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REPRO Flashcards

1
Q

3 important branches of the pudendal nerve

A

Inferior rectal nerve
Dorsal nerve of the penis/clitoris
Perineal nerves – posterior scrotal/labial nn.

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2
Q

Emission of sperm is primarily controlled by what nerve?

A

Hypogastric n (sympathetic NS)

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3
Q

Ejaculation of sperm is primarily controlled by what nerve?

A

Pudendal n (sympathetic NS)

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4
Q

Venous drainage of left ovary/testis

A

Left ovary/testis – > left gonadal vein –> left renal vein –> IVC

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5
Q

Lymphatic drainage of proximal 2/3 of vagina/uterus

A

Obturator, external iliac, and hypogastric nodes

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6
Q

What do the paramesonephric ducts develop into? What cell type suppresses the development of these ducts?

A

These are mullerian ducts that develop into female internal structures like the fallopian tubes, uterus, and upper portion of the vagina. Sertoli cells secrete Mullerian inhibitor factor.

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7
Q

Which cell type induces the mesonephric ducts to develop?

A

These are the Wolffian ducts which develop into male internal structures –seminal vesicles, epididymis, ejaculatory duct, and ductus deferens. Leydig cells secrete androgens which stimulate the development of these ducts.

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8
Q

What helps with the development of male external genitalia?

A

SRY gene on Y chromosome produces testis-determining factor which promotes testes development.

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9
Q

Which male reproductive organ does NOT form from mesonephric ducts??

A

Prostate

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10
Q

Pathology that results from incomplete fusion of paramesonephric ducts

A

Bicornuate uterus – leads to UT abnormalities and miscarriages.

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11
Q

2 homologue pairs originating from genital tubercle (2 male, 2 female)

A

Male: glans penis
Female: Glans clitoris

Male: corpus cavernosum, spongiosum
Female: vestibular bulbs

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12
Q

2 homologue pairs originating from urogenital sinus (2 male, 2 female)

A

Male: bulbourethral glands of cowper
Female: greater vestibular glands of Bartholin

Male: Prostate gland
Female: urethral and paraurethral glands of Skene

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13
Q

Homologue pair that originates from urogenital folds

A

Male: ventral shaft of penis (penile urethra)
Female: labia minora

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14
Q

If an individual either has no sertoli cells or lacks Mullerian inhibitory factor, what will be their phenotypic makeup?

A

Develop both male and female internal genitalia and male external genitalia

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15
Q

Abnormal opening of penile urethra on dorsal side of penis.

  • What is this due to?
  • What other abnormality do you expect to find?
A

Epispadias is due to faulty positioning of genital tubercle.

Exstrophy of the bladder is associated with epispadias.

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16
Q

Abnormal opening of penile urethra on ventral side of penis is most likely due to failure of what?

A

Urethral folds to close

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17
Q

Suspensory ligament of ovaries connects?

A

Ovaries to lateral pelvic wall.

Contains ovarian vessels.

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18
Q

Cardinal ligament connects?

A

Cervix to side wall of pelvis

Contains uterine vessels.

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19
Q

Round ligament of the uterus connects?

A

Uterine fundus to labia majora

Contains artery of Sampson

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20
Q

2 structures derived from gubernaculum in female

A

Round ligament of the uterus

Ligament of the ovary

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21
Q

Broad ligament connects what?

A

Uterus, fallopan tubes, and ovaries to pelvic side wall.

Contains ovaries, fallopian tubes, and round ligaments of uterus.

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22
Q

Ligament of the ovary connects what?

A

Medal pole of ovary to lateral uterus

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23
Q

Histology of vagina

A

Stratified squamous epithelium, non-keratinized

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24
Q

Histology of ectocervix

A

Stratified squamous epithelium

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25
Q

Histology of endocervix

A

Simple columnar epithelium

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26
Q

Histology of uterus

A

Simple columnar epithelium, pseudostratified tubular glands

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27
Q

Histology of fallopian tube

A

Ciliated simple columnar

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28
Q

Histology of ovary

A

Simple cuboidal eptiehlium

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29
Q

Spermiogenesis involves what 2 events?

A

Loss of cytoplasmic contents

Gain of acrosomal cap

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30
Q

Failure of meiosis I in a male

A

Accumulation of primary spermatocytes (2N, 4C)

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31
Q

Failure of meiosis II in a male

A

Accumulation of secondary spermatocytes (1N, 2C)

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32
Q

Role of FSH in a male

A

Stimulates Sertoli cells to produce ABP (maintains testosterone levels in seminiferous tubules to help mature those spermatogonium)

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33
Q

What is the responsibility of DHT early on?

A

Differentiation of penis, scrotum, and prostate

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34
Q

What 2 locations are testosterone and androstenedione converted to estrogen?

A

Adipose tissue
Leydig cells

Due to aromatase

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35
Q

Causative agent in prostatic hyperplasia

A

DHT

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36
Q

Most likely cause of lumps in the labia majora and pathogenesis

A

Most of the time these will be testes and the patient has Androgen Insensitivity Syndrome. These patients will have increased testosterone, estrogen, and LH levels. She will have female external genitalia with rudimentary vagina and scant sexual hair. However, the uterus and fallopian tubes are generally absent.

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37
Q

Describe what 5a-reductase deficiency looks like phenotypically.

A

Inability to convert testosterone to DHT causes male to have ambiguous genitalia until puberty when finally the increase in testosterone causes masculinization and increased growth of external genitalia. Testosterone/estrogen and LH levels are all normal. Internal genitalia is also normal.

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38
Q

What happens when a pregnant mom takes exogenous androgens during her pregnancy?

A

She gets a pseudohermaphroditic kid that is STILL XX. Ovaries are present but the child will have virilized or ambiguous external genitalia.

CAH will also cause this.

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39
Q

Most common type of testicular tumor

A

Germ cell tumors

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40
Q

2 risk factors for germ cell tumors in males

A

Cryptorchidism

Klinefelter syndrome

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41
Q

25 y.o. male presents with painless testicular mass. What do you expect to see histologically?

A

SEMINOMA!
Large cells in lobules with watery cytoplasm and central nuclei
Homogenous mass with no hemorrhage or necrosis

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42
Q

4 male germ cell tumors that produce increased B-hCG

A

Seminoma
Embryonal CA
Choriocarcinoma*
Teratoma

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43
Q

25 y.o. male presents with painful testicular mass. What do you expect to see histologically?

A

Embryonal CA comprised of immature primitive cells that may produce glands
Forms a hemorrhagic mass with necrosis

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44
Q

Most common testicular tumor in children and histological appearance

A

Yolk sac (endodermal sinus) tumor contains Schiller Duval bodies which are glomerulus like structures

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45
Q

3 male germ cell tumors that produce increased AFP

A

Embryonal CA
Yolk sac tumor
Teratoma

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46
Q

Mechanism by which choriocarcinomas spread

A

Hematogenously because its composed of placenta-like tissue. The placenta is genetically programemd to find blood vessels.

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47
Q

How is prognosis determined in a mixed germ cell tumor?

A

Based on the worst component (teratoma in males is bad, embryonal CA, etc.)

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48
Q

Increased placental alkaline phsophatase levels in a male may indicate?

A

Seminoma

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49
Q

Most likely cause of hydrocele

A

Increased fluid secondary to incomplete fusion of processus vaginalis

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50
Q

Most common testicular cancer in older men

A

Testicular lymphoma d/t metastases –usually of diffuse large B cell type

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51
Q

This testicular tumor is golden brown in color and contains Reinke crystals on histology

A

Leydig cell tumor –produces androgen causing precocious puberty in children or gynecomastia in adults

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52
Q

50 y.o. male presents concerned about this gradually enlarging, well-demarcated erythematous plaque with an irregular border and surface crusting or scaling located on the glans of his penis. What are you most worried about this progressing into?

A

This is a precursor in situ lesion for SCC. Its also known as Bowen disease and presents as leukoplakia.

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53
Q

55 y.o. male patient presents to you with a red velvety plaque on the glans of his penis. What is the most likely dx?

A

Erythroplasia of Queyrat – a precursor in situ lesion of SCC of the penis.

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54
Q

A 35 y.o. male patient presents with multiple reddish papules on his penis. STD tests are negative. What is the most likely dx?

A

Bowenoid papulosis

55
Q

Peyronies disease is due to formation of what?

A

This is a bent penis due to acquired fibrous tissue formation.

56
Q

5 Rx that can cause priapism

A 
Anticoagulants
PDE5 inhibitors
Antidepressants
Alpha blockers
Cocaine
57
Q

2 underlying conditions associated with balanitis

A

Probably due to Candida.
You think about this in patients with Diabetes or uncircumsized.

Treat with ketoconazole.:)

58
Q

What do prostatic secretions show in chronic Prostatitis?

A

WBCs

Negative cultures

59
Q

Where does BPH occur in the prostate?

A

Central periurethral zone of the prostate

60
Q

What do you suspect in an older male that presents with nocturia?

A

BPH

61
Q

Biopsy of the prostate shows small infiltrating glands with prominent nucleoli. What is your dx?

A

Prostatic adenocarcinoma

62
Q

What effect does estrogen have on SHBG, HDL, and LDL?

A

Increases SHBG
Increases HDL
Decreases LDL

63
Q

Which phase of the menstrual cycle can vary in length?

A

Follicular phase.

64
Q

What causes ovulation?

A

Increased estrogen and increased GnRH receptors on anterior pituitary stimulates release of LH causing the rupture of the follicle. Progesterone induced rise in temperature occurs about 24 hours after ovulation.

65
Q

What are the 3 layers of the endometrium and which 2 are shed during menstruation?

A

Stratum basalis

Stratum spongiosum, stratum compactum (these 2 layers are the ones shed)

66
Q

Which hypothalamic nucleus is involved in ovulation?

A

Arcuate nucleus (GnRH production)

67
Q

When does oogenesis begin?

A

Prior to birth

68
Q

Where does meiosis I arrest in females and when does it resume?

A

Arrested in prophase I until ovulation where it progresses into secondary oocytes, which are haploid 1N, 2C.

69
Q

Where does meiosis II arrest in females and when does it resume?

A

Arrested in metaphase II until fertilization (an egg MET a sperm), when it progresses into a haploid ovum (1N, 1C). 3 polar bodies.

70
Q

What phase are most of your oocytes in?

A

Primary oocytes in prophase I

71
Q

Which cells secrete beta hCG?

A

Syncytiotrophoblasts of the placenta

72
Q

3 hormones structurally similar to beta hCG

A

TSH
FSH
LH

73
Q

How often does the beta hCG level double?

A

Every 2 days initially

74
Q

Lactation is brought on by a decrease in hwat 2 hormones?

A

Progesterone and estrogen.

After labor, the decrease in progesterone levels disinhibits lactation.

75
Q

Which hormones are stimulated by suckling?

A

Prolactin and oxytoxin

76
Q

What enzyme converts progesterone into androstenedione?

A

17 alpha hydroxylase

77
Q

What enzyme converts estrogen into estradiol?

A

17 beta HSD 1

78
Q

Best test to confirm menopause

A

INCREASED FSH due to loss of negative feedback from estrogen

79
Q

Hormonal changes associated with menopause

A

Decreased estrogen
VERY increased FSH
Increased LH
Increased GnRH

80
Q

What is the actual cause of menopause?

A

Decreased estrogen production due to age-linked decline in # of ovarian follicles

81
Q

How does HPV 16 cause its effect?

A

E6 gene product inhibits p53 suppressor.

82
Q

How does HPV 18 cause its effect?

A

E7 gene product inhibits Rb suppressor.

83
Q

Describe histological appearance of a rhabdomyoblast and associated positive stains.

A

Exhibits cytoplasmic cross-striations and positive IHC staining for desmin (immature filament of myocytes) and myogenin/myoglobin.

84
Q

Where does cervical dysplasia begin?

A

Basal layer of squamo-columnar junction

85
Q

4 risk factors for cervical dysplasia

A

Multiple sexual partners
Smoking
Early sexual intercourse
HIV infection

86
Q

Invasive cervical carcinoma can lead to failure of what organ?

A

Renal failure due to lateral invasion blocking ureters –this is a common cause of death!

87
Q

Middle aged woman presenting with post-coital bleeding and vaginal discharge. Most likely dx?

A

Cervical CA

88
Q

Pain of endometriosis classically begins at what stage of the menstrual cycle?

A

1 week prior to menstruation

89
Q

“Gun powder” nodules are seen in what pathology?

A

Endometriosis of soft tissue

90
Q

Patient presents with menorrhagia with an enlarged uterus and no pelvic pain. Gross exam reveals what?

A

Multiple, well-defined, white whorled masses that may distort the uterus and impinge on pelvic structures – Leiomyoma

91
Q

Histological appearance and associated mutation of sporadic endometrial carcinoma

A

Serous and characterized by papillary structures with psammoma body formation
p53 mutation * –arises in elderly
Tumor is aggressive :(

92
Q

Most important predictor for progression of endometrial hyperplasia to CA

A

Cellular atypia

93
Q

Hormonal characteristic of PCOS

A

Increased LH and low FSH (LH:FSH>2)
Increased LH induces excess androgen production from theca cells resulting in hirsutism. Androgen is converted to estrone in adipose tissue. This estrone feedback decreases FSH resulting in cystic degeneration of follicles.
Some patients also have insulin resistance.

94
Q

Which type of surface epithelial tumors are BRCA1 mutation carriers at increased risk for?

A

Serous carcinoma of the ovary and fallopian tube

95
Q

Which characteristic of cystic teratomas in women indicates malignant potential?

A

Presence of immature tissue (usually neural) or somatic malignancy (usually SCC of skin)

96
Q

Most common germ cell tumor in childen and 2 classic characteristics

A

Endodermal sinus tumor –elevated serum AFP and schiller duval bodies (glomerulus like structures)

97
Q

Triad of Meig’s syndrome

A

Ovarian tumor + ascites + pleural effusions

98
Q

Characteristics of tumor that has Call-Exner bodies

A

Call Exner bodies are classically seen in granulosa cell tumors which secrete estrogen, leading to precocious puberty.

99
Q

Which ovarian tumor is lined with fallopian tube-like epithelium?

A

Serous cystadenoma

100
Q

Which ovarian tumor contains psammoma bodies?

A

Serous cystadenocarcinoma

101
Q

When does division occur in diamniotic/dichorionic placentation twinning?

A

Prior to morula stage (within 3 days of fertilization)

102
Q

When does division occur in diamniotic/monochorionic placentation twinning

A

4-8 days post fertilization (blastocyst)

103
Q

When does division occur in monoamniotic/monochorionic placentation twinning

A

8-12 days after fertilization (epiblast/hypoblast)

104
Q

2 indications that you have monoamniotic/monochorionic twins

A

One yolk sac and 2 fetal poles

Cord entanglement

105
Q

When does division occur for conjoined twins?

A

At or after 13 days

106
Q

Only cause of pre-eclampsia prior to 20 weeks gestation

A

Hydatidiform mole

107
Q

Most common organ of metastases from hydatidiform mole

A

Lung

108
Q

Most common precursor of choriocarcinoma

A

Hydatidiform mole

109
Q

Placenta previa presentation

A

Implantation of placenta in lower uterine segment and placenta overlies cervical os. PAINLESS vaginal bleeding during 3rd trimester. Need a C-section.

110
Q

Placental abruption presentation

A

Separation of placenta from decidua prior to delivery of fetus presenting with very painful abdomen +/- vaginal bleeding. It is associated with cocaine use, tobacco, trauma, abuse, or MVA. Common cause of still birth. :(

111
Q

Placenta accreta presentation

A

Improper implantation of placenta into myometrium with little or no intervening decidua. Presents with difficult delivery of the placenta and post-partum bleeding. Often requires hysterectomy.

112
Q

What gene is affected in Fragile X syndrome and what is its normal function?

A

FMR1 which codes for FMRP, a cytoplasmic protein in the brain and testes involved in mRNA translation of nerve axons and dendrites.

113
Q

Results of pregnancy quad screen in Down Syndrome

A

Decreased alpha feto protein and estriol

Increased B-hCG and inhibin A.

114
Q

Results of pregnancy quad screen in trisomy 18 as well as 7 common findings in these patients

A

Decreased alpha feto protein, B-hCG, and estriol. Normal inhibin A.
Findings include severe MR, rocker-bottom feet, micrognathia, low-set ears, clenched hands, prominent occiput, and congenital heart disease.

115
Q

Results of first-trimester pregnancy screen in Trisomy 13 as well as the 3 P’s that distinguish this from Trisomy 18

A

This is Patau’s syndrome. First trimester screen shows decreased free B-hCG, decreased PAPP-A (pregnancy associated plasma protein) and increased nuchal translucency (also seen in Down syndrome). Distinguishing features from Edward’s syndrome include cleft liP/Palate, holoProsencephaly, and Polydactyly.

116
Q

Describe a Robertsonian translocation

A

Non reciprocal chromosoam ltranslocation. Occurs when the long arms of 2 acrocentric chromosomes (Chromosomes with centromeres near the ends) fuse at the cnetromere and the 2 short arms are lost.

117
Q

Findings in a patient with a microdeletion of short arm of chromosome 5

A

Cri-du-chat

Microcephaly, moderate to severe MR, high-pitched crying/mewing, epicanthal folds, and cardiac abnormalities like VSD.

118
Q

Findings in a patient with congenital microdeletion of long arm of chromosome 7

A

Williams syndrome – note that the deleted region includes the elastin gene. Findings include distinctive “elfin” facies, intellectual disability, hypercalcemia (increased sensitivity to Vitamin D), well-developed verbal skills, extreme friendliness with strangers, and cardiovascular problems.

Think of the movie Elf and Will Farrell’s character.

119
Q

Where can breast tissue develop?

A

Anywhere along the milk line which runs from the axilla to the vulva. This is why we can get extra nipples along the way too.

120
Q

Describe the 2 layers of epithelium that line the lobules and ducts of the breaset.

A

Luminal cell layer – inner cell layer lining ducts and lobules; responsible for milk production in lobules
Myoepithelial cell layer–outer cell layer responsible for contractile function that propels milk toward the nipple

121
Q

Where can you find the highest density of lobules and ducts in the breast?

A

Upper outer quadrant

122
Q

Describe the pathology of mammary duct ectasia including classic presentation and biopsy findings.

A

This is inflammation with dilation of the subareolar ducts classically arising in multiparous post-menopausal women. It presents as a peri-areolar mass wit hgreen-brown nipple discharge (inflammatory debris) –chronic inflammation with plasma cells seen on bx.

123
Q

How does an individual get fat necrosis of the breast? How does this present on mammography and bx?

A

Usually related to trauma.
Presents as mass on PE or abnormal calcification on mammography due to saponification. Bx reveals necrotic fat with associated calcifications and giant cells.

124
Q

Most common change of pre-menopausal breast

A

Fibrocystic change. Cysts have a blue dome appearance. SOME changes are associated with an increased risk for invasive CA.

125
Q

2 forms of fibrocystic change associated with increased risk for invasive CA and one type that is not

A

Fibrosis, cysts, and APOCRINE metaplasia is NOT associated with increased risk.
Ductal hyperplasia and sclerosing adenosis is 2x increased risk.
Atypical hyperplasia is 5x increased risk.

126
Q

This pathology classically presents as blood nipple discharge in a pre-menopausal woman.

A

Intraductal papilloma characterized by fibrovascular projections lined by epithelial (luminal) and myoeithelial cells. Must be distinguished from papillary CA.

127
Q

Major 2 differences between intraductal papilloma and papillary CA.

A

Papillary CA is characterized by fibrovascular projections lined by epithelial cells as well, but WITHOUT underlying myoepithelial cells. Additionally, as the risk increases with age, its more commonly seen in POST menopausal women.

128
Q

Most common benign neoplasm of the breast usually seen in pre-menopasual women

A

Fibroadenoma – well circumscribed, marble like mass that is estrogen sensitive.

129
Q

“Leaf-like” projections seen on breast bx

A

Phyllodes tumor – fibroadenoma like tumor with overgrowth of the fibrous component. Most commonly seen in post-menopausal women and can be malignant.

130
Q

Most useful prognostic factor in breast cancer

A

Spread to axillary lmph nodes –thus sentinel lymph node biopsy is used to assess these nodes.

131
Q

Dyscohesive cells lacking E-cadherin adhesion protein with no invasion of the basement membrane seen on breast biopsy

A

Lobular CA in situ – often multifocal and bilateral and disocvered incidentally. More of a risk factor.

132
Q

Invasive CA that characteristically grows in a single file pattern and may exhibet signet ring morphology on breast bx

A

Invasive lobular CA

No duct formation due to lack of E-cadherin

133
Q

Epidemiology of women more likely to get triple negative CA

A

African American women

Triple negative tumors are negative for ER, PR, and HER2/neu, thus have a poor prognosis

134
Q

This invasive ductal carcinoma subtype is characterized by large, high-grade cells growing in sheets with associated lymphocytes and plasma cells on breast biopsy.

A

Medullary CA

Increased incidence in BRCA1 carriers

DIT FACTS (16 decks)

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