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The hard parts of the animal body are collectively known as skeletal system or simply skeleton. The vertebrates possess the hard parts inside the body. It is known as endo skeleton. The endo skeletal structures are formed with cartilages and bones which are the living tissues. The endo skeleton has been divided into:The hard parts of the animal body are collectively known as skeletal system or simply skeleton. The vertebrates possess the hard parts inside the body. It is known as endo skeleton. The endo skeletal structures are formed with cartilages and bones which are the living tissues. The endo skeleton has been divided into:
  1. Axial skeleton - includes the skull and vertebral column.
  2. Appenducular skeleton - includes the girdles and limb bones.
The skull develops in the head of animal body. The skull includes two major parts - 'Cranium' enclosing the brain and the organs of special sense and Visceral arches' which form the jaws and frame work of pharyngeal wall.

The cranium is developed from the mesodermal cells soon after the appearance of the brain. It is also known as brain box. Cranium includes three pairs of capsules for smell, sight and hearing. These are known as olfactory, optic and auditory capsules respectively. The cartilaginous cranium is called chondro cranium and bony cranium is called dermato cranium.

The visceral arches develop around anterior (Pharyngeal) part of the embryonic gut from the cells of neural crests. Mostly seven visceral arches are present. The first one is the largest and highly modified - 'Mandibular arch. It has dorsal & ventral halves. Each side of the dorsal half is termed the palato -pterygoid Quadrate Cartilage. It bears teeth and forms the upper jaw. The ventral half of the mandibular arch is called Meckel's cartilage. It also bears the teeth and form the lower jaw. The wide gap between the two jaws is the mouth. The two jaws articulate their hind ends by hinge joints which enable the mouth to open & close. The second arch is hyoid arch and the remaining five arches are termed bronchial arches. The visceral arches are collectively known as the splanchno cranium. The upper jaw and lower jaw are known as Maxilla and Mandible respectively: See images. 
1. Skull is formed with cartilage tissues. 1. Skull is formed most­ly with bony tissues (but tadpole skull is cartilaginous) 1. Skull is formed most­ly with bony tissues. 1. Skull is formed mostly with bony tissue. 1. Skull is formed with mostly bony tissue.
2. It consists of crani­um, sense capsules and visceral arches. 2. It consists of cran­ium, sense capsules, jaws and hyoid ap­paratus. 2. It consists of crani­um, sense capsules, jaws and hyoid apparatus. 2. Same as in calotes. 2. Same as in calotes.
3. It is the axial portion of the skull. It is more or less a violin box open in front and be­hind with an arched roof and flattened floor. It is divided into occipital, auditory, orbital and ethmoidal regions. 3. It forms the middle hollow part of the skull. It is divided into auditory, olfactory and occipital regions. 3. It forms the median hollow part of the skull. It is divided into occipital, audi­tory, orbital, olfacto­ry and optic regions. 3. It forms the posterior median hollow part of the skull. It is divided into occipital, audito­ry, optic orbital and ol­factory regions. 3. It forms the middle hollow part of the skull. It is divided into occipital auditory, optic orbital & olfac­tory regions.
4. Foramen magnum is posteriorly present. 4. Same. 4. Same. 4. Same. 4. Same.
5. Beneath the foramen magnum a deep concavity is present. On either side of this concavity is a pro­minence - occipital condyle articulates with the first verte­bra, occipital crest is formed. Dicondylic skull. 5. Beneath the foramen magnum there are two occipital con­dyles. On either side of the foramen mag­num dorsolaterally exoccipital bones are present. Dicondylic skull 5. Beneath the fora­men magnum a sin­gle occipital condyle is present.suupraoccipitai, exo occipitals,& basi occipital bones are also present in the occipital region. Monocondylic skull. 5. Beneath the foramen magnum single occip­ital condyle is present. Supra occipital, Exocci pitals & basioccipital bones are also present. Monocondylic skull. 5. Beneath the fora­men magnum two occipital condyles with paroccipital process are present. Supraoccipital, exo-ccipitai, & basio-ccipital bones are also present. Dico­ndylic skull.
6. Auditory region has a mid dorsal depres­sion - parietal fossa. It contain two pairs of apertures. Anteri­orly smaller open­ings of endolymp­hatic ducts and pos­teriorly larger open­ings of perilymphatic spaces are present. 6.— 6.— 6.— 6.—
7. Auditory capsules lie on the poster lat­eral sides of the cranium. Which enclose & protect the ears. Post orbital groove is present on the ven­tral side 7. Auditory capsules enclose the internal ear. Its roof is formed by pro-otic bone, fenestra ovalis, sta­pedial plate and columella auris are present. 7. Each auditory capsule is formed by small, single vertical prootic bone which is lying outside the supra occipital. Epiotic & opisthotic are not differentiat­ed. 7. Each auditory capsule is formed largely by the prooticbone. Fenestra ovalis, fenestra rotun da, columella auris, stapes are also present. 7. Each auditory cap­sule in the adult animal consists only periotic. Flask - like Tympanic bulla bone is significant.
8.— 8. Dorsally the cranium is formed, by frontoparietals, ven­trally by parasphenoid and laterally by sphen ethmoid bones. 8. The dorsal part of the cranium is formed by parietals, frontals interparietal foramen, and ven­trally by basisphenoid, parasphenoid bones. 8. The dorsal part of the cranium is formed by Parietals, frontals a rostum, alisphenoids; ventrally basisphenoid, basitemporal bones. 8. The cranium is formed dorsally by 'Parietals, frontals, inter parietal, and ventrally by basisphenoids, presphenoid bones along with alisphenoids and orbit sphenoids. The cra­nial cavity is closed infront by a narrow vertical bone cibriform plate.
9.  Each orbit lies on the sides of the middle part of the cranium. It is bordered by dor­sal super orbital ridge,anterior preorbital process, posterior post orbital process and ventraily by infra orbital ridge. The orbital region has a large oral cavity anterior fontanelle. 9. On either side of the cranium is large gap - orbit which lodges the eye. 9. In the middle of the cranium laterally two orbits are present. Each orbit is bounded by prefrontal supra orbital, lacri­mal, post frontal and jugal bones. The jugal bone forms the ventral border of the orbit. Supratemporal arch is present. 9. The two orbits are very large cavities present infront of the cranium. Each orbit is bounded dorsally by frontal, antero - dorsally by lac­rimal and posteriorly by the zygomatic process. Orbit is incomplete on the ventral side. The two orbits are separated by inter orbital septum. 9. These are two orbits are large sockets present on the sides of frontal segment of cranium. The orbit is bounded dorsally by frontal, anteriorly by maxilla and lacrimal, posteriorly by squa­mosal and alisp-henoid and external­ly by the zygomatic arch.
10. The olfactory cap­sules lie at the anteri­or side of the cranium. Each capsule possesses a short sic at ethmopalatine ridge. 10. The olfactory cap­sules are separated, from each other by mesethmoid. Each capsule is formed by a large triangular nasal on the dorsal side and a smaller triradiate vomer on the ventral side vomers possess vomerine teeth. 10. Each olfactory capsule is formed by three bones Nasal, septo maxillary and vomer. 10. Each olfactory capsule is formed by two bones - Nasal and vomer. Nasals fuse with frontals and form into super and inferior processes. 10. Each olfactory cap­sule is bounded by dorsally by long na­sal bone and laterally by jaw bones. The two capsules are sep­arated by mesethmoid bone. The lower end of mesethmoid fits into a vomer bone. Vomer is formed by the fusion of a pair of bones.
11. Ethmoidal region tapers anteriorly. It consists of a basal slender barventro-median rostral carti­lage and a pair of similar barsdorso - lateral rostral cartilages aris­en from the roof of ihe olfactory capsules. 11. Absent. 11. Absent. 11. Absent. 11. Absent.
12. Scoliodon has seven visceral arches which are cartilagienous. The first arch forms the jaws and it is catted Mandibular arch the second one is the hyoid arch the remain­ing five arches are called branchial arch­es. 12. Branchial arches are absent.There are upper and lower jaws to support the borders of the mouth. The upper jaw is formed by union of two similar halves. Each half is formed by the Pre-maxilla, maxilla and quadratojugal. The inner set of the jaw has palatine, ptery goid and squamosal bones. The lower consists of two halves and unite an­teriorly by mento-meckelian cartilage. Each half consists of dentary and angio -splenial bones. Just infroni of the articu­lar fact a small coro-nary process is present. Upper jaw alone has teeth. 12. Branchial arches are absent. 12. Branchial arches are absent. 12.   Branchial arches absent.These are upper and lower jaws. Each half of the upper jaw is formed by premax-illa, maxilla jugular, palatine, pterygoid and squamosal.
13. The mandibular arch consists of two halves. Each half of this arch possess an upper paleto-pterygo quadrate cartilage and a lower meckel s cartilage.The pale topterygo Quadrate gives off anteriorly palatine. The two sides of it from the upper jaw with teeth. The two meckel's cartilages united antero medially by lig­ament form the lower jaw with teeth.   13. These are upper and lower jaws. Each half of the upper jaw consists of an outer set of bones - pre maxilla, maxilla, jugal and quadrate and the inner set in­cludes pterygoid, palatine, transp-alatine, epiptery-goid and squamo­sal. Each half of the lower jaw consists of six bones -dentary, angular, supra angular, ar­ticular, splenial and coronoid. Both the jaws possess teeth. 13. These are upper and lower jaws. Each half of the upper jaw is formed by premaxilla, maxilla, quadra tojugal, and jugal bones. The inner ar­cade of the upper jaw forms the roof of bucco pharyngal cav­ity which consists of palatine, pterygoid, and quadrate. Each half of the lower jaw is formed by articu­lar, angular supra an­gular, dentary and splenial. Both the jaws are lacking the teeth. 13. The lower jaw also con­sists of two halves. Each half is formed by a single, large dentary bone. The posterior of the dentary possess con­dylar, coronoid and angular process. Both the jaws pos­sess the codent type of teeth which are having different (Heterodont teeth in mammals) shap­es. Diastema is present in both the jaws because of the absence of canines.
14. Hyostylic jaw suspension. 14. Auto stylic jaw suspension. 14. Auto stylic jaw suspension. 14. Auto stylic jaw suspension. 14. Craniostylic jaw suspension.
Last modified on Tuesday, 11 July 2017 13:22

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    The ovaries are the sites of production of female gametes or ova by the process of oogenesis. The ova are released by the process of ovulation in a cyclical manner at regular intervals. Ovary contains numerous follicles that contain ova in various stages of development. During each menstrual cycle, up to 20 primordial follicles are activated for maturation; however, only one follicle becomes fully mature; this dominant follicle ruptures to release the secondary oocyte from the ovary. Maturation of the follicle is stimulated by follicle stimulating hormone (FSH) secreted by anterior pituitary (Figure 862.1). Maturing follicle secretes estrogen that causes proliferation of endometrium of the uterus (proliferative phase). Follicular cells also secrete inhibin which regulates release of FSH by the anterior pituitary. Fall in FSH level is followed by secretion of luteinizing hormone (LH) by the anterior pituitary (LH surge). This causes follicle to rupture and the ovum is expelled into the peritoneal cavity near the fimbrial end of the fallopian tube. The fallopian tubes conduct ova from the ovaries to the uterus. Fertilization of ovum by the sperm occurs in the fallopian tube.
    Figure 862.1 The hypothalamus pituitary ovarian axis
    Figure 862.1 The hypothalamus-pituitary-ovarian axis 
    The ovum consists of the secondary oocyte, zona pellucida and corona radiata. The ruptured follicle in the ovary collapses and fills with blood clot (corpus luteum). LH converts granulose cells in the follicle to lutein cells which begin to secrete progesterone. Progesterone stimulates secretion from the endometrial glands (secretory phase) that were earlier under the influence of estrogen. Rising progesterone levels inhibit LH production from the anterior pituitary. Without LH, the corpus luteum regresses and becomes functionless corpus albicans. After regression of corpus luteum, production of estrogen and progesterone stops and endometrium collapses, causing onset of menstruation. If the ovum is fertilized and implanted in the uterine wall, human chorionic gonadotropin (hCG) is secreted by the developing placenta into the maternal circulation. Human chorionic gonadotropin maintains the corpus luteum for secetion of estrogen and progesterone till 12th week of pregnancy. After 12th week, corpus luteum regresses to corpus albicans and the function of synthesis of estrogen and progesterone is taken over by placenta till parturition.
    The average duration of the normal menstrual cycle is 28 days. Ovulation occurs around 14th day of the cycle. The time interval between ovulation and menstruation is called as luteal phase and is fairly constant (14 days) (Figure 862.2).
    Figure 862.2 Normal menstrual cycle
    Figure 862.2 Normal menstrual cycle
    Causes of Female Infertility
    Causes of female infertility are shown in Table 862.1.
    Table 862.1 Causes of female infertility
    1. Hypothalamic-pituitary dysfunction:
    • Hypothalamic causes
      – Excessive exercise
      – Excess stress
      – Low weight
      – Kallman’s syndrome
    • Pituitary causes
      – Hyperprolactinemia
      Hypopituitarism (Sheehan’s syndrome, Simmond’s disease)
      – Craniopharyngioma
      – Cerebral irradiation
     2. Ovarian dysfunction:
    • Polycystic ovarian disease (Stein-Leventhal syndrome)
    • Luteinized unruptured follicle
    • Turner’s syndrome
    • Radiation or chemotherapy
    • Surgical removal of ovaries
    • Idiopathic
     3. Dysfunction in passages:
    • Fallopian tubes
      Infections: Tuberculosis, gonorrhea, Chlamydia
      – Previous surgery (e.g. laparotomy)
      – Tubectomy
      Congenital hypoplasia, non-canalization
    • Uterus
      – Uterine malformations
      – Asherman’s syndrome
      – Tuberculous endometritis
    • Cervix: Sperm antibodies
    • Vagina: Septum
     4. Dysfunction of sexual act: Dyspareunia
    Evaluation of female infertility is shown in Figure 862.3.
    Figure 862.3 Evaluation of female infertility
    Figure 862.3 Evaluation of female infertility. FSH: Follicle stimulating hormone; LH: Luteinizing hormone; DHEA-S: Dihydroepiandrosterone; TSH: Thyroid stimulating hormone; ↑ : Increased; ↓ : Decreased
    Tests for Ovulation
    Most common cause of female infertility is anovulation.
    1. Regular cycles, mastalgia, and laparoscopic direct visualization of corpus luteum indicate ovulatory cycles. Anovulatory cycles are clinically characterized by amenorrhea, oligomenorrhea, or irregular menstruation. However, apparently regular cycles may be associated with anovulation.
    2. Endometrial biopsy: Endometrial biopsy is done during premenstrual period (21st-23rd day of the cycle). The secretory endometrium during the later half of the cycle is an evidence of ovulation.
    3. Ultrasonography (USG): Serial ultrasonography is done from 10th day of the cycle and the size of the dominant follicle is measured. Size >18 mm is indicative of imminent ovulation. Collapse of the follicle with presence of few ml of fluid in the pouch of Douglas is suggestive of ovulation. USG also is helpful for treatment (i.e. timing of coitus or of intrauterine insemination) and diagnosis of luteinized unruptured follicle (absence of collapse of dominant follicle). Transvaginal USG is more sensitive than abdominal USG.
    4. Basal body temperature (BBT): Patient takes her oral temperature at the same time every morning before arising. BBT falls by about 0.5°F at the time of ovulation. During the second (progestational) half of the cycle, temperature is slightly raised above the preovulatory level (rise of 0.5° to 1°F). This is due to the slight pyrogenic action of progesterone and is therefore presumptive evidence of functional corpus luteum.
    5. Cervical mucus study:
      Fern test: During estrogenic phase, a characteristic pattern of fern formation is seen when cervical mucus is spread on a glass slide (Figure 862.4). This ferning disappears after the 21st day of the cycle. If previously observed, its disappearance is presumptive evidence of corpus luteum activity.
      Spinnbarkeit test: Cervical mucus is elastic and withstands stretching upto a distance of over 10 cm. This phenomenon is called Spinnbarkeit or the thread test for the estrogen activity. During the secretory phase, viscosity of the cervical mucus increases and it gets fractured when stretched. This change in cervical mucus is evidence of ovulation.
    6. Vaginal cytology: Karyopyknotic index (KI) is high during estrogenic phase, while it becomes low in secretory phase. This refers to percentage of super-ficial squamous cells with pyknotic nuclei to all mature squamous cells in a lateral vaginal wall smear. Usually minimum of 300 cells are evaluated. The peak KI usually corresponds with time of ovulation and may reach upto 50 to 85.
    7. Estimation of progesterone in mid-luteal phase (day 21 or 7 days before expected menstruation): Progesterone level > 10 nmol/L is a reliable evidence of ovulation if cycles are regular (Figure 862.5). A mistimed sample is a common cause of abnormal result.
    Figure 862.4 Ferning of cervical mucosa
    Figure 862.4 Ferning of cervical mucosa
    Figure 862.5 Serum progesterone during normal menstrual cycle
    Figure 862.5 Serum progesterone during normal menstrual cycle
    Tests to Determine the Cause of Anovulation
    1. Measurement of LH, FSH, and estradiol during days 2 to 6: All values are low in hypogonadotropic hypogonadism (hypothalamic or pituitary failure).
    2. Measurement of TSH, prolactin, and testosterone if cycles are irregular or absent:
      Increased TSH: Hypothyroidism
      Increased prolactin: Pituitary adenoma
      Increased testosterone: Polycystic ovarian disease (PCOD), congenital adrenal hyperplasia (To differentiate PCOD from congenital adrenal hyperplasia, ultrasound and estimation of dihydroepiandrosterone or DHEA are done).
    3. Transvaginal ultrasonography: This is done for detection of PCOD.
    Investigations to Assess Tubal and Uterine Status
    1. Infectious disease: These tests include endometrial biopsy for tuberculosis and test for chlamydial IgG antibodies for tubal factor in infertility.
    2. Hysterosalpingography (HSG): HSG is a radiological contrast study for investigation of the shape of the uterine cavity and for blockage of fallopian tubes (Figure 862.6). A catheter is introduced into the cervical canal and a radiocontrast dye is injected into the uterine cavity. A real time X-ray imaging is carried out to observe the flow of the dye into the uterine cavity, tubes, and spillage into the uterine cavity.
    3. Hysterosalpingo-contrast sonography: A catheter is introduced into the cervical canal and an echocontrast fluid is introduced into the uterine cavity. Shape of the uterine cavity, filling of fallopian tubes, and spillage of contrast fluid are noted. In addition, ultrasound scan of the pelvis provides information about any fibroids or polycystic ovarian disease.
    4. Laparoscopy and dye hydrotubation test with hysteroscopy: In this test, a cannula is inserted into the cervix and methylene blue dye is introduced into the uterine cavity. If tubes are patent, spillage of the dye is observed from the ends of both tubes. This technique also allows visualization of pelvic organs, endometriosis, and pelvic adhesions. If required, endometriosis and tubal blockage can be treated during the procedure.
    Possible pregnancy and active pelvic or vaginal infection are contraindications to tubal patency tests.
    Figure 862.6 Hysterosalpingography
    Figure 862.6 Hysterosalpingography
    The male reproductive system consists of testes (paired organs located in the scrotal sac that produce spermatozoa and secrete testosterone), a paired system of ducts comprising of epididymis, vasa deferentia, and ejaculatory ducts (collect, store, and conduct spermatozoa), paired seminal vesicles and a single prostate gland (produce nutritive and lubricating seminal fluid), bulbourethral glands of Cowper (secrete lubricating mucus), and penis (organ of copulation).
    The hypothalamus secretes gonadotropin releasing hormone (GnRH) that regulates the secretion of the two gonadotropins from the anterior pituitary: luteinizing hormone (LH) and follicle stimulating hormone (FSH) (Figure 861.1). Luteinizing hormone primarily stimulates the production and secretion of testosterone from Leydig cells located in the interstitial tissue of the testes. Testosterone stimulates spermatogenesis, and plays a role in the development of secondary sexual characters. Testosterone needs to be converted to an important steroidal metabolite, dihydrotestosterone within cells to perform most of its androgenic functions. Testosterone inhibits LH secretion by negative feedback. Follicle stimulating hormone acts on Sertoli cells of seminiferous tubules to regulate the normal maturation of the sperms. Sertoli cells produce inhibin that controls FSH secretion by negative feedback.
    Figure 861.1 Hypothalamus-pituitary-testis axis. + indicates stimulation; – indicates negative feedback
    Figure 861.1 Hypothalamus-pituitary-testis axis. + indicates stimulation; – indicates negative feedback
    During sexual intercourse, semen is deposited into the vagina. Liquefaction of semen occurs within 20-30 minutes due to proteolytic enzymes of prostatic fluid. For fertilization to occur in vivo, the sperm must undergo capacitation and acrosome reaction. Capacitation refers to physiologic changes in sperms that occur during their passage through the cervix of the female genital tract. With capacitation, the sperm acquires (i) ability to undergo acrosome reaction, (ii) ability to bind to zona pellucida, and (iii) hypermotility. Sperm then travels through the cervix and uterus up to the fallopian tube. Binding of sperm to zona pellucida induces acrosomal reaction (breakdown of outer plasma membrane by enzymes of acrosome and its fusion with outer acrosomal membrane, i.e. loss of acrosome). This is necessary for fusion of sperm and oocyte membranes. Acrosomal reaction and binding of sperm and ovum surface proteins is followed by penetration of zona pellucida of ovum by the sperm. Following penetration by sperm, hardening of zona pellucida occurs that inhibits penetration by additional sperms. A sperm penetrates and fertilizes the egg in the ampullary portion of the fallopian tube (Figure 861.2).
    Figure 861.2 Steps before and after fertilization of ovum
    Figure 861.2 Steps before and after fertilization of ovum
    Causes of Male Infertility
    Causes of male infertility are listed in Table 861.1.
    Table 861.1 Causes of male infertility 
    2. Hypothalamic-pituitary dysfunction (hypogonadotropic hypogonadism)
    3. Testicular dysfunction:
    • Radiation, cytotoxic drugs, antihypertensives, antidepressants
    • General factors like stress, emotional factors, drugs like marijuana, anabolic steroids, and cocaine, alcoholism, heavy smoking, undernutrition
    • Mumps orchitis after puberty
    • Varicocele (dilatation of pampiniform plexus of scrotal veins)
    • Undescended testes (cryptorchidism)
    • Endocrine disorders like diabetes mellitus, thyroid dysfunction
    • Genetic disorders: Klinefelter’s syndrome, microdeletions in Y chromosome, autosomal Robertsonian translocation, immotile cilia syndrome (Kartagener’s syndrome), cystic fibrosis, androgen receptor gene defect
    4. Dysfunction of passages and accessory sex glands:
     5. Dysfunction of sexual act:
    • Defects in ejaculation: retrograde (semen is pumped backwards in to the bladder), premature, or absent
    • Hypospadias
    Investigations of Male Infertility
    1. History: This includes type of lifestyle (heavy smoking, alcoholism), sexual practice, erectile dysfunction, ejaculation, sexually transmitted diseases, surgery in genital area, drugs, and any systemic illness.
    2. Physical examination: Examination of reproductive system should includes testicular size, undescended testes, hypospadias, scrotal abnormalities (like varicocele), body hair, and facial hair. Varicocele can occur bilaterally and is the most common surgically removable abnormality causing male infertility.
    3. Semen analysis: See article Semen Analysis. Evaluation of azoospermia is shown in Figure 861.3. Evaluation of low semen volume is shown in Figure 861.4.
    4. Chromosomal analysis: This can reveal Klinefelter’s syndrome (e.g. XXY karyotype) (Figure 861.5), deletion in Y chromosome, and autosomal Robertsonian translocation. It is necessary to screen for cystic fibrosis carrier state if bilateral congenital absence of vas deferens is present.
    5. Hormonal studies: This includes measurement of FSH, LH, and testosterone to detect hormonal abnormalities causing testicular failure (Table 861.2).
    6. Testicular biopsy: Testicular biopsy is indicated when differentiation between obstructive and non-obstructive azoospermia is not evident (i.e. normal FSH and normal testicular volume).
    Table 861.2 Interpretation of hormonal studies in male infertility 
    Follicle stimulating hormone Luteinizing hormone Testosterone Interpretation
    Low Low Low Hypogonadotropic hypogonadism (Hypothalamic or pituitary disorder)
    High High Low Hypergonadotropic hypogonadism (Testicular disorder)
    Normal Normal Normal Obstruction of passages, dysfunction of accessory glands
    Figure 861.3 Evaluation of azoospermia
    Figure 861.3 Evaluation of azoospermia. FSH: Follicle stimulating hormone; LH: Luteinizing hormone
    Figure 861.4 Evaluation of low semen volume
    Figure 861.4 Evaluation of low semen volume
    Figure 861.5 Karyotype in Klinefelter's Syndrome
     Figure 861.5 Karyotype in Klinefelter’s syndrome (47, XXY)
    Common initial investigations for diagnosis of cause of infertility are listed below.
    Anatomically, stomach is divided into four parts: cardia, fundus, body, and pyloric part. Cardia is the upper part surrounding the entrance of the esophagus and is lined by the mucus-secreting epithelium. The epithelium of the fundus and the body of the stomach is composed of different cell types including: (i) mucus-secreting cells which protect gastric mucosa from self-digestion by forming an overlying thick layer of mucus, (ii) parietal cells which secrete hydrochloric acid and intrinsic factor, and (iii) peptic cells or chief cells which secrete the proteolytic enzyme pepsinogen. Pyloric part is divided into pyloric antrum and pyloric canal. It is lined by mucus-secreting cells and gastrin-secreting neuroendocrine cells (G cells) (Figure 859.1).
    Figure 859.1 Parts of stomach and their lining cells
    Figure 859.1 Parts of stomach and their lining cells 
    In the stomach, ingested food is mechanically and chemically broken down to form semi-digested liquid called chyme. Following relaxation of pyloric sphincter, chyme passes into the duodenum.
    There are three phases of gastric acid secretion: cephalic, gastric, and intestinal.
    • Cephalic or neurogenic phase: This phase is initiated by the sight, smell, taste, or thought of food that causes stimulation of vagal nuclei in the brain. Vagus nerve directly stimulates parietal cells to secrete acid; in addition, it also stimulates antral G cells to secrete gastrin in blood (which is also a potent stimulus for gastric acid secretion) (Figure 859.2). Cephalic phase is abolished by vagotomy.
    • Gastric phase: Entry of swallowed food into the stomach causes gastric distension and induces gastric phase. Distension of antrum and increase in pH due to neutralization of acid by food stimulate antral G cells to secrete gastrin into the circulation. Gastrin, in turn, causes release of hydrochloric acid from parietal cells.
    • Intestinal phase: Entry of digested proteins into the duodenum causes an increase in acid output from the stomach. It is thought that certain hormones and absorbed amino acids stimulate parietal cells to secrete acid.
    The secretion from the stomach is called as gastric juice. The chief constituents of the gastric juice are:
    • Hydrochloric acid (HCl): This is secreted by the parietal cells of the fundus and the body of the stomach. HCl provides the high acidic pH necessary for activation of pepsinogen to pepsin. Gastric acid secretion is stimulated by histamine, acetylcholine, and gastrin (Figure 859.2). HCl kills most microorganisms entering the stomach and also denatures proteins (breaks hydrogen bonds making polypeptide chains to unfold). Its secretion is inhibited by somatostatin (secreted by D cells in pancreas and by mucosa of intestine), gastric inhibitory peptide (secreted by K cells in duodenum and jejunum), prostaglandin, and secretin (secreted by S cells in duodenum).
    • Pepsin: Pepsin is secreted by chief cells in stomach. Pepsin causes partial digestion of proteins leading to the formation of large polypeptide molecules (optimal function at pH 1.0 to 3.0). Its secretion is enhanced by vagal stimulation.
    • Mucus
    • Intrinsic factor (IF): IF is necessary for absorption of vitamin B12 in the terminal ileum. It is secreted by parietal cells of stomach.
    Figure 859.2 Stimulation of gastric acid secretion
    Figure 859.2 Stimulation of gastric acid secretion. Three receptors on parietal cells stimulate acid secretion: histamine (H2) receptor, acetylcholine or cholinergic receptor, and gastrin/CCK-B receptor. Histamine is released by enterochromaffin-like cells in lamina propria. Acetylcholine is released from nerve endings. Gastrin is released from G cells in antrum (in response to amino acids in food, antral distention, and gastrin-releasing peptide). After binding to receptors, H+ is secreted in exchange for K+ by proton pump

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