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FEMALE reproductive > reproductive: EMBRYOLOGY > Flashcards

reproductive: EMBRYOLOGY Flashcards

1
Q

key roles of Sonic Hedgehog Gene (SHH gene) (2)

NOTE: embryonic SIGNALING protein

A

1- CNS development
2- Limb development

^^sonic like human with limbs and cns :)

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2
Q

Sonic Hedgehog Gene (SHH gene)

FUNCTION + MUTATION (+symptoms)

A

1- normal development of the hemispheres of brain
-abnormal: Holoprosencephaly
-remb: prosencephaly at wk3-4, at wk5 (telencephaly and diencephaly)
-symptoms:
a- single lobed brain
b- facial abnormalities (cleft lip/palate or cyclopia)

2- limb AP axis development: SHH is active in the zone of polarizing activity so influences the AER

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3
Q

limb development: 3 planes

A 
1- Proximal to distal 
(humerus->radium->wrist)
2- dorsal- ventral axis
(dorsal-extensor, ventral-flexors) 
^^old famous drawing
3-Anterior-posterior axis
Anterior towards head (radius and thumb)
posterior (ulna fingers)
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4
Q

4 imp embryonic genes

A

1- Sonic Hedgehog
2- FGF
3- Wnt-7a
4- Homeobox (Hox) genes

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5
Q

proximal to distal development genes and description

A

structure called: Apical Ectodermal Ridge (AER); area of limb bud formation above “progress zone” in the mesoderm.
-key transcriptional factor: Fibroblast growth factor (FGF gene)

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6
Q

what happens if the AER is removed in proximal to distal development? is it replaceable?

A

LIMB stops growing

-replaced with FGF: normal growth

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7
Q

Wnt-7a gene

  • function?
  • gene deletion?
A

in the dorsal-ventral development

  • KEY for DORSAL
  • activates LMX-1 gene in mesoderm
  • thus, DORSALIZES mesoderm

deletion: TWO VENTRAL sides
NOTE: ventral (Engrailed 1) represses Wnt-7 !!!

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8
Q

Wnt genes fxn
early embryo?
late embryogenisis?

A

early: DORSAL-VENTRAL axis
late: ANTERO- POSTERIOR axis

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9
Q

HOX genes fxn and mutation

A
  • regulators of AP axis development
  • mutation: abnormal limb (digits/toes) formations
    e. g: fruit flies, polydactyly, syndactyly
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10
Q 
(?N, ?C) in 
haploid spermatozoon ?
haploid ovum ? 
zygote ? 
AFTER DNA SYNTHESIS IN ZYGOTE ? 
AFTER DIVISION ?
A 
(1N, 1C) 
(1N, 1C) 
(2N, 2C) 
(2N, 4C) 
(2N, 2C)+(2N, 2C)
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11
Q

When does the two cell stage occur in fetus ?

A

first 1-2 days after ferilization

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12
Q

what forms after 2 cell stage? (2 steps)

A 
MORULA (ball of cells) 
then BLASTULA (humans;blastocyst)
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13
Q

whats the difference b/w morula and blastula?

A

blastula contains fluid cavity (called BLASTOCOEL)

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14
Q

2 layers of blastocyst:

and their fxn

A 
1- OUTER cells: Trophoblast 
-polarized (2 diff sides)
-secrete watery fluid of blastocoel
2- INNER cell mass 
-apolar
-give rise to ALL TISSUES of body (i.e embryonic stem cells)
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15
Q

what is implanted in implantation and when ?

A
  • blastocyst in uterus

- day 6-10

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16
Q

when does B-hCG secretion begins?
what structure secretes it?
when pregnancy is detected?

A
  • after implantation
  • placenta
  • day 6-10
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17
Q

what happens to the blastula?

A 
GRANULATION 
3 layered (gastrula) 
Ecto meso endo
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18
Q

describe the process of gastrulation. from what structures the 3 layers arise ?

A 
-inner cell mass form bilaminar disc (2 layers separated by BM)
1- Epiblast
GIVE RISE TO 3 germ layers
2- Hypoblast
yolk sac (in womb) + other structures 
i.e not embryonic structures
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19
Q

what indicates the start of gastrulation ?

A

invagination of epiblast cells creates a VISIBLE LINE (primitive STREAK) in blastocyst

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20
Q

Ectoderm gives rise to (2)

A

1- epidermis
(outer surface skin, nailbed, hair)
2- NERVOUS system

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21
Q

what is the adult remnant of the notochord?

A

Nucleus pulposus of spine

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22
Q

NS development

A

notochord (from mesoderm) induces ectoderm to become neural plate that folds to give neural tube

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23
Q

Neural tube gives rise to

A

CNS structures

  • CNS neurons, oligodendroctes, astrocytes
  • retina
  • spinal cord
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24
Q

Neural crest gives rise to

A

PNS structures

  • cranial nerves
  • dorsal root ganglia
  • autonomic ganglia
  • shwann cells
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25
Q

what CNS structures arise from the mesoderm ??

A

Microglia

Meninges

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26
Q

Endoderm gives rise to

A
  • GI epithelium (and liver, gall bladder, pancreas)

- inner lung (alveoli, epithelium of trachea/bronchi)

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27
Q

airway cartilage

from what embryonic layer?

A

mesoderm

note alveoli, epithelium of trachea/bronchi from endoderm

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28
Q

mesoderm gives rise to

A
  • muscle, bone, CT
  • CV structures
  • kidneys
  • lymphatics
  • blood
  • airway cartilage
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29
Q

congenital defects from mesoderm derivatives (3)

A

1- congenital heart disease
2- limb deformities
3- renal defects

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30
Q

what is mesenchyme?
derived from what layer?
its tumors known as?

A

-embryonic CT
(in adults only found as stem cells)
-mostly mesoderm
-sarcmas

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31
Q

what is the embryonic period/ fetal period?

A

embryonic:

  • 1st 8 weeks
  • organogenesis

fetal:

  • adult structures established
  • organ/ structures grow
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32
Q

most vulnerable period for teratogens

A

EMBRYONIC PERIOD

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33
Q

Heart development wks?

A

week 4
heart begins beating

week 6
Transvaginal US detects fetal heart movement

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34
Q

Limbs development wks?

A

week 4
limbs form

week 8
baby begins moving

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35
Q

genitalia development wks?

identification of sex

A

prior to week 10 (genitalia looks similar)

  • SRY gene (Y chromosome) : penis development
  • lack of SRY: clitoris development

Ultrasound identification: usually weeks 15-20

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36
Q

Pituitary gland (anterior vs posterior) arises from

A

Anterior:
ECTODERM (rathke’s pouch)
outpouching of upper mouth

Posterior:
NEURAL TUBE

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37
Q

Adrenal gland (cortex vs medulla) arises from

A

Cortex:
MESODERM
aldosterone, cortisol, androgen

Medulla:
NEURAL CREST
epinephrine, norepinephrine

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38
Q

2 types of errors of morphogenesis +define briefly

A

Intrinsic: failure of embryo to develop
Extrinsic: external force impacts normal development

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39
Q

types of Intrinsic errors of morphogenesis (4)

A
  1. Agenesis
  2. Aplasia
  3. Hypoplasia
  4. Malformation
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40
Q

types of extrinsic errors of morphogenesis (2)

A
  1. Disruption

2. Deformation

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41
Q

difference between Agenesis and Aplasia

with EXAMPLE !

A
  • Agenesis: missing organ caused by MISSING EMBRYONIC TISSUE
    e. g: Renal agenesis
  • Aplasia: missing organ caused by GROWTH FAILURE OF EMBRYONIC TISSUE (present!)
    e. g: thymic aplasia (DiGeorge syndrome)
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42
Q

what is hypoplasia ? e.g?

A

incomplete organ development

-microcephaly

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43
Q
  1. neural tube defects
  2. cleft lip palate
  3. congenital heart defects
    what error of morphogenisis (intrinsic/extrinsic) and what type?
A

INTRINSIC
MALFORMATION:
abnormal development of structure

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44
Q

difference between disruption and deformation with examples

A
  • Disruption: normal tissue GROWTH ARRESTED due to external force
    e. g: AMNIOTIC BAND SYNDROME
  • Deformation: external force leads to ABNORMAL GROWTH (NOT ARREST)
    e. g: Potter’s syndrome
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45
Q

diagnose:
-fetal structure entrapped by fibrous bands in utero (often involves limbs or digits)
and what type of errors in morphogenisis

A
  • EXTRINSIC
  • DISRUPTION
  • AMNIOTIC BAND SYNDROME
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46
Q

what is potter’s syndrome? cause?

A

fetus exposed to ABSENT or LOW amniotic fluid!!
so amniotic fluid is frim fetal urine :)
caused by SEVERE RENAL MALFUNCTION (i.e reduced amniotic fluid)
leads to loss of fetal cushioning to external forces (fxn of normal amniotic fluid)

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47
Q

what is potter’s SEQUENCE ?

A

sequence of fetal abnormalities, all resulting from single problem: RENAL DYSFUNCTION
leads to:
1- External compression of the fetus (abnormal face/limb formation)
2- alteration in lung liquid content (abnormal lung formation)
(SUMMARY:
-PULMONARY HYPOPLASIA, LIMB/SKELETAL DEFORMITIES)

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48
Q

what trimester has the highest risk of teratogens fetal exposure

A

1st (i.e embryonic period)

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49
Q

first 2 weeks teratogens leads to:

A

“ALL or NONE” period

  • spontaneous abortion
  • no effect
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50
Q

in wks 2-8, teratogens lead to

A

Structural defects (organogenesis)

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51
Q

after wk 8 teratogens lead to

A
  • decreased growth
  • CNS dysfunction
  • usually NO BIRTH DEFECTS
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52
Q

CATEGORIES A-D,X

A 
A: no risk to fetus in HUMAN studies
B: no risk to fetus in OTHER studies
C: risk CANNOT BE RULED OUT 
D: POSITIVE evidence of risk
X: CONTRAINDICATED IN PREGNANCY
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53
Q

ACEIs and ARBs in pregnancy

  • class?
  • 1st, 2nd, 3rd trimester?
A

1st: numerous congenital malformations
2nd 3rd !!!!!: OLIGOHYDRAMNIOS
(thus can lead to potter’s syndrome - sequence) (RAAS interferes w/ kidney)

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54
Q

seizure drugs in pregnancy

  • most common effect on fetus?
  • high risk drugs?
  • in case of EPILEPSY women needs to take it, what do you give with it?
A
  • NEURAL TUBE DEFECTS
  • VALPROIC ACID!!, phenytoin, phenobarbital, carbamazepine
  • HIGH dose folic acid supplementation
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55
Q

use of PHENYTOIN in pregnancy leads to:

A 
Fetal Hydantoin Syndrome 
A) growth deficiency 
B) abnormal facial features 
-MICROCEPHALY 
-CLASSICALLY CLEFT LIP/PALATE  
-nose: broad, short
-eyes: wide-spaced
-ears: malformed
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56
Q

what malignancy is common in pregnant women ?

A

HODGKIN LYMPHOMA

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57
Q

ideally chemotherapy deferred to: what periods?

A
  • after birth
  • 2nd/3rd trimester

(note 1st trimester: high risk of fetal malformation)

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58
Q

What are the chemotherapeutics with the highest risks? (2)

what is their classic symptom?

A

1-Alkylating agents
2- antimetabolites
classically: MISSING DIGITS

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59
Q

embryopathy:
-abnormal facial features (low ears, wide spread eyes)
-congenital heart disease
-hydrocephalus
or spontaneous abortion

what drug did the mom take? class?

A

-Isotretinoin (derivative of vit A)
used to treat acne
-class X

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60
Q

women of reproductive age taking isotretinoin, should take what with it?

A

birth control mandatory

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61
Q 
Vitamin A excess (dose much higher than RDA recommended daily allowance) 
TERATOGENIC IN 1ST TRIMESTER 
leads to (3):
A

1- spontaneous abortion
2- microcephaly
3- cardiac anomalies

62
Q

what anti-inflammatory is used to induce abortion in ectopic pregnancy?
leads to what if given to pregnant women?

A 
-Methotrexate (inhibits folate mechanism) 
CLASS X (contraindicated) 
-leads to neural tube defects
63
Q 
1- neural tube defects 
2- abnormal skull/face shape 
3- cleft palate 
4- hydrocephalus 
5- limb anomalies

what drug leads to these in embryos?

A

Aminopterin/ methotrexate

64
Q

warafrin can lead to (4) in fetus?

A 
1- fetal hemorrhage 
2- spontaneous abortion 
3- optic atrophy (vision loss) 
4- bone and cartilage abnormalities:
*stippled epiphyses (SMALL, ROUND DENSITIES ON XRAY) 
*nasal hypoplasia 
*limb hypoplasia
65
Q

MISSING PATCH SKIN/HAIR IN BABY
(aplasia cutis: absence of epidermis on scalp)
what did the mother take (IN 1ST TRIMESTER)? to treat what? what class?
what she had to use instead?

A

-Methimazole
-to treat hypethyroidism
(NOTE: may cause FETAL and NEONATAL HYPOthyroidism) !!!!!!
-class D
-should use Proplthiouracil (PTU) in 1st trimester

66
Q

what is the most common anomaly when pregnant take lithium for psychiatric disorder (class D)

A

mostly involve the heart

EBSTEIN’S ANOMALY OF THE TRICUSPID VALVE- displaced toward the apex of the RV

67
Q

what antibiotics leads to the following in fetus?
1- permenant deafness
2- permanently discolor fetal teeth (due to accumulation in teeth and long bones)
3- fetal cartilage damage
4- neural tube defects (due to disruption of folate metabolism in fetus)
5- Kernicterus (permenant brain damage d/t high bilirubin lvls) - displace bilirubin from albumin

A 
1- Aminoglycosides
2- Tetracycline 
3- Fluoroquionolones 
4- Trimethoprim 
5- Sulfonamide
68
Q 
what drug used to treat multiple myeloma and was given as sedative IN THE PAST to pregnant women? 
leads to: 
-amelia: no limb 
-micromelia: short limb
-phocomelia: abnormal limb
A

Thalidomide (class X)

69
Q

main risk to -mother -baby (if mom takes diethylstilbestrol - nonsteroidal estrogen during pregnancy)
NOTE: WAS used before to prevent miscarriage and premature birth

A
  • Mother: slightly increased risk of breast cancer

- FEMALE babies: reproductive tract abnormalities

70
Q 
Female baby with:
-hypoplastic uterus 
- cervical hypoplasia
-vaginal adenosis 
3 questions: 
1- what drug did the mom take? 
2- explain vaginal adenosis findings
3- what further complications could happen later on?
A

1- DES: diethylstilbestrol
2- metaplasia (cervical and endometrial epithelium found in VAGINA!!) d/t persistent Mullerian tissue after birth
3- a- VAGINAL CLEAR CELL ADENOCARCINOMA
b- INFERTILITY

71
Q

what are the 4 characteristics of fetal alcohol syndrome (FAS)

A

1- facial features
2- congenital heart disease
3- skeletal anomalies
4- INTELLECTUAL DISABILITY (REDUCED IQ LIFELONG)

72
Q

what are the facial features in fetal alcohol syndrome? 3

A

1- smooth philtrum : groove from base of nose to upper lip
2- short palpebral fissures: small opening of eyes
3- Thin vermillion border: upper lip

73
Q

what are the growth skeletal anomalies in fetal alcohol syndrome? 3

A
  • below average height, weight
  • LIMB DEFECTS :
  • *Finger contractions
  • *congenital hip dislocations
74
Q

alcohol in
1st trimester
3rd trimester

A

1st: facial, brain, heart
3rd: size, growth
due to each trimester role

75
Q

HOW SMOKING AFFECTS FETUS? 2 WAYS

A

RESULT: impaired oxygen delivery to fetus
1- NICOTINE: nicotine-induced vasoconstriction
(reduced placental blood flow)
2- CARBON MONOXIDE: CO competes with O2
(reduced oxyhemoglobin)

76
Q

main characteristic of smoking in fetus?

A

IUGR (intrauterine growth restriction)
and low birthweight

PLUS association with SIDS (sudden infant death syndrome)

77
Q

effect of mother taking cocaine on fetus?

A

VASOCONSTRICTION
-SAME as nicotine
IUGR, low birthweight, etc…

78
Q

why pregnant women should avoid FISH/SEAFOOD?

esp swordfish, shark, tilefish, mackerel king

A

contains METHYLmercury (not removed by cooking)
-fetal brain highly sensitive to mercury (mother -nothing)
leads to:
1- delayed milestones
2-rarely blindness, deafness, cerebral palsy

79
Q

high dose of XRAY in 8-15 wks in pregnancy may cause: 3:

how can we protect fetus?

A

1- intellectual disability !
2- microcephaly !
3- growth restriction

—> LEAD SHIELDING !!!!!

80
Q

what is a common characteristic in babies for DIABETIC MOMS?
and can lead to what?

A

MACROSOMIA (LARGE BABY)

can lead to birth injury (shoulder dystocia-shoulder cannot pass through birth canal) —> EMERGENCY C-section

81
Q

what is the most common congenital heart defect for maternal diabetes ?

A

TRANSPOSITION OF THE GREAT VESSELS (TGA)

82
Q

why maternal diabetes can lead to neonatal hypoglycemia?

A

-baby is in hyperinsulinemic state
-glucose lvls drop
(TRANSIENT usually first 24 hrs)

83
Q

what to do for babies with maternal diabetics when they are born?

A

CLOSE GLUCOSE MONITORING is essential

84
Q

children of insulin-dependent mothers usually suffer from what syndrome ?
what are the 3 main characteristic of this syndrome:

A 
CAUDAL REGRESSION SYNDROME 
aka sacral agenesis 
1-incomplete development of SACRUS
2- may include SIRENOMELIA (MERMAID SYNDROME)-fused legs 
3- often neural tube defect
85
Q

women with PKU put their babies at risk of what?

what changes should be made during pregnancy?

A

PHENYLKETONURIA (same dx:))

  • serum PHENYLALANINE should be monitored
  • dietary restriction of PHENYLALANINE
    (note: high levels of phenylalanine acts as teratogen)
86
Q 
1- IUGR 
2- microcephaly 
3- intelectual disability 
4- congenital heart defects 
*COARCTATION of the aorta
*hypoplastic left heart syndrome

note similar to alcohol effects on fetus
whats the diagnosis?

A

PHENYLKETONURIA

87
Q

branchial/ pharyngeal apparatus consist of (3):

A

1- pharyngeal arches
2- pharyngeal clefts
3- pharyngeal pouches

88
Q

from what embryonic layer does each of the following arise from:
1- pharyngeal arches
2- pharyngeal clefts
3- pharyngeal pouches

A

1- pharyngeal arches: MESODERM (MESENCHYME)
2- pharyngeal clefts: ECTODERM
3- pharyngeal pouches: ENDODERM

89
Q

what BONES arise from the first arch?

A 
1- MAXILLARY process
*maxilla
*zygomatic bone
2- MANDIBULAR process 
*mandible
*MECKEL’S cartilage (Incus and malleus)
90
Q

what (only main) MUSCLES arise from the first arch?

A

MUSCLES OF MASTICATION
1-temporalis
2-masseter
3-pterygoids

91
Q

what NERVE arise from the first arch?

A

TRIGEMINAL NERVE

mandibular and maxillary divisions

92
Q

which artery of the AORTIC ARCH arise from the first arch?

A

portion of the MAXILLARY ARTERY

93
Q

what BONES arise from the second arch?

A

REICHERTS CARTILAGE
1-stapes
2- styloid process of temporal bone
3- LESSER horn of hyoid

94
Q

what main MUSCLES arise from the second arch?

A

STAPEDIUS

-smallest in body

95
Q

what NERVE arise from the second arch?

A

FACIAL NERVE

96
Q

what ARTERIES arise from the second arch? 2

A

not v imp (both embryonic vessels-involutes later)
1-stapedial artery
2-hyoid artery

97
Q

what CARTILAGE/BONES arise from the third arch?

A

HYOID BONE

BODY AND GREATER horn

98
Q

what MUSCLES arise from the third arch?

A

STYLOPHARYNGEUS

99
Q

what NERVE arise from the third arch?

A

GLOSSOPHARYNGEAL NERVE (IX)

100
Q

what happens to the 5th pharyngeal arch

A

does not persist in humans

101
Q

what NERVE innervates the fourth and sixth arches?

A

VAGUS NERVE

4th: superior laryngeal
6th: recurrent laryngeal

102
Q

what CARTILAGE arises from the fourth and sixth arches?

A

both arches fuse to form LARYNX CARTILAGE

103
Q

what (general) MUSCLES arises from the fourth and sixth arches?

A

LARYNGEAL MUSCLES

104
Q

what ARTERIES arises from the fourth and sixth arches?

A

4TH

lt: aortic arch
rt: proximal rt subclavian artery

6TH (PULMONARY ARCH)

lt: proximal pulmonary artery and ductus arteriosus
rt: proximal pulmonary artery

105
Q

PHARYNGEAL ARCHES SOS SUMMARY
mention the nerve and main structures for each: (6 arches)
4 points

A
  • 1st: CN 5 trigeminal: maxilla/mandible
  • 2nd: CN 7 facial: hyoid
  • 3rd: CN 9 glossopharyngeal: hyoid
  • 4th&6th: CN X vagus: larynx
106
Q 
children presents w/
facial abnormalities: 
-small: mandibular hypoplasia
- small jaw: micrognathia 
-absent/small ears 
-glossoptosis;retraction of tongue
WITH DIFFICULTY BREATHING 
-diagnosis? + mechanism
-what caused difficulty breathing? 
-is intelligence affected?
A

-TREACHER COLLINS SYNDROME
1st and 2nd arch syndrome
due to failure of neural crest cell migration
-d/t underdeveloped lower jaw, thus obstruction of airway by tongue
-NO

107
Q

sos TONGUE DEVELOPMENT

  • SENSATION
  • TASTE
  • MOTOR
A

ant 2/3: (1st and 2nd arches)

  • sensation: CN V: 1st arch
  • taste: CN VII: 2nd arch

post 1/3: (3rd and 4th arches)

  • sensation: CN IX: 3rd arch
  • taste: CN X: 4th arch

MOTOR: hypoglossal XII
—>exception: palatoglossus (CN X)

108
Q

most common craniofacial malformation +cause

A

CLEFT LIP

-mltifactorial etiology

109
Q
  • how is the primary palate formed?

- failure leads to —-?

A
  • by fusion of:
    1- maxillary prominences (from 1st arch) with
    2- medial nasal prominence (from philtrum)
    -leads to cleft lip
110
Q

note for clefts check these:

A

1- unilateral/bilateral
2- complete/incomplete
3- lip or palate or both

111
Q
  • how is the secodary palate formed?

- failure leads to —-?

A
  • fusion of lateral PALATAL SHELVES (PROCESSES)

- failure leads to cleft palate

112
Q 
how many 
pharyngeal arches
pharyngeal clefts
pharyngeal pouches 
is there
A

6
4
4

113
Q

what is mainly formed from the 1st pouch?

A

inner ear: EUSTACHIAN TUBE

114
Q

what is mainly formed from the 2nd pouch?

A

PALATINE TONSILS

115
Q

what is mainly formed from the 3rd pouch?

A
  • THYMUS

- lt and rt INFERIOR PARATHYROID GLANDS

116
Q

what is mainly formed from the 4th pouch?

A

-SUPERIOR PARATHYROID GLANDS
-ULTIMOBRANCHIAL BODY
forms C-cells (thyroid)
derived from neural crest cells

117
Q

failure of the 3rd/4th pharyngeal pouch to form leads to —?

A

DiGeorge syndrome

-thymic aplasia

118
Q

most common deletion in DiGeorge syndrome

A

22q11 chromosomal deletion

119
Q

CLASSIC TRIAD OF DIGEORGE SYNDROME

A 
1- loss of thymus 
loss of T-cells, RECURRENT INFECTION
2- loss of parathyroid gland
HYPOCALCEMIA, TETANY 
3- congenital heart defects 
CONOTRNCAL
120
Q

pharyngeal clefts develops into:

A

1st: EXTERNAL AUDITORY MEATUS

2nd 3rd 4th: CERVICAL SINUS (temporary cavity)

121
Q

NECK MASS IN CHILDREN DD

how to differentiate?

A 
1- branchial cleft cyst 
-does NOT move with swallowing
2-thyroglossal duct cyst
-moves with swallowing 
(remember physical exam we check)
122
Q

what is the most common location for BRANCHIAL CLEFT CYST?

How is it noticed?

A 
2nd pharyngeal CLEFT
-below angle of the mandible 
-anterior to SCM muscle 
>>when it becomes infected 
also, may develop fistula to skin (OOZE PUS)
123
Q

how gonads development start?
what week?
what layers?
failure of what leads to no development?

A

GONADAL RIDGES form at wk 7
(derived from MESENCHYME)
+GERM CELLS (derived from EPIBLAST) invade the gonadal ridges

124
Q

SRY gene codes for

-forms what cells?

A

testis determining factor

forms sertoli and leydig cells

125
Q

what cell produce testesterone in fetus

A

Leydig cells

126
Q

what cords develop in testis vs ovaries

A

testis: MEDULLARY (testis) cords
ovary: CORTICAL cords develop (form clusters) NOTE: surrind germ cells

127
Q

what cells form the primordial follicles 2

A
  • oogenia

- follicular cells

128
Q

Genital ducts (internal genitalia)
2
DEVELOP INTO :

A 
Mesonephric (wolffian)
-epididymis
-vas deferens 
-seminal vesicles
-ejaculatory duct 
parsmesonephric (mullerian) 
-fallopian tube
-uterus 
-upper 2/3 vagina
129
Q

how does genital ducts develop into a male (2 main things/2 cells + fxn)

A

1- SERTOLI CELLS
release MIF mullerian inhibitory factor: suppress mullerian
2- LEYDIG CELLS
release ANDROGENS: stimulate wolfian

130
Q

REMNANTS of suppression of WOLFFIAN/MULLERIAN ducts in males and females

A

males: appendix testis (tissue at upper testis)
females: gartner’s duct (found on vaginal walls) note: may form cyst :(

131
Q

what part of male genitals secrete about 75% of fluid in semen

A

glands: seminal vesicles

132
Q

ejaculatory duct passes through —- to connect to the ——

A
  • prostate

- urethra

133
Q

PARAMESONEPHRIC ducts ONLY occur in absence of: 2

A
  • MIF

- ANDROGENS

134
Q

what other structure gives rise to INTERNAL GENITALIA (other than genital ducts)?
arises from ?

A

UROGENITAL SINUS

arises from the cloaca

135
Q

cloaca divides into 2

A

1- urogenital sinus

2- anal canal

136
Q

Upper portion of the urogenital sinus forms :

  • males?
  • females?
A

BOTH: bladder

137
Q

MIDDLE (pelvic) portion of the urogenital sinus forms :

  • males?
  • females?
A

males: prostate and prostatic urethra
NOTE: -phalic portion in males forms the penile urethra

females: inferior vagina

138
Q

what is the MOST COMMON defect that can lead to uterine anomalies? complications?

A

LATERAL FUSION DEFECTS
(failed fusion of the 2 sides of uterus)
-infertility, pregnancy loss

139
Q

Most common lateral fusion defects (uterine anomalies)? mechanism

A

SEPTATE UTERUS

  • septum divides uterus
  • 2 endometrial cavities
  • defects in resorption of septum b/w Mullerian ducts
140
Q

treatment for septate uterus

A

septoplasty

141
Q

how to diagnose uterine anomalies?

A

HYSTEROSALPINGOGRAPHY

inject dye in the uterus

142
Q

external genitalia 4 key structures

A

1- genital tubercle
2- urogenital sinus (from cloaca)
3- urogenital folds (from cloaca)
4- labioscrotal (genital) swellings

143
Q

external genitalia:

genital tubercle elongates to form what structures in male/female

A

male: phallus
female: clitoris

144
Q

external genitalia:

urogenital folds to form what structures in male/female

A

1- male:
urogenital folds close to form penile urethra

2- female:
no fusion, forms labia minora

145
Q

external genitalia: urogenital sinus form what structures in male/female

A

GLANDS

male: prostate gland, bulbourethral glands (of Cowper)
female: paraurethral glands (Skene), bartholin glands

146
Q

external genitalia:

labioscrotal swelling form what structures in male/female

A

male: scrotum
female: labia majora

147
Q

what is required for female external genitalia to form?

A

ESTROGEN MUST BE HIGHER THAN ANDROGEN

148
Q

what is required for male external genitalia to form?

sos

A

DIHYDROTESTESTERONE

testesterone —5a-reductase—-> DHT

149
Q

5a-reductase fxn and deficiency

A

fxn: converts testosterone into DHT
deficiency: ambiguous genitalia until PUBERTY
and at puberty (testosterone increases)

150
Q

what is hypospadia?
mechanism?
occurs with ?

Vs
what is epispadia?
mechanism?
-occurs with?

which one is more common?

A
  • VENTRAL opening of urethra
  • failure of urethral FOLDS to close
  • CRYPTORCHIDISM 10%

vs

  • DORSAL opening of urethra
  • abnormal position/formation of GENITAL TUBERCLE
  • BLADDER EXSTROPHY

hypospadia is more common

FEMALE reproductive (6 decks)

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