DIT review - Reproduction 1 Flashcards

1
Q

Describe the difference between a direct and indirect hernia

A
  • Indirect inguinal hernia
    • Goes through the internal (deep) inguinal ring, external (superficial) inguinal ring, and into the scrotum
    • Enters internal inguinal ring lateral to inferior epigastric vessels
  • Direct inguinal hernia
    • Protrudes through the inguinal triangle
    • Goes through the external (superficial) inguinal ring only
    • Covered by external spermatic fascia
    • Bulges directly through parietal peritoneum, medial to the inferior epigastric vessels but lateral to the rectus abdominis
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2
Q

During genital embryology, what is produces by Leydig cells and what is produced by Sertoli cells?

A

Leydig = testosterone

Sertoli = AMH

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3
Q

Describe the sequence of events caused by the SRY gene during genital embryologic development

A
  • SRY gene on chr Y produces testes determining factor (TDF)
  • TDF stimulates the development of testes
  • Tested produce Sertoli cells and Leydig cells
    • Sertoli cells produce Anti-Mullerian hormone
      • AMH causes degeneration of paramesonephric ducts
    • Leydig cells produce Testosterone
      • Testosterone causes Wolffian duct to develop into male internal genitalia (except the prostate)
      • Testosterone is also converted to DHT via 5 a-reductase in order to cause the development of male external structures + prostate
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4
Q

What cell is responsible for maintaining high levels of testosterone in the testes?

A

Sertoli cells

o Androgen-binding protein (ABP) within the seminiferous tubules binds testosterone and DHT to make them less lipophilic and reduce diffusion out of the luminal fluid

o ABP is synthesized by Sertoli cells in response to FSH

o Sertoli cell dysfunction may manifest as normal serum testosterone (hypothalamus, pituitary, and Leydig cells are fine) with low concentration of testosterone in the seminiferous tubules due to inadequate ABP production

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5
Q

What is the presentation, histology, and prognosis of seminoma?

A
  • Most common type of testicular cancer
  • Malignant
  • Painless, homogenous testicular enlargement
  • “Fried egg” appearance under histology
  • Radiosensitive – excellent prognosis
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6
Q

What is the histology, lab values, and most commonly affected population of yolk sac tumor of the testes?

A
  • Yellow, mucinous
  • Schiller duval bodies (resemble glomeruli)
  • Increased AFP
  • Most common testicular tumor in boys < 3 y/o
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7
Q

What are the relevant lab values of choriocarcinoma of the testes?

A
  • Malignant
  • Increased hCG
  • Disordered syncytiotrophoblasts and cytotrophoblasts
  • Hematogenous metastasis
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8
Q

What is the difference between teratoma in males and females

A

Malignant in males but not females

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9
Q

What is the presentation and lab values of embryonal carcinoma of the testes?

A
  • Malignant tumor comprised of immature, primitive cells that may produce glands
  • Painful, hemorrhagic mass with necrosis
  • Increased hCG and normal AFP
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10
Q

What are the 3 non-germ cell tumors of the testes?

A

Leydig cell, Sertoli, and testicular lymphoma

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11
Q

Presentation and histology of Leydig cell tumor

A
  • Golden brown color
  • Contains Reinke crystals (eosinophilic cytoplasmic inclusions)
  • Produce androgens:
    • Gynecomastia in men
    • Precocious puberty in boys
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12
Q

Population most affected by testicular lymphoma

A
  • Most common testicular cancer in older men > 60 y/o
  • Not a primary cancer – arises from metastatic lymphoma
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13
Q

What is Peyronie disease?

A
  • Abnormal curvature of the penis due to fibrous plaque within the tunica albuginea
  • Associated with erectile dysfunction
  • May cause pain or anxiety
  • Can consider surgical repair
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14
Q

What are precursor lesions/increased risk of squamous cell carcinoma of the penis?

A
  • Bowen disease - presents as leukoplakia in the shaft
  • Erythroplasia of Queyrat - presents as erythroplakia of the glans
  • Bowenoid papulosis - presents as reddish papules
  • HPV
  • Lack of circumcision
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15
Q

Is BPH due to hypertrophy or hyperplasia

A

Hyperplasia

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16
Q

Treatment of BPH

A
  • Alpha-1-antagonists
  • 5a-reductase inhibitors
17
Q

Common metastatic location of prostatic adenocarcinoma

A

Bone

18
Q

What pathology occurs in the lateral/middle vs. posterior lobe of the prostate

A

BPH = lateral/middle (compression of urethra into vertical slit)

Prostatic adenocarcinoma = posterior (felt on rectal exam)

19
Q

Describe the differences between the different types of estrogen (estradiol, estrone, and estriol)

A
  • THINK: 1, 2, 3 = man, woman, baby
    • Estrone = one = 1 = man
      • Found in men and women
      • Produced by fat cells in the periphery via aromatase
    • Estradiaol = di = 2 = women
      • Produced in ovaries
      • Strongest and most abundant form of estrogen in women
    • Estriol = tri = 3 = babies
      • Produced by the placenta
20
Q

Describe what parts of meiosis I and meiosis II the egg is arrested in, and what allows the egg to continue on in the process

A
  • Primary oocytes arrested tin Prophase I until ovulation
  • Secondary oocytes arrested in Metaphase II until fertilization (an egg met a sperm)
21
Q

Describe the steps of ovulation, from rise in estrogen to rise in basal body temperature

A
  • Estrogen causes increased production of its own receptors, as well as LH and GnRH receptors (positive feedback)
  • Estrogen surge stimulates an LH surge
  • LH surge leads to release of the egg
  • Corpus luteum secretes progesterone
  • Basal body temperature rises about 24 hours after ovulation in response to increased progesterone
22
Q

What is Mittelschmerz

A
  • Transient mid-cycle ovulatory pain
  • Associated with peritoneal irritation
23
Q

What are the stimulators and products of theca and granulosa cells?

A
    • Theca cells
      * Stimulated by LH
      * Produce androstenedione from cholesterol via desmolase
      • Granulosa cells
        • Stimulated by FSH
        • Produce estrogen (estradiol) from androstenedione via aromatase
24
Q

What is vaginal adenosis?

A
  • Persistence of columnar epithelium within the upper vagina
    • Lower 1/3 of vagina derived from urogenital sinus à squamous epithelium
    • Upper 2/3 of vagina derived from Mullerian duct à columnar epithelium
    • Normally, squamous epithelium will grow upwards to replace the columnar epithelium
  • Associated with diethylstilbestrol (DES) in utero and clear cell adenocarcinoma
25
Q

What is the risk factor for vaginal clear cell carcinoma

A

Diethylstilbestrol (DES)

26
Q

What is sarcoma botryoides?

A
  • Sarcoma botryoides (embryonal rhabdomyosarcoma)
    • Malignant mesenchymal proliferation of immature skeletal muscle
    • Presents as a grape-like mass protruding from the vagina of a child (usually < 5 y/o)
27
Q

What is the positve lab finding in sarcoma botryoides

A

Desmin +

28
Q

Serious complication of invasive cervical carcinoma

A
  • Lateral invasion can block ureters leading to hydronephrosis and postrenal failure
29
Q

Most common type of cervical carcinoma

A
  • Usually squamous cell carcinoma, but occasionally adenocarcinoma
30
Q

Risk factors for cervical carcinoma

A

Anything that increases risk for HPV, multiple sexual partners, smoking and HIV (decrease immune system)

31
Q

What is Asherman syndrome?

A
  • Secondary amenorrhea due to loss of basalis and scarring
  • Caused by overaggresive D&C
32
Q

Describe the differences between leiomyoma and leimyosarcoma of the uterus

A
  • Leiomyoma (fibroids)
    • Benign neoplastic proliferation of smooth muscle arising from myometrium
    • Related to estrogen exposure
    • Arises is premenopausal women
    • Multiple, well-define, white, whorled masses
    • Usually asymptomatic
  • Leiomyosarcoma
    • Malignant proliferation of smooth muscle arising from myometrium
    • Usually arises de nova (not a progression from leiomyoma)
    • Arises in post menopausal women
    • Single lesion with areas of necrosis and hemorrhage
33
Q

Describe the pathogenesis of PCOS

A
  • Increases LH
  • stimulation of theca cells
  • increased androgen production by theca cells
  • increased peripheral conversion of androgens into estrone in adipose tissue
  • decreased FSH (negative feedback)
  • decreased stimulation of granulosa cells
  • degeneration of follicles
  • cystic follicles
34
Q

Diagnostic criteria of PCOS

A
  • Diagnostic criteria (2/3):
    • (1) Oligo- or anovulation
    • (2) Hyperandrogenism
    • (3) Polycystic ovaries on US
    • Obesity
    • Insulin resistance
35
Q

What serum hormone levels are indicative of PCOS?

A
  • Elevated LH:FSH ratio (LH:FSH > 2)
36
Q

Why are obesity and insuline resistance associated with PCOS

A
  • Obesity - increased adipose tissue for androgen conversion to estrone
  • Insulin resistance - elevated insulin levels - insulin stimulates androgen production in theca cells
37
Q

Complication of PCOS

A
  • Complications:
    • Increased risk of endometrial cancer secondary to unopposed estrogen from repeated anovulatory cycles
38
Q

Treatment of PCOS:

A
  • Weight loss - less adipose tissue to convert androgens to estrone
  • Metformin - treatment of insulin resistance
  • Progesterone - protection from endometrial cancer
  • OCPs - increase androgen binding proteins so there is less free androgens
  • Ovulation induction:
    • Clomiphene
    • Leuprolide (pulsatile)
  • Spironolactone - hirsutism
39
Q

What is the mechanism of action of Clomiphene

A
  • Partial agonist at estrogen receptors in hypothalamus
  • Decreases negative feedback from estrogen since it binds to estrogen receptors but is less potent
  • Increases FSH