus’ page 116

8. Give the clinical importance of placenta? (05 Jan)9. What is placenta praevia?

Answer: When placenta is implanted in lower uterine segment near internal os or in the os, the placenta is called placenta praevia.

10. What is polyhydroamnions? Give its cause & effect. Answer: See Main ‘Fetus’ page 220

Explain anatomically / Developmentally11) Human placenta is heamochorial type. (05 Ju)

Answer: Because the maternal blood in the intervillous spaces is separated from the fetal blood by a chorionic derivative, the human placenta is considered to be of the hemochorial type.(Langman, 10th edition)

GeneticsWhat do you mean by Trisomy / Monosomy The normal human somatic cell contains 46 chromosomes; the normal gamete contains 23. Normal somatic cells are diploid, or 2 n; normal gametes are haploid, or n. Euploid refers to any exact multiple of n, e.g., diploid or triploid. Aneuploid refers to any chromosome number that is not euploid; it is usually applied when an extra chromosome is present (trisomy) or when one is missing (monosomy).

(Langman, 10th edition)

Full trisomy of an individual occurs due to non-disjunction when the cells are dividing (meiosis I or II) to form egg and sperm cells (gametogenesis). This can result in an extra or missing chromosome (either 24 or 22 chromosomes instead of the typical 23) in a sperm or egg cell. After fertilization, the resulting fetus has 47 chromosomes instead of the typical 46.

A partial trisomy/mosaic occurs when part of an extra chromosome is attached to one of the other chromosomes, or if one of the chromosomes has two copies of part of its chromosome.

Figure A: Normal meiosis. B. Nondisjunction in the first meiotic division. C. Nondisjunction in the second meiotic division.

6. Give cause & features of klinefelter syndrome. Klinefelter syndrome is a term used to describe males who have an extra X chromosome in most of their cells. Instead of having the usual XY chromosome pattern that most males have, these men have an XXY pattern.

Cause:Nondisjunction of the XX homologues is the most common causative event in klinefelter syndrome.

(Langman, 10th edition)

Features:a. The clinical features of Klinefelter syndrome, found only in males and usually detected at puberty, are sterility,

testicular atrophy, hyalinization of the seminiferous tubules, and usually gynecomastia. b. The cells have 47 chromosomes with a sex chromosomal complement of the XXY type, and a sex chromatin body

(Barr body) is found in 80% of cases. c. Occasionally, patients with Klinefelter syndrome have 48 chromosomes: 44 autosomes and 4 sex chromosomes

(XXXY). d. Although mental retardation is not generally part of the syndrome, the more X chromosomes there are, the more

likely there will be some degree of mental impairment.(Langman, 10th edition)

7. Give cause & features of Turner syndrome.

Cause In 80% of these women, nondisjunction in the male gamete is the cause. In the remainder of women, structural abnormalities of the X chromosome or mitotic nondisjunction resulting in

mosaicism are the cause. (Langman, 10th edition)

Featuresa. 45,X karyotype. b. 98% of all fetuses with the syndrome are spontaneously aborted. c. The few that survive are unmistakably female in appearance and are characterized by the absence of ovaries (gonadal

dysgenesis) and short stature. Other common associated abnormalities are webbed neck, lymphedema of the extremities, skeletal deformities, and a broad chest with widely spaced nipples. Approximately 55% of affected women are monosomic for the X and chromatin body negative because of nondisjunction. .

(Langman, 10th edition)

8. Give cause & features of Down syndrome.

Cause In 95% of cases, the syndrome is caused by trisomy 21 resulting from meiotic nondisjunction, in 75% of these instances, nondisjunction occurs during oocyte formation. In approximately 4% of cases of Down syndrome, there is an unbalanced translocation between chromosome 21 and

chromosome 13, 14, or 15. The final 1% is caused by mosaicism resulting from mitotic nondisjunction. These individuals have some cells with a

normal chromosome number and some that are aneuploid. They may exhibit few or many of the characteristics of Down syndrome

(Langman, 10th edition)

Figure: A. Translocation of the long arms of chromosomes 14 and 21 at the centromere. Loss of the short arms is not clinically significant, and these individuals are clinically normal, although they are at risk for producing offspring with unbalanced translocations. B. Karyotype of translocation of chromosome 21 onto 14, resulting in Down syndrome.

Features growth retardation; varying degrees of mental retardation; craniofacial abnormalities, including upward slanting eyes, epicanthal folds (extra skin folds at the medial corners of

the eyes), flat facies, and small ears;

cardiac defects; hypotonia. These individuals also have relatively high incidences of leukemia, infections, thyroid dysfunction, and premature

aging. Furthermore, nearly all develop signs of Alzheimer disease after age 35.

(Langman, 10th edition)

Congenital malformationsExplain anatomically / Developmentally

e) Embryonic period is highly sensitive to teratogen why? (05Jan)Answer: In embryonic period gastrulation is initiated. At this time, fate maps can be made for various organ systems, such as the eyes and brain anlage, and these cell populations may be damaged by teratogens. For example, high doses of alcohol at this stage kill cells in the anterior midline of the germ disc, producing a deficiency of the midline in craniofacial structures and resulting in holoprosencephaly

(Langman, 10th edition)

SPECIAL EMBRYOLOGY

Cardiovascular System :1. How interatrial septum is developed?

Answer: See Main ‘Fetus’ page 1602. Give the development of interventricular septum. (03M)

Answer: See Main ‘Fetus’ page 161 to 1633. Describe the foetal circulation.

Answer: See Main ‘Fetus’ page 1854. What are the circulatory changes occur at birth? (00J)

Answer: See Main ‘Fetus’ page 1875. Give the development & derivatives of aortic arches. (03J, 04M)

Answer: See Main ‘Fetus’ page 1696. Give the development of superior / Inferior venacava. (03M)

Answer: See Main ‘Fetus’ page 176 to 1777. Give the development of aorta / Arch of the aorta.

Answer: See Main ‘Fetus’ page 1688. Give the development of coronary sinus.

Answer: See Main ‘Fetus’ page 1809. Give the fates of the different parts of primitive heart tube.

Answer: See Main ‘Fetus’ page 15710. What are the developmental source of different parts of right atrium / left atrium/ right Ventricle/ left ventricle

Answer: See Main ‘Fetus’ page 15711. Give the mechanism of closure of foramen ovale.

Answer: See Main ‘Fetus’ page 16012. Give the fates of vitelline / umbilical artery.

Answer: See Main ‘Fetus’ page 17113. Give the development of pericardium.

Clinical correlate1. Name the developmental anomalies of heart (00M, 04M)

Answer: See Main ‘Fetus’ page 1632. Name the developmental anomalies of interatrial septum.

Answer: See Main ‘Fetus’ page 1653. Name the developmental anomalies of interventricular septum / What is Fallot’s tetralogy?

Answer: See Main ‘Fetus’ page 165 to 1674. What is coarctation of aorta? Give its region, type.

Answer: See Main ‘Fetus’ page 1745. What is double aortic arch.

Answer: See Main ‘Fetus’ page 1746. Give congenital anomalies associated with aortic arch development. (04M)

Answer: See Main ‘Fetus’ page 173

Explain anatomically / Developmentallyb) How circulation is maintained in post ductal aortic coarctation?Answer: See Main ‘Fetus’ page 175 and 187

Respiratory System

1. Give the stages (J-08) development of lung / Larynx (00J) / Trachea.Answer: See Main ‘Fetus’ page 232

2. Give the maturation process of lung.Answer: See Main ‘Fetus’ page 233

3. When respiration is possible & why?Answer: See Main ‘Fetus’ page 234

4. Give the developmental anomalies of lung/trachea.Answer: See Main ‘Fetus’ page 234

5. What is respiratory distress syndrome? Give its treatment. (03M, 02S, 00J)Answer: See Main ‘Fetus’ page 235

Explain anatomically / Developmentally

a) Fetus reaches viable ages at alveolar stages & of lung development.Answer: See Main ‘Fetus’ page 234

b) Respiration is possible at alveolar stage of lung development.Answer: See Main ‘Fetus’ page 234

c) Right recurrent laryngeal nerve hooks around the right subclavian artery but left recurrent laryngeal nerve hooks around the ligamentum arteriosum.Answer: See Main ‘Fetus’ page 171

d) How tracheo-oesophageal fistula occurs? (05 Jan)Answer: See Main ‘Fetus’ page 235

Urinary System

1. Give the development of kidney (00M, 00J, 04M, 03S)Answer: See Main ‘Fetus’ page 243 and 246

2. Give the fate of mesonephric duct & tubules in both sex.Answer: See Main ‘Fetus’ page 242

3. Give the process of ascend of kidney.Answer: See Main ‘Fetus’ page 243

4. Mention of developmental source of urinary bladder / Urethra / Ureter (03S)Answer: See Main ‘Fetus’ page 259, 254 and 256

5. Give the fate of mesonephric & paramesonephric ducts in both sexes. (04M)Answer: See Main ‘Fetus’ page 271 and 272

6. What are the developmental anomalies of kidney? (01J, 00M, 00J)Answer: See Main ‘Fetus’ page 247

7. What is polycystic kidney? Give its causes. (03S)Answer: See Main ‘Fetus’ page 250

8. What is horseshoe shaped kidney? Give its cause.Answer: See Main ‘Fetus’ page 247

9. What do you mean by floating kidney?10. Explain developmentally – Renate agenesis cause oligohydromnios. (06JU)

Genital System

1. Mention of developmental source of different parts of testis (03M)/ ovary.Answer: See Main ‘Fetus’ page 261

2. Give the pathway & duration of descend of testis. Mention the factors that cause the descend of testis.Answer: See Main ‘Fetus’ page 265

3. Give the development of uterus (02J, 00) / Uterine tube (04M, 03J) / vas deference prostate. (03J)Answer: See Main ‘Fetus’ page 273, 275 and 259

4. Give the fate of the paramesonephric duct.Answer: See Main ‘Fetus’ page 272

Genital System

1. Mention about the possible anomalies which could happen during development of testis. (03M)Answer: See Main ‘Fetus’ page 265

2. What is hypospadias & epispadias?Answer: See Main ‘Fetus’ page 156 and 157

3. What do you mean by ectopic testis? Give its possible sites & features.Answer: See Main ‘Fetus’ page 265

4. What is undescended testis.Answer: See Main ‘Fetus’ page 265

5. Give the congenital anomalies of uterus.Answer: See Main ‘Fetus’ page 273

Diaphragm and septum transversum

1. Give the development & derivatives of septum transversum.Answer: See Main ‘Fetus’ page 237

2. Give the nerve supply of diaphragm of developmental back ground.Answer: See Main ‘Fetus’ page 240

3. Mention the developmental source of diaphragm. (00M, 02S, 02M, 01S)Answer: See Main ‘Fetus’ page 239

4. Why the central tendon of diaphragm is closely attached with the pericardium?Answer: See Main ‘Fetus’ page 238

Digestive system1. Name the derivatives of primitive gut. (03J) Describe the rotation of midgut.

Answer: See Main ‘Fetus’ page 1922. Give artery supply of gut on the developmental back ground.

Answer: See Main ‘Fetus’ page 1933. Name the developmental source of stomach. (00J) Write about the rotational changes of it.

Answer: See Main ‘Fetus’ page 1964. Give the developmental of liver / pancreas (02S, 00J, 00S) / spleen.

Answer: See Main ‘Fetus’ page 214 and 2155. Name the derivative of four gut with its arterial supply. Mention possible anomalies.

(03S)Answer: See Main ‘Fetus’ page 192

Clinical correlate1. What is Meckel's diverticulum (ileal diverticulum) ? Give its featuresAnswer: In 2% to 4% of people, a small portion of the Vitelline duct persists, forming an outpocketing of the ileum. This is called Meckel's diverticulum or ileal diverticulum.

(Langman, 10th edition)

Features:In the adult, this diverticulum, approximately 40 to 60 cm from the ileocecal valve on the antimesenteric border of the ileum, does not usually cause any symptoms. However, when it contains heterotopic pancreatic tissue or gastric mucosa, it may cause ulceration, bleeding, or even perforation.

(Langman, 10th edition)

2. Give the developmental anomalies of liver / pancreas/ gall bladder.Answer: See Main ‘Fetus’ page 228

3. What is omphalocele?4. Give the developmental anomalies of rectum & anal canal.

Answer: See Main ‘Fetus’ page 225 to 2275. What is congenital megacolon? Give its cause.

Answer: See Main ‘Fetus’ page 2256. Give the developmental anomalies stomach.

Answer: See Main ‘Fetus’ page 221

Head and Neck

1. Enumerate the derivatives of pharyngeal arches (05Ju, 04M, 06JU)/ pouches. (06JU); Clefts (06J).Answer: See Main ‘Fetus’ page 279, 282 and 285

2. Mention the developmental sources of face. (05 Ju, 04J, 02J, 02S, 00J)Answer: See Main ‘Fetus’ page 292

3. Give the developmental of tongue. (04M, 01S, 00J, 00S, 06J)Answer: See Main ‘Fetus’ page 286

4. Give the nerve supply of tongue on developmental back ground.(04M, 01S, 00J, 00S, 06J, 08J)Answer: See Main ‘Fetus’ page 286 and 287

5. Give the development of thyroid gland (00M, 02J, 01J)/ parathyroid gland.Answer: See Main ‘Fetus’ page 287

6. Why cleft lift is usually accompanied by congenital heart defect?Answer: See Main ‘Fetus’ page 298

7. Why cleft lift is more common in upper lip?Answer: See Main ‘Fetus’ page 296

39. What is pharyngeal arch? Give its development. (03S, 04M, 02M) / Mention the derivatives of pharyngeal arches.Answer: See Main ‘Fetus’ page 281, 282 and 285

41. Mention the derivatives of pharyngeal pouches.Answer: See Main ‘Fetus’ page 285

Clinical correlate

1. Give the developmental anomalies of tongue. (01S, 00S, 00J)Answer: See Main ‘Fetus’ page 287

2. What is tongue tie (ankyloglossia)Answer: See Main ‘Fetus’ page 287

3. Give the developmental anomalies of face (02J, 02S, 00J)/ soft palate/ thyroid gland/ cleft plate.Answer: See Main ‘Fetus’ page 296 and 289

4. Give the developmental anomalies of soft palate.

Answer: See Main ‘Fetus’ page 296

Explain anatomically / Developmentally

f) Neural crest cell plays a great role to development of head and neck region. How?(05JAn)Answer: See Main ‘Fetus’ page 303

Ns and Endocrine gland

1. What is neural crest? Give the general account of structures develop from it. (00M, 00J, 00S, 01S)Answer: See Main ‘Fetus’ page 308 and 309

2. Give the development & derivatives of neural tube (05 Jan). Where from the meanings develop? (03M) Answer: See Main ‘Fetus’ page 305 and 307

3. Give the development of pituitary (02M, 01M) / adeernal gland (03J)Answer: See Main ‘Fetus’ page 317

4. Spina bifida.Answer: See Main ‘Fetus’ page 316

5. Neural crest (00M, 00J, 00S, 01S)Answer: See Main ‘Fetus’ page 308

6. Give the neural tube defects. (05 Jan)Answer: See Main ‘Fetus’ page 316

Skeletal systemExplain anatomically / Developmentallya) Bone is rigid form of connective tissue. (05 Ju)

Answer: See Main ‘Fetus’ page 325