COMPARATIVE ANATOMY: VENOUS SYSTEM OF FROG AND FISH

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FROG - VENOUS SYSTEM: 1) External Jugular Vein. 2) Innominate Vein 3) Subclavian Vein 4) Pulmonary Vein 5) Hepatic Vein 6) Renal Vein 7) Gonadial.Vein 8) Dorso-Lumbarvein 9) Renal Portal Vein 10) Femororenal Vein 11) Pelvic. Vein 12) Femoral Vein 13) Sciatic Vein 14) Lingual Vein 15) Mandibular Vein 16) Internal Jugular Vein 17) Sub Scapular Vein 18) Brachial Vein 19) Musculo Cutaneous Vein 20) Cardiac Vein 21) Hepatic Portalvein 22) Anterior Abdominal Vein FROG - VENOUS SYSTEM: 1) External Jugular Vein. 2) Innominate Vein 3) Subclavian Vein 4) Pulmonary Vein 5) Hepatic Vein 6) Renal Vein 7) Gonadial.Vein 8) Dorso-Lumbarvein 9) Renal Portal Vein 10) Femororenal Vein 11) Pelvic. Vein 12) Femoral Vein 13) Sciatic Vein 14) Lingual Vein 15) Mandibular Vein 16) Internal Jugular Vein 17) Sub Scapular Vein 18) Brachial Vein 19) Musculo Cutaneous Vein 20) Cardiac Vein 21) Hepatic Portalvein 22) Anterior Abdominal Vein
Scoliodon commonly called as shark fish is a poikilothermic (cold blooded) animal. It is cartilaginous fish. Rana (frog) is also poikilothermic and amphibious animal. The circulation of blood in vertebrates is of closed type. The blood vessels which collect blood from various parts of the body are known as veins. The walls of the veins are thin and possess valves. Their lumen is wide. They collect deoxygenated blood from different parts of the body and carry to the heart. The veins are formed by means of capillaries in the respective tissues or organs. The deoxygenated blood first enter into the sinus venosus which is the part of the heart. The portal veins are having capillaries at their both ends. The pulmonary veins possess oxygenated blood.
 
 
FISH (SHARK) - VENOUS SYSTEM FROG (RANA) - VENOUS SYSTEM
1. The venous system comprises a system of large thin walled sinuses which collect blood from the different body organs 1. The venous system comprises of thin walled tubular veins.
2. It consists of the following systems i) Anterior cardinal system ii) Posterior cardinal system iii) Hepatic porta! system iv) Ventral veins vi) Cutanecious system 2. It is divided into i) Anterior system of veins ii) Posterior system of veins iii) Portal systems.
3. The anterior cardinal system and the interior jugular sinuses collect blood from the head region through a number of sinuses. 3. The blood from the head region is collected by a pair of precoval veins. Each precaval vein is formed by External jugular, innominate and subclavian veins.
4. The blood from gills is collected by five pairs of dorsal nutrient sinuses and five pairs of ventral nutrient sinuses. 4.The blood from the lungs is collected by a pair of pulmonary veins.
5. The nutrient sinuses carry deoxygenated blood. 5. The pulmonary veins carry oxygenated blood.
6. The nutrient sinuses empty into anterior cardinal and interior jugular sinuses which inturn open into the ductus cuvieri. Thus the blood finally carried to the sinus venosus. 6. The pulmonary veins open into the left auricle.
7. From the posterior part of the body the blood is collected by i) a pair of posterior cardinal sinuses ii) a pair of lateral abdominal veins iii) a pair of brachial veins. 7. The blood from the posterior part of the body is collected by i) renal portal system and ii) Post caval vein.
8. The renal portal system includes the caudal vein and the renal postal veins & Iliac veins. The blood from the pelvic fins is not carried to the kidneys. 8. The renal portal system consists of veins hind limbs i.e. femoral, sciatic and renal portal veins. The caudal vein is absent.
9. It is absent. 9. A part of the blood from the hind-body is transported to the liyer by an anterior abdominal vein.
10. The blood from the kidneys is collected by renal veins which open into posterior cardinals, opening into the cuvierian sinus. 10. The blood from kidneys is collected by four pairs of renal veins which open into the post caval vein.
11. The brachial veins join the lateral abdominals to form sub clavian veins which open into the ductus cuvieri. 11. The brachial veins open into the precaval veins particularly into the subclavian veins.
12. Three pairs cutaneous veins collect blood from the muscles of skin and open into the cardinal sinuses, lateral abdominals and brachial veins. 12. The cutaneous veins are only one pair which join with muscular & brachial and finally open into the subclavian veins.
13. The venus blood does not enter the sinus venosus directly. But it is collected first by the cuvierian sinus present transversely. 13. The blood collected by the two precavals and one post caval veins directly enters into the sinus venosus.
14. The blood from the parts of the alimentary canal is collected by the Hepatic portal vein and empties into the liver and from there it is transported by Hepatic sinuses into the sinus venosus. 14. The Hepatic portal vein collects blood from the different parts of the alimentary canal and empties into the liver. From the blood is transported into the sinus venosus through the hepatic veins and post caval vein.
Last modified on Saturday, 15 July 2017 03:44

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  • FEMALE INFERTILITY: CAUSES AND INVESTIGATIONS
    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
      Idiopathic
    • 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
      Endometriosis
    • Uterus
      – Uterine malformations
      – Asherman’s syndrome
      – Tuberculous endometritis
      Fibroid
    • Cervix: Sperm antibodies
    • Vagina: Septum
     4. Dysfunction of sexual act: Dyspareunia
     
    Investigations
     
    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
  • MALE INFERTILITY: CAUSES AND INVESTIGATIONS
    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.
     
  • NORMAL GASTRIC ANATOMY AND PHYSIOLOGY
    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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