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Boards - Step 1 > First Aid: Repro > Flashcards

First Aid: Repro Flashcards

1
Q

Effects on fetus of the following teratogens

a) ACEi
(b) Aminoglycosides (Gentamycin, Tobramycin, Amikacin
(b) Lithium

A

Teratogens

(a) ACEi = renal developmental abnormalities
(b) Gentamycin/tobramycin (aminoglycosides) = CN VIII abnormalities => hearing difficulty
(c) Lithium and Epstein’s anomaly = messed up tricuspid valve

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2
Q

Effects on fetus of the following teratogens

(a) DES
(b) Valproate
(c) Warfarin

A

(a) DES: vaginal clear cell adenocarcinoma, congenital Mullerian anomalies
(b) Valproate inhibits maternal folate absorption => neural tube defects
(c) Warfarin: bone deformities, fetal hemorrhage, abortion, ophthalmologic abnormalities
“keep baby heppy w/ heparin”

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3
Q

Maternal substance abuse associated w/

(a) Placental abruption
(b) Low birth weight in fetus

A

Maternal substance abuse

(a) Placental absorption associated w/ cocaine
(b) Low birth weight in fetus associated w/ smoking

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4
Q

Thalidomide

(a) 2 indications
(b) Teratogenic effects

A

Thalidomide = immunomodulator

(a) Used in some malignancies (multiple myeloma) and Lyme’s disease
(b) Teratogenic = limb defects

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5
Q

Mechanism of ID and other abnormalities seen in fetal alcohol syndrome

A

Mechanism is failure of cell migration

  • MR, microcephaly, facial abnormalities, limb dislocation, heart defects
  • heart-lung fistulas, holoprosencephaly
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6
Q

Differentiate consequence of mutation in sonic hedgehog vs. hox gene

A

Sonic hedgehog codes anterior-posterior, while hox (homeobox) for craniocaudal direction

Sonic hedgehog mutation = holoprosencephaly (failure of prosencephalon to develop into 2 hemispheres)

Hox mutation = appendages in wrong location

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7
Q

Differentiate function of sonic hedgehog vs. hox gene

A

Sonic hedgehog patterns along anterior-posterior axis

Hox/homeobox gene patterns along craniocaudal direction

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8
Q

How long after fertilization do the following occur

(a) Implantation
(b) Gastrulation
(c) Organogenesis

A

Fertilization = day 0

(a) Fertilization –> morula –> blastula –> implants between days 6-10
(b) Gastrulation (formation of 3 layers) starts around week 3 (3 weeks, 3 layers)
(c) Organogenesis: weeks 3-8 weeks

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9
Q

Etiology of the VACTERL association

A

VACTERL association = nonrandom co-occurence of birth defects due to defect in mesoderm (all mesodermal structures)

Vertebral
Anal atresia
Cardiac defects
TE fistula
Renal defects
Limb defects
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10
Q

Differentiate patent urachus from patent vitelline duct

A

Urachus (from allantois) connects yolk sac to fetal bladder, sopatent urachus => urine comes out of umbilicus

Vitelline duct connects yolk sac to midgut lumen, so patent vitelline duct = poops comes out of belly button

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11
Q

Complications of

(a) Urachal cyst
(b) Meckel diverticulum

A

(a) Urachal cyst = partial failure of urachus (attaching yolk sac to bladder) to obliterate => fluid filled cavity lined w/ uroepithelium
- can lead to infection or adenocarcinoma

(b) Meckel diverticulum = partial failure of vitelline duct (attaching yolk sac to intestinal lumen) to obliterate => true diverticulum
- can be filled w/ heterotypic gastric or pancreatic tissue => melena, hematochezia, abdominal pain

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12
Q

Differentiate cytotrophoblast and syncytiotrophoblast

A

Cytotrophoblast is the inner cell layer of the fetal side of the placenta, cytotrophoblast makes the cells

Then syncytiotrophoblast is the outer layer that secretes beta-hCG to maintain endometrial lining

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13
Q

Function of beta-hCG to maintain pregnancy

A

Beta-hCG is structurally similar to LH, so it stimulates the corpus luteum (cells leftover in ovary after ovulation) to secrete progesterone

Progesterone maintains lining

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14
Q

Which parts of the brachial apparatus are derived from each of the three layers?

A

‘CAP’

Brachial clefts from ectoderm
Brachial arches from mesoderm and neural crest
Brachial pouches from endoderm

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15
Q

Functions of the derivatives of the 6 brachial arches

A

“when at the golden arches: first chew, then smile, then swallow, the speak”

  • 1st arch: CN V2 and V3, muscles of mastication for chewing
  • 2nd arch: CN VII, muscles of facial expression
  • 3rd arch: CN IX innervating stylopharyngess to swallow
  • 4th arch: CN X (superior laryngeal branch) innervates pharyngeal constrictors for swallowing
  • 6th: CN X (recurrent laryngeal branch) for intrinsic muscles of the larynx for speaking
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16
Q

What is unique about the nerves that innervate derivates of the brachial arches

A

CN V3 (arch 1), CN VII (2nd), CN IX (3rd), CN X (4 and 6) are the only cranial nerves that carry both motor and sensory components

One exception = CN V2 (only sensory, no motor) that innervates part of 1st arch

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17
Q

Differentiate brachial/pharyngeal touch d/o

(a) Treacher Collins
(b) DiGeorge Syndrome

A

CAP: brachial clefts from ectoderm, brachial arches from mesoderm, brachial pouches from endoderm

(a) Treacher collins = syndrome of the first brachial arch from failure of 1st arch neural crest cells to migrate (so mesodermal issue)
(b) DiGeorge syndrome = defect of brachial pouch (endoderm)

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18
Q

Treacher Collins syndrome

A

D/o of first brachial arch = Treacher Collins- 1st arch neural crests fail to migrate => mandibular hypoplasia and facial abnormalities

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19
Q

Using the embryologic derivatives of the 3rd and 4th brachial pouches, name the main features of DiGeorge syndrome

A

DiGeorge syndrome = aberrant development of the 3rd and 4th pouches

  • 3rd pouch => inferior parathyroid and thymus
  • 4th pouch => superior parathyroid glands

Thymic aplasia => T cell deficiency
No parathyroid glands = no PTH => hypocalcemia

Also associated cardiac defects = conotruncal anomalies

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20
Q

Paramesonephric duct

(a) Males
(b) Females

A

Paramesonpehric duct = Mullerian duct

(a) Degenerates in males due to MIF (mullerian inhibitory factor) produced by Sertoli cells
(b) Females (default, aka w/o MIF that won’t be present w/o testes which require SRY gene for development)- Paramesonephric duct => fallopian tubes, uterus, upper vagina

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21
Q

Clinical presentation of Mullerian agenesis

A

Mullerian agenesis = lack of devleopmnt of the paramesonephric duct
-still have ovaries, but no fallopian tube or uterus

So presents as primary amenorrhea (b/c no uterus) in female w/ fully developed secondary sex characteristics (ovaries are functional)

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22
Q

Mesonephric duct

(a) Males
(b) Females

A

Mesonephric (Wollfian) duct

(a) Males- develops ‘SEED’ = seminiferous tubules, epididmyis, ejaculatory duct, ducutus deferens
(b) Remnant in females becomes Gartner duct

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23
Q

Clinically what would result from lack of Mullerian inhibitor factor from Sertoli cells?

A

W/o MIF: paramesonpehric duct doesn’t degenerate => get female internal genitalia (fallopian tubes, uterus, upper vagina)

But still testoersone from Leydig cels => also get male internal and external genitalia

So have both male and female internal and male external genitalia

-same presentation if lack of Serotoli cells

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24
Q

What happens to the gubernaculum in males vs. females

A

Gubernaculum = band of fibrous tissue

In males the gubernaculum anchors the testes w/in the scrotum

In females the gubernaculum forms the ovarian ligament and round ligament of the uterus

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25
Q

LN that drain

(a) Ovaries/testes
(b) Distal vagina/scrotum
(d) Proximal vagina and uterus

A

(a) Ovaries and testes come from the abdominal cavity so bring their lymphatics and blood supply w/ them- drain into para-aortic LN
(b) Distal vagina and scrotum to the superficial inguinal nodes
(c) Proximal vagina and uterus to obturator, external iliac, and hypogastric nodes

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26
Q

Explain mechanism by which Sildenafil tx ED

A

Sildenafil = PDE5 inhibitor that decreases breakdown of cGMP

More cGMP (normally mediated by NO release) relaxes smooth muscle causing vasodilation and increased blood to penis

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27
Q

Which part of the testes makes them temperature sensitive

A

Sertoli cells are temperature sensitive- reduction in sperm production (b/c Sertoli cells support sperm production) and increased inhibin (inhibits FSH release) at higher temperatures

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28
Q

Male homolog of female granulosa cells

A

Granulosa cells in F are stimulated by FSH to take androgens (from theca cells) and convert into estradiol

Male homolog = Sertoli cells which are inside seminiferous tubules and support developing spermatogonia

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29
Q

Male homolog of female theca cells

A

Theca cells line peripherally to granulosa cells and are stimulated by LH to produce androgens later converted to estradiol

Male homolog = Leydig cells which lie in interstitium (instead of inside seminiferous tubules like Leydig cells) and are stimulated by LH to produce testosterone

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30
Q

Differentiate affect of temperature on Leydig vs. Sertoli cells

A

Only Sertoli cells are temperature sensitive: in response to higher temp => increased inhibin and decreased sperm production

While Leydig cells and their testosterone production are unaffected by temp

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31
Q

Rank by potency: type of estrogen from fat, ovary, and placenta

A

Estriadiol > estrione > estriol

  • estradiol is produced by the ovary (in granulosa cells stimulated by FSH)
  • estrione aromatized in peripheral adipose tissue
  • estriol produced by placenta
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32
Q

4 places progesterone is produced

A

Progesterone production

  1. Corpus lutuem- what supports the pregnancy before placenta is large enough
  2. Placenta- takes over from corpus luteum to support the pregnancy
  3. Adrenal cortex- zona reticulatum
  4. Testes
33
Q

Explain the role of progesterone in causing lactation

A

Progesterone produced by placenta, after delivery (bye bye placenta) there is a loss of the progesterone inhibition on prolactin

So prolactin rises and stimulates lactation

34
Q

Which phase of the menstrual cycle varies in length?

A

Follicular phase (proliferative) can vary in length, while the luteal phase (secretory) is always just 14 days

So if you have 40 day cycle, follicular phase is super long while luteal phase is still the same 2 weeks
-this is b/c after ovulation the corpus luteum only a certain amount of time before regressing and therefore removing progesterone

35
Q

What causes menstruation?

A

Corpus luteum regresses => no more progesterone => endometrial cells no longer stabilized

Apoptosis of endometrial cells => shedding = menstruation

36
Q

MC location of egg fertilization

(a) How many days after ovulation

A

Egg MC fertilized (a) 1 day after ovulation) in the ampulla (upper end) of the fallopian tube

37
Q

What part of the placenta secretes beta-hCG?

(a) When does this become detectable in blood vs. urine

A

Syncytiotrophoblasts (outer lining) of placenta forms beta-hCG

(a) Detectable in blood 1 week after conception, detectable on home test in urine 2 weeks after conception

38
Q

Contrast role of prolactin and oxytocin in lactation

A

Prolactin stimulates milk production

Oxytocin assists in milk letdown (also promotes uterine contraction for labor)

39
Q

Breast milk

(a) Baby requires what supplementation?
(b) Benefit to mother

A

Breast milk

(a) Exclusively breast fed babies require vitamin D supplementation
(b) Reduced risk of breast and ovarian carcinoma

40
Q

Explain the function of beta-hCG from the syncytiotrophoblasts

A

beta-hCG looks like LH (same alpha subunit, diff beta subunit which is why we test for beta), LH needed to maintain the corpus luteum to produce progesterone for first 8-10 weeks of pregnancy

B/c only until 8-10 weeks is placenta mature enough to synthesize its own estriol and progesterone, then corpus luteum degenerates

41
Q

Conditions of

(a) High hCG
(b) Low HCG

A

(a) High hCG seen in multiple gestations (twins), hydatidiform mole (just placenta tissue), choriocarcinoma, Down syndrome
(b) Low hCG: ectopic/failing pregnancies (not functional placenta), Edward and Patau syndrome

42
Q

Clinical presentation of premature ovarian failure

A

Premature ovarian failure presents as menopause before the age of 40

B/c menopause is physiologically due to reduced estrogen from age-related decline in number of ovarian follicles, if premature failure of these follicles => menopause before that age-related decline

43
Q

What forms the blood-testis barrier

(a) Fxn

A

Blood-testes barrier formed by tight junctions btwn adjacent Sertoli cells (sertoli cells are within the seminiferous tubules)

(a) Fxn = isolate from autoimmune attack or infection

44
Q

Differentiate location of production and potency of the three male androgens

A

Testosterone and DHT made in the testis, while androstenedione is produced in the adrenal cortex

DHT most potent, then T, then androstenedione

45
Q

How can exogenous testosterone cause infertility

A

Exogenous testosterone inhibits HPA axis => reduced intratesticular production of testosterone => reduced testicular size and activity => azoospermia

46
Q

How may aromatase deficiency present during pregnancy?

A

Aromatase deficiency = can’t convert androgens into estrogen => get masculinization (ambiguous genitalia) of female infants

Elevated fetal androgens can cross placenta and cause maternal virilization during pregnancy

47
Q

Clinical presentation of androgen insensitivity syndrome in (46,XY)

(a) Lab values

A

Normal-appearing females, female external genitalia but uterus and fallopian tubes absent (b/c MIF present)
-develop testes

(a) Elevated testosterone, estrogen, and LH

48
Q

18 pre-pubertal boy p/w anosmia- dx?

A

Kallmann syndrome = form of hypogonadotropic hypogonadism due to defective migration of GnRH cells and defective formation of olfactory bulb => reduced GnRH secretion (causing failure to complete puberty in both M and F) and anosmia

Reduced GnRH, FSH, and LH
Infertility 2/2 low sperm count in males and amenorrhea in F

49
Q

Tx of gestational HTN

A

Antihypertensives safe during pregnancy: alpha-methyldopa, labetolol, hydralazine, nifedipine

Deliver at 37-39 weeks

50
Q

Tx of preeclampsia

A

Preeclampsia: tx w/ antihypertensives and IV Mg to prevent seizures

Only definitive therapy is delivery of fetus

51
Q

Tx of eclampsia

A

Eclampsia = preeclampsia and seizures

IV magnesium sulfate

  • antihypertensives
  • ***immediate delivery (can’t wait at this point)
52
Q

Why is delivery necessary to treat eclampsia

A

Once mother has preeclampsia plus seizures the fetus needs to be delivered 2/2 risk of maternal death due to stroke, intracranial hemorrhage, or ARDS

53
Q

HELLP

(a) What does it stand for?
(b) Cause
(c) Blood smear finding
(d) Tx

A

HELLP

(a) hemolysis, elevated liver enzymes, and low platelets
(b) Manifestation of severe preeclampsia
(b) Schistocytes on smear- b/c microvascular clots sheer RBC
(d) Tx = immediate delivery

54
Q

Preeclampsia definition

(a) Cause

A

Preeclampsia = new onset HTN w/ either proteinuria or end-organ dysfunction after 20th week of gestation

(a) Caused by a problem w/ the placenta, it’s the placenta causing the HTN

Abnormal placental spiral arteries => endothelial dysfunction, vasoconstriction, ischemia

55
Q

Complications of preeclampsia

A 
Complications:
placental abruption
coagulopathy
renal failure
uteroplacental insufficiency 
eclampsia
56
Q

Why is preeclampsia defined as new-onset HTN after 20th week, what about before?

A

Before 20th week if new-onset HTN w/ either proteinuria or end-organ dysfunction arises, it suggests molar pregnancy

57
Q

Define gestational HTN

A

BP over 140/90 for the first time after 20th week of gestation

  • no preexisting HTN
  • no proteinuria or end organ damage (or else it’s preeclampsia instead)
58
Q

Mothers w/ increased risk of preelampsia

A

Pre-existing HTN, diabetes, chronic renal disease, autoimmune d/o

59
Q

RF for ectopic pregnancy

A

RF for ectopic pregnancy = fallopian tube scarring

-h/o PID or prior tubal surgery

60
Q

Endometrial, cervical, ovarian cancers

(a) Rank by incidence in the US
(b) Rank by prognosis

A

(a) Incidence: endometrial MC, then ovarian, then cervical (more common worldwide w/o screening and HPV vaccine)
(b) Ovarian has worst prognosis, then cervical, endometrial has best

61
Q

Two medication options for pts w/ PCOS who desire pregnancy

A

Induce ovulation w/ clomiphene citrate

Usually put on OCPs to reduce symptoms but not if desire pregnancy…

62
Q

Which ovarian neoplasm associated w/

(a) Psammoma bodies
(b) Pseudomyxoma peritonei

A

Ovarian neoplasm

(a) Psammoma bodies seen in serous cystadenocarcinoma (serous surface epithelial tumor)- MC ovarian neoplasm
(b) Pseudomyxoma peritonei (intraperitoneal mucus accumulation ‘jelly belly’) associated w/ mucinous cystadenocarcinoma

63
Q

Germ cell choriocarcinoma- composition

(a) Why may present w/ hemoptysis/SOB

A

Germ cell choriocarcinoma = malignancy of trophoblastic tissue (cytotrophoblasts and synctiotrophoblasts) but NO chorionic villi!!! (so just the trophoblast tissue, no villi)

(a) Placenta tissue is made to invade BVs, so quickly hematogenously spreads and often to lungs => SOB and hemoptysis

64
Q

Tx options for adenomysosis

A

Adenomyosis = extension of glandular endometrial tissue into the uterine myometrium

Tx include GnRH agonists (disrupt pulsatile GnRH) or hysterectomy

65
Q

Intraductal papilloma

(a) Association w/ cancer
(b) Typical location
(c) Clinical presentation

A

Intraductal papilloma

(a) Benign itself but slight (1.5-2x) increased in risk for carcinoma
(b) Small tumor of the lactiferous ducts, typically beneath the areola
(c) Serous or bloody nipple discharge

66
Q

Name some drugs that can cause gynecomastia

A

Spironolactone, ketoconazole

B/c gynecomastia (breast enlargement in males) is due to high estrogen, both these drugs inhibit steroid (androgen) synthesis

67
Q

Which sympathetic-acting drug can be used to tx priapism

A

Intracavernosal phenylephrine (selective alpha1 agonist) for vasoconstriction

68
Q

Testosterone levels in b/l vs. unilateral cryptorchidism

A

T reduced in b/l, but normal in unilateral since Leydig cells are unaffected by temperature

69
Q

Varicocele

(a) Etiology
(b) Why left sided
(c) Physical exam finding

A

Varicocele = MC cause of scrotal enlargement in adult males

(a) Dilated veins in pampiniform plexus due to increased venous pressure
(b) 2/2 increased resistance of flow from L gonadal vein into the L renal vein (it’s at a right angle)
(c) ‘Bag of worms’ on palpation

70
Q

MC location of extragonadal germ cell tumor

A

Can arise midline, MC sacrococcygeal teratomas in children/infants

71
Q

2 RF for testicular germ cell tumors

A
  1. Cryptorchidism (testes in abdomen 2/2 failure to descend)

2. Klinefelter syndrome

72
Q

MC testicular tumor

(a) Histologic appearance
(b) Serum marker
(c) Prognosis

A

95% testicular tumors are germ cell tumors, and MC germ cell tumor = seminoma

(a) Fried egg appearance appearance: large cells in lobules w/ watery cytoplasm
(b) Elevated alk phos
(c) Excellent prognosis, late mets

73
Q

Teratomas in M vs. F

A

Mature teratomas in females aren’t malignant, while they can be malignant in adult males

-still benign in male children

74
Q

Drugs to treat androgenic symptoms of PCOS

A
  1. Ketoconazole inhibits 17,20 desmolase to inhibit steroid synthesis
  2. Spironolactone inhibits steroid binding and synthesis
75
Q

How do OCPs prevent pregnancy?

A

OCPs provide exogenous hromones => inhibit release of LH/FSH
No estrogen surge = no LH peak = no ovulation, no ovluation of eggs = can’t get preggers!

76
Q

Contraindications to OCPs

A

Smokers over 35 (2/2 risk of caridovascular events)
H/o stroke or thromboembolic events
H/o estrogen-dependent tumor

77
Q

How does tamsulosin exert selective effects

A

Tamsulosin specifically inhibits alpha1 receptors on the prostate to inhibit smooth muscle contraction, while not inhibiting alpha1 receptors on vasculature (therefore not causing vasodilation peripherally)

78
Q

Mechanism of minoxidil

A

Minoxidil = direct arteriolar vasodilator

Applied topically for androgenetic alopecia, systemically for severe refractory HTN

79
Q

Rogaine vs. propecia

A

Rogaine = minoxidil for androgenetic alopecia, works by direct arteriolar vasodilation

Propecia = Finesteride = 5alpha reductase inhibitor to reduce T to DHT

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