Reproductive Medicine Pathology

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jknell
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Reproductive Medicine Pathology
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2013-03-20 10:51:15
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  1. Cervical Dysplasia and Carcinoma in situ
    • Risk Factors:
    • -multiple sex partners (#1)
    • -smoking
    • -early sexual intercourse
    • -HIV infection

    • Pathophysiology:
    • -associated with HPV infection
    • -HPV 16: E6 inhibits p53
    • -HPV 18: E7 inhibits Rb

    • Pathology:
    • -disordered epithelial growth
    • -begins at basal layer of squamo-columnar junction and extends outward
    • -koilocytic change (raisinoid nucleus)
    • -nuclear atypia
    • -increased mitotic activity
    • -progressive stepwise from CIN I to CIS

    • Classification:
    • -cervical intraepithelial neoplasia
    • -CIN I: involves < 1/3 of thickness
    • -CIN II: involves < 2/3 of thickness
    • -CIN III: involves slightly less than the entire thickness
    • -Carcinoma in situ (CIS): full thickness

    • *may progress to invasive carcinoma if left untreated
    • **CIN I often regresses

    • Screening:
    • -PAP smear can catch cervical dysplasia before it develops into carcinoma
    • -low grade (CIN I)
    • -high grade (CIN II and CIN III)
    • **has not decreased incidence of adenocarcinoma

    • Immunization:
    • -quadrivalent vaccine (6, 11, 16, 18)
    • -6, 11 protect against condylomas
    • -16, 18 protect against CIN and carcinoma
    • -still need PAP smears (doesn't cover all strains)
  2. Invasive Cervical Carcinoma
    • Epidemiology:
    • -middle aged women (40-50y)

    • Risk Factors:
    • -high risk HPV infection
    • -smoking
    • -immunodeficiency (AIDS-defining illness)

    • Presentation:
    • -vaginal bleeding (especially post-coital)
    • -cervical discharge

    • Pathology:
    • -squamous cell carcinoma (80%)
    • -adenocarcinoma (15%)

    • Complications:
    • -tumor grows locally and metastasizes late
    • -lateral invasion can block ureters (→ hydronephrosis and renal failure)
  3. Asherman Syndrome
    • Pathophysiology:
    • -loss of basalis and scarring
    • -result of overaggressive D&C

    • Presentation:
    • -secondary amenorrhea
  4. Acute Endometritis
    • Pathophysiology:
    • -bacterial infection (from vagina or intestinal tract) of the endometrium
    • -usually due to retained products of conception following delivery/miscarriage/abortion
    • -also associated with IUD

    • Presentation:
    • -fever
    • -abnormal uterine bleeding
    • -pelvic pain

    • Treatment:
    • -gentamycin + clindamycin
    • -with or without ampicilin
  5. Chronic Endometritis
    • Pathophysiology:
    • -chronic inflammation of the endometrium

    • Diagnosis:
    • -lymphocytes and plasma cells in endometrium (lymphocytes normally present; plasma cells required for diagnosis)

    • Causes:
    • -retained products of conception
    • -chronic pelvic inflammation (chlamydia)
    • -IUD
    • -TB

    • Presentation:
    • -abnormal uterine bleeding
    • -pain
    • -infertility
  6. Endometriosis
    • Pathophysiology:
    • -non-neoplastic endometrial glands/stroma in abnormal locations outside the uterus
    • -most common site of involvement is ovary
    • -uterine ligaments, pouch of Douglas, bladder wall, bowel serosa, fallopian tube serosa

    • Theories:
    • 1. Retrograde menstruation
    • 2. Metaplastic theory
    • 3. Lymphatic dissemination (lungs)

    • Presentation:
    • -dysmenorrhea (severe pain during menstruation)
    • -painful intercourse
    • -infertility
    • -menorrhagia
    • -dysparenuria

    • Pathology:
    • -ovaries → chocolate cysts
    • -yellow brown, gun powder nodules
    • -uterus normal sized

    • Complications:
    • -increased risk of carcinoma (esp in the ovary)

    • Treatment:
    • -OCPs
    • -NSAIDs
    • -Leuprolide
    • -danazol
  7. Adenomyosis
    • Pathophysiology:
    • -endometrium within the myometrium

    • Presentation:
    • -menorrhagia
    • -dysmenorrhea
    • -pelvic pain
    • -uterus is enlarged! (vs endometriosis)

    • Treatment:
    • -hysterectomy
  8. Endometrial Hyperplasia
    • Risk Factors:
    • -obesity
    • -anovulatory cycles
    • -hormone replacement therapy
    • -PCOS
    • -granulosa cell tumor

    • Pathophysiology:
    • -consequence of unopposed estrogen

    • Presentation:
    • -postmenopausal vaginal bleeding

    • Biopsy:
    • -too many glands
    • -with or without atypia (with atypia → high risk for endometrial carcinoma)
  9. Endometrial Carcinoma
    • Epidemiology:
    • -most common gynecologic malignancy
    • -peak occurrence 55-65 years

    • Risk Factors:
    • -prolonged use of estrogen without progestins
    • -obesity
    • -diabetes
    • -HTN
    • -nulliparity
    • -late menopause

    • Two Pathways
    • 1. Hyperplasia
    • -75%
    • -avg age 60 years
    • -histology shows endometrioid pathology
    • 2. Sporadic
    • -arises with no evident precursor lesion
    • -avg age 70 years
    • -histology is serous with papillary structures and psammoma bodies
    • -p53 mutations common
    • -more aggressive

    • Clinical Presentation:
    • -vaginal bleeding (postmenopausal bleeding)
  10. Leiomyoma
    "Fibroids"

    • Epidemiology:
    • -most common tumor in females
    • -common in premenopausal women (20-40 years)
    • -increased incidence in blacks

    • Pathophysiology:
    • -benign smooth muscle tumor arising from myometrium
    • -related to estrogen exposure
    • -increase size with pregnancy
    • -decrease size with menoapuse

    • Pathology:
    • -multiple
    • -well defined, white, whorled masses

    • Presentation:
    • -commonly asymptomatic
    • -abnormal uterine bleeding
    • -severe bleeding may lead to iron deficiency anemia
    • -miscarriage
    • -pelvic mass

    DOES NOT PROGRESS TO LEIOMYOSARCOMA
  11. Leiomyosarcoma
    • Epidemiology:
    • -affect postmenopausal women (70-80 years)
    • -increase incidence in blacks

    • Pathophysiology:
    • -malignant proliferation of smooth muscle of myometrium
    • -typically arise de novo!

    • Pathology:
    • -usually a single lesion
    • -bulky, irregularly shaped tumor
    • -areas of necrosis and hemorrhage

    • Presentation:
    • -may protrude from cervix and bleed

    • Prognosis:
    • -highly aggressive tumor with tendency to recur
  12. Gynecologic Tumor Epidemiology
    • Incidence:
    • endometrial > ovarian > cervical
    • **worldwide ovarian most common

    • Worst Prognosis:
    • ovarian > cervical > endometrial
  13. Premature Ovarian Failure
    • Pathophysiology:
    • -premature atresia of ovarian follicles in women of reproductive age

    • Presentation:
    • -signs of menopause after puberty but before age 40

    • Hormones:
    • -↓ estrogen
    • -↑ LH
    • -↑ FSH
  14. Most common causes of anovulation
    • -pregnancy
    • -PCOS
    • -obesity
    • -HPO axis abnormalities
    • -premature ovarian failure
    • -hyperprolactinemia
    • -thyroid disorders
    • -eating disorders
    • -Cushing's syndrome
    • -adrenal insufficiency
  15. Polycystic Ovarian Syndrome
    • Epidemiology:
    • -affects 5% of women of reproductive age

    • Pathophysiology:
    • -increased LH production leads to anovulation and therefore no progesterone
    • -LH causes hyperandrogenism (increased androgen secretion by theca cells
    • -Androgens are converted to estrone peripherally in adipose tissue
    • -high levels of androgen inhibit FSH
    • -without FSH stimulation granulosa cells don't produce estradiol and oocytes do not mature
    • -this leads to cystic degeneration of the follicles

    • Pathology:
    • -bilaterally enlarged, cystic ovaries

    • Clinical Presentation:
    • -amenorrhea/oligomenorrhea
    • -infertility
    • -obesity
    • -hirsutism

    • Associated with:
    • -insulin resistance
    • -increased risk of endometrial cancer (increased estrogen without opposing progesterone)

    • Hormones:
    • -↑ LH
    • -↓ FSH
    • -↑ testosterone
    • -↑ estrogen (from testosterone aromatization)

    • Treatment:
    • -weight reduction
    • -low dose OCPs or medroxyprogesterone (reduce LH and androgenesis)
    • -spironolactone (acne and hirsutism)
    • -clomiphene (for women who want to get pregnant)
    • -metformin (diabetes
  16. Ovarian Cysts
    • -Follicular cyst
    • -Corpus Luteum cyst
    • -Theca-lutein cyst
    • -Hemorrhagic cyst
    • -Dermoid cyst
    • -Endometrioid cyst
  17. Follicular Cyst
    • Pathophysiology:
    • -distention of unruptured graafian follicle
    • -may be associated with hyperestrinism and endometrial hyperplasia

    Most common ovarian mass in young women
  18. Corpus Luteum Cyst
    • Pathophysiology:
    • -hemorrhage into persistent corpus luteum
    • -commonly regresses spontaneously
  19. Theca-lutein cyst
    • Pathophysiology:
    • -often bilateral/multiple
    • -due to gonadotropin stimulation

    Associated with choriocarcinoma and moles
  20. Hemorrhagic Cyst
    • Pathophysiology:
    • -blood vessel rupture in cyst wall
    • -cyst grows with increased blood retention
    • -usually self resolves
  21. Dermoid Cyst
    • Pathophysiology:
    • -mature teratoma
    • -cystic growths filled with various types of tissue such as fat, hair, teeth, bits of bone and cartilage
  22. Endometrioid Cyst
    • Pathophysiology:
    • -endometriosis within ovary with cyst formation
    • -varies with menstrual cycle
    • -"chocolate cyst" when filled with dark reddish-brown blood
  23. Ovarian Germ Cell Tumors
    • Epidemiology:
    • -second most common type of ovarian tumors (15%)-most common in adolescents/women of reproductive age

    • Types:
    • 1. Dysgerminoma (oocytes)
    • 2. Choriocarcinoma (placental tissue)
    • 3. Endodermal sinus tumor (yolk sac)
    • 4. Teratoma (fetal tissue)
    • 5. Embryonal carcinoma (fetal tissue)
  24. Dysgerminoma
    • Epidemiology:
    • -malignant
    • -rare (1% of GCT in females)
    • -male counterpart = seminoma (30% of GCT in males)
    • -associated with Turner Syndrome

    • Pathology:
    • -sheets of uniform cells
    • -large cells with clear cytoplasm and central nuclei (resemble oocytes)

    • Tumor Markers:
    • -hCG
    • -LDH

    • Prognosis/Treatment:
    • -good prognosis
    • -responds to radiotherapy
  25. Choriocarcinoma
    • Epidemiology:
    • -rare but malignant
    • -can develop during or after pregnancy in mother or baby
    • -gestational trophoblastic neoplasia

    • Pathophysiology:
    • -malignancy of trophoblastic tissue
    • -chorionic villi are ABSENT
    • -small hemorrhagic tumor with hematogenous spread to lungs
    • -increased frequency of theca-lutein cysts

    • Tumor Markers:
    • -hCG

    • Prognosis/Treatment:
    • -poor response to chemo
  26. Endodermal Sinus Tumor
    • Epidemiology:
    • -most common GCT in children

    • Pathophysiology:
    • -malignant tumor that mimics yolk sac
    • -of ovaries (testes in boys) and sacrococcygeal area

    • Pathology:
    • -yellow, friable solid masses
    • -50% have Schiller-Duval bodies (resemble glomeruli)

    • Tumor Markers:
    • -AFP
  27. Teratoma
    • Epidemiology:
    • -90% of ovarian GCTs
    • -bilateral in 10%
    • -benign

    • Pathophysiology:
    • -contains tissue from 2 or 3 germ layers

    • Mature Teratoma
    • -"dermoid cyst"
    • -mostly benign
    • -most common ovarian GCT

    • Immature Teratoma
    • -aggressively malignant
    • -usually neural tissue
    • *can also have tumors of tissue in teratoma (most commonly squamous cell carcinoma of skin)

    • Struma Ovarii
    • -contains functional thyroid tissue
    • -can present as hyperthyroidism
  28. Embryonal Carcinoma
    • Pathophysiology:
    • -malignant tumor composed of large primitive cells

    Aggressive with early metastasis
  29. Ovarian Non-Germ Cell Tumors
    -tumors that arise from surface epithelium or sex cords

    • Surface Epithelial Tumor
    • 1. Serous Cystadenoma
    • 2. Serous Cystadenocarcinoma
    • 3. Mucinous Cystadenoma
    • 4. Mucinous Cystadenocarcinoma
    • 5. Brenner Tumor

    • Sex-Cord Stromal Tumor
    • 6. Fibromas
    • 7. Granulosa Cell Tumor
    • 8. Sertoli-Leydig Cell Tumor

    • Metastases
    • 9. Krukenberg Tumor
  30. Serous Cystadenoma
    • Epidemiology:
    • -45% of ovarian tumors
    • -benign
    • -most commonly in premenopausal women (30-40 years)

    • Pathology:
    • -frequently bilateral
    • -lined with fallopian tube-like epithelium
    • -single cyst with flat lining

    • Tumor Marker
    • -CA-125 (good for monitoring progression, not screening)
  31. Serous Cystadenocarcinoma
    • Epidemiology:
    • -45% of ovarian tumors
    • -malignant
    • -more common in postmenopausal women (60-70 years)

    • Pathology:
    • -frequently bilateral
    • -psammoma bodies-complex cyst with a thick, shaggy lining

    • Risk Factors:
    • -BRCA1, BRCA2, HNPCC
    • -significant genetic predisposition makes family history the most important risk factor
  32. Mucinous Cystadenoma
    • Epidemiology:
    • -45% of ovarian tumors
    • -benign
    • -most commonly in premenopausal women (30-40 years)

    • Pathology:
    • -multilocular cyst lined by mucus-secreting epithelium
    • -intestine like tissue
  33. Mucinous Cystadenocarcinoma
    • Epidemiology
    • -45% of ovarian tumors (with serous)
    • -malignant
    • -most commonly in postmenopausal women (60-70 years)

    • Pathology:
    • -pseudomyxoma peritonei: intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor ("Jelly Belly")
  34. Brenner Tumor
    • Pathology:
    • -benign
    • -unilateral
    • -looks like Bladder
    • -solid tumor, pale yellow-tan color
    • -appears encapsulated
    • -"coffee bean" nuclei
  35. Fibromas
    • Pathology:
    • -benign tumor of fibroblasts
    • -bundles of spindle-shaped fibroblasts

    • Meigs' Syndrome
    • 1. Ovarian fibroma
    • 2. Ascites
    • 3. Hydrothorax

    Pulling sensation in groin
  36. Granulosa Cell Tumor
    • Presentation:
    • -often produce estrogen
    • -Children: precocious puberty
    • -Reproductive age: menorrhagia and metrorrhagia
    • -Postmenopause: endometrial hyperplasia, postmenopausal uterine bleeding (risk for carcinoma)

    • Pathology:
    • -Call-Exner bodies: small follicles filled with eosinophilic secretions
  37. Sertoli-Leydig Cell Tumor
    • Pathophysiology:
    • -Granulosa-Theca cells and Sertoli-Leydig cells have a similar embryonic precursor

    • Pathology:
    • -composed of sertoli cells that form tubules and Leydig cells inbetween
    • -Reinke crystals

    • Presentation:
    • -may produce androgen
    • -associated with hirsutism and virilization
  38. Krukenberg Tumor
    • Pathophysiology:
    • -metastatic mucinous tumor that involves both ovaries
    • -most commonly due to diffuse type gastric carcinoma

    • Pathology:
    • -signet ring cells

    Krukenberg tumor is usually bilateral, distinguishes from primary mucinous carcinoma of the ovary (usually unilateral)
  39. Adenosis
    • Normal Development:
    • -squamous epithelium derived from the urogenital sinus lines the lower 2/3 of the vagina
    • -columnar epithelium derived from the Mullerian ducts lines the upper 1/3 of the vagina
    • -normally squamous epithelium replaces the columnar epithelium

    • Pathogenesis:
    • -focal persistence of columnar epithelium in the upper 1/3 of the vagina

    • Risk Factors:
    • -DES exposure in utero

    Increased risk for clear cell adenocarcinoma
  40. Bartholin Cyst
    • Epidemiology:
    • -women of reproductive age

    • Pathogenesis:
    • -cystic dilation of the Bartholin gland (on either side of the vaginal canal, secrete mucus-like fluid)
    • -dilation arises due to inflammation and obstruction of the gland

    • Presentation:
    • -unilateral, painful cystic lesion at the lower vestibule
  41. Condyloma
    • Pathophysiology:
    • -most commonly due to HPV 6, 11
    • -less commonly due to syphilis

    • Presentation:
    • -warty neoplasm of vulvar skin, often large

    Rarely progress to carcinoma
  42. Lichen Sclerosis
    • Epidemiology:
    • -postmenopausal women

    • Pathophysiology:
    • -thinning of the epidermis and fibrosis (sclerosis) of the dermis

    • Presentation:
    • -white patch (leukoplakia) with parchment like vulvar skin

    Benign but slight increased risk for squamous cell carcinoma
  43. Lichen Simplex Chronicus
    • Pathophysiology:
    • -associated with chronic irritation and scratching
    • -hyperplasia of vulvar squamous epithelium

    • Presentation:
    • -leukoplakia with thick, leathery skin

    Benign, no increased risk of squamous cell carcinoma
  44. Vulvar Carcinoma
    • Epidemiology:
    • -relatively rare
    • -HPV-related: reproductive age women
    • -non-HPV related: women > 70 years

    • Pathophysiology:
    • -may be HPV related (arises from VIN)
    • -or non-HPV related (long standing lichen sclerosis)

    • Presentation:
    • -leukoplakia
    • -biopsy needed to distinguish from other causes of leukoplakia
  45. Extramammary Paget Disease
    • Pathophysiology:
    • -carcinoma in situ (usually no underlying carcinoma)
    • -vs Paget disease of the nipple (always underlying carcinoma)

    • Presentation:
    • -erythematous
    • -pruritic
    • -ulcers

    • Distinguish from Melanoma:
    • -Paget Cells: PAS+, keratin+, S100-
    • -Melanoma: PAS-, keratin-, S100+
  46. Vaginal Tumors
    • 1. Squamous Cell Carcinoma
    • 2. Clear Cell Adenocarcinoma
    • 3. Sarcoma botryoides (Rhadomyosarcoma)
  47. Squamous Cell Carcinoma of Vagina
    • Pathophysiology:
    • -usually secondary to cervical SCC
    • -primary VERY rare
  48. Clear Cell Adenocarcinoma
    • Epidemiology:
    • -women who had DES exposure in utero

    • Pathology:
    • -malignant proliferation of glands with clear cytoplasm
  49. Sarcoma Botryoides
    "Embryonal Rhabdomyosarcoma"

    • Epidemiology:
    • -very rare
    • -usually child (<5 years)

    • Pathophysiology:
    • -malignant mesenchymal proliferation of immature skeletal muscle

    • Presentation:
    • -bleeding and grape-like mass that protrudes from the vagina or penis of a child

    • Pathology:
    • -cytoplasmic cross-striations
    • -IF positive for desmin and myogenin
  50. Vaginal Carcinoma
    • Pathophysiology:
    • -usually related to high-risk HPV
    • -precursor lesion VAIN

    • Lymph Node Spread
    • -lower 2/3 of vagina (UGS) → inguinal nodes
    • -upper 1/3 of vagina (Mullerian Duct) → regional iliac nodes
  51. Localization of Breast Pathology


    • Nipple:
    • -Paget's Disease
    • -Breast abscess

    • Lactiferous Sinus:
    • -intraductal papilloma
    • -breast abscess
    • -mastitis

    • Major Duct:
    • -fibrocystic change
    • -ductal cancer

    • Terminal Duct:
    • -tubular carcinoma

    • Lobules:
    • -lobular carcinoma
    • -sclerosing adenosis

    • Stroma:
    • -Fibroadenoma
    • -Phyllodes tumor
  52. Benign Breast Tumors
    • 1. Fibroadenoma
    • 2. Intraductal Papilloma
    • 3. Phyllodes Tumor
  53. Fibroadenoma
    • Epidemiology:
    • -most common tumor in those < 35 years

    • Pathophysiology:
    • -tumor of fibrous tissue and glands
    • -estrogen sensitive (increase size and tenderness)

    • Pathology:
    • -small, mobile, firm mass
    • -sharp edges

    • Prognosis:
    • -no increased risk of carcinoma
  54. Intraductal Papilloma
    • Epidemiology:
    • -typically premenopausal women

    • Pathology:
    • -small projection that grows into lactiferous ducts
    • -typically beneath areola
    • -lined by both epithelium and myoepithelial cells

    • Presentation:
    • -bloody nipple discharge

    • Prognosis:
    • -slight (1.5-2x) increase risk for carcinoma

    • Must distinguish from Papillary Carcinoma!!!
    • -risk increases with age (commonly in postmenopausal women)
    • -lacks myoepithelial cell layer
  55. Phyllodes Tumor
    • Epidemiology:
    • -most common in 6th decade (postmenopausal women)

    • Pathophysiology:
    • -fibroadenoma-like tumor with overgrowth of fibrous component

    • Pathology:
    • -large bulky mass of connective tissue and cysts
    • -"leaf like" projections

    • Prognosis:
    • -some may become malignant
  56. Fibrocystic Disease
    • Epidemiology:
    • -most common cause of "breast lumps" from age 25 to menopause

    • Pathophysiology:
    • -thought to be hormone mediated
    • -cysts of glands/ducts stretch connective tissue leading to fibrosis

    • Pathology:
    • -cysts have a blue dome appearance on gross exam

    • Presentation:
    • -premenstrual breast pain
    • -multiple lesions
    • -often bilateral
    • -fluctuation in size of mass

    • Histologic Types:
    • 1. Fibrosis:
    • -hyperplasia of breast stroma

    • 2. Cystic:
    • -fluid filled
    • -blue dome
    • -ductal dilation

    • 3. Sclerosing Adenosis:
    • -increased acini and intralobular fissures
    • -calcifications
    • -often confused with cancer
    • -slight increased risk of cancer (2x)

    • 4. Epithelial Hyperplasia/Apocrine hyperplasia
    • -increase in number of epithelial cell layers in terminal duct lobule
    • -increased risk of carcinoma with atypical cells (5x)
    • -occurs in women > 30 years old
  57. Inflammatory Conditions of the Breast
    • 1. Acute Mastitis
    • 2. Periductal Mastitis
    • 3. Mammary Duct Ectasia
    • 4. Fat Necrosis
  58. Acute Mastitis
    • Epidemiology:
    • -associated with breast feeding (fissures develop in nipple allowing microbe entry)

    • Pathophysiology:
    • -most common organism = S. aureus

    • Presentation:
    • -erythematous breast
    • -purulent nipple discharge
    • -may develop abscess (can lead to a mass)

    • Treatment:
    • -continued drainage (breast feeding)
    • -antibiotics (dicloxacillin)
  59. Periductal Mastitis
    • Pathophysiology:
    • -inflammation of subareolar ducts
    • -usually seen in smokers: lactiferous ducts surrounded by highly specialized epithelium that is dependent on vitamin A
    • -vitamin A deficiency leads to squamous metaplasia → duct blockage and inflammation

    • Presentation:
    • -subareolar mass
    • -nipple retraction
  60. Mammary Duct Ectasia
    • Epidemiology:
    • -rare
    • -classically arises in multiparous, postmenopausal women

    • Pathophysiology:
    • -inflammation with dilation (ectasia) of the subareolar ducts

    • Presentation:
    • -periareolar mass
    • -green-brown nipple discharge
    • -plasma cells seen on bx
  61. Fat Necrosis
    • Epidemiology:
    • -forms after trauma (50% may not report trauma)

    • Presentation:
    • -benign, usually painless lump
    • -calcification on mammography
  62. Gynecomastia
    • Epidemiology:
    • -occurs in males

    • Pathophysiology:
    • -hyperestrogenism (cirrhosis, testicular tumor, puberty, old age)
    • -Klinefelter's syndrome
    • -Drugs (estrogen, marijuana, heroin, psychoactive drugs)

    • "Some Drugs Create Awkward Knockers"
    • -Spironolactone
    • -Digitalis
    • -Cimetidine
    • -Alcohol
    • -Ketoconazole
  63. Malignant Breast Tumors
    • Epidemiology:
    • -common post-menopause
    • -second most common cause of cancer mortality in women

    • Risk Factors:
    • -increased estrogen exposure
    • -increased total number of menstrual cycles
    • -older age at first live birth
    • -obesity (increased estrogen due to peripheral adipose conversion)
    • -BRCA1/2

    • Pathophysiology:
    • -usually arise from terminal duct lobular unit
    • -usually located in upper outer quadrant of breast

    • Molecular Factors:
    • -overexpression of estrogen/progesterone receptors or Her2/Neu is common
    • -affect therapy and prognosis

    • Prognosis:
    • -axillary LN metastasis is the most important prognostic factor (usually caught before peripheral metastasis)

    • Noninvasive Types:
    • 1. Ductal Carcinoma In Situ
    • 2. Comedocarcinoma (subtype of DCIS)
    • 3. Lobular Carcinoma In Situ

    • Invasive Types:
    • 1. Invasive Ductal Carcinoma
    • 2. Invasive Lobular Carcinoma
    • 3. Medullary Carcinoma
    • 4. Inflammatory Carcinoma
    • 5. Paget's Disease
  64. Ductal Carcinoma In Situ (DCIS)
    • Characteristics:
    • -fills ductal lumen
    • -arises from ductal hyperplasia
    • -no invasion of basement membrane

    • Presentation:
    • -often detected as calcification on mammography (biopsy often needed to distinguish between malignant and benign calcifications)
    • -doesn't usually produce a mass

    • Histologic Types:
    • 1. Comedo type
    • 2. Paget disease of the breast
  65. Comedocarcinoma
    Subtype of DCIS

    • Characteristics:
    • -ductal, caseous necrosis
    • -dystrophic calcification at the center of ducts
  66. Paget's Disease of the Breast
    • Pathophysiology:
    • -DCIS that extends up the ducts to involve the skin of the nipple

    • Paget Cells
    • -large cells in epidermis with clear halo

    • Presentation:
    • -nipple ulceration and erythema
    • -almost always associated with underlying carcinoma (vs. Paget's in the vulva)
  67. Lobular Carcinoma In Situ (LCIS)
    • Pathophysiology:
    • -malignant proliferation of lobules with no invasion of basement membrane
    • -dyscohesive cells (due to lack of E cadherin)

    • Presentation:
    • -does not produce a mass or calcifications
    • -usually discovered incidentally on biopsy
    • -often multifocal and bilateral

    • Treatment:
    • -tamoxifen (reduce risk of subsequent carcinoma)
    • -close follow up

    Currently seen as more of a risk factor than a malignancy
  68. Invasive Ductal Carcinoma
    • Epidemiology:
    • -most common type of invasive carcinoma (>80%)

    • Presentation:
    • -firm, fibrous, "rock hard" mass with sharp margins
    • -detected by mammography (>1cm) or on physical exam (>2cm)

    • Pathology:
    • -small, glandular duct-like cells
    • -duct-like structures with desmoplastic stroma

    • Subtypes:
    • 1. Tubular: well differentiated, relatively good prognosis
    • 2. Mucinous: "tumor cells floating in a pool of mucus", older women (>70), good prognosis
    • 3. Medullary carcinoma
    • 4. Inflammatory carcinoma
  69. Medullary Carcinoma
    • Epidemiology:
    • -increased incidence in BRCA1 carriers

    • Pathology:
    • -fleshy, cellular
    • -well-circumscribed mass
    • -lymphocytic infiltrate (plasma cells)
    • -mimic fibroadenoma

    • Prognosis:
    • -relatively good
  70. Inflammatory Carcinoma
    • Presentation:
    • -inflamed swollen breast
    • -no discrete mass
    • **can be mistaken for acute mastitis
    • -Peau d'orange (skin resembles orange peel)

    • Pathophysiology:
    • -tumor cells block lymphatic drainage

    • Prognosis:
    • -very poor
    • -50% survival at 5 years
  71. Invasive Lobular Carcinoma
    • Pathology:
    • -grows in a single file pattern (Indian file)
    • -no duct formation due to lack of E cadherin
    • -may have signet-ring morphology

    • Presentation:
    • -often multiple lesions and bilateral
  72. Prostatitis
    • Presentation:
    • -dyuria
    • -frequency
    • -urgency
    • -fever and chills
    • -low back pain
    • -prostate tender and boggy on DRE
    • Acute (bacterial)
    • -Young adults (C. trachomatis, N. gonorrhea)
    • -Older adults (E. coli, Pseudomonas)

    Chronic (abacterial)
  73. Benign Prostatic Hyperplasia (BPH)
    • Epidemiology:
    • -age-related change
    • -common in men > 50 years

    • Pathophysiology:
    • -hyperplasia (NOT hypertrophy) of prostate gland
    • -related to DHT (causes hyperplasia)

    • Pathology:
    • -nodular enlargement of periurethral (lateral and middle) lobes → compress the urethra

    • Presentation:
    • -increased frequency of urination
    • -nocturia
    • -difficulty starting and stopping stream
    • -dysuria
    • -increased PSA

    • Complications:
    • -distention and hypertrophy of bladder
    • -hydronephrosis
    • -UTI

    • Prognosis:
    • -NOT considered premalignant

    • Treatment:
    • 1. α1-antagonists (terazosin, tamsulosin)
    • -relaxation of smooth muscle
    • -also lowers BP
    • 2. 5a-reductase inhibitor (finasteride)
    • -takes months to work
    • -also used for male pattern baldness
    • -AE: gynecomastia, sexual dysfunction
  74. Prostate Adenocarcinoma
    • Epidemiology:
    • -common in men > 50 years
    • -most common cancer in men

    • Risk Factors:
    • -age
    • -race (African Americans > Caucasians > Asians)
    • -diet high in saturated fats

    • Pathophysiology:
    • -usually arises in the peripheral, posterior region of the prostate (rarely urinary sx early on)

    • Presentation:
    • -most often clinically silent

    • Screening:
    • -increased total PSA (>10)
    • -decreased free PSA
    • -needle core bx (invasive glands, prominent nucleoli)

    • Gleason Grading System
    • -based on architecture alone
    • -assess multiple regions (pick two most common presentations and add scores: 2-10)

    • Metastases:
    • -spread to lumbar spine and pelvis is common (osteoblastic mets → lower back pain and ↑Alk Phos)

    • Treatment:
    • -prostatectomy for localized disease
    • -GnRH analogs (leuprolide)
    • -Androgen Receptor Antagonist (Flutamide)
  75. Cryptorchidism
    Undescended testicle

    • Epidemiology:
    • -most common congenital male reproductive abnormality
    • -1% of male infants
    • -increased risk with prematurity

    • Pathophysiology:
    • -normally testicles develop in the abdomen and then descend into the scrotum

    • Hormones:
    • -can have normal testosterone (Leydig cells unaffected by temperature)
    • -↓ inhibin
    • -↑ FSH
    • -↑ LH
    • -↓ testosterone in bilateral (normal in unilateral)

    • Complications:
    • -testicular atrophy
    • -infertility (increased temperature)
    • -increased risk for seminoma (GCT)

    • Treatment:
    • -usually resolve spontaneously
    • -orchioplexy before 2 years if not
  76. Orchitis
    Inflammation of the testicle

    • Young Adults:
    • -Chlamydia trachomatis (D-K)
    • -Neisseria gonorrhea
    • -increased risk of sterility
    • -libido not affected (Leydig cells spared)

    • Older Adults:
    • -E. Coli
    • -Pseudomonas
    • -UTI pathogens spread into reproductive tract

    • Teenage Males:
    • -Mumps virus
    • -increased risk for infertility
    • -testicular inflammation usually absent in children < 10

    • Autoimmune orchitis:
    • -granulomas of seminiferous tubules
    • -distinguish from TB
  77. Testicular Torsion
    • Pathophysiology:
    • -twisting of the spermatic cord
    • -thin walled veins become obstructed by arterial flow remains intact (blood can get in but can't get out)
    • -usually due to congenital failure of testes to attach to inner lining of scrotum (by processus vaginalis)

    • Presentation:
    • -sudden testicular pain
    • -absent cremasteric reflex
  78. Vericocele
    • Epidemiology:
    • -most common cause of scrotal enlargement in males

    • Pathophysiology:
    • -dilated veins in pampiniform plexus
    • -result of increased venous pressure (impaired drainage)
    • -usually left testicle (increased resistance of flow from left gonadal vein drainage into left renal vein)

    • Presentation:
    • -scrotal enlargement
    • -bag of worms appearance

    • Complications:
    • -infertility (increased temperature)
    • -associated with L sided renal cell carcinoma

    • Treatment:
    • -varicocelectomy
    • -embolization
  79. Hydrocele
    Fluid collection in the tunica vaginalis

    • Pathophysiology:
    • -associated with incomplete closure of the processus vaginalis leading to communication with peritoneal cavity (infants)
    • -blockage of lymphatics (adults)

    • Presentation:
    • -scrotal swelling
    • -can be transilluminated (vs tumor)
  80. Spermatocele
    Dilated epididymal duct

    Testicular mass that can be transilluminated (vs. tumor)
  81. Testicular Germ Cell Tumors
    • ~95% of all testicular tumors
    • -most often malignant
    • -can present as mixed germ cell tumors
    • -usually occur btwn 15-40 years of age

    • Risk Factors:
    • -crytorchidism
    • -Klinefelter syndrome

    • Presentation:
    • -testicular mass that does not illuminated

    • Types:
    • 1. Seminoma (55%, radioresponsive, metastasize late, excellent prognosis)

    • Non-seminoma (45%, variable response to tx, mets early)
    • 2. Yolk Sac (Endodermal sinus)
    • 3. Choriocarcinoma
    • 4. Teratoma
    • 5. Embryonal Carcinoma
  82. Testicular Seminoma
    • Epidemiology:
    • -most common testicular tumor
    • -mostly males age 15-35
    • -resembles ovarian dysgerminoma

    • Presentation:
    • -painless, homogenous testicular enlargement

    • Pathology:
    • -malignant
    • -large cells in lobules with watery cytoplasm and "fried" egg appearance
    • -no hemorrhage or necrosis

    • Tumor Markers:
    • -↑ placental alkaline phosphatase (PLAP)
    • -rare cases produce b-hCG
  83. Yolk Sac (Endodermal Sinus) Tumor
    • Epidemiology:
    • -most common testicular tumor in children

    • Pathology:
    • -yellow, mucinous
    • -Schiller-Duval bodies (resemble glomeruli)

    • Tumor Markers:
    • -↑AFP
  84. Choriocarcinoma
    • Pathology:
    • -malignant
    • -disordered syncytiotrophoblastic and cytotrophoblastic elements (absent villi)
    • -spreads early by blood (lungs)

    • Tumor Markers:
    • -↑ β-hCG
    • -subunit of hCG is similar to FSH, LH and TSH → gynecomastia and hyperthyroidism
  85. Teratoma
    • Pathophysiology:
    • -composed of mature fetal tissue derived from 2 to 3 embryonic layers
    • -MALIGNANT in males (as opposed to females)
    • -benign in children

    • Tumor Markers:
    • -↑ AFP/ ↑ β-hCG in 50%
  86. Embryonal Carcinoma
    • Pathophysiology:
    • -malignant
    • -painful
    • -aggressive with early hematogenous spread
    • -pure embryonal carcinoma is rare (usually mixed)

    • Pathology:
    • -often glandular/papillary morphology

    • Tumor Markers:
    • -Pure: ↑ hCG, normal AFP
    • -Mixed: ↑ AFP

    • Prognosis:
    • -worse than seminoma
    • -chemotherapy may result in differentiation into another type of GCT
  87. Testicular Non-Germ Cell Tumors
    • Sex Cord-Stromal Tumors
    • 1. Leydig cell tumor
    • 2. Steroli cell tumor

    Testicular Lymphoma
  88. Leydig Cell Tumor
    • Presentation:
    • -produce androgen
    • → gynecomastia in men
    • → precocious puberty in boys

    • Pathology:
    • -golden brown color
    • -Reinke crystals
  89. Sertoli Cell Tumor
    • Presentation:
    • -usually clinically silent

    • Pathology:
    • -composed of tubules
  90. Testicular Lymphoma
    • Epidemiology:
    • -most common cause of a testicular mass in males > 60 years old

    • Pathophysiology:
    • -not a primary cancer, arises from lymphoma metastasis to testes

    • Pathology:
    • -often bilateral
    • -diffuse large B cell type

    • Prognosis:
    • -aggressive
  91. Penile Squamous cell carcinoma
    • Epidemiology:
    • -more common in Asia, Africa, South America

    • Risk Factors:
    • -high risk HPV-lack of circumcision

    • Precursor Lesions
    • 1. Bowen Disease:
    • -in situ carcinoma on shaft or scrotum
    • -leukoplakia
    • 2. Erythroplasia of Queyrat
    • -in situ carcinoma on the glans
    • -erythroplakia
    • 3. Bowenoid papulosis
    • -multiple reddish papules
    • -seen in younger patients
    • -does not progress to invasive carcinoma
  92. Peyronie's Disease
    Bent penis due to acquired fibrous tissue formation
  93. Priapism
    Painful sustained erection not associated with sexual stimulation or desire

    • Associated with:
    • -trauma
    • -SCD
    • -medications (anticoagulants, PDE5 inhibitors, antidepressants, α-blockers, cocaine)

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