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Reproductive pathophysiology > Pathology > Flashcards

Pathology Flashcards

1
Q

Bartholin gland

A

present on each side of vaginal canal

produces mucus-like fluid that drains into lower vestibule

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2
Q

Bartholin cyst

A

cystic dilation of Bartholin gland

etiology: inflammation and obstruction of gland usually due to UTI or STD –> usually occurs in women of reproductive age
presentation: unilateral painful cystic lesion at lower vestibule adjacent to vaginal canal

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3
Q

Vulvar condyloma

A

warty neoplasm, often large

Etiology: sexually transmitted; usually due to HPV 6 or 11 (low risk) - condyloma acuminatum or less commonly secondary syphilis (condyloma latum)

Histology: HPV-associated condylomas have koilocytic nuclei (look like raisins)

*Condylomas rarely progress to cancer

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4
Q

Lichen sclerosis

A

Etiology: Possibly autoimmune, usually seen in postmenopausal women; Thinning of epidermis and fibrosis (sclerosis) of dermis

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

*benign, but can slightly increase risk for squam. cell carcinoma

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5
Q

Lichen simplex chronicus

A

Hyperplasia of vulvar squamous epithelium

Etiology: chronic irritation/scratching

Presentation: leukoplakia w/ thick vulvar skin

*Benign, NO increase risk of squam. cell carcinoma

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6
Q

Vulvar carcinoma

A

Rare, carcinoma from squamous epithelium of vulva

Presentation: leukoplakia -> need biopsy to distinguish

Etiology:
- HPV related (HPV 16,18,31,33 - high risk), usually in women of reproductive age

  • non-HPV related (long-standing lichen sclerosis), usually elderly women >70yo
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7
Q

Extramammary Paget Disease

A

Malignant epithelial cells in epidermis of vulva; carcinoma in situ usually with no underlying carcinoma (contrast with Paget of nipple which almost always associated with underlying breast cancer)

Presentation: erythematous, pruritic, ulcerated vulvar skin

Distinguish from melanoma:
Paget cells: PAS+, keratin+, S100-
Melanoma: PAS-, keratin-, S100+

[keratin=intermediate filament in epithelial cells –> carcinoma]

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8
Q

What kind of cells line the vaginal canal?

A

non-keratinizing squamous epithelium

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9
Q

What are the epithelium of the upper 2/3 and lower 1/3 of the vaginal canal derived from?

A

upper 2/3: from Mullerian duct (columnar epithelium that is later replaced by squamous epithelium from lower 1/3)

lower 1/3: from urogenital sinus (squamous epithelium)

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10
Q

Vaginal adenosis

A

focal persistence of columnar epithelium in upper vagina

increased incidence when exposed to DES (diethylstilbestrol) in utero

*Can (rarely) lead to clear cell adenocarcinoma

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11
Q

Clear cell adenocarcinoma of vagina

A

malignant proliferation of glands w clear cytosol

-Rare complication of DES-associated vaginal adenosis

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12
Q

What complications can arise from DES exposure?

A

Mother exposed to DES: slight increased risk of breast cancer

Daughter exposed to DES: 1. vaginal adenosis -> clear cell adenocarcinoma, 2. abnormalities of smooth muscle -> abnormal shape of uterus -> increased ectopic pregnancies and fertility problems

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13
Q

Embryonal Rhabdomyosarcoma

A

Rare. Malignant mesenchymal proliferation of immature skeletal muscle

Presentation: bleeding and “grape-like” mass protruding from vagina or penis of child

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14
Q

Vaginal carcinoma

A

Carcinoma of squamous epithelium lining vaginal mucosa

Etiology: high-risk HPV (16,18,31,33); precursor lesion is vaginal intraepithelial neoplasia (VAIN) which is dysplastic

Spreads to lymph nodes:
from lower 1/3 of vagina -> superficial inguinal nodes
from upper 2/3 of vagina -> external iliac nodes

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15
Q

What type of cells line the exocervix and the endocervix?

A

exocervix - nonkeratinizing squamous epithelium

endocervix - single layer of columnar cells

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16
Q

Where does HPV usually infect?

A

lower genital tract, especially cervical transformation zone

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17
Q

What causes the increased risk associated with high-risk HPV versus low-risk HPV?

A

High-risk HPV (16,18,31,33) produce E6 and E7 proteins

E6 destroys p53 –> less regulation of cell cycle
E7 destroys Rb –> E2F can be released and progress cells from G0 to G1

*loss of tumor suppressors -> increase risk for CIN

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18
Q

Cervical intraepithelial neoplasia (CIN)

A

Characteristics: koilocytic change (raisin nuclei), disordered maturation, nuclear atypia, increased mitotic activity

Grades based on epithelial involvement by immature dysplastic cells

CIN I: WILL PROGRESS to cervical carcinoma

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19
Q

Cervical carcinoma

A

invasive carcinoma (goes through basement membrane) arising from cervical epithelium

  • squamous cell (80%) and adenocarcinoma subtypes
  • most common in women 40-50yo (HPV takes 20-30years to develop into carcinoma)

Presentation: vaginal bleeding, especially postcoital, or cervical discharge
Advanced tumors- invade into bladder blocking ureters -> hydronephrosis w/ post-renal failure (most common cause of death)

Risk factors: HPV**, smoking, immunodeficiency

*AIDS-defining illness

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20
Q

What are the characteristics of high-grade dysplastic cells on Pap smear?

A

hyperchromatic (dark) nuclei, high nuclear to cytosol ratio

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21
Q

What are the limitations of Pap smear?

A

inadequate sampling -> false negative

more difficult to detect adenocarcinoma (incidence of adenocarcinoma has not decreased significantly)

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22
Q

What HPV types are covered in immunization?

A

6, 11 (low risk), 16, 18 (high risk)

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23
Q

What are the characteristics of the endometrium and myometrium?

A

endometrium: mucosal lining of uterine cavity; hormonally sensitive ->
1. growth driven by estrogen (prolif. phase)
2. preparation for implantation driven by progesterone (secretory phase)
3. shedding with loss of progesterone (menstruation)

myometrium: smooth muscle underlying endometrium

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24
Q

Asherman syndrome

A

Secondary amenorrhea from loss of basalis (stem cells) layer that is result of overaggressive dilation and curettage (D&C)

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25
Q

Acute endometritis

A

Bacterial infection of endometrium

  • usually due to retained products of conception (after delivery or miscarriage)
  • Presents with fever, abnormal uterine bleeding and pelvic pain
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26
Q

Chronic endometritis

A

Chronic inflammation of endometrium characterized by lymphocytes and plasma cells*

Caused by retained products of conception, chronic PID (Chlamydia ex), IUD, TB (granulomas)

Presentation: abnormal bleeding, pain, infertility

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27
Q

How is endometritis treated?

A

gentamicin + clindamycin w or w/out ampicillin

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28
Q

enodmetrial polyp

A

well circumscribed hyperplastic protrusion of endometrium

Presents as abnormal bleeding

Can arise as side effect of tamoxifen (weak pro-estrogenic effects on endometrium)

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29
Q

Endometriosis

A

Endometrial glands and stroma outside of uterine endometrial lining, most commonly affecting ovaries

Etiology: 3 theories

  1. retrograde menstruation w ectopic implantation
  2. metaplastic transformation of multipotent cells
  3. transportation of endometrial tissue via lymphatics

Presentation: dysmenorrhea (menstrual pain)and pelvic pain , dyschezia (pain w/ defecation) - pouch of Douglas, dyspareunia (painful intercourse), infertility

In ovary appears as ‘chocolate cyst’ endometrioma
In soft tissue appears as ‘gun powder’ nodules

Treatment: NSAIDs, OCPs, progestins, GnRH agonists, danazol, laparoscopic removal

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30
Q

Adenomyosis

A

Endometriosis in myometrium caused by hyperplasia of basal layer of endometrium

Presents with dysmenorrhea, menorrhagia, enlarged soft globular uterus

Treatment: GnRH agonists, hysterectomy

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31
Q

Endometrial hyperplasia

A

Hyperplasia of endometrial glands relative to stroma

Etiology: unopposed estrogen (obesity, PCOS, estrogen replacement)

Presentation: usually postmenopausal uterine bleeding

Histology: cellular atypia is most important predictor for progression to carcinoma

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32
Q

Endometrial carcinoma

A

Most common invasive carcinoma of female GU tract

Presentation: postmenopausal bleeding

2 etiologies:

  1. Endometrial hyperplasia (75%)
    - risk factors related to increased estrogen exposure
    - age ~60
    - histology: endometrioid
  2. Sporadic (25%)
    - no evident precursor lesion, p53 mutation common
    - aggressive behavior of tumor
    - histology: serous papillary structures w psammoma bodies
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33
Q

Leiomyoma (fibroids)

A

most common tumor in females, higher incidence in African Americans

benign neoplastic proliferation of smooth muscle of myometrium, related to estrogen exposure

Presents: PREmenopausal women
Multiple, well-defined, white, whorled masses -> may distort uterus
*Usually asymptomatic, if presents- symptoms of abnormal uterine bleeding, infertility, pelvic mass

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34
Q

Leiomyosarcoma

A

Malignant proliferation of myometrium smooth muscle

  • Arises de-novo DO NOT arise from leiomyoma (fibroids)
  • POSTmenopausal women
  • Gross exam: single lesion with necrosis and hemorrhage
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35
Q

Common causes of anovulation

A 
pregnancy
PCOS
obesity
HPO axis abnormalities
premature ovarian failure 
hyperprolactinemia
thyroid disorders
eating disorders
competitive sports
Cushing syndrome
adrenal insufficiency
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36
Q

Follicular cyst

A

distention of unruptured graafian follicle, associated with hyperestrogenism, endometrial hyperplasia. most common ovarian mass in young women. Small numbers are common and no clinical significance

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37
Q

Polycystic Ovarian Syndrome (PCOS) aka Stein-Leventhal syndrome

A

Multiple ovarian follicular cysts from hormone imbalance

Characterized by increased LH and low FSH (LH:FSH >2)

Hyperinsulinemia (increase free testosterone via decreased sex hormone binding globulin) and/or insulin resistance (stimulates theca cells to produce more androgens) may alter hormonal feed back response ->

Increased LH:FSH -> increased androgens from theca -> hirsutism, estrone in adipose negative feedback decreases FSH -> cystic degeneration of follicles + anovulation

Associated with obesity, increases risk of endometrial cancer secondary to unopposed estrogen from repeated anovulatory cycles

Treatment: weight reduction, OCPs, clomiphene citrate (SERM), ketoconazole (anti-androgen), spironolactone (anti-androgen)

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38
Q

Surface epithelial ovarian tumors- what are they derived from and what are the most common subtypes?

A

Most common type of ovarian tumor

Derived from coelomic epithelium that lines ovary - embryologically produces lining of fallopian tube (serous cells), endometrium and endocervix (mucinous cells)

Common subtypes:
Cystadenomas
Cystadenocarcinomas
Endometriod tumors
Brenner tumors

They often present late with vague symptoms: pain and fullness or signs of compression - urinary frequency

Poor prognosis of surface epithelial carcinoma and tend to spread locally, especially peritoneum

(CA-125 marker to monitor treatment response)

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39
Q

Cystadenomas

A

Benign tumors

composed of single cyst with simple flat lining - contain serous (most common) or mucinous epithelium and fluid

-commonly in PREmenopausal women (30-40yo

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40
Q

Cystadenocarcinomas

A

Malignant tumors

  • Serous cystadenocarcinoma - most common ovarian neoplasm, freq bilateral, psammoma bodies
  • Mucinous - pseudomyxoma peritonei-intraperitoneal accumulation of mucinous material from ovarian or appendical tumor
  • composed of multiple complex cysts with thick shaggy lining
  • commonly in POSTmenopausal women (60-70yo)
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41
Q

BRCA1 mutation carries increased risk for what kind of carcinomas in the female GU tract?

A

serous carcinoma of ovary and fallopian tube

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42
Q

Endometrioid tumors

A

Usually malignant

composed of endometrial-like glands, may arise from endometriosis

15% associated with an independent endometrial carcinoma (endometriod type)

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43
Q

Brenner tumors

A

Usually benign, composed of urothelium (bladder-like epithelium)

Solid tumor is pale yellow and appears encapsulated. ‘coffee bean’ nuclei on H&E

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44
Q

Germ cell tumors

A

2nd most common type of ovarian tumor

-usually women of reproductive age

Subtypes:

  1. Fetal tissue- cystic teratoma and embryonal carcinoma
  2. Oocytes (germ cell) - dysgerminoma
  3. Yolk sac - endodermal sinus tumor
  4. Placental tissue - choriocarcinoma
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45
Q

Cystic teratoma (dermoid cyst)

A

Most common ovarian tumor in women 20-30yo

Cystic mass with elements from all 3 germ layers (bilateral 10% of time)

Can present with pain secondary to ovarian enlargement

Benign, but presence of immature tissue (neural) or somatic malignancy (tumor w/in teratoma, usually squamous cell carcinoma of skin) –> malignant potential

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46
Q

Struma ovarii

A

Cystic teratoma comprised mostly of thyroid tissue –> hyperthyroidism presentation

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47
Q

Dysgerminoma

A

Most common in adolescents

Malignant tumor composed of large cells with clear cytosol and central nuclei; Seminoma is counterpart in males

Good prognosis, responds to RT

Serum LDH may be elevated

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48
Q

Endodermal sinus tumor (yolk sac tumor)

A

Aggressive tumor in ovaries or testes and sacrococcygeal area in kids

Most common germ cell tumor in children

Yellow, friable (hemorrhagic) solid mass

Histo: Schiller-Duval bodies (resemble glomeruli)

AFP= tumor marker

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49
Q

Choriocarcinoma

A

Rare, can develop during or after pregnancy in mom or baby/

Malignant tumor composed of cytotrophoblasts and syncytiotrophoblasts; mimics placental tissue but villi absent

Small, hemorrhagic tumor with early hematogenous spread -> to lung

Presentation: shortness of breat, hemoptysis and *High beta-hCG is characteristic –> may lead to thecal cysts in ovaries

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50
Q

Granulosa-theca cell tumor

A

Malignant sex cord-stromal tumor, neoplastic proliferation of granulosa and theca cells (usually don’t metastasize)

  • Presents with signs of excess estrogen
  • Predominantly women in 50s - endometrial hyperplasia with postmenopausal bleeding
  • prior to puberty can cause precocious puberty
  • reproductive age- menorrhagia or metrorrhagia

Histology: Call-Exner bodies (granulosa cells arranged around collections of eosinophilic fluid, resembles primordial follicles)

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51
Q

Sertoli-Leydig cell tumor

A

Sex cord-stromal tumor of ovary

  • composed of sertoli cells and Leydig cells with characteristic Reinke crystals

May produce androgen -> virilization

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52
Q

Fibroma

A

Benign ovarian tumor of fibroblasts

Bundles of spindle-shaped fibroblasts

Associated with Meigs syndrome: triad of ovarian fibroma, ascites and hydrothorax.

presentation: “pulling” sensation in groin

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53
Q

Krukenberg tumor

A

Metastatic mucinous tumor involving both ovaries

Usually due to metastatic gastric carcinoma (diffuse type)

See mucin secreting signet ring cells

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54
Q

Ectopic pregnancy

A

Implantation of fertilized ovum at site other than uterine wall

Most commonly site is ampulla of fallopian tube

Presentation: pain w or w/out bleeding, hx of amenorrhea, lower-than expected rise in hCG, sudden lower abdominal pain

Confirm w US

Risk factors- scarring of fallopian tube:
Hx of infertility
Salpingitis (PID)
Ruptured appendix
Prior tubal surgery

Major complications: hematosalpinx (bleeding into fallopian tube) and rupture

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55
Q

Spontaneous abortion

A

Miscarriage before 20 weeks

Presentation: vaginal bleeding, cramping, passage of fetal tissues

Usually due to chromosomal anomalies, also hypercoagulable states (ex SLE antiphospholipid syndrome), infection, teratogens

56
Q

polyhydramnios

A

Too much amniotic fluid (>1.5-2L)

Associated with fetal malformations (inability to swallow amniotic fluid)

  • esophageal/duodenal atresia
  • anencephaly

Associated with maternal diabetes, fetal anemia, multi gestations

57
Q

oligohydramnios

A
58
Q

Vasa previa

A

Fetal vessels run over or near cervical os

May result in vessel rupture, exsanguination, fetal death

Presents: triad of membrane rupture, painless vag bleeding, fetal bradycardia ( fetal vessels travel unprotected by Wharton jelly)

59
Q

Placenta previa

A

Attachment of placenta to lower uterine segment over or

60
Q

Placental abruption

A

Prematureseparation of placenta from uterine wall

Presentation: abrupt painful bleeding in 3rd trimester; possible DIC, maternal shock, fetal distress. Life threatening to mom and fetus

Risk factors:
Trauma, HTN, smoking, preeclampsia, cocaine abuse

61
Q

Placenta accreta/ increta/ precreta

A

Defective decidual layer -> abnormal attachment of placenta

Presentation: usually detected early on US
No separation of placenta after delivery -> postpartum bleeding -> can cause Sheehan syndrome

Risk factors: prior C-section, inflammation, placenta previa

3 types based on depth:

  1. placenta accreta - attaches to myometrium w/out penetrating it (most common)
  2. placenta increta - placenta penetrates into myometrium
  3. placenta precreta - placenta penetrates through myometrium and into serosa, can cause attachment to rectum or bladder
62
Q

Preeclampsia

A

Pregnancy induced HTN (may cause HA and vision changes), proteinuria and edema

  • usually in 3rd trimester (if less than 20 weeks suggest molar pregnancy)
  • abnormalities of spiral arteries (maternal-fetal vascular interface) in placenta; resolves w delivery

Risk factors:
pre-existing HTN, diabetes, chronic renal disease, autoimmune disorders

Complications:
placental abruption, coagulopathy, renal failure, uteroplacental insufficiency, eclampsia

Treatment: antihypertensives, IV magnesium sulfate (prevent seizure), definitive treatment is delivery of baby

63
Q

Retained placental tissue

A

may cause postpartum hemorrhage, increases risk of infection

64
Q

Eclampsia

A

Preeclampsia + seizures

Maternal death due to stroke, intracranial hemorrhage or ARDS

Treatment: IV magnesium sulfate, antihypertensives, immediate delivery

65
Q

HELLP syndrome

A

Hemolysis, Elevated Liver enzymes, Low Platelets

Severe preeclampsia manifestation with thrombotic microangiopaty involving liver –>

Blood smear shows schistocytes

Can lead to hepatic hematomas -> rupture -> severe hypotension

Treatment: immediate delivery

66
Q

Sudden infant death syndrome (SIDS)

A

death of healthy infant (1mo-1yr) w/out obvious cause

usually during sleep

Risk factors: sleeping on stomach, second hand smoke, prematurity

67
Q

Gestational HTN (pregnancy-induced HTN)

A

BP>140/90mmHg after 20th week gestation when no pre-existing HTN

No proteinuria or end-organ damage

Treatment: antihypertensives (alpha-methyldopa, labetalol, hydralazine, nifedipine); deliver at 37-39 wks

68
Q

Hydatidiform mole

A

abnormal conception characterized by swollen and edematous villi with proliferation of trophoblasts

Associated with theca-lutein cysts, hyperemesis gravidarum, hyperhtyroidism

Treatment: dilation and curettage and methotrexate. Monitor beta-hCG

69
Q

Partial mole

A

Genetics: 69XXX, 69XXY, 69XYY

Components: 2 sperm +1egg

fetal parts: Yes

hCG: elevated

Uterine size: ~normal

Convert to choriocarcinoma: rare

Risk of complications: low risk of malignancy

Symptoms: vaginal bleeding, abdominal pain

Imaging: fetal parts

villous edema: some villi hydropic, some normal

Trophoblastic proliferation: focal proliferation around villi

70
Q

Complete mole

A

Genetics: 46XX, 46XY

Components: enucleated egg+ single sperm that duplicates or 2 sperm

fetal parts: no

hCG: very high!

Uterine size: much larger for date of gestation

Convert to choriocarcinoma: 2%

Risk of complications: 15-20% malignant trophoblastic disease

Symptoms: 1st trimester bleeding, enlarged uterus, hyperemesis, pre-eclampsia, hyperthyroidism

Imaging: “honeycombed” uterus or “clusters of grapes”/ “snowstorm” on US

villous edema: almost all villi are hydropic

Trophoblastic proliferation: diffuse, circumferential proliferation around villi

71
Q

Hyposadias

A

Opening of urethra on inferior surface (ventral side) due to failure of urethral folds to fuse

72
Q

Epispadias

A

(very rare) opening on uretra on superior (dorsal) surface of penis due to abnormal positioning of the genital tubercle

Associated with exstrophy of bladder (complete exposure of bladder wall)

73
Q

Lymphogranuloma venereum

A

necrotizing inflammation of inguinal lymphatics and lymph nodes

Etiology: STDs caused by Chlamydia trachomatis (L1-L3 serotypes)

Eventually heals w fibrosis, perianal involvement may cause rectal stricture

74
Q

Squamous cell carcinoma of the penis

A

risk factors: high risk HPV (16,18,31,33), lack of circumcision and improperly maintained foreskin

-More common in Asia, Africa and S. America

Precursor in situ lesions:
1. Bowen disease - in situ carcinoma of penile shaft, presents as leukoplakia

  1. Erythroplasia of Queyrat - in situ carcinoma on glans presenting with erythroplakia
  2. Bowenoid papulosis - in situ carcinoma presenting with reddish papules, seen in younger patients (40s), does NOT progress to carcinoma
75
Q

Cryptorchidism

A

Failure of testicle to descend into scrotal sac

-impaired spermatogenesis (sperm develop best at

76
Q

Orchitis

A

Inflammation of testicle

Causes:
1. young adults- C. trachomatis (D-K serotypes) or N. gonorrhoeae. Increased risk of sterility, but libido spared since Leydig unaffected

  1. older adults - E. coli and Pseudomonas. UTI spread into repro tract
  2. teenage males -> Mumps virus, increased risk for infertility (mumps also causes parotitis, meningitis, pancreatitis)
  3. Autoimmune - granumolas involving seminiferous tubules
77
Q

Peyronie disease

A

Abnormal curvature of penis due to fibrous plaque within tunica albuginea

Associated w erectile dysfunction

78
Q

Priapism

A

painful erection >4 hours

Associated with trauma, sickle cell disease (sickled RBCs get stuck), meds (sildenafil, trazodone)

Treat with corporal aspiration, intracavernosal phenylephrine or surgical decompression to prevent ischemia

79
Q

varicocele

A

dilation of spermatic vein due to impaired drainage gives ‘bag of worms’ appearance

  • usually L sided, associated with L sided RCC since often invades L renal vein
  • seen in many infertile males (warm blood piles up)
80
Q

testicular torsion

A

twisting of spermatic cord -> veins become obstructed -> congestion and hemorrhagic infarction

  • usually congenital failure of testes to attach inner lining of scrotum via processus vaginalis
  • presents as sudden testicular pain and absent cremasteric reflex
81
Q

congenital hydrocele

A

common cause of scrotal swelling in infants due to incomplete obliteration of proccessus vaginalis

-transilluminating swelling

82
Q

acquired hydrocele

A

benign scrotal fluid collection usually secondary to infection, trauma, tumor
-transilluminating

-if bloody: hematocele

83
Q

spermatocele

A

cyst due to dilated epididymal duct or rete testis

paratesticular fluctuant nodule

84
Q

extragonadal germ cell tumors

A

arise in midline locations

Adults- retroperitoneum, mediastinum, pineal and supraseller regions

Infants and young kids- sacrococcygeal teratomas most common

85
Q

Testicular germ cell tumors

A

~95% of testicular tumors

  • Seminomas (55% of cases, good prognosis)
  • Non-seminomas (45% of cases, variable response and metastasize early): embryonal carcinoma, yolk sac (endodermal sinus) tumor, choriocarcinoma, teratoma
  • usually young men (15-40yr)
  • risk factors: cryptorchidism, Klinefelter syndrome
  • can present as mixed germ cell tumor
  • Ddx for painless testicular mass that doesn’t transilluminate is cancer
86
Q

Seminoma

A

Malignant, painless, homogenous testicular enlargement

  • most common testicular tumor, most common in 30s, never in infancy
  • large cells in lobules with clear cytoplasm and ‘fried egg’ appearance (resembles dysgerminoma in ovary)
  • increased placental ALP
  • responds to RT, late metastasis, very good prognosis
87
Q

Embryonal carcinoma

A

malignant, hemorrhagic mass with necrosis; painful; worse prognosis than seminoma- aggressive with early spread

  • glandular/papillary morphology, usually mixed with other tumor types
  • chemo can cause differentiation into other germ cell tumors
  • may have increased hCG and normal AFP levels when pure, increased AFP if mixed
88
Q

Yolk sac (endodermal sinus) tumors

A

malignant tumor that resembles yolk sac elements- yellow, mucinous

-most common testicular tumor in children

89
Q

Choriocarcinoma

A

malignant tumor of syncytiotrophoblasts (produces hCG) and cytotrophoblasts (placenta like with absent villI)

  • high hCG
  • spreads early via blood –> lungs and brain, may present with ‘hemorrhagic stroke’
  • may produce gynecomastia, symptoms of hyperthyroidism (hCG structurally similar to LH, FSH, TSH)
90
Q

Teratomas

A

Unlike in females, mature teratoma in adult males may be malignant! Benign in children

Increased hCG and/or AFP in 50% cases

91
Q

Sex cord-stromal tumors

A

~5% of all testicular tumors, mostly benign

92
Q

Leydig cell tumor

A

produces androgen -> precocious puberty in children or gynecomastia in adults

-Characteristic Reinke crystals (eosinophilic cytoplasmic inclusions)

93
Q

Sertoli cell tumor

A

Androblastoma from sex cord stroma, comprised of tubules and clinically silent

94
Q

Testicular lymphoma

A

most common in older men. bilateral masses

  • not a primary cancer-> arises from metastatic lymphoma to testes, usually diffuse large B cell
  • aggressive
95
Q

Acute prostatitis

A

-usually bacterial: 1. young adults STDs: chlamydia and gonorrhoeae, 2. old (UTIs): E. coli and Pseudomonas

  • presents with dysuria, fever and chills
  • prostate tender on DRE
  • prostatic secretions show WBCs and bacteria on culture
96
Q

Chronic prostatitis

A
  • chronic inflammation, usually abacterial
  • dysuria with pelvic or low back pain
  • secretios show WBCs with negative culture
97
Q

Benign prostatic hyperplasia (BPH)

A

hyperplasia of prostatic stroma and glands -> smooth, elastic, firm nodular enlargement (since no hypertrophy, just hyperplasia) of periurethral lobes (lateral and middle)

  • common in men >50yr
  • NOT precursor to cancer
  • related to DHT -> acts on androgen receptors of stromal and epithelial cells -> hyperplastic nodules

Clinical features:

  • problems starting and stopping urine stream
  • dysuria
  • increased frequency of urination
  • free PSA elevated

Complications: impaired bladder emptying increases risk for UTIs, hydronephrosis, hypertrophy of bladder wall

Treatment:
-alpha1 antagonists: terazosin (if also have HTN), tamsulosin (in normotensive patients) -> relax smooth muscle

  • PDE-5 inhibitors
  • 5a-reductase inhibitors (finasteride) -> blocks conversion to DHT but takes months to produce results
98
Q

Prostate adenocarcinoma

A

malignant proliferation of prostatic glands, usually arises in posterior lobe (peripheral zone)

  • common in men >50
  • diagnosed by increased total PSA, decreased fraction of free PSA (tumor produces bound PSA) and needle core biopsy
  • Prostatic acid phosphatase (PAP) also good tumor marker
  • Osteoblastic mets in bone may develop late -> presents with low back pain and increased serum ALP and PSA

Treatment: prostatectomy for localized disease; advanced disease treated with hormone suppression: continuous GnRH analogs (leuprolide), Flutamide competitive inhibitor at androgen receptor

99
Q

What are the 2 layers of epithelium that line the lobules and ducts of the breast?

A

luminal cell layer- inner cell layer, responsible for milk production in lobules

myoepithelial cell layer- outer cell layer lining ducts and lobules, contractile fxn propels milk

100
Q

Acute mastitis

A

Bacterial infection of breast, usually Staph aureus

  • associated with fissures in nipple- breast feeding usually
  • presents as erythematous breast w purulent nipple discharge; may progress to abscess

Treatmet: drainage (continued feeding), antibiotics (dicloxacillin)

101
Q

Periductal mastitis

A

inflammation of subareolar ducts (highly specialized epithelia dependent on vitamin A)

  • common in smokers (vitamin A deficiency)
  • > squamous metaplasia of lactiferous ducts blocks duct and causes inflammation

-presents as subareolar mass w nipple retraction (myofibroblasts contract)

102
Q

Mammary duct ectasia

A

Inflammation with dilation (ectasia) of subareolar ducts

-rare, usually in multiparous postmenopausal women

**green-brown nipple discharge and periareolar mass

-plasma cells seen on biopsy

103
Q

Fat necrosis of breast

A

benign, usually painless lump, usually blunt trauma related (50% do not report trauma)

-abnormal calcifications on mammogram

Biopsy shows necrotic fat and giant cells

104
Q

Proliferative breast disease

A

Most common cause of ‘breast lumps’ from 25-menopause.

-presents w pre-menstrual breast pain and multiple lesions, usually bilateral in upper outer quadrant. Fluctuates size

NO increased risk for invasive carcinoma:

  • Fibrosis- hyperplasia of breast stroma
  • cystic change - fluid filled, blue dome. ductal dilation
  • apocrine metaplasia (abundant eosinophilic cytosol)
  1. 5-2x increased risk for invasive carcinoma:
    - Ductal hyperplasia
    - sclerosing adenosis: associated with calcification and often mistaken for cancer

Atypical hyperplasia -> 5x increased risk

105
Q

Intraductal papilloma

A

benign papillary growth into large duct, slight increase risk for cancer

  • fibrovascular projections lined by epithelial (luminal) AND myoepithelial cells (normal cell layers)
  • presents as bloody nipple discharge in PREmenopausal woman
  • must be distinguished from papillary CARCINOMA: no myoepithelial cells, usually POSTmenopausal woman
106
Q

Fibroadenoma

A

Most common benign neoplasm of breast in premenopausal women

  • small, mobile, firm mass with well-circumscribed edges
  • estrogen sensitive-> grows during pregnancy and pain during menstrual cycle
  • benign with NO increased risk of carcinoma
107
Q

Phyllodes tumor

A

Fibroadenoma-like tumor with overgrowth of fibrous component

Large, bulky mass with ‘leaf-like’ projections on biopsy

  • most common in postmenopausal women (50s)
  • can be malignant
108
Q

Breast cancer risk factors

A

increased estrogen exposure

  1. F»M
  2. Age
  3. Early menarche/late menopause
  4. obesity (adipose converts androgens to estrone)
  5. atypical hyperplasia
  6. 1st degree relative with breast cancer (BRCA1/2 mutations)
  7. African American ethnicity (increases risk of triple negative breast cancer)
109
Q

Ductal carcinoma in situ (DCIS)

A

Malignant proliferation of cells in ducts (fills lumen) with NO invasion of basement membrane

  • often detected as calcification on mammography, does NOT usually produce mass
  • Biopsy calcification to distinguish difference between malignant and benign
110
Q

Comedo type DCIS

A

subtype of DCIS

  • high-grade cells with necrosis and dystrophic calcification in center of ducts
111
Q

Paget disease of breast

A

DCIS or invasive breast cancer that extends up to ducts to involve skin of the nipple

Presentation: nipple ulceration and erythema
-almost always associated with underlying carcinoma

Paget cells= large cells in epidermis with clear halo

112
Q

Invasive ductal carcinoma

A

Most common type of invasive carcinoma in breast, most invasive breast cancer

  • presents as firm, fibrous ‘rock-hard’ mass with sharp margins, detected by physical exam (>2cm) or mammography (1cm or larger)
  • Advanced tumors may result in dimpling of skin or retraction of nipple
  • biopsy usually shows duct-like structures in desmoplastic stroma
113
Q

Tubular carcinoma

A

subtype of invasive ductal carcinoma

  • well-differentiated tubules that lack myoepithelial cells
  • good prognosis
114
Q

Mucinous carcinoma

A

subtype of invasive ductal carcinoma

  • carcinoma w abundant extracellular mucin ‘tumor cells floating in a mucus pool’
  • older women (70yrs)
  • relatively good prognosis
115
Q

Medullary carcinoma

A

subtype of invasive ductal carcinoma

  • large, high-grade cells growing in sheets with associated lymphocytes and plasma cells
  • grow as well-circumscribed mass that can mimic fibroadenoma on mammography
  • good prognosis
  • increased incidence in BRCA1
116
Q

Inflammatory carcinoma

A

subtype of invasive ductal carcinoma

  • carcinoma in dermal lymphatics
  • presents as inflamed- erythematous, peau d’ orange- swollen breast (tumor blocks lymphatics)
  • no discrete mass, can be mistaken for mastitis
  • very poor prognosis
117
Q

Lobular carcinoma in situ (LCIS)

A

malignant proliferation of cells in lobules without basement membrane proliferation

  • no mass or calcifications -> found incidentally on biopsy
  • lacks E-cadherin
  • multifocal and bilateral
  • treat with tamoxifen to reduce risk of carcinoma, close follow-up
118
Q

Invasive lobular carcinoma

A

invasive, orderly row of cells ‘Indian file’ due to lack of E-cadherin expression (no duct formation)

  • usually multifocal and bilateral
  • may show signet-ring morphology
119
Q

Prognostic and predictive factors of breast cancer

A

Metastasis is most important factor, but since most present before metastasis –> axillary lymph node spread is most USEFUL factor

Predictive factors to treatment response:
Estrogen receptor (ER)
Progesterone receptor (PR)
HER2/neu gene amplification

ER and PR (+) –> antiestrogenic agents (tamoxifen)

HER2/neu (+)–> trastuzumab (Herceptin)

120
Q

BRCA1 and BRCA2 mutations

A

BRCA1 mutation associated with breast and ovarian (serous, also in fallopian tubes) carcinoma

BRCA2 also associated with breast carcinoma in males

121
Q

Male breast cancer

A

very rare

  • subareolar mass in older males, may produce discharge
  • most common is invasive ductal carcinoma

Associated with BRCA2 and Klinefelter syndrome

122
Q

Klinefelter syndrome

A

47, XXY [male]

Testicular atrophy, eunuchoid body shape, tall, long extremities, gynecomastia, female hair distribution, mild intellectual disability

  • usually diagnosed in puberty, common cause of hypogonadism in infertility work up (azoospermia)

Primary testicular failure:

hyalinization and fibrosis of seminiferous tubules -> decreased inhibin -> high FSH

Leydig disfunction -> decreased testosterone -> increased LH -> increased estrogen

123
Q

Turner syndrome

A

45, XO [female] resulting from mitotic or meiotic error; can be complete monosomy (45 XO) or mosaicism (45XO/46XX)

  • short stature (untreated)
  • ovarian dysgenesis (streak ovary)
  • shield chest
  • bicuspid aortic valve
  • preductal coarctation (femoral high LH, FSH
  • cystic hygromas (lymphatic malformations) usually on neck- painless doughy mass that transluminates
124
Q

Double Y males

A

XYY

Phenotypically normal, very tall

Random nondisjunction event (paternal meiosis II)

-normal fertility, associated with severe acne, learning disability, autism spectrum disorders

125
Q

True hermaphroditism

A

46 XX or 47 XXY

Also called ovotesticular disorder of sex development

-Both ovarian and testicular tissue present; ambiguous genitalia

126
Q

What are the relative testosterone and LH levels with defective androgen receptor?

A

Testosterone: high
LH: high

127
Q

What are the relative testosterone and LH levels with testosterone secreting tumor or exogenous steroids?

A

Testosterone: high
LH: low

128
Q

What are the relative testosterone and LH levels with primary hypogonadism?

A

Testosterone: low
LH: high

129
Q

What are the relative testosterone and LH levels with hypogonadotropic hypogonadism?

A

Testosterone: low
LH: low

130
Q

Female pseudo-hermaphrodite (XX)

A

ovaries present but external genitalia are virilized or ambiguous

-excessive/inappropriate exposure to androgenic steroids during early gestation (congenital adrenal hyperplasia, exogenous androgens during pregnancy)

131
Q

Male pseudo-hermaphrodite (XY)

A

testes present but external genitalia are female or ambiguous

most commonly caused by androgen insensitivity syndrome (testicular feminization)

132
Q

Aromatase deficiency

A

Inability to synthesize estrogen from androgens

  • masculinization of female infants (ambiguous genitalia)
  • increased testosterone and androstenedione
  • can present with maternal virilization during pregnancy since androgens cross the placenta
133
Q

Androgen insensitivity syndrome (46XY)

A

Defect in androgen receptor -> normal appearing female; female external genitalia with scant sexual hair, rudimentary vagina

  • uterus and fallopian absent
  • patients develop testes (found in labia majora; surgically removed to prevent malignancy)
  • increased testosterone, estrogen and LH
134
Q

5alpha reductase deficiency

A

AR, sex limited to genetic males 46XY

Inability to convert testosterone to DHT

-normal internal genitalia, ambiguous external genitalia until puberty when increased testosterone causes increased growth of external genitalia

  • Testosterone/estrogen levels normal
  • LH normal or elevated
135
Q

Kallmann syndrome

A

Failure to complete puberty

-hypogonadotropic hypogonadism -> defective migration of GnRH cells and formation of olfactory bulb

  • anosmia (no sense of smell)
  • decreased GnRH, FSH, LH, testosterone
  • infertility (low sperm in males, amenorrhea in females)

Reproductive pathophysiology (3 decks)

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