reproductive: EMBRYOLOGY Flashcards

(150 cards)

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
what CNS structures arise from the mesoderm ??
Microglia | Meninges
26
Endoderm gives rise to
- GI epithelium (and liver, gall bladder, pancreas) | - inner lung (alveoli, epithelium of trachea/bronchi)
27
airway cartilage | from what embryonic layer?
mesoderm | note alveoli, epithelium of trachea/bronchi from endoderm
28
mesoderm gives rise to
- muscle, bone, CT - CV structures - kidneys - lymphatics - blood - airway cartilage
29
congenital defects from mesoderm derivatives (3)
1- congenital heart disease 2- limb deformities 3- renal defects
30
what is mesenchyme? derived from what layer? its tumors known as?
-embryonic CT (in adults only found as stem cells) -mostly mesoderm -sarcmas
31
what is the embryonic period/ fetal period?
embryonic: - 1st 8 weeks - organogenesis fetal: - adult structures established - organ/ structures grow
32
most vulnerable period for teratogens
EMBRYONIC PERIOD
33
Heart development wks?
week 4 heart begins beating week 6 Transvaginal US detects fetal heart movement
34
Limbs development wks?
week 4 limbs form week 8 baby begins moving
35
genitalia development wks? | identification of sex
prior to week 10 (genitalia looks similar) - SRY gene (Y chromosome) : penis development - lack of SRY: clitoris development Ultrasound identification: usually weeks 15-20
36
Pituitary gland (anterior vs posterior) arises from
Anterior: ECTODERM (rathke’s pouch) *outpouching of upper mouth* Posterior: NEURAL TUBE
37
Adrenal gland (cortex vs medulla) arises from
Cortex: MESODERM aldosterone, cortisol, androgen Medulla: NEURAL CREST epinephrine, norepinephrine
38
2 types of errors of morphogenesis +define briefly
Intrinsic: failure of embryo to develop Extrinsic: external force impacts normal development
39
types of Intrinsic errors of morphogenesis (4)
1. Agenesis 2. Aplasia 3. Hypoplasia 4. Malformation
40
types of extrinsic errors of morphogenesis (2)
1. Disruption | 2. Deformation
41
difference between Agenesis and Aplasia | with EXAMPLE !
- 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)
42
what is hypoplasia ? e.g?
incomplete organ development | -microcephaly
43
1. neural tube defects 2. cleft lip palate 3. congenital heart defects what error of morphogenisis (intrinsic/extrinsic) and what type?
INTRINSIC MALFORMATION: abnormal development of structure
44
difference between disruption and deformation with examples
- 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
45
diagnose: -fetal structure entrapped by fibrous bands in utero (often involves limbs or digits) and what type of errors in morphogenisis
- EXTRINSIC - DISRUPTION - AMNIOTIC BAND SYNDROME
46
what is potter’s syndrome? cause?
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)
47
what is potter’s SEQUENCE ?
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)
48
what trimester has the highest risk of teratogens fetal exposure
1st (i.e embryonic period)
49
first 2 weeks teratogens leads to:
“ALL or NONE” period - spontaneous abortion - no effect
50
in wks 2-8, teratogens lead to
Structural defects (organogenesis)
51
after wk 8 teratogens lead to
- decreased growth - CNS dysfunction - usually NO BIRTH DEFECTS
52
CATEGORIES A-D,X
``` 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 ```
53
ACEIs and ARBs in pregnancy - class? - 1st, 2nd, 3rd trimester?
1st: numerous congenital malformations 2nd 3rd !!!!!: OLIGOHYDRAMNIOS (thus can lead to potter’s syndrome - sequence) (RAAS interferes w/ kidney)
54
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?
- NEURAL TUBE DEFECTS - VALPROIC ACID!!, phenytoin, phenobarbital, carbamazepine - HIGH dose folic acid supplementation
55
use of PHENYTOIN in pregnancy leads to:
``` Fetal Hydantoin Syndrome A) growth deficiency B) abnormal facial features -MICROCEPHALY -CLASSICALLY CLEFT LIP/PALATE -nose: broad, short -eyes: wide-spaced -ears: malformed ```
56
what malignancy is common in pregnant women ?
HODGKIN LYMPHOMA
57
ideally chemotherapy deferred to: what periods?
- after birth - 2nd/3rd trimester (note 1st trimester: high risk of fetal malformation)
58
What are the chemotherapeutics with the highest risks? (2) | what is their classic symptom?
1-Alkylating agents 2- antimetabolites classically: MISSING DIGITS
59
embryopathy: -abnormal facial features (low ears, wide spread eyes) -congenital heart disease -hydrocephalus or spontaneous abortion what drug did the mom take? class?
-Isotretinoin (derivative of vit A) used to treat acne -class X
60
women of reproductive age taking isotretinoin, should take what with it?
birth control mandatory
61
``` Vitamin A excess (dose much higher than RDA recommended daily allowance) TERATOGENIC IN 1ST TRIMESTER leads to (3): ```
1- spontaneous abortion 2- microcephaly 3- cardiac anomalies
62
what anti-inflammatory is used to induce abortion in ectopic pregnancy? leads to what if given to pregnant women?
``` -Methotrexate (inhibits folate mechanism) CLASS X (contraindicated) -leads to neural tube defects ```
63
``` 1- neural tube defects 2- abnormal skull/face shape 3- cleft palate 4- hydrocephalus 5- limb anomalies ``` what drug leads to these in embryos?
Aminopterin/ methotrexate
64
warafrin can lead to (4) in fetus?
``` 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
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?
-Methimazole -to treat hypethyroidism (NOTE: may cause FETAL and NEONATAL HYPOthyroidism) !!!!!! -class D -should use Proplthiouracil (PTU) in 1st trimester
66
what is the most common anomaly when pregnant take lithium for psychiatric disorder (class D)
mostly involve the heart | EBSTEIN’S ANOMALY OF THE TRICUSPID VALVE- displaced toward the apex of the RV
67
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
``` 1- Aminoglycosides 2- Tetracycline 3- Fluoroquionolones 4- Trimethoprim 5- Sulfonamide ```
68
``` 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 ```
Thalidomide (class X)
69
main risk to -mother -baby (if mom takes diethylstilbestrol - nonsteroidal estrogen during pregnancy) NOTE: WAS used before to prevent miscarriage and premature birth
- Mother: slightly increased risk of breast cancer | - FEMALE babies: reproductive tract abnormalities
70
``` 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? ```
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
what are the 4 characteristics of fetal alcohol syndrome (FAS)
1- facial features 2- congenital heart disease 3- skeletal anomalies 4- INTELLECTUAL DISABILITY (REDUCED IQ LIFELONG)
72
what are the facial features in fetal alcohol syndrome? 3
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
what are the growth skeletal anomalies in fetal alcohol syndrome? 3
- below average height, weight - LIMB DEFECTS : * *Finger contractions * *congenital hip dislocations
74
alcohol in 1st trimester 3rd trimester
1st: facial, brain, heart 3rd: size, growth due to each trimester role
75
HOW SMOKING AFFECTS FETUS? 2 WAYS
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
main characteristic of smoking in fetus?
IUGR (intrauterine growth restriction) and low birthweight PLUS association with SIDS (sudden infant death syndrome)
77
effect of mother taking cocaine on fetus?
VASOCONSTRICTION -SAME as nicotine IUGR, low birthweight, etc…
78
why pregnant women should avoid FISH/SEAFOOD? | esp swordfish, shark, tilefish, mackerel king
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
high dose of XRAY in 8-15 wks in pregnancy may cause: 3: | how can we protect fetus?
1- intellectual disability ! 2- microcephaly ! 3- growth restriction —> LEAD SHIELDING !!!!!
80
what is a common characteristic in babies for DIABETIC MOMS? and can lead to what?
MACROSOMIA (LARGE BABY) | can lead to birth injury (shoulder dystocia-shoulder cannot pass through birth canal) —> EMERGENCY C-section
81
what is the most common congenital heart defect for maternal diabetes ?
TRANSPOSITION OF THE GREAT VESSELS (TGA)
82
why maternal diabetes can lead to neonatal hypoglycemia?
-baby is in hyperinsulinemic state -glucose lvls drop (TRANSIENT usually first 24 hrs)
83
what to do for babies with maternal diabetics when they are born?
CLOSE GLUCOSE MONITORING is essential
84
children of insulin-dependent mothers usually suffer from what syndrome ? what are the 3 main characteristic of this syndrome:
``` 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
women with PKU put their babies at risk of what? | what changes should be made during pregnancy?
PHENYLKETONURIA (same dx:)) - serum PHENYLALANINE should be monitored - dietary restriction of PHENYLALANINE (note: high levels of phenylalanine acts as teratogen)
86
``` 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?
PHENYLKETONURIA
87
branchial/ pharyngeal apparatus consist of (3):
1- pharyngeal arches 2- pharyngeal clefts 3- pharyngeal pouches
88
from what embryonic layer does each of the following arise from: 1- pharyngeal arches 2- pharyngeal clefts 3- pharyngeal pouches
1- pharyngeal arches: MESODERM (MESENCHYME) 2- pharyngeal clefts: ECTODERM 3- pharyngeal pouches: ENDODERM
89
what BONES arise from the first arch?
``` 1- MAXILLARY process *maxilla *zygomatic bone 2- MANDIBULAR process *mandible *MECKEL’S cartilage (Incus and malleus) ```
90
what (only main) MUSCLES arise from the first arch?
MUSCLES OF MASTICATION 1-temporalis 2-masseter 3-pterygoids
91
what NERVE arise from the first arch?
TRIGEMINAL NERVE | mandibular and maxillary divisions
92
which artery of the AORTIC ARCH arise from the first arch?
portion of the MAXILLARY ARTERY
93
what BONES arise from the second arch?
REICHERTS CARTILAGE 1-stapes 2- styloid process of temporal bone 3- LESSER horn of hyoid
94
what main MUSCLES arise from the second arch?
STAPEDIUS | -smallest in body
95
what NERVE arise from the second arch?
FACIAL NERVE
96
what ARTERIES arise from the second arch? 2
not v imp (both embryonic vessels-involutes later) 1-stapedial artery 2-hyoid artery
97
what CARTILAGE/BONES arise from the third arch?
HYOID BONE | BODY AND GREATER horn
98
what MUSCLES arise from the third arch?
STYLOPHARYNGEUS
99
what NERVE arise from the third arch?
GLOSSOPHARYNGEAL NERVE (IX)
100
what happens to the 5th pharyngeal arch
does not persist in humans
101
what NERVE innervates the fourth and sixth arches?
VAGUS NERVE 4th: superior laryngeal 6th: recurrent laryngeal
102
what CARTILAGE arises from the fourth and sixth arches?
both arches fuse to form LARYNX CARTILAGE
103
what (general) MUSCLES arises from the fourth and sixth arches?
LARYNGEAL MUSCLES
104
what ARTERIES arises from the fourth and sixth arches?
4TH lt: aortic arch rt: proximal rt subclavian artery 6TH (PULMONARY ARCH) lt: proximal pulmonary artery and ductus arteriosus rt: proximal pulmonary artery
105
PHARYNGEAL ARCHES SOS SUMMARY mention the nerve and main structures for each: (6 arches) 4 points
- 1st: CN 5 trigeminal: maxilla/mandible - 2nd: CN 7 facial: hyoid - 3rd: CN 9 glossopharyngeal: hyoid - 4th&6th: CN X vagus: larynx
106
``` 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? ```
-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
sos TONGUE DEVELOPMENT - SENSATION - TASTE - MOTOR
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
most common craniofacial malformation +cause
CLEFT LIP | -mltifactorial etiology
109
- how is the primary palate formed? | - failure leads to —-?
- by fusion of: 1- maxillary prominences (from 1st arch) with 2- medial nasal prominence (from philtrum) -leads to cleft lip
110
note for clefts check these:
1- unilateral/bilateral 2- complete/incomplete 3- lip or palate or both
111
- how is the secodary palate formed? | - failure leads to —-?
- fusion of lateral PALATAL SHELVES (PROCESSES) | - failure leads to cleft palate
112
``` how many pharyngeal arches pharyngeal clefts pharyngeal pouches is there ```
6 4 4
113
what is mainly formed from the 1st pouch?
inner ear: EUSTACHIAN TUBE
114
what is mainly formed from the 2nd pouch?
PALATINE TONSILS
115
what is mainly formed from the 3rd pouch?
- THYMUS | - lt and rt INFERIOR PARATHYROID GLANDS
116
what is mainly formed from the 4th pouch?
-SUPERIOR PARATHYROID GLANDS -ULTIMOBRANCHIAL BODY forms C-cells (thyroid) derived from neural crest cells
117
failure of the 3rd/4th pharyngeal pouch to form leads to —?
DiGeorge syndrome | -thymic aplasia
118
most common deletion in DiGeorge syndrome
22q11 chromosomal deletion
119
CLASSIC TRIAD OF DIGEORGE SYNDROME
``` 1- loss of thymus loss of T-cells, RECURRENT INFECTION 2- loss of parathyroid gland HYPOCALCEMIA, TETANY 3- congenital heart defects CONOTRNCAL ```
120
pharyngeal clefts develops into:
1st: EXTERNAL AUDITORY MEATUS | 2nd 3rd 4th: CERVICAL SINUS (temporary cavity)
121
NECK MASS IN CHILDREN DD | how to differentiate?
``` 1- branchial cleft cyst -does NOT move with swallowing 2-thyroglossal duct cyst -moves with swallowing (remember physical exam we check) ```
122
what is the most common location for BRANCHIAL CLEFT CYST? | How is it noticed?
``` 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
how gonads development start? what week? what layers? failure of what leads to no development?
GONADAL RIDGES form at wk 7 (derived from MESENCHYME) +GERM CELLS (derived from EPIBLAST) invade the gonadal ridges
124
SRY gene codes for | -forms what cells?
testis determining factor | forms sertoli and leydig cells
125
what cell produce testesterone in fetus
Leydig cells
126
what cords develop in testis vs ovaries
testis: MEDULLARY (testis) cords ovary: CORTICAL cords develop (form clusters) NOTE: surrind germ cells
127
what cells form the primordial follicles 2
- oogenia | - follicular cells
128
Genital ducts (internal genitalia) 2 DEVELOP INTO :
``` Mesonephric (wolffian) -epididymis -vas deferens -seminal vesicles -ejaculatory duct parsmesonephric (mullerian) -fallopian tube -uterus -upper 2/3 vagina ```
129
how does genital ducts develop into a male (2 main things/2 cells + fxn)
1- SERTOLI CELLS release MIF mullerian inhibitory factor: suppress mullerian 2- LEYDIG CELLS release ANDROGENS: stimulate wolfian
130
REMNANTS of suppression of WOLFFIAN/MULLERIAN ducts in males and females
males: appendix testis (tissue at upper testis) females: gartner’s duct (found on vaginal walls) note: may form cyst :(
131
what part of male genitals secrete about 75% of fluid in semen
glands: seminal vesicles
132
ejaculatory duct passes through —- to connect to the ——
- prostate | - urethra
133
PARAMESONEPHRIC ducts ONLY occur in absence of: 2
- MIF | - ANDROGENS
134
what other structure gives rise to INTERNAL GENITALIA (other than genital ducts)? arises from ?
UROGENITAL SINUS | arises from the cloaca
135
cloaca divides into 2
1- urogenital sinus | 2- anal canal
136
Upper portion of the urogenital sinus forms : - males? - females?
BOTH: bladder
137
MIDDLE (pelvic) portion of the urogenital sinus forms : - males? - females?
males: prostate and prostatic urethra NOTE: -phalic portion in males forms the penile urethra females: inferior vagina
138
what is the MOST COMMON defect that can lead to uterine anomalies? complications?
LATERAL FUSION DEFECTS (failed fusion of the 2 sides of uterus) -infertility, pregnancy loss
139
Most common lateral fusion defects (uterine anomalies)? mechanism
SEPTATE UTERUS - septum divides uterus - 2 endometrial cavities - defects in resorption of septum b/w Mullerian ducts
140
treatment for septate uterus
septoplasty
141
how to diagnose uterine anomalies?
HYSTEROSALPINGOGRAPHY | inject dye in the uterus
142
external genitalia 4 key structures
1- genital tubercle 2- urogenital sinus (from cloaca) 3- urogenital folds (from cloaca) 4- labioscrotal (genital) swellings
143
external genitalia: | genital tubercle elongates to form what structures in male/female
male: phallus female: clitoris
144
external genitalia: | urogenital folds to form what structures in male/female
1- male: urogenital folds close to form penile urethra 2- female: no fusion, forms labia minora
145
external genitalia: urogenital sinus form what structures in male/female
GLANDS male: prostate gland, bulbourethral glands (of Cowper) female: paraurethral glands (Skene), bartholin glands
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external genitalia: | labioscrotal swelling form what structures in male/female
male: scrotum female: labia majora
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what is required for female external genitalia to form?
ESTROGEN MUST BE HIGHER THAN ANDROGEN
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what is required for male external genitalia to form? | sos
DIHYDROTESTESTERONE | testesterone —5a-reductase—-> DHT
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5a-reductase fxn and deficiency
fxn: converts testosterone into DHT deficiency: ambiguous genitalia until PUBERTY and at puberty (testosterone increases)
150
what is hypospadia? mechanism? occurs with ? Vs what is epispadia? mechanism? -occurs with? which one is more common?
- 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