Reproductive embryology and anatomy

Question 1

What are some important genes of embryogenesis?

Answer 1

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

Question 2

Where is the sonic hedgehog gene produced? What is it involved in? what can mutation cause?

Answer 2

Base of limbs in zone of polarizing activity

Patterning along A/P axis
CNS development

Holoprosencephaly

Question 3

Where is the Wnt-7 gene produced? What is it necessary for?

Answer 3

Apical ectodermal ridge (thickened ectoderm at distal end of each developing limb)

Proper organization along dorsal-ventral axis)

Question 4

Where is FGF gene produced? What is its function?

Answer 4

Apical ectodermal ridge

Stimulates mitosis of underlying mesoderm, limb lengthening

Question 5

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

Answer 5

Segmental organization of embryo in craniocaudal direction

Transcription factors

Appendages in wrong locations

Question 6

Early fetal development

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

Answer 6

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

Question 7

What is gastrulation? How does it start?

Answer 7

Process that forms trilaminar embryonic disc

Establishes ectoderm, mesoderm, and endoderm germ layers

epiblast invaginating to form the primitive streak

Question 8

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

Answer 8

Ectoderm=external
Mesoderm=middle/meat
Endoderm=internal

Surface ectoderm
neuroectoderm
neural crest

Question 9

What is made of surface ectoderm?

Answer 9

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

Question 10

What is made of neuroectoderm?

Answer 10

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

Question 11

What is made of neural crest cells?

Answer 11

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

Question 12

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

Answer 12

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

Question 13

What is made up of endoderm?

Answer 13

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)

Question 14

What is

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

Answer 14

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)

Question 15

When are fetuses most susceptible to teratogens? What happens before that? After that?

Answer 15

3rd to 8 weeks

Before-all or none
After-growth and function affected

Question 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:

Answer 16

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.

Question 17

What effects do these substances have on the fetus?

Alcohol:
Cocaine:
Smoking (nicotine/CO):

Answer 17

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)

Question 18

What does a lack or excess of iodine lead in the fetus? Maternal diabetes? Vitamin A excess? x-rays?

Answer 18

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

Question 19

Epid of FAS? What does it lead to in newborns? In most severe form? Mechanism?

Answer 19

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

Question 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

Answer 20

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.

Question 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?

Answer 21

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

Question 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?

Answer 22

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

Question 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?

Answer 23

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

Question 24

Decribe the destruction of vitelline duct. Timeline? What is a vitelline fistula? Result? What is pathophys of meckel diverticulum? Symptoms?

Answer 24

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

Question 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?

Answer 25

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

Question 26

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

Answer 26

Pharyngeal apparatus Clefts, arches, and pouches CAP covers from outside to inside Cleft/Groove=ectoderm Arches=mesoderm and neural crest Pouches=Endoderm

Question 27

What does the 1st cleft turn into? 2nd through 4th? What is a persistent cervical sinus? Location?

Answer 27

1st=external auditory meatus 2-4=temporary cervical sinuses, obliterated by prolif. of 2nd arch mesenchyme Branchial cleft cyst within lateral neck

Question 28

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

Answer 28

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)

Question 29

What is Treacher Collins syndrome? Congenital pharyngocutaneous fistula?

Answer 29

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.

Question 30

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

Answer 30

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

Question 31

What is DiGeorge syndrome? symptoms?

Answer 31

Aberrant development of 3rd/4th pouches ``` T cell deficiency Hypocalcemia Cardiac defects (conotruncal anomalies) ```

Question 32

What is MEN 2A? Findings?

Answer 32

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)

Question 33

What is pathophys of cleft lip? Pathophys of cleft palate?

Answer 33

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)

Question 34

Describe the initial process/pathway of sex differentiation in the embryo.

Answer 34

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)

Question 35

What does the paramesonephric duct develop into in female? How does mullerian agenesis present?

Answer 35

Female internal structures: fallopian tubes, uterus, upper portion of vagina primary amenorrhea (no uterus) with fully developed secondary sex characteristics (functional ovaries)

Question 36

What does the mesonephric duct develop into? What is a gartner duct?

Answer 36

Male internal structures (except prostate): seminal vesicles, epididymis, ejaculatory duct, ductus deferens In females, remnant of mesonephric duct.

Question 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?

Answer 37

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)

Question 38

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

Answer 38

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

Question 39

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

Answer 39

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

Question 40

What hypospadias? Association? What is epispadias? ASsociation?

Answer 40

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

Question 41

What is the gubernaculu? What is its function in males? Females? Processus vaginalis? Function in males Females?

Answer 41

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

Question 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?

Answer 42

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.

Question 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?

Answer 43

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:

Question 44

``` What is histo of vagina: Ectocervix: Transformation zone: Endocervix: Uterus: Fallopian tube: Ovary, outer surface: ```

Answer 44

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)

Question 45

Describe the steps of the female sexual response cycle. How is it mediated? systemic effects?

Answer 45

Phase of excitement (uterus elevates, vaginal lubrication) Plateua (expansion of inner vagina) Orgasm (contraction of uterus) Resolution ANS Tachycardia and skin flushing

Question 46

What is the pathway of sperm during ejaculation?

Answer 46

SEVEN UP ``` Semniferous tubules Epididymis Vas deferens Ejaculatory ducts Nothing Urethra Penis ```

Question 47

When should a urethral injury be suspected? Causes of posterior urethral injury? Findings? Anterior?

Answer 47

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

Question 48

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

Answer 48

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

Question 49

What is the progression of male germ cells?

Answer 49

spermatogonia line semniferous tubules. They produce primary spermatocytes, to secondary spermatocytes to spermatids to spermatozoon (in each succession they move closer middle of tubule

Question 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?

Answer 50

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)

Question 51

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

Answer 51

Interstitium (around tubules) Homolog of theca interna cells Respond to LH Secrete testosterone Unaffected by temp.

Question 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?

Answer 52

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

Question 53

What are the sources of progesterone? Functions? Effect on lactation ?

Answer 53

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.

Question 54

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

Answer 54

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

Question 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.

Answer 55

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).

Question 56

What is dysmenorrhea? Oligomenorrhea? Polymenorrhea?Metrorrhagia? Menorrhagia? Menometrorrhagia?

Answer 56

Pain with menses; often associated with endometriosis >35 day cycle 80 mL blood loss or days of menses Heavy, irregular bleeding

Question 57

Describe oogenesis. What are primary and secondary oocytes like? Ovum?

Answer 57

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.

Question 58

What occurs in ovulation? What is mittelschmerz?

Answer 58

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

Question 59

Where does fertilzation occur and when? Where does implantation occur and when? What happens after that?

Answer 59

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.

Question 60

What effect do estrogen, progesterone, suckling, prolactin, oxytocin have on lactation?

Answer 60

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

Question 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?

Answer 61

Infant

Question 62

What is the source of hCG? Function? Structure? What conditions increase it? Decrease it?

Answer 62

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

Question 63

What is the pathophys of menopause? Epid? Hormone changes? Findings? How is it detected? Waht does menopause under 40 indicate?

Answer 63

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.

Question 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?

Answer 64

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)

Question 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?

Answer 65

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.