Reproductive 2 Flashcards

1
Q

Lichen sclerosus

A

Thinning of epidermis with fibrosis/sclerosis of dermis.

Porcelain-white plaques with a red or violet border.

Skin fragility with erosions can be observed.

Postmenopausal women. Benign, but risk for SCC.

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2
Q

Lichen simplex chronicus

A

Hyperplasia of vuIvar squamous epithelium.

Leathery, thick vulvar skin with enhanced skin markings due to chronic rubbing or scratching.

Benign, no risk of SCC.

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3
Q

Vulvar carcinoma - Presentation

A

Carcinoma from squamous epithelial lining of vulvar - Rare.

Leukoplakia - biopsy often required to distinguish carcinoma from other causes.

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4
Q

Extramammary Paget disease

A

intraepithelial adenocarcinoma.

Carcinoma in situ, low risk of underlying carcinoma (vs Paget disease of the breast, which is always associated with underlying carcinoma).

Presents with pruritus, erythema, crusting, ulcers

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5
Q

imperforate hymen

A

Failure of hymen central epithelial cells to degenerate at birth.

Accumulation of vaginal mucus at birth -> self-resolving bulge in introitus.

If untreated, leads to 1° amenorrhea, cyclic abdominal pain, hematocolpos (accumulation of menstrual blood in vagina - bulging and bluish hymenal membrane).

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6
Q

Sarcoma botryoides

A

Embryonal rhabdomyosarcoma variant.

Affects girls< 4 years old; spindle-shaped cells; desmin (+)

Presents with clear, grape-like, polypoid mass emerging from the vagina.

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7
Q

Vaginal tumors

A

Vaginal squamous cell carcinoma - Usually 2° to cervical SCC

Clear cell adenocarcinoma - Affects women who had exposure to DES in utero.

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8
Q

Dysplasia and carcinoma in situ of cervix - pathology and Sx.

A

begins at the basal layer of squamocolumnar junction (transformation zone) and extends outward.

ClN 1, ClN 2, or ClN 3

Koilocytes are pathognomonic of HPV infection. May progress slowly to invasive carcinoma if left untreated.

Typically asymptomatic or vaginal bleeding (often postcoital).

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9
Q

Dysplasia and carcinoma in situ of cervix - risk factors

A

Associated with HPV-16 and HPV-18, which produce both the:

E6 gene product (inhibits TP53)
E7 gene product (inhibits pRb)

Risk factors:
D - DES exposure
I - immunocompromise (eg, Hl\/, transplant)
S - smoking
C - coitarche (early)
S - sexual partners - multiple (#1)
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10
Q

Primary ovarian insufficiency

A

Also known as premature ovarian failure - Premature atresia of ovarian follicles in women of reproductive age.

Idiopathic - associated with chromosomal abnormalities (especially in females< 30 years) -> Need karyotype screening.

Patients present with signs of menopause after puberty but before age 40.

Dec. estrogen, Inc LH and FSH

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11
Q

Most common causes of anovulation

A

OB/GYN:
Pregnancy
Polycystic ovarian syndrome
Premature ovarian failure.

Endocrine: 
P - hyperProlactinemia
A - adrenal insufficiency
T -  thyroid disorders
C - Cushing syndrome
H - HPO axis abnormalities/immaturity

Caloric/ chromosomal:
A - athletics
C - chromosomal abnormalities (eg, Turner syndrome)
E - eating disorders/obesity

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12
Q

Functional hypothalamic amenorrhea

A

exercise-induced amenorrhea.

Severe caloric restriction, Inc energy expenditure, and/or stress -> functional disruption of pulsatile GnRH secretion -> dec. LH, FSH, estrogen.

Dec. Leptin (dec fat)
Inc. Cortisol

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13
Q

Polycystic ovarian syndrome - Pathophysiology

A

Stein-Leventhal syndrome
Hyperinsulinemia and/or insulin resistance hypothesized to alter hypothalamic hormonal feedback response

  • > Inc LH: FSH
  • > androgens (eg, testosterone - theca interna cells)
  • > Estrogen (from fat)
  • > Dec rate of follicular maturation
  • > unruptured follicles (cysts) + anovulation.

A common cause of dec fertility in women.

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14
Q

Polycystic ovarian syndrome - Presentation

A

A - amenorrhea/oligomenorrhea
F - fertility (dec.)
A - acanthosis nigricans

C - cystic ovaries (Enlarged bilateral)
H - hirsutism
A - acne
O - obesity

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15
Q

Polycystic ovarian syndrome - Presentation

A

A - amenorrhea/oligomenorrhea
F - fertility (dec.)
A - acanthosis nigricans

C - cystic ovaries (Enlarged bilateral)
H - hirsutism
A - acne
O - obesity

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16
Q

Polycystic ovarian syndrome - Tx:

A

C - clomiphene
o
W - weight reduction (cycle regulation via dec. peripheral estrone formation)
S - spironolactone (to treat hirsutism)

O - OCPs (prevent endometrial hyperplasia due to unopposed estrogen)
F - finasteride (to treat hirsutism)
F - flutamide (to treat hirsutism)

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17
Q

Ovarian cysts

A

Follicular cyst - Distention of unruptured Graafian follicle -> Most common ovarian mass in young women.
May be associated with hyperestrogenism, endometrial hyperplasia.

Theca-lutein cyst - Often bilateral/multiple (Due to gonadotropin stimulation).
Associated with choriocarcinoma and hydatidiform moles.

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18
Q

Ovarian neoplasms - Inc risk:

A
Risk:
P - PCOS
A - advanced age
I - infertility
G - genetic predisposition (eg, BRCA-1 or BRCA-2 mutation, strong family history})
E - endometriosis

Lynch - Lynch syndrome

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19
Q

Ovarian neoplasms - Dec risk:

A

B - breastfeeding
O - OCPs
T - tubal ligation

+ previous pregnancy

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20
Q

Ovarian neoplasms - presentation

A

Presents with an adnexal mass, abdominal distension, bowel obstruction, pleural effusion.

Monitor response to therapy/relapse by measuring CA 125 levels (not good for screening)

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21
Q

Ovarian neoplasms - Surface epithelium tumors (benign)

A

Serous cystadenoma - Most common ovarian neoplasm. Lined with fallopian tube-like epithelium. Often bilateral.

Mucinous cystadenoma - Multiloculated, large. Lined by mucus-secreting epithelium

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22
Q

Ovarian neoplasms - Germ cell tumors (benign)

A

Mature cystic teratoma (dermoid cyst)

Most common in I0- 30 years old.

Cystic mass w/ all 3 germ layers (eg, teeth, hair, sebum).

pain 2° to ovarian enlargement or torsion.

A monodermal form with thyroid tissue (struma ovarii) uncommonly presents with hyperthyroidism.

Malignant transformation rare (usually to squamous cell carcinoma).

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23
Q

Ovarian neoplasms - Sex cord-stromal tumor (benign)

A

Fibroma

Sertoli-Leydig cell tumor

Thecoma

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24
Q

Ovarian neoplasms - Other (benign)

A

Brenner tumor

Resembles bladder epithelium (transitional cell tumor).

Solid tumor that is pale yellow-tan and appears encapsulated.

“Coffee bean” nuclei on H&E stain.

Usually benign.

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25
Q

Fibroma

A

Fibroma - Bundles of spindle-shaped fibroblasts.

Meigs syndrome- triad of ovarian fibroma, ascites, pleural effusion.

“Pulling” sensation in groin.

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26
Q

Sertoli-Leydig cell tumor

A

May produce androgens - virilization (eg, hirsutism, male pattern baldness, breast atrophy, clitoral enlargement, oligomenorrhea/amenorrhea).

Small, grey to yellow-brown mass and resembles testicular histology.

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27
Q

Thecoma

A

Thecoma - Like granulosa cell tumors, may produce estrogen.

Usually presents as abnormal uterine bleeding in a postmenopausal woman.

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28
Q

Surface epithelium tumors (malignant)

A

Serous cystadenocarcinoma - Most common malignant ovarian neoplasm, frequently bilateral.
Psammoma bodies.

Mucinous cystadenocarcinoma - Rare malignant mucinous ovarian epithelial tumor. Maybe metastatic from appendiceal or other GI tumors.
Can result in pseudomyxoma peritonei- intraperitoneal accumulation of mucinous material.

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29
Q

Germ cell tumors (malignant)

A

Dysgerminoma

Immature teratoma

Yolk sac tumor

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30
Q

Germ cell tumors (malignant) - Dysgerminoma

A

Most common in adolescents.

Equivalent to male seminoma but rarer.

1 % of all ovarian tumors, 30% of germ cell tumors.

Sheets of uniform “fried egg” cells.

hCG, LDH = tumor markers.

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31
Q

Germ cell tumors (malignant) - Immature teratoma

A

Aggressive, contains fetal tissue, neuroectoderm.

Commonly diagnosed before age 20.

Typically represented by immature/embryonic-like neural tissue.

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32
Q

Germ cell tumors (malignant) - Yolk sac tumor

A

Also known as ovarian endodermal sinus tumor.

Aggressive, in ovaries or testes and sacrococcygeal area in young children.

Yellow, friable (hemorrhagic), solid mass.

50% have Schiller-Duval bodies (resemble glomeruli).

AFP =tumor marker.

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33
Q

Sex cord-stromal tumors (malignant) - Granulosa cell tumor

A

Most common malignant stromal tumor.

Women in their 50’s.

Often produces estrogen and/or progesterone -> presents with postmenopausal bleeding, endometrial hyperplasia, sexual precocity (in pre-adolescents), breast tenderness.

Histology shows Call-Exner bodies (granulosa cells arranged haphazardly around collections of eosinophilic fluid, resembling primordial follicles.

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34
Q

Krukenberg tumor

A

GI malignancy that metastasizes to ovaries -> mucin-secreting signet cell adenocarcinoma.

Commonly presents as bilateral ovarian masses.

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35
Q

Primary dysmenorrhea

A

Painful menses, caused by uterine contractions to dec blood loss -> ischemic pain.

Mediated by prostaglandins -> Treatment: NSAIDs.

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36
Q

Endometriosis Tx

A
G - GnRH agonists
O - OCPs (continuous)/progestins
N - NSAIDs
D - danazol
e
L - laparoscopic removal
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37
Q

Endometritis Tx

A

gentamicin + clindamycin +/- ampicillin.

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38
Q

Endometrial carcinoma

A

Endometrioid - Histology shows abnormally arranged endometrial glands.
Early pathogenic events include loss of PTEN or mismatch repair proteins.

Serous - associated with endometrial atrophy in postmenopausal women. Aggressive.
Characterized by the formation of papillae and tufts. TP53 mutations common.

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39
Q

Adenomyosis Tx

A

GnRH agonists

hysterectomy

excision of an organized adenomyoma

40
Q

Endometriod Endometrial carcinoma - Risk factors:

A

Unopposed estrogen exposure and endometrial hyperplasia, usually in perimenopausal women.

Risk factors include obesity, DM, HTN, infertility.

41
Q

Benign breast diseases - Fibrocystic changes

A

Premenopausal women 20-50 years old.

Present with premenstrual breast pain or lumps; often bilateral and multifocal.

Nonproliferative lesions include simple cysts (fluid-filled duct dilation, blue dome), papillary apocrine change/metaplasia, stromal fibrosis.

Risk of cancer is usually not increased.

42
Q

Benign breast diseases - Inflammatory

processes

A

Fat necrosis - benign, usually painless, lump due to injury to breast tissue. Calcified oil cyst on mammography; necrotic fat and giant cells on biopsy.
Up to 50% of patients may not report trauma.

Lactational mastitis - occurs during breastfeeding, risk of bacterial infection through cracks in nipple.
S aureus is most common pathogen.
Treat with antibiotics and CONTINUE breastfeeding.

43
Q

Benign breast tumors - Fibroadenoma

A

Most common in women < 35 years old. Small, well-defined, mobile mass.

Inc size and tenderness with inc estrogen (eg, pregnancy, prior to menstruation).

Risk of cancer is usually not increased.

44
Q

Benign breast tumors - lntraductal papilloma

A

Small fibroepithelial tumor within lactiferous ducts, typically beneath areola.

Most common cause of nipple discharge (serous or bloody).

Slight Inc risk for cancer.

HAS myoepithelial cells.

45
Q

Benign breast tumors - Phyllodes tumor

A

a large mass of connective tissue and cysts with “ leaf-like” lobulations.

Most common in the 5th decade.

Some may become malignant.

46
Q

Sclerosing adenosis

A

Acini and stromal fibrosis, associated with calcifications.

Slight inc risk for cancer.

47
Q

Fibrocystic changes of the breast - Epithelial hyperplasia

A

cells in terminal ductal or lobular epithelium.

Inc risk of carcinoma with atypical cells.

48
Q

Breast cancer - risk factors

A

A - age /alcohol consumption
B - BRCA1 or BRCA2 gene mutations/ breastfeeding (-absence of).
C - Caucasian (African Americans at risk for triple (-) breast cancer)

H - history ( atypical hyperplasia, family history
O - obesity (adipose tissue converts androstenedione to estrone)
M - menstrual cycles (inc)
E - estrogen exposure (eg, nulliparity)

In men: BRCA2 mutation, Klinefelter syndrome.

49
Q

Breast cancer - The most important prognostic factor in early-stage disease.

A

Axillary lymph node metastasis.

50
Q

Ductal carcinoma in situ

A

Arises from ductal atypia.

Often seen early as microcalcifications on mammography.

Early malignancy without basement membrane penetration.

Usually does not produce a mass.

51
Q

Paget disease

A

Extension of underlying DCIS/invasive breast cancer up the lactiferous ducts and into the contiguous skin of nipple -> eczematous patches over nipple and areolar skin

Paget cells= intraepithelial adenocarcinoma cells.

52
Q

Lobular carcinoma in situ

A

Does not produce mass or calcifications -> incidental biopsy finding.

Inc risk of cancer in either breast (vs DCIS, same breast, and quadrant).

53
Q

Comedocarcinoma

A

A subtype of DCIS.

Cells have high-grade nuclei with extensive central necrosis and dystrophic calcification.

54
Q

Breast cancer - Invasive ductal

A

Firm, fibrous, “rock-hard” mass with sharp margins and small, glandular, duct-like cells in desmoplastic stroma.

Subtypes:
tubular- well-differentiated tubules that LACK myoepithelium.
mucinous- abundant extracellular mucin, seen in older women.

55
Q

Breast cancer - Invasive lobular

A

Dec. E-cadherin expression - orderly row of cells (“single file”) and no duct formation.

Often lacks desmoplastic response.

“Lots of lesions” - Often bilateral with multiple lesions in the same location.

“Lines of cells” = Lobular.

56
Q

Breast cancer - Medullary

A

Large, anaplastic cells growing in sheets with associated lymphocytes and plasma cells.

A well-circumscribed tumor can mimic fibroadenoma.

57
Q

Breast cancer - Inflammatory

A

Invasion of dermal lymphatic spaces - painful breast with warm, swollen, erythematous skin, peau d’orange

Poor prognosis (50% survival at 5 years).

Often mistaken for mastitis or Paget disease.

Usually lacks a palpable mass.

58
Q

Peyronie disease

A

Abnormal curvature of the penis due to fibrous plaque within tunica albuginea.

Consider surgical repair or treatment with collagenase injections once curvature stabilizes.

Distinct from penile fracture (rupture of corpora cavernosa due to forced bending).

59
Q

lschemic priapism

A

lasting> 4 hours.

Associated with sickle cell disease and medications (eg, sildenafil, trazodone).

Treat immediately with to prevent ischemia:

P - phenylephrine (intracavernosal)
A - aspiration (corporal)
D - decompression (surgical)

60
Q

Squamous cell carcinoma of penis - Precursor in situ lesions:

A

Precursor in situ lesions:

BoWen disease - in penile shaft, presents as leukoplakia “white plaque”.

Erythroplasia of Queyrat - carcinoma in situ of the glans, presents as erythroplakia “red plaque”.

Bowenoid papulosis - carcinoma in situ of unclear malignant potential, presenting as reddish papules.

61
Q

Testicular torsion - presentation

A

Rotation of testicle around spermatic cord and vascular pedicle.

12- 18 years old.

After an inciting event (eg, trauma) or spontaneously.

Acute, severe pain, high-riding testis, and absent cremasteric reflex.

62
Q

Varicocele - presentation

A

Dilated veins in pampiniform plexus due to inc venous pressure;

Most common cause of scrotal enlargement in adult males;

Most often on left side because of inc resistance to flow from left gonadal vein drainage into left renal vein;

Can cause infertility because of Inc temperature;

63
Q

Cryptorchidism

A

Descent failure of one or both testes;

impaired spermatogenesis (since sperm develop best at temperatures< 37°C);

Associated with risk of germ cell tumors.

Prematurity inc risk of cryptorchidism.

Dec inhibin B - > Inc FSH and LH;

testosterone dec in bilateral cryptorchidism, normal in unilateral.

64
Q

Testicular torsion -Tx

A

Surgical correction (orchiopexy) within 6 hours

manual detorsion if surgical option unavailable in the timeframe.

If testis is not viable, orchiectomy.

Orchiopexy, when performed, should be bilateral because the contralateral testis is at risk for subsequent torsion.

65
Q

Varicocele - Tx & Dx

A

diagnosed by standing clinical exam / Valsalva maneuver or ultrasound with Doppler

Distension on inspection and “bag of worms” on palpation; augmented by VaIsava.

does not transilluminate.

Treatment: consider surgical ligation or embolization if associated with pain or infertility.

66
Q

Vulvar carcinoma - subtypes:

A

HPV-related vulvar carcinoma- associated with high-risk HPV types 16, 18.
Risk factors: multiple partners, early coitarche. Reproductive-age females.

Non-HPV vulvar carcinoma - usually from long-standing lichen sclerosis.
Females> 70 years old.

67
Q

Extragonadal germ cell tumors

A

Arise in midline locations.

In adults, most commonly in retroperitoneum, mediastinum, pineal, and suprasellar regions.

In infants and young children, sacrococcygeal teratomas are most common.

68
Q

Scrotal masses

A

Congenital hydrocele - incomplete obliteration of processes vaginalis. Most spontaneously resolve by 1-year old (Transilluminating swelling).

Acquired hydrocele - Scrotal fluid collection usually 2° to infection, trauma, tumor. If bloody -> hematocele.

Spermatocele - Cyst due to a dilated epididymal duct or rete testis. Paratesticular fluctuant nodule.

69
Q

Seminoma

A

Malignant, does not occur in infancy - most common testicular tumor.

painless, homogenous testicular enlargement;

Large cells in lobules with watery cytoplasm and “fried egg’’ appearance - similar to dysgerminoma in females.

Inc placental ALP (PALP).

Highly radiosensitive, late metastasis, excellent prognosis.

70
Q

Testicular yolk sac tumor

A

Testicular endodermal sinus tumor.

Yellow, mucinous. Aggressive malignancy of testes, analogous to ovarian yolk sac tumor.

Schiller-Duval bodies resemble primitive glomeruli.

Inc. AFP is highly characteristic.

Most common testicular tumors in boys < 3 years old.

71
Q

Testicular choriocarcinoma

A

Malignant, Inc hCG.

Disordered syncytiotrophoblastic and cytotrophoblastic elements.

Hematogenous metastases to lungs and brain.

May produce gynecomastia, symptoms of hyperthyroidism (a -subunit of hCG same in FiLTH).

72
Q

Testicular embryonal carcinoma

A

Malignant, hemorrhagic mass with necrosis - worse prognosis than seminoma;

painful.

Often glandular/papillary morphology.

“Pure” embryonal carcinoma is rare (inc hCG and normal AFP levels);

most commonly mixed with other tumor types (inc AFP when mixed).

73
Q

Teratoma: malignant vs benign.

A

Malignant:
Immature - females
Mature - males

Benign:
Mature - females
Mature - kids

74
Q

Hormone levels in testicular germ cell tumors

A

Teratoma - NONE

Beta hCG - ALL (big rise in Choriocarcinoma)

PALP - Seminoma

AFP - embryonal (when mixed)/ yolk sac

75
Q

Testicular non-germ cell tumors

A

Leydig cell tumor - Golden brown color and Reinke crystals (eosinophilic cytoplasmic inclusions). Produces androgens or estrogens ->gynecomastia in men, precocious puberty in boys.

Sertoli cell tumor - Androblastoma from sex cord stroma.

Testicular lymphoma - Not a 1° cancer; arises from metastatic lymphoma to testes. Aggressive. Most common testicular cancer in older men.

76
Q

Epididymitis & Orchitis

A

Epididymitis: pain, and tenderness over posterior testis. Prehn sign (pain relief with scrotal elevation).

Orchitis:
young men - C trachomatis and N gonorrhoeae
elderly men - E coli and Pseudomonas
boys <1O years old - Mumps
Autoimmune - granulomas involving seminiferous tubules

77
Q

Benign prostatic hyperplasia - presentation

A

men > 50 years old.

periurethral (lateral and middle) lobes

May lead to distention and hypertrophy of bladder, hydronephrosis, UTis.

Inc free prostate-specific antigen (PSA).

78
Q

Prostatitis

A

Acute bacterial prostatitis:
Older men - E coli;
Young men - C trachomatis/ N gonorrhoeae.

Chronic prostatitis - either bacterial or nonbacterial (eg, 2° to previous infection, nerve problems, chemical irritation).

79
Q

Prostatic adenocarcinoma

A

men> 50 years old.

posterior lobe (peripheral zone)

Dx: Inc PSA and subsequent needle core biopsies.

useful tumor markers: Prostatic acid phosphatase (PAP) and PSA (inc total PSA, with I fraction of free PSA)

Osteoblastic metastases in bone - to the spine often occurs via Batson (vertebral) venous plexus.

80
Q

Benign prostatic hyperplasia Tx:

A

alfa1-antagonists (terazosin, tamsulosin) - which cause relaxation of smooth muscle;

5 alfa-reductase inhibitors (eg, finasteride);

PDE-5 inhibitors (eg, tadalafil);

surgical resection (eg, TURP, ablation).

81
Q

Leuprolide - MECHANISM

A

GnRH analog with agonist properties when used in pulsatile fashion;

Antagonist properties when used in a continuous fashion (downregulates GnRH receptor in pituitary
-> dec FSH and LH).

82
Q

Estrogens use contraindications

A

ER (+) breast cancer

history of DVTs

tobacco use in women > 35 years old.

83
Q

Clomiphene

A

Antagonist at estrogen receptors in hypothalamus.

Prevents normal feedback inhibition and inc release of LH and FSH from the pituitary, which stimulates ovulation.

Used to treat infertility due to anovulation (eg, PCOS).

SERMs may cause:

F - hot flashes
E - enlargement of ovaries
M - multiple simultaneous pregnancies

V - visual disturbances

84
Q

Tamoxifen vs Raloxifene

A

Both:

  • agonist in the bone.
  • antagonist in the breast.
  • risk of thromboembolic events (especially with smoking)

Raloxifene - antagonisint in the endometrium -> “Relax”

Tamoxifen -agonist in the endometrium -> risk of endometrial cancer.

85
Q

Aromatase inhibitors eamples

A

Anastrozole

letrozole

exemestane - “no aroma in the exam”

86
Q

Leuprolide - CLINICAL USE

A

Uterus - Uterine fibroids, endometriosis

Fertility - precocious puberty, infertility.

Prostate - prostate cancer

87
Q

Progestins examples

A

Levonorgestrel

medroxyprogesterone

etonogestrel

norethindrone - “Northen drone”

megestrol.

88
Q

Antiprogestins

A

Mifepristone, ulipristal - Competitive inhibitors of progestins at progesterone receptors.

Termination of pregnancy (mifepristone with misoprostol); emergency contraception (ulipristal).

“Priests against pregnancy”

89
Q

Combined contraception - mechanism

A

Estrogen and progestins inhibit LH/FSH and thus prevent estrogen surge.
No estrogen surge -> no LH surge -> no ovulation.

Progestins cause thickening of cervical mucus, thereby limiting access of sperm to uterus.

Progestins also inhibit endometrial proliferation -> endometrium is less suitable to the implantation of an embryo.

90
Q

Copper intrauterine device

A

I - Produces local inflammatory reaction toxic to sperm and ova, preventing fertilization and implantation;

H - Hormone-free.
E - emergency contraception (most effective) .
L - Long-acting reversible contraception.
P - PID risk with insertion (contraindicated in active pelvic infection).

91
Q

Tocolytics

A

Used to dec contraction frequency in preterm labor and allow time for administration of steroids (to promote fetal lung maturity) or transfer to an appropriate medical center with obstetrical care.

T - terbutaline
N - nifedipine
I - indomethacin

92
Q

Danazol - Use and mechanism

A

Synthetic androgen that acts as a partial agonist at androgen receptors - used Endometriosis, hereditary angioedema.

93
Q

Testosterone, methyltestosterone - Use and A/E

A

Treat hypogonadism and promote the development of 2° sex characteristics; stimulate anabolism to promote recovery after burn or injury.

Masculinization in females;

Dec intratesticular testosterone in males by inhibiting release of LH (via negative feedback) ->gonadal atrophy.

Premature closure of epiphyseal plates.

Inc LDL and Dec HDL

94
Q

Antiandrogens - Ketoconazole vs. Spironolactone

A

Ketoconazole - Inhibits steroid SYNTHESIS (inhibits 17,20 desmolase/17a-hyd roxylase).

Spironolactone - Inhibits steroid BINDING (inhibits 17,20 desmolase/17a-hyd roxylase).

Used in PCOS to reduce androgenic symptoms.

Both can cause gynecomastia and amenorrhea.

95
Q

Tamsulosin

A

alfa1-antagonist used to treat BPH by inhibiting smooth muscle contraction.

Selective for alfa -1A/D receptors (found on the prostate) vs vascular alfa-1B receptors.

96
Q

Phosphodiesterase type 5 inhibitors -ADVERSE EFFECTS

A

Headache, flushing, dyspepsia, cyanopia (blue-tinted vision).

Risk of life-threatening hypotension in patients taking nitrates.

“Hot and sweaty, but then Headache, Heartburn, Hypotension”

97
Q

Flutamide

A

Nonsteroidal competitive inhibitor at androgen receptors.

Used for prostate carcinoma.