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Flashcards in Reproductive embryology and anatomy Deck (65):
1

What are some important genes of embryogenesis?

Sonic hedgehog gene
Wnt-7 gene
FGF gene
Homeobox (Hox) genes

2

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
CNS development

Holoprosencephaly

3

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)

4

Where is FGF gene produced? What is its function?

Apical ectodermal ridge

Stimulates mitosis of underlying mesoderm, limb lengthening

5

What is the Homeobox gene involved in? What does it code for? What do mutations lead to?

Segmental organization of embryo in craniocaudal direction

Transcription factors

Appendages in wrong locations

6

Early fetal development

Day 0:
Week 1:
W2:
W3:
W3-8:
Week 4:
Week 6:
Week 10:

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

7

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

8

What are the 3 embryologic derivatives? Location? What are the 3 types of ectoderm?

Ectoderm=external
Mesoderm=middle/meat
Endoderm=internal

Surface ectoderm
neuroectoderm
neural crest

9

What is made of surface ectoderm?

Epidermis
Adenohypophysis (Rathke pouch)
Lens of eye
Epithelial linings of oral cavity
Sensory organs of ear
Olfactory epithelium
Epidermis
Anal canal below pectinate line
Parotic, sweat, and mammary glands

10

What is made of neuroectoderm?

Brain (neurohypophysis, CNS neurons, oligodendrocytes, astrocytes, ependymal cells, pineal gland)
Retina and optic nerve
Spinal cord

11

What is made of neural crest cells?

PNS (dorsal root ganglia, schwann cells, CNs, celiac ganglion, ANS)
Melanocytes
Chromaffin cells of adrenal medulla
Parafollicular C cells of thyroid
Pia and arachnoid
Bones of the skull
Odontoblasts
Aorticopulmonary septum

12

What is made of mesoderm? What do mesoderm defects lead to?

Muscles
Bone
CT
Serous linings of body cavities (peritoneum)
spleen (foregut mesentary)
CV structures
Lymphatics
Blood
Wall of gut tube
Vagina
Kidneys
Adrenal cortex
Dermis
Testes
Ovaries
Notochord (nucleus pulposus)

Vertebral defects
Anal Atresia
Cardiac defects
TEF
Renal defects
Limb defects

13

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)

14

What is

Agenesis:
Aplasia:
Hypoplasia:
Deformation:
Disruption:
Malformation:
Sequence:

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)

15

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

16

What effects do these drugs have on fetus?

ACEI:
Alkylating agents
Aminoglycosides:
Carbamazepine:
DES:
Folate antag:
Isotretinoin:
Lithium:
Methimazole:
Phenytoin:
Tetracyclines:
Thalidomide:
Valproate:
Warfarin:

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.

17

What effects do these substances have on the fetus?

Alcohol:
Cocaine:
Smoking (nicotine/CO):

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)

18

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

19

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
microcephaly
facial abnormalities (smooth filtrum, hypertelorism)
Limb dislocation
heart defects

Severe: Heart/lung fistulas, holoprosencephaly

Failure of cell migration

20

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
Dichorionic diamniotic

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.

21

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

Decidua basalis=endometrium

22

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

23

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

24

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

25

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
Second=Stapedial

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

26

What is the branchial apparatus? Another name? What is it composed of? What are branchial clefts (another name), arches, and pouches derived from?

Pharyngeal apparatus

Clefts, arches, and pouches

CAP covers from outside to inside
Cleft/Groove=ectoderm
Arches=mesoderm and neural crest
Pouches=Endoderm

27

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

28

What does the 1st arch turn into (cartilage, muscles, and nerves)? 2nd? 3rd? 4th-6th?

1st
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)

2nd
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)

3rd
C: greater horn of hyoid
M: Stylopharyngeus (innervated by glossopharyngeus)
N: CNIX (glossopharyngeal) (swallow stylishly)

4-6
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)

29

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.

30

What are the derivatives of the 1st branchial pouch? 2nd? 3rd? 4th?

1st
Middle ear cavity, eustachian tube, mastoid air cells (endoderm lined structures of ear)

2nd: Epithelial lining of palatine tonsil

3rd
Dorsal wings-inferior parathyroids
Ventral wings=thymus

4th
Dorsal wings=superior thyroids

Ear, tonsils, bottom to top

1=ear
2=tonsils
3=inferior thyroids, thymus
4=superior thyroids

31

What is DiGeorge syndrome? symptoms?

Aberrant development of 3rd/4th pouches

T cell deficiency
Hypocalcemia
Cardiac defects (conotruncal anomalies)

32

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)

33

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)

34

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)

35

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)

36

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.

37

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)

38

What is a septate uterus? Results? treatment? Bicornuate uterus? Results? Uterus didelphys? Results?

Incomplete resorption of septum
Decr. fertility
Septoplasty

Incomplete fusion of mullerian ducts
Incr. risk of complicated pregnancy

Complete failure of fusion
Double uterus, vagina, and cervix
pregancy possible

39

What are the undifferentiated external genitalia? What do they become in males and in females and in response to what?

M: DHT
F: Estrogen

Genital tubercle
M:Glans penis
F: glans clitoris

Genital tubercle:
M: Corpus cavernosum and spongiosum
F: Vestibular bulbs

Urogenital sinus
M: bulbourethral glands (of cowper)
F: greater vestibular glands (of bartholin

Urogenital sinus
M: prostate gland
F: urethral and paraurethral glands (of skene)

Urogenital folds
M: ventral shaft of penis (penile urethra)
F: Labia minora

Labioscrotal swelling
M: Scrotum
F:Labia majora

40

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

41

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
F: Obliterated

42

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.

43

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?

SUSPENSORY
Connects: ovaries to lateral pelvic wall
Contained: ovarian vessels
Notes: ligate vessels to avoid bleeding during oophorectomy; urerer courses retroperitoneally; risk of injury

CARDINAL
Connects: cervix to side wall of pelvis
Contained: uterine vessels
Notes: ureter at risk during ligation for hysterectomy

ROUND
Connects: uterine fundus to labia majora
Contained:
Notes: derivative of gubernaculum. Travels through round inguinal canal

BROAD
Connects: uterus, fallopian tubes, and ovaries to pelvice side wall
Contained: Ovary, fallopian tubes, round ligaments of uterus
Notes: Mesosalpinx, mesometrium, mesoovarium

OVARIAN
Connects: edial pole of ovary to lateral uterus
Contained:
Notes:

44

What is histo of
vagina:
Ectocervix:
Transformation zone:
Endocervix:
Uterus:
Fallopian tube:
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)

45

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)
Resolution

ANS

Tachycardia and skin flushing

46

What is the pathway of sperm during ejaculation?

SEVEN UP

Semniferous tubules
Epididymis
Vas deferens
Ejaculatory ducts
Nothing
Urethra
Penis

47

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

48

Describe the innervation of the male erection? Pathways behind erection and relaxtion. Innervation of emission? Innervation of ejaculation? What does sildenafil do?

Erection=parasympathetic=pelvic nerve

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

Emission=symp=hypogastric nerve

Ejaculation-visceral and somatic nerves (pudendal)

Sildenafil-PDE inhib=more cGMP

49

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

50

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
Regulate spermatogenesis
Produce MIF

Incr in temp=decr. sperm production and decr. inhibin (varicocele and cryptorchidism)

51

Where are leydig cells located? Homolog in females? Respond to? Function? Temp effect?

Interstitium (around tubules)

Homolog of theca interna cells

Respond to LH

Secrete testosterone

Unaffected by temp.

52

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
Placenta=estriol
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

53

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.

54

How are tanner stages assigned? Stage I, II, III, IV, V?

Independently to genitalia, pubic hair, and breast

I=childhood (prepubertal)
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

55

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).


56

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

57

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.

58

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

59

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.

60

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

61

When is breast milk ideal nutrition? What does it contain? How does it help infant? What does it lack? How does it help mother?

Infant

62

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

63

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

HAVOCS

Hot flashes
atrophy of vagina
osteoporosis
coronary artery disease
sleep disturbances

Greatly increased serum FSH is diagnostic

under 40=premature ovarian failure.

64

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)

65

What are 3 forms of androgens? What are the sources of each? Potency? Interconversion? Function of Finasteride? How are they converted to estrogen in males? Where? What does exogenous test lead to? Functions?

Testosterone, DHT, Androstenedione

DHT and testosterone (testis), Androstenedione (Adrenal)

DHT > test > Androstene

Test to DHT by 5 alpha reductase (inhib by finasteride)

Androgens to estrogen by aromatase
In males: By P450 aromatase in adipose and testis

Exogenous=inhibition of HPGA leading to decr. intratesticular testosterone leading to decr. testicular size to azoospermia

Testosterone
Differentiation of epididymis, vas deferens, seminal vesicles
Growth spurt: penis, seminal vesicles, sperm, muscle, RBCs
Deepening of voice
Closing of epiphyseal plates (via estrogen from testosterone)
Libido

DHT
Early=differentiation of penis, scrotum, prostate
Late=prostate growth, balding, sebaceous gland activity.