Reproductive Flashcards

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1
Q

when do you get 3 layers?

A

3 weeks- 3 layers-endoderm, mesoderm, ectoderm

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2
Q

where does the notochord come from? where does the neural plate arise from?

A

notochord over midline mesoderm

neural plate comes from ectoderm

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3
Q

where does the neural tube come from and when does it close?

A

neural tube comes from neuroectoderm and closes week 4- very susceptible to teratogens

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4
Q

what does the ectoderm consist of?

A

neural tube and neural crest

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5
Q

what comes from the neural crest?

A

MMOtEL PPASS- melanocytes, myenteric (auerbach plexus), ondontoblasts, , endocardial cushions,, larygneal cartilage, parafollicular C cells of thyroid, PNS, adrenal medulla, spiral membrane (aorticpulmonary septum) schwann cells

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6
Q

in utero aminoglycosides?

A

ototoxicity

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7
Q

which is safe in pregnancy-warfarin or heparin?

A

heparin!

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8
Q

what is the urachus?

A

the allantois develops into the urachus which is the connection between the fetal bladder and umbilicus, it involutes to the median umbilical ligament (failure can be patent, cyst or vesicourachal diverticulum)

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9
Q

how do you remember the brachial pouches?

A
ear, tonsils, bottom to top
ear-1
tonsils-2
inferior parathyroid-3
to-thymus
superior parathyroid-4
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10
Q

what is 22q11 an example of?

A

failure of 3th-4th brachial pouches (thymus and the superior parathyroids-why you get thymic aplasia and hypocalcemia

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11
Q

what does 5 alpha reductase do?

A

converts testosterone to DHT

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12
Q

what causes hypospadias?

A

failure of urethral folds to fuse so you get urethral opening on ventral surface as opposed to epispadias which is dorsal and less common

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13
Q

how do you get an erection? emission? ejaculation?

A

erection (parasympathetic) pelvic splanchnic nerves S2-4
emission-hypogastric (sympathetic) T11-L2
ejaculation-visceral and somatic nerves

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14
Q

what do sertoli cells secret?

A

MIF-mullerian inhibitory factor- cause paramesonephric duct to degenerate and also secrete inhibin B which inhibits FSH
-homolog to female granulosa cells

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15
Q

what does aromatase do?

A

converts testosterone to estrogen

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16
Q

what do leydig cells do?

A

secrete testosterone in response to LH

homolog to the theca interna cells

17
Q

what produces progesterone? what does it do?

A

corpus luteum, placenta, adrenal cortex, testes

  • thick cervical mucus, prevents sperm entering uterus
  • prevents endometrial hyperplasia
  • maintains pregnancy (inhibits LH and FSH
  • prevents contractions
18
Q

which part of the menstrual cycle varies and what stays the same?

A

follicular varies, but luteal is 14 days

19
Q

when does hcg peak?

A

week 8-10, after 8-10 weeks, the placenta secretes its own estriol and progesterone and corpus luteum degenerates

20
Q

what is human placental lactogen?

A

increases insulin so you get lipolysis and conserve glucose and AA for fetus

21
Q

what is kallman syndrome?

A

failure of gnRH secreting neurons so you get hypogonadotrophic hypogonadism, anosmia, low sperm count in males and amenorrhea in females

22
Q

what is the difference between a complete and partial mole?

A

Complete: 46XX or 46XY, empty egg with 1 sperm, duplicates paternal DNA, no fetal parts, higher risk choriocarcinoma, higher hcg-snowstorm, cluster of grapes
Partial- 69XXX or XXY, XYY, fetal parts, lower hcg, smaller uterus

23
Q

what is velamentous umbilical cord insertion?

A

inserts into the chorioamnotic membrane instead of placenta- associated with vasa previa

24
Q

what is the path finding for a serous cystadenocarcinoma

A

psammoma bodies

25
Q

what increasing with estrogen?

A

leiomyoma size so increased in pregnancy and decreased with menopause

26
Q

What is the pattern on histology for leiomyoma?

A

whorled pattern of smooth muscle bundles with well demarcated borders

27
Q

What are the benign breast lesions?

A

fibroadenoma, intraductal papilloma (in the lactiferous duct-causes discharge), phyllodes tumour (large connective tissue mass)

28
Q

What is the mutation associated with breast tumours?

A

c-erbB2 (HER) EGF receptor

ER -, PR - Her2/Neu - is the most aggressive

29
Q

What are the types of noninvasive breast cancers?

A
  1. DCIS (ductal carcinoma in situ)-microcalcifications
  2. Comedocarcinoma
  3. Paget disease (eczematous changes on nipple) underlying DCIS
30
Q

What are the invasive breast cancers?

A
  1. Invasive ductal carcinoma- most common (suspensory ligament damage can cause dimpling) stellate on histology
  2. Invasive lobular carcinoma (often bilateral- dec e cadherin, lines of cells)
  3. Medullary carcinoma
  4. Inflammatory breast cancer (dermal invasion of the lymphatics, cooper suspensory ligament has edema so dimpling of the breast, peau d’orange
31
Q

Which side is a variocele more common on and why?

A

L because of increased pressure into the L gonadal then renal vein
-bag of worms appearance

32
Q

What is a hydrocele?

A

patent processus vaginalis, usually resolves within 1 year

33
Q

What are the testicular germ cell tumours? (95%)

A
  1. Seminoma (most common-fried egg withlarge cells in lobules) high ALP
  2. Yolk sac- yellow, mucinous, schiller duval bodies, high AFP
  3. Choriocarcinoma (disordered syncytiotrophoblasts) high hcg
  4. Teratoma
  5. Embryonal carcinoma (hemorrhagic with necrosis)
34
Q

What are the testicular non germ cell tumours? (5%)

A
  1. Leydig- golden brown, androgens and estrogen, gynecomastia
  2. Sertoli
  3. Testicular lymphoma
35
Q

what do you use tamoxifen for?

A

ER/PR positive breast cancer

  • can increase risk of endometrial cancer
  • antagonist in breast, agonist in bone
36
Q

what are aromatase inhibitors?

A

decrease conversion of testosterone to estrogen

-for ER positive breast cancer

37
Q

what does progesterone do?

A

thickens cervical mucus, increases vascularization of endometrium, but decreases growth

38
Q

what are common tocolytics?

A

NSAIDS, terbutaline, nifedipine

39
Q

what is finasteride?

A

antiandrogen, decreases testosterone conversion to DHT

-can use for BPH