Flashcards in Reproductive embryology and anatomy Deck (65):
What are some important genes of embryogenesis?
Sonic hedgehog gene
Homeobox (Hox) genes
Where is the sonic hedgehog gene produced? What is it involved in? what can mutation cause?
Base of limbs in zone of polarizing activity
Patterning along A/P axis
Where is the Wnt-7 gene produced? What is it necessary for?
Apical ectodermal ridge (thickened ectoderm at distal end of each developing limb)
Proper organization along dorsal-ventral axis)
Where is FGF gene produced? What is its function?
Apical ectodermal ridge
Stimulates mitosis of underlying mesoderm, limb lengthening
What is the Homeobox gene involved in? What does it code for? What do mutations lead to?
Segmental organization of embryo in craniocaudal direction
Appendages in wrong locations
Early fetal development
Day 0:fertilization by sperm, forming zygote, initiating embryogenesis
Week 1: hCH secretion begins around the time of implantation of blastocyst ("sticks" at day 6)
W2: Bilaminar disc (epiblast, hypoblast) (2 weeks=2 layers)
W3: Trilaminar disc (3W=3 layers), gastrulation, primitive streak, notochord, mesoderm and its organization, and neural plate begins to form
W3-8: Embryonic period (neural tube formed by neuroectoderm and closes by week 4; organogenesis; extremely susceptible to teratogens)
Week 4: Heart begins to beat; upper and lower limbs begin to form (4 limbs, 4 chambers=4 weeks)
Week 6: Fetal cardiac activity visible by T/V U/S
Week 10: Genitalia have male/female characteristics
What is gastrulation? How does it start?
Process that forms trilaminar embryonic disc
Establishes ectoderm, mesoderm, and endoderm germ layers
epiblast invaginating to form the primitive streak
What are the 3 embryologic derivatives? Location? What are the 3 types of ectoderm?
What is made of surface ectoderm?
Adenohypophysis (Rathke pouch)
Lens of eye
Epithelial linings of oral cavity
Sensory organs of ear
Anal canal below pectinate line
Parotic, sweat, and mammary glands
What is made of neuroectoderm?
Brain (neurohypophysis, CNS neurons, oligodendrocytes, astrocytes, ependymal cells, pineal gland)
Retina and optic nerve
What is made of neural crest cells?
PNS (dorsal root ganglia, schwann cells, CNs, celiac ganglion, ANS)
Chromaffin cells of adrenal medulla
Parafollicular C cells of thyroid
Pia and arachnoid
Bones of the skull
What is made of mesoderm? What do mesoderm defects lead to?
Serous linings of body cavities (peritoneum)
spleen (foregut mesentary)
Wall of gut tube
Notochord (nucleus pulposus)
What is made up of endoderm?
Gut tube epithelium (including anal canal above pectinate line)
Most of urethra (urogenital sinus)
Luminal epithelial derivatives (lungs, liver, gallbladder, pancreas, eustachian tube, thymus, parathyroid, thyroid follicular cells)
Agenesis: Absent organ due to absent primordial tissue
Aplasia: Absent organ despite presence of primordial tissue
Hypoplasia: incomplete organ develop.; primordial tissue present
Deformation: Extrinsic disruption; occurs after embryonic period
Disruption: secondary breakdown of previously normal tissue or structure (amniotic band syndrome)
Malformation: intrinsic disruption; occurs during embryonic period
Sequence: Abnormalities result from single embryological event (potter sequence)
When are fetuses most susceptible to teratogens? What happens before that? After that?
3rd to 8 weeks
Before-all or none
After-growth and function affected
What effects do these drugs have on fetus?
ACEI: Renal damage
Alkylating agents: Absence of digits
Aminoglycosides: CN VIII toxicity
Carbamazepine: Facial dysmorphism, devel. delay, neural tube defects, phalanx/fingernail hypoplasia
DES: Vaginal clear cell adenoCA, congenital mullerian anomalies
Folate antag: Neural tube defects
Isotretinoin: multiple severe birth defects (Contraception mandatory
Lithium: Ebstein anomaly
Methimazole: Aplasia cutis congenita
Phenytoin: Fetal hydantoin syndrome=cleft palate, cardiac defects, phalanx/fingernail hypoplasia
Tetracyclines: discolored teeth
Thalidomide: limb defects (phocomelia, micromelia)
Valproate: inhibition of maternal folate absorption leading to neural tube defects
Warfarin: bone deformities, fetal hemorrhage, abortion, opthalmologic abnorm.
What effects do these substances have on the fetus?
Alcohol: Common cause of birth defects; FAS
Cocaine: Abnormal fetal growth and fetal addiction; placental abruption
Smoking (nicotine/CO): Low birth weight, preterm labor, placental problems, IUGR, ADHD (nicotine leads to vasoconstriction; CO leads to impaired O2 delivery)
What does a lack or excess of iodine lead in the fetus? Maternal diabetes? Vitamin A excess? x-rays?
Iodine: congenital goiter or hypothyroidism (cretinism)
MDM: Caudal regression syndrome (anal atresia to sirenomelia), congenital heart defects, neural tube defects
Vit. A: Extremely high risk for spontaneous abortions and birth defects (cleft palate, cardiac)
X-rays: microcephaly, intellectual disability
Epid of FAS? What does it lead to in newborns? In most severe form? Mechanism?
Leading cause of intellectual disability in the u.s.
Incr. incidence of congenital abnormalities:
Prenatal and postnatal developmental retardation
facial abnormalities (smooth filtrum, hypertelorism)
Severe: Heart/lung fistulas, holoprosencephaly
Failure of cell migration
What do dizygotic twins come from? Results in placenta? HOw common? What do monozygotic twins arise from? What is the result if the cleavage occurs during days 0-4? What is this period called? How common is this? Same questions for 4-8, 8-12, >13
Dizygotic (80%)=2 eggs and two sperms
Monozygotic=1 egg and 1 sperm that split into 2 zygotes early on.
0-4 days (25%)=zygote splits leading to dichorionic diamniotic with either fused placenta or separate placenta
4-8 days (75%)=morula splits leading to monochorionic diamniotic
8-12 days (13 days=embryonic disc is already formed then splits leading to monochorionic monoamniotic conjoined twins.
What is the function of the placenta? Describe basic anatomy of placenta. Origin of cytotrophoblast? Location? Function? Origin of syncytiotrophoblast? Location? Function? What does it lack? Origin of decidua basalis?
Primary site of nutrient and gas exchange between mother and fetus
Baby is surrounded by amniotic fluid. On the other side of the amniotic lining, there are fetal arteries and veins. These arteries branch up into lacunae toward the mothers side of the placenta. Inside of the lacunae is the mother's blood. On the other side of the lacunae (mother's side), there is the decidua basalis. The maternal artery and vein directly connect with lacuna. The villi are lined with cytotrophoblasts on its inner side, and syncytiotrophoblasts on its outer layer. Therefore, the lacunae are lined by sync on its inner layer and cyto on its outer layer. The villi communicate with the mother's blood in lacunae. The fetal arteries and veins form into the umbilical arteries and vein in the umbilical cord.
Cytotrophoblast: Makes cells (fetal component)
Sync: Secrete hCG (similar to LH; stimulates corpus luteum to secrete progesterone during 1st tri)
Lacks MHC-I=decr. chance of attack by maternal immune system
How many umbilical arteries are there? function? What is the function of the umbilical veins? How many? What are they derived from? What else is located within the umbilical cord? What is single umbilical artery associated with?
UA (2)=return deoxygenated blood from fetal internal iliac arteries to placenta
UV (1)=supplies oxygenated blood from placenta to fetus; drains into IVC via liver or ductus venosus
Derived from allantois
Single UA is associated with congen and chromosom abnormal.
Allantoic duct and wharton jelly
Describe the development of the urachus. Timeline? What is a patent urachus? Result? What is a urachal cyst? Pathphys? Complications? What is a vesicourachal diverticulum? Result?
3rd week-yolk sac forms the allantois, which extends into urogenital sinus. Allantois becomes the uraches, a duct b/w the fetal bladder and yolk sac
Total failure of urachus to obliterate leads to urine d/c from umbilicus
partial failure of urachus to obliterate
Fluid filled cavity line with uroepithelium b/w umbilicus and bladder
Infection and AdenoCA
Slight failure of urachus to obliterate leads to outpouching of bladder
Decribe the destruction of vitelline duct. Timeline? What is a vitelline fistula? Result? What is pathophys of meckel diverticulum? Symptoms?
7th week-obliteratation of vitelline duct (omphalo-mesenteric duct), which connects yolk sac to midgut lumen
Vitelline fistula=vitelline duct fails to close=meconium d/c from umbilicus
Meckel=partial closure of vitelline duct, with patent portion attached to ileum.
Heteropic gastric/panc tissue
melena, hematochezia, abdominal pain
What do the aortic arch derivatives develop into? What deriv 1-6 result in? Where do right and left recurrent laryngeal nerves loop around?
1st=part of maxillay artery (external carotid)
1st arch is maximal
2nd=stapedial artery and hyoid artery
3rd=Common carotid artery and proximal part of ICA
C is third letter of alphabet
4th=On left, aortic arch; on right, proximal part of right subclavian artery
4th arch=4 limbs=systemic
6th=proximal part of pulmonary arteries and ductus arteriosus
6th=pulmonary and pulmonary to systemic shunt
Right=beneath right subclavian
Left=beneath aortic arch
What is the branchial apparatus? Another name? What is it composed of? What are branchial clefts (another name), arches, and pouches derived from?
Clefts, arches, and pouches
CAP covers from outside to inside
Arches=mesoderm and neural crest
What does the 1st cleft turn into? 2nd through 4th? What is a persistent cervical sinus? Location?
1st=external auditory meatus
2-4=temporary cervical sinuses, obliterated by prolif. of 2nd arch mesenchyme
Branchial cleft cyst within lateral neck
What does the 1st arch turn into (cartilage, muscles, and nerves)? 2nd? 3rd? 4th-6th?
C: Meckel cartilage: Mandible, malleus, incus, sphenomandibular ligament
M: Muscles of mastication (temporalis, masseter, pterygoids), Mylohyoid, anterior belly of digastric, tensor tympani, tensor veli palatini (lots of M's)
N: V2 and V3 (chew)
C: Reichert cartilage: stapes, styloid process, lesser horn of hyoid, stylohyoid ligament
M: Facial expression muscles, stapedius, stylohyoid, platysma, posterior belly of digastric (S's)
N: Facial (smile)
C: greater horn of hyoid
M: Stylopharyngeus (innervated by glossopharyngeus)
N: CNIX (glossopharyngeal) (swallow stylishly)
C: thyroid, cricoid, arytenoids, corniculate, cuneiform
M: 4=most pharyngeal constrictors, cricothyroid, levator veli pelatini; 6=all intrinsic muscles of larynx except cricothyroid
N: 4th=CN X (superior laryn) (simply swallow); 6=CN X (recurrent laryngeal) (speak)
Nerves included are the only ones with both sensory and motor components
What at the restaurant of the golden arches, children tend to chew (1), then smile (2), then swallow stylishly (3), then simply swallow (4), and then speak (6)
What is Treacher Collins syndrome? Congenital pharyngocutaneous fistula?
TCS: 1st arch neural crest fails to migrate leading to mandibular hypoplasia, facial abnormalities
CPF: Persistence of cleft and pouch leads to fistula b/w tonsillar area and lateral neck.
What are the derivatives of the 1st branchial pouch? 2nd? 3rd? 4th?
Middle ear cavity, eustachian tube, mastoid air cells (endoderm lined structures of ear)
2nd: Epithelial lining of palatine tonsil
Dorsal wings-inferior parathyroids
Dorsal wings=superior thyroids
Ear, tonsils, bottom to top
3=inferior thyroids, thymus
What is DiGeorge syndrome? symptoms?
Aberrant development of 3rd/4th pouches
T cell deficiency
Cardiac defects (conotruncal anomalies)
What is MEN 2A? Findings?
Germline RET mutation (neural crest cells)
Adrenal medulla (pheochromocytoma), parathyroid tumor (3rd/4th pharyngeal pouch), parafollicular cells (medullary thyroid cancer=derived from NC cells, associated with 4th/5th pouches)
What is pathophys of cleft lip? Pathophys of cleft palate?
Lip: failure of fusion of the maxillary and medial nasal processes (formation of primary plate)
Palate: failure of fusion of the two lateral palatine processes or failure of fusion of lateral palatine processes with the nasal septum and/or median palatine process (secondary palate)
Describe the initial process/pathway of sex differentiation in the embryo.
Males: SRY gene on y chromosome codes for testis determining factor which causes the testes to develop.
When testes develop, sertoli cells secrete Mullerian inhibitory factor which suppresses development of paramesonephric ducts. Leydig cells secret androgens that stimulate development of mesonephric ducts.
Females: No SRY, no TDF, no testes, no MIF, no androgens. Mesonephric duct degenerates and paramesonephric duct develops (default development)
What does the paramesonephric duct develop into in female? How does mullerian agenesis present?
Female internal structures: fallopian tubes, uterus, upper portion of vagina
primary amenorrhea (no uterus) with fully developed secondary sex characteristics (functional ovaries)
What does the mesonephric duct develop into? What is a gartner duct?
Male internal structures (except prostate): seminal vesicles, epididymis, ejaculatory duct, ductus deferens
In females, remnant of mesonephric duct.
What induces male external genitalia formation? What happens if that doesn't work? What happens if there are no sertoli cells or no MIF?
Testosterone is converted by 5 alpha reductase to DHT, which induces formation of male external genitalia and the prostate.
In 5 alpha reductase deficiency, there are male internal genitalia and ambigous external genitalia until puberty, at which point incr. testosterone leads to masculinization.
If no sertolli or no MIF, develop both male (testosterone=mesonephric ducts) and female (No MIF=paramesonephric) internal genitalia, and male external genitalia (DHT)
What is a septate uterus? Results? treatment? Bicornuate uterus? Results? Uterus didelphys? Results?
Incomplete resorption of septum
Incomplete fusion of mullerian ducts
Incr. risk of complicated pregnancy
Complete failure of fusion
Double uterus, vagina, and cervix
What are the undifferentiated external genitalia? What do they become in males and in females and in response to what?
F: glans clitoris
M: Corpus cavernosum and spongiosum
F: Vestibular bulbs
M: bulbourethral glands (of cowper)
F: greater vestibular glands (of bartholin
M: prostate gland
F: urethral and paraurethral glands (of skene)
M: ventral shaft of penis (penile urethra)
F: Labia minora
What hypospadias? Association? What is epispadias? ASsociation?
Abnormal opening of penile urethra on ventral surface of penis due to failure of urethral folds to fuse
Inguinal hernia and cryptorchidism
Abnormal opening of penile urethra on dorsal surface of penis due to faulty positioning of genital tubercle
Exstrophy of the bladder
What is the gubernaculu? What is its function in males? Females? Processus vaginalis? Function in males Females?
Gubernaculum: Band of fibrous tissue
M: anchors testes in scrotum
F: Ovarian ligament + round ligament of uterus
Processus: Evagination of peritoneum
M: Tunica vaginalis
What is the venous drainage of left ovary/testis? Right ovary/testis? What is the lymph drainage of ovaries/testes? Distal vagina/vulva/scrotum? Proximal vagina/uterus? Why is a varicocele more common on left?
Left: gonadal vein, renal vein, IVC
Right: Gonadal vein, IVC
Ovaries/testes: para-aortic LNs
Distal vagina/vulva/scrotum: superficial inguinal
Proximal vagina/uterus: obturator, external iliac, hypogastric
Into left renal vein (right angle=flow less laminar), can be obstructed.
What does the infundibulopelvic ligament (suspensory ligament of the ovary) connect? Structures contained? Clinical correlations? Same Q's for cardinal ligament. Round ligament? Broad ligament? Parts? Ovarian?
Connects: ovaries to lateral pelvic wall
Contained: ovarian vessels
Notes: ligate vessels to avoid bleeding during oophorectomy; urerer courses retroperitoneally; risk of injury
Connects: cervix to side wall of pelvis
Contained: uterine vessels
Notes: ureter at risk during ligation for hysterectomy
Connects: uterine fundus to labia majora
Notes: derivative of gubernaculum. Travels through round inguinal canal
Connects: uterus, fallopian tubes, and ovaries to pelvice side wall
Contained: Ovary, fallopian tubes, round ligaments of uterus
Notes: Mesosalpinx, mesometrium, mesoovarium
Connects: edial pole of ovary to lateral uterus
What is histo of
Ovary, outer surface:
vagina: strat. squam, non keratin
Ectocervix: strat squam, non kerat
Transformation zone: squamocolumnar junction (cerv. cancer)
Endocervix: simple columnar
Uterus: simple columnar with long tubular glands in follicular phase, coiled glands in luteal phase
Fallopian tube: simple columnar, ciliated
Ovary, outer surface: simple cuboidal (germinal epithelium covering surface of ovary)
Describe the steps of the female sexual response cycle. How is it mediated? systemic effects?
Phase of excitement (uterus elevates, vaginal lubrication)
Plateua (expansion of inner vagina)
Orgasm (contraction of uterus)
Tachycardia and skin flushing
What is the pathway of sperm during ejaculation?
When should a urethral injury be suspected? Causes of posterior urethral injury? Findings? Anterior?
Blood seen at urethra meatus
Post: Membranous urethra prone to injury from pelvic fracture; bulbar urethra susceptible to blunt force. Urine into retropubic space
Ant: Penile urethra at risk of damage to perineal straddle injury. Urine to leak beneath deep fascia of Buck. If fascia torn, into superficial perineal space
Describe the innervation of the male erection? Pathways behind erection and relaxtion. Innervation of emission? Innervation of ejaculation? What does sildenafil do?
NO leads to incr. cGMP to incr. SM relaxation to vasodilatio n to erection
NE leads to incr. IC Ca, which leads to SM contraction to vasoconstriction to antierectile
Ejaculation-visceral and somatic nerves (pudendal)
Sildenafil-PDE inhib=more cGMP
What is the progression of male germ cells?
spermatogonia line semniferous tubules.
They produce primary spermatocytes, to secondary spermatocytes to spermatids to spermatozoon (in each succession they move closer middle of tubule
Where are sertoli cells located? Homolog in females? What is their function? What do they respond to? What effect does temperature have on them? Examples?
Line semniferous tubules
Granulosa cells in females
Respond to FSH
Secrete inhibin (inhibit FSH)
Secrete androgen binding protein (maintain local levels of testosterone)
Convert test and androstenedione to estrogens via aromatase
Tight junctions b/w adjacent ones form blood-testis barrier which prevents gametes from autoimmune attack
Support and nourish developing spermatazoa
Incr in temp=decr. sperm production and decr. inhibin (varicocele and cryptorchidism)
Where are leydig cells located? Homolog in females? Respond to? Function? Temp effect?
Interstitium (around tubules)
Homolog of theca interna cells
Respond to LH
Unaffected by temp.
What are the sources of estrogen? Forms in source? Which form is most potent? Functions? Describe its formation/regulation in the ovaries? Where are its receptors located? Changes in pregnancy?
Ovary=17 beta estradiol
Adipose=estrone via aromatization
Estradiol > estrone >estriol
Development of genitalia and breast, female fat distribution
Growth of follicle, endometrial prolif, incr. myometrial excitability
Upregulation of estrogen, LH, and progesterone receptors; feedback inhibition of FSH and LH, then LH surge; stimulation of prolactin secretion
Incr. transport proteins, SHBG; incr. HDL, decr. LDL
ER in cytoplasm, translocate to nucleus
Pulsatile GnRH leads to FSH and LH from pit.
LH stimulates desmolase in theca interna cell, which converts cholesterol to androgens.
Androgens transported to granulosa cell
FSH stimulates aromatase in granulosa cell, which converts androgens to estrogens
What are the sources of progesterone? Functions? Effect on lactation ?
Corpus luteum, placenta, adrenal cortex, testes
Stimulation of endometrial glandular secretions and spiral artery development
Maintenance of pregnancy
Decr. myometrial excitability
Production of thick cervical mucus, which inhibits sperm entry to uterus
Incr. body temp
Inhibition of gonadotropins
Uterine smooth muscle relaxation (no contractions)
Decr. estrogen receptor expression
Prevents endometrial hyperplasia
Fall in progesterone post delivery disinhibits prolactin leading to lactation.
Incr. progesterone is indicative of ovulation.
How are tanner stages assigned? Stage I, II, III, IV, V?
Independently to genitalia, pubic hair, and breast
II=pubic hair appears (pubarche); breast buds form (thelarche)
III=Pubic hair darkens and become curly; penis size/lenght incr.; breasts enlarge
IV: penis width incr., darker scrotal skin, development of glans; raised areolae
V=Adult; areolae no longer raised
How long is the follicular phase? When does it start? What is it like in ovary and uterus? How long is luteal phase? Start? Uterus and ovary? Describe the hormone levels during these periods and the cycle in general.
Follicular: Varies in length, begins at menstruation. FSH begins incr. before menstruation and by doing so, it starts to cause follicles to grow. It then starts decreasing which effectively selects just one follicle. That follicle matures and begins secreting estrogen. Estrogen reaches a peak at the end of the follicular phase and this peak causes an LH surge (FSH slightly peaks to).
Called the proliferative phase in the uterus b/c estrogen causes the endometrium to proliferate.
Luteal phase: Begins at ovulation; always 14 days. LH surge causes ova to be released from graafian follicle into the salpinx, leaving behind the corpus luteum. The corpus luteum secretes progesterone. Progesterone maintains endometrium to support implantation (spiral arteries and secretions). If there is no implantation, the ova does not secrete hCG, and the luteum eventually stops secreting progesterone, causing endometrial cells to apoptose and slough off. Estrogen levels decr. during this phase, but have a second peak at progesterones peak (after about 5 days).
What is dysmenorrhea? Oligomenorrhea? Polymenorrhea?Metrorrhagia? Menorrhagia? Menometrorrhagia?
Pain with menses; often associated with endometriosis
>35 day cycle
80 mL blood loss or days of menses
Heavy, irregular bleeding
Describe oogenesis. What are primary and secondary oocytes like? Ovum?
Primary oocytes begin meiosis I during fetal life but meiosis I is arrested in prophase I until ovulation (primary oocytes=2N, 4C=46 sister chromatids). Ovulation=prOphase
At ovulation, it splits into a secondary oocyte and a polar body and proceeds until METaphase II, where it stays until fertilization (secondary oocytes=1N, 2C (23 sister chromatids)) An egg MET a sperm
If fertilization does not occur in one day, the oocyte degenerates.
If fertilization occurs, the cycle continues forming an ovum (1N, 1C) which combines with sperm.
What occurs in ovulation? What is mittelschmerz?
Incr. estrogen, incr. GnRH receptors on anterior pit. Estrogen surge then stimulates LH release which leads to rupture of follicle
Incr. temp (progesterone)
Transient mid cycle ovulatory pain; associated with peritoneal irritation (follicular swelling/rupture, tuebe contraction). Can mimic appendicitis
Where does fertilzation occur and when? Where does implantation occur and when? What happens after that?
Upper end of fallopian tube (ampulla).
Within 1 day of ovulation
Implantation within wall of uterus occur 6 days after fertilization. Syncytiotrophoblasts secrete hCH, which is detectable in blood 1 week after coneption and on home test in urine 2 weeks after conception.
What effect do estrogen, progesterone, suckling, prolactin, oxytocin have on lactation?
After labor, estrogen and progesterone decr. which disinhibits lactation.
Suckling required to maintain milk production, since incr. nerve stimulation increases oxytocin and prolactin
Prolactin=induces and maintains lactation and decr. reproductive function.
Oxytocin=assists in milk letdown; promotes uterine contractions
When is breast milk ideal nutrition? What does it contain? How does it help infant? What does it lack? How does it help mother?
What is the source of hCG? Function? Structure? What conditions increase it? Decrease it?
Syncytiotrophoblast of placenta
Maintains corpus luteum (and thus progesterone) for first 8-10 weeks of pregnancy by acting like LH. After 8-10 weeks, placenta synthesizes its own estriol and progesterone and corpus luteum degenerates.
Used to detect pregnancy b/c it enters urine early
Has identical alpha subunit as LH, FSH, and TSH. Beta subunit is unique.
Increase: multiple gestations, hydatiform moles, chorioCAs, DS
Decr.: ectopic or failing pregnancies, Edward syndrome, Patau syndrome
What is the pathophys of menopause? Epid? Hormone changes? Findings? How is it detected? Waht does menopause under 40 indicate?
Decr. estrogen production due to age linked decline in number of ovarian follicles.
51 years old ( earlier in smokers)
Usually preceded by 4-5 yeras of abnormal menstrual cycles.
Source of estrogen becomes estrone from peripheral conversion of androgens.
Incr. androgens leads to hirsutism.
Decr. estrogen, really incr. FSH, incr. LH (no surge), incr. GnRH
atrophy of vagina
coronary artery disease
Greatly increased serum FSH is diagnostic
under 40=premature ovarian failure.
When does spermatogenesis begin? How long does development take? Location? What is result? What happens after? Describe the maturation. What are the parts of a spermatozoon?
Spermatogonium (2N, 2C, 46 single chromosomes, XY) goes through blood-testis barrier, then dupicates to become a primary spermatocyte
Prim. sperm. (2N, 4C, 46 sister chromatids, XX and XY) undergo meiosis I to become secondary spermatocytes
Secondary sperm. (1N, 2C, 23 sister chromatids, XX or XY) undergo meiosis II to become spermatids.
Spermatids (1N, 1C, 23 single chromatids, X or Y) undergo spermiogenesis (loss of cytoplasmic contents, gain of acrosomal cap) to form mature spermatozoon (1n, 1C)
Zoon is zooming to egg
Gonium is going to be a sperm
Acrosome cap on head, neck, middle piece, tail (imparired mobility (kartageners)=infertility)