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REPRO DISEASES Disease Name Sexual Determination Dx Gonadal Agensis if no germ cell => no gonad bowing of the can

look femur and tibia phenotypically (long bones); female anomalies of ribs from Sox9 - on an autosome; if you have an XY female with bowing of the long bones - think Sox 9 mutation Clinical presentation Associated Signs/ Symptoms Genetics Labs / Imaging Gross LM Tx Notes

Campomelic Dysplasia

phenotypic female 46, XY; with small vagina, Gonads = Androgen no uterus, testes but Insensitivity (aka intraabdominal receptors are Testicular testes; scant pubic bad => can't Feminization) hair and large recognize the breasts T or DHT phenotypic female (or ambiguous 46,XY; genitalia) with gonads are small vagina, no testes but 5-alpha reductase uterus, can't convert deficiency ("penis undescended amenorrhea T to DHT at 13") testes; AT => can't PUBERTY: virilize "override" external androgen receptor genitalia and start to phenotypic female 46,XX but Mullerian with small vagina, Mullerian Agenesis (Mayer- no uterus, normal amenorrhea (b/c ducts just Rokitansky-Kuster- ovaries; normal no uterus) regress (it just Hauser Syndrome) pubic hair and happens) breasts

Normale MALE T range; LH = elevated; E = elevated

T & E = normal LH = normal or increased

looks same as androgen insensitivity but at puberty, you override the hormones and get a penis;

webbed neck, cubitus valgus, short 4th metacarpal, shield phenotypic female chest, wide with normal spaced nipple; vagina, normal other anomalies: uterus, streak renal anomalies, ovaries, scant hearing loss, Turner Syndrome pubic hair, small 45, X autoimmune dx breasts, primary (10% amenorrhea, hypothyroid), CV delayed puberty anomalies (33%) or primary like bicuspid amenorrhea aortic valve, coarctation of aorta, aortic aneurysms SRY deletion or Dax O/E 46 XY Females (b/c Dax-9 inhibits Sox9) SRY translocation to X chromosome

high FSH, high LH, low estradiol, normal androgens; ultrasound/MRI : prepubertal uterus (normal), no gonads seen

provide estrogen/progestin (BC pills) for breast dev, bone density, increase uterine size, stimulates endometrium; FERTILITY: egg donation, adoption

early oocyte death => streak ovaries; LH induces enzymes that convert cholesterol into androstendione and testosterone => SCANT PUBIC HAIR (from low T)

46 XX Males

Menstrual Cycle Disorders Kallman's Syndrome (extreme ex of hypothalamic amenorrhea)

Oligomenorrhea: menstrual interval greater than 35 days (i.e. infrequent menstrual cycles); Polymenorrhea: menstrual interval less than 21 days; Menorrhagia: normal interval, excessive flow (>80mL, >7 days); Metrorrhagia: irregular intervals, bleeding btwn menses; Menometrorrhagia: heavy & irregular bleeding congenital - x linked form anosmia/ (Xp22.3 = Kal1 => anosmin 1) hyposmia; absent and anosmin 1 is required for olfactory sulci in migration of GnRH and rhinencephalon olfactory neurons

no GnRH neurons in hypothalamus

phenotypic female with normal Hypergonadotropi vagina, normal c Hypogonadism uterus, streak (aka ovarian ovaries possible, failure - ex. scant pubic hair, Turner's small breasts, Syndrome) primary or secondary amenorrhea

summary: high gonadotropins (FSH, LH), low estrogen, often abnormal karyotype (ex. 45,X), ovarian failure (no more eggs, no more hormone production)

high FSH, high LH, low estradiol, normal androgens; ultrasound/MRI : prepubertal uterus (normal)

as T increases => increased body hair > facial hair > menstrual disturbances > clitorimegaly > muscle mass abnormal female and/or balding; Hyperandrogenic hair pattern (more see acanthosis Anovulation AKA male pattern), nigracans and PCOS (Polycystic usually skin tags from Ovarian overweight/obese hyperinsulinemic Syndrome) , normal uterus, state; KEY normal ovaries POINTS: anovulation, hyperandrogenis m, hyperinsulinemia, risk obesity, HTN, DM, endometrial Pediatric / Adolescent GYN Issues Neonatal Findings

androgens (DHEA, DHEAS, androstenedione , T) increased, LH/FSH ratio > 3:1; progesterone is low; basal body temp is monophasic/an ovulatory; ultrasound multiple peripheral cysts < 10mm ("string of pearls")

etiology: idiopathic, autoimmune, provide estrogen/progestin (BC gonadal pills) for breast dev, bone density, agenesis/dysgenesis, increase uterine size, stimulates genetic, "resistant endometrium; FERTILITY: egg ovaries", donation, adoption, 10% POI chemo/radiation, ovulation (sporadic, unpredictable infection (mumps), NOT genetic causes surgery, SCD, trauma, StAR defect provide hormonal factors estrogen/progestin affecting HPO axis: (BC pills) to cycle androgens converted endometrium to estrogens in fat (prevent (by aromatase); more hyperplasia), lower fat => more FSH and LH, conversion; prevent ovarian estrogens => ~ cysts, decrease increase in LH and androgens, and estrogens (low increase SHBG; levels) => decrease FERTILITY: in FSH; LH => ovulation induction increase in ovarian with clomiphene androgens - cycle citrate (estrogen just continues; antagonist --> insulin => increase increase FSH), in LH, decrease in gonadotropins SHBG => more (FSH), insulin free androgens (why sensitizers tx with metformin); (METFORMIN) i.e. too many GnRH

Normal Findings: breast buds, nipple discharge, white vaginal discharge (from mom's estrogen in utero) - resolve in 6-8 weeks; vaginal bleeding (from maternal estrogen withdrawal) - resolve in 10 days adjacent edges labia minora adhere (commonly posteriorly) no impact on puberty, growth, sex, fertility; due to low estrogen +/inflammation

Labial Agglutination

Congenital Adrenal Hyperplasia (CAH) Neonatal Vulvar Disorders

ambiguous genitalia at birth (ex. clitoral enlargement) Candidiasis: diaper rash (candida albicans); Molluscum Contagiosum: smooth papules with central cheesy plug, "umbilicated"; condyloma acuminata: genital warts (HPV, perinatal transmission)

need to determine the source (vaginal, vulvar, endometrial); etiology: inflammatory (most common): vulvovaginitis (atrophy, inflammation, pruritis); Premenarchal STD (condyloma acuminata), parasite (shigella); hormonal: precocious puberty, exogenous hormones, sex hormone tumors; trauma: exclude sexual Disorders: Vaginal abuse, physical activities (straddle injuries), foreign body (toilet paper); urologic: urethral prolapse ("angry red donut"), UTI, hematuria, neoplasms; Bleeding vulvar lesions: Lichen sclerosis (flat ivory colored papules, may coalesce into plaques; tumors: sarcoma botryoides, ovarian germ cell tumor etiology: most common is idiopathic; McCune Albright Syndrome: polyostotic fibrous dysplasia, caf au lait skin pigment lesions, activating mutations of G-protein coupled receptors; exogenous hormones; sex hormone tumors Etiology: 1) non-specific (70%) secondary to urinary/fecal hygiene (mixed bacterial / e. coli) 2) specific vulvovaginitis: enteric = shigella; respiratory = H. influenzae; skin = staph, strep; STD = sexual abuse (G & C); candida; pinworm = enterobius vermicularis (scotch tape test) risk factors: anatomic (no pubic hair, no labial fat pads, close to rectum); poor hygiene (wipe front to back, diapers); hormonal (thin atrophic vagina pH 6.5 7.5); others: obesity, DM, other vulvar dermatoses, immune status; most common prepubertal GYN complaint (50% outpt visits)

Precocious Puberty

secondary sex characteristics (<7 y/o W, <6 y/o AA)


discharge (50%), presents in dysuria, pruritis, pediatrics; pain, genital inflammation of irritation, vulvar and vaginal erythema, tissues excoriation, vaginal bleeding inability to conceive after 1 year of trying

Infertility / Pregnancy


primary: never been pregnant before; secondary: has been pregnant in the past

Testing Female for Ovulation: BBT, luteal progesterone (3 weeks after last period); test for sub-clinical endocrinopathies (hyper/hypo thyroid, hyperprolactin, hypergonadotropic; Test Female anatomy: hystersalpingogram (HSG), laparoscopy, hysteroscopy; Test Male via Semen Analysis (volume, count, motility, morphology) and for anti-sperm antibodies; Female-Male Evaluation: sexual intercourse (timing, frequency), postcoital test, female anti-sperm antibodies

Ovulation Induction: clomiphene citrate, gonadotropins, dopamine agonists, side effects of many steroids; IVF infertility tx = (harvest eggs after multiple gestations induction by gonadotropins and mix egg & sperm in dish then reimplant in uterus)


placenta previa: placenta implants too low in the uterine cavity (covers cervical os); placenta accreta: placenta invades uterine wall too deeply; ** placenta previa and placenta accreta tend to occur together! abruptio placentae: early separation of placenta from uterus => hemorrhage (etiology of abruptio = 1) trauma 2) some sort of pathophysiologic injury to spiral arteries e.g. infection => inflammation => rupture of spiral artery) CMV: immunocompromise d pts; hematogenous spread; Acute chorioamnionitis: ascending bacterial infection in placenta (group B strep, e coli) from bacteria that colonize vaginal/cervical tract Single Umbilical Artery; Velamentous Insertion (cord inserts into fetal membranes then travels w/in membranes to placenta => exposed vessels vulnerable to rupture); True Knot; Pseudoknot; Helical Coiling; Nuchal Cord placenta = thin; chronic infarct = tan/yellow appearance & acute = hemorrhagic i.e. red and congested; infarct has well defined borders ghost villi; chorionic villi that are no longer identifiable; coagulative necrosis or sometimes liquefactive necrosis (large cysts)

2 types of infection in placenta: 1) organisms cross over placental barrier Placental Infection (transplacental infection) or 2) infections arise by hematogenous spread (mostly viral like

Acute chorioamnionitis: preterm = serious problem (infection = most common cause of spontaneous preterm birth)

TORCH infections

CMV: see CMV inclusions in nucleus and cytoplasm; Acute Chorioamnionit is: PNMs present

Umbilical Cord Pathology

see single umbilical artery think fetal CV abnormalities

Placental Infarct

chronic placental malperfusion => placentas that are small for gestational age (IUGR)

Benign Breast Pathology

Disorder of Development: Persistent Milk Line

heterotopic breast tissue; supernumerary nipples or breasts

bilaterally from the mid-axillae through normal breasts then inferior to medial groins; embryological milk line atrophies except for short segment at pectoral region to make breasts needs to be considered when considering cancer uncommon; need to include "inflammatory breast cancer" (peau d'orange) in the differential dx localized necrosis of fat tissues; related to trauma (32%), surgery and radiation can cause it

Disorder of palpable mass Development: with lactational Accessory Axillary change Breast Inflammatory Disorders erythematous swollen painful breast Etiologies: fat necrosis, duct ectasia, acute mastitis, recurrent subareolar abscess, granulomatous mastitis, lymphocytic mastopathy mammogram can reveal spiculated poorly defined mass w/ calcifications (i.e. mimic cancer) features depend on stage: necrotic fat surrounded by foamy macrophages, giant cells, fibroblasts and fibrosis; +/Ca++ dilated ducts with insipissated secretions; epithelial degeneration and periductal chronic lymphocytic reaction antibiotics SMOLD (squamous metaplasia of lactiferous ducts - Zuska dx); keratinizing squamous metaplasia surgery of nipple duct; intense Cl and granulomatous inflammation collagenized stroma surround atrophic lobule with Cl and circumferential inflammation

Fat Necrosis

painless mass, palpable and firm mimics cancer (usually present clinically w/o any significant hx)

Duct Ectasia

intermittent clear nipple discharge acute infection (with staph aureus), abscess secondary infection

Acute Mastitis

from breast feeding

Periductal Mastitis some periductal (aka recurrent chronic subareolar inflammation abscess) Lymphocytic Mastopathy (aka Diabetic Mastopathy)

palpable mass

type 1 DM, autoimmune dx

Nonproliferative Breast Changes (fibrocystic change)

palpable lump, some pts have nipple discharge

cysts (lined by thin wall), fibrosis, mammographic adenosis (increased # lobular density or units); calcifications (blue), calcifications apocrine change (pink) **increased risk of invasive breast cancer 1.5 to 2.0 more than 2 cell layers (usually inner cell layer that proliferates); architecture: irregular space, peripheral fenestration, cells look streaming or whirling; cytological: heterogenous variations in size and shape of cells and nuclei

epithelial hyperplasia usual type, Proliferative Breast sclerosing adenosis, complex dx w/o Atypia sclerosing lesion, papillomas

Epithelial Hyperplasia Usual Type

usually incidental


nipple discharge (can even be bloody) imaging density, calcification or mass that mimics invasive carcinoma radiographic images show central mass with long projections

fibrovascular cores extend into duct lumens covered by epithelium; epithelium can have epithelial hyperplasia, apocrine metaplasia, sometimes atypia or DCIS increased number of acinar (distorted and compressed), may be present with other FCC or form mass itself sclerosing adenosis, papilloma, epithelial hyperplasia, stroma is distorted with entrapped benign cords and ducts/lobules

Sclerosing Adenosis

palpable mass

Radial Sclerosing Lesion / Complex Sclerosing Lesion Atypical Ductal Proliferative Breast Hyperplasia & Dx w/ Atypia Atypical Lobular Hyperplasia

benign mimicker of invasive cancer

** 4-5x risk of developing invasive breast cancer

Atypical Ductal Hyperplasia

harbor acquired genetic gain or loss present in DCIS

Atypical Lobular Hyperplasia

most common benign tumor of female breast; young Fibroadenoma women (20-30 yo), hormonal responsive (increase during pregnancy) localized or most common diffuse, tender, male breast only has ducts (no clinical and assymmetric area lobules), increased dense associated with pathological of firmness and collagenous CT; in the ducts, see Gynecomastia hyperestrinism abnormality of male enlargement some epithelial hyperplasia with and medications breast; etiology: (unilateral or micropapillary type hormonal imbalance bilateral) ; pt (ex. Klinefelter's) presents with Risk Factors: first degree relative w/ breast ca; genetic predisposition (BRCA1&2, Li-Fraumeni syndrome (germ line mutation of p53), Cowden dx (multiple hamartoma syndrome)); increasing age; age at first full term pregnancy over 30 or nulliparous; early onset menstruation/late menopause; previous bx dx of proliferative breast dx; race (caucasian: highest rates; AA: present at higher stage, higher grade, younger age, receptor neg; hispanic: fastest growing rate of ca); obesity (decrease in young women, increase in older women); hormonal imbalance (estrogen excess); radiation Breast Carcinoma exposure; dietary fat (increases risk); smoking NOT associated; Prognostic Factors: Tumor size (<1 cm 98% 10 year survival); Lymph Node Status (MOST IMPT): neg LN - 70-80% 10 year survival; Distant Metastasis; Other Prognostic Factors: histologic subtypes that aren't NOS, ER/PR + is better; lymphovascular invasion is worse; oncogene expression (Her-2/Neu) is worse; loss of tumor suppressor gene fxn (p53 mutation) is worse; Tx: pts undergo surgery +/- adjuvant therapy (hormonal manipulation - PR/ER+; external radiation, brachytherapy; chemotherapy; antibody therapy (Herceptin against Her2)) early onset (15-20 years earlier); occurrence in several close relatives; more than 1 type of ca; bilateral in Familial Cancer 80% of families with Syndrome (BRCA paired organs; occurrence in less cancers are from 1&2, Li-Fraumeni) affected sex (males w/ breast ca); sporadic mutations mult ca across generations; rare ca clusters

monotonous (diff from hetero in typical) cells forming complex architecture (cribiform, micropapillary etc); forms arcades (diff from whirling in typical); nuclei are evenly spaced with distinct cell borders cytologically like LCIS (lobular carcinoma in situ) but only partially involving a lobular unit; punched out holes (cookie cutter appearance), cells look monotonous w/ uniform evenly spaced nuclei hyalinized or oval, white, myxoid stroma rubbery, mobile compress mass, well epithelium (i.e. circumscribed prolif of stroma)

seen in 5-17% bx calcifications; cellular proliferation resembling DCIS but quantitative and qualitative insufficiency

mostly incidental

BRCA 1 & 2

no palpable lesion (in-situ carcionmas, sm invasive lesions) OR breast mass, skin retraction/dimpling, peau d'orange / changes of inflammatory carcinoma, nipple retraction, discharge (invasive carcinoma, palpable tumors 2cm) ductal carcinoma in situ (DCIS) / intraductal carcinoma (80%) ; lobular carcinoma in situ (LCIS) (20%)

hereditary AD breast ca susceptibility genes

detection: incidental finding on palpation (women find themselves), yearly clinical breast exams and monthly self; screening: mammography starts at 40, screening MRI for high risk pts

<5 % of breast ca but 30% of breast ca in pts <30 yo; risk of other tumors; Ashkenazi Jewish ancestry

In situ/ noninvasive carcinoma (1530%)

proliferation of epithelial cells that have undergone malignant transformation but remain at site of origin (i.e. w/in duct or lobule) confined by a BM; metastatic spread CANNOT occur by definition calcifications on mammogram (screening begins at 40 yo look for changes over time); pathologic evaluation: ?invasion, grade, size, margins incidence = 30% (was rare 20 years ago b/c of not screening); grade based on nuclear features & necrosis; considered precursor lesion to invasive carcinoma

rarely forms a mass, rarely bilateraly (10Ductal Carcinoma 20%) - as In Situ (DCIS) opposed to lobular carcinoma which tends to be bilateral contiguous intraductal spread from nipple ducts ulcerating oozing to nipple skin and nipple areola => scale crust on skin surface

4 types: solid, cribiform, comedocarinoma, micropapillary; low grade = uniform, smaller nuclei w/ infrequent necrosis; high grade = large bizarre nuclei w/ central necrosis little balloons w/ dots in the middle = cancer cells

Paget's Dx of the Nipple

underlying DCIS, invasion present in ~60% of cases

bilateral (in Lobular approx 40%) => Carcinoma In Situ no palpable mass more risk of (LCIS) invasive tumor in both breasts

proliferation of small uniform cells w/in terminal ducts and lobules (acini); no necrosis or microcalcifications

close observation

incidental finding; significance: considered a marker of increased risk for developing invasive carcinoma (8-10x)

Invasive carcinoma (70%) aka infiltrating carcinoma; adenocarcinoma

neglected tumors present needle loc usually presents mets first to as large invasive ductal mammogram as a (palpable) axillary nodes ulcerating carcinoma (90%); (use needle to mass; can cause then to liver, lesions; invasive lobular locate lesion for skin dimpling and lung, bones, scirrhous (= carcinoma (10%) excision during nipple retraction CNS stony hard), surgery) gritty consistency w/

surgery, tamoxifen, lymph node evaluation, ER/PR receptor antagonist

proliferation of epithelial cells that have undergone malignant transformation and have grown beyond the confines of the BM (of the duct / lobule) into breast parenchyma; metastatic spread CAN occur

Invasive Ductal Carcinoma

mets to bone, liver, lungs

colloid/mucinous: nest of ca cells floating in mucinous tissue; tubular: ca cells in nests in tubules; medullary: looks like high grade ca, lot's of inflammatory rxn (esp lymphocytes) pleomorphic cells; tubules, nests, sheets

NOS = 90%; colloid (mucinous) = 1-6%; tubular = 2%; medullary = 1-5%; all look diff under microscope and behave better than NOS (less aggressive and invasive); grading: modified bloom richardson score - nuclear pleomorphism (1-3); tubule formation (1-3); mitotic activity (1-3) best differentiated => total = 3

Invasive Lobular Carcinoma

bilateral and multicentric

mets to abdomen and retroperitoneum

ill defined firm areas

single file pattern and targetoid patterns present NOT graded -uniform cells; single cells, multicentric

invade in a diffuse pattern

Problems in Puberty Kallman's Syndrome (see above) Hypothalamic Hamartoma form of central precocious puberty if happens in fetal life => micropenis in boys (b/c no GH, FSH, LH, ACTH, TSH in fetal life) document with MRI (but usually leave alone) congenital (structural or midline abnormalities; mutations in pituitary TFs) or acquired (CNS insult, trauma, basal skull fracture, radiation, chemo) medical therapy heterotopic mass of GnRH secreting neurons; present from birth may involve isolated or multiple hormones


delayed puberty

idiopathic central precocious precocious puberty puberty Turner's Syndrome (see above)

early fusion of epiphysial growth plates (severe short stature)

GnRH stimulation test to dx (do FSH measurement after GnRH stim => normal levels when should be prepubertal); then can do head MRI

premature activation of HPG axis; more common in girls

delayed puberty

classic triad: precocious puberty, caf au McCune-Albright lait skin Syndrome pigmentation & fibrous bone dysplasia Cervical Pathology Non Neoplastic Lesions usually Polyps (Nonasymptomatic but neoplastic Lesion) can cause vaginal spotting Follicular Cervicitis (Nonneoplastic lesion) Infections infections and inflammation of cervix

activating mutation in Gs alpha lg ovarian cysts in => hyper fxn of endocrine tissues; somatic mutation in girls mosaic distribution

looks red when glandular and white when squamous often caused by chlamydia

fibromuscular stroma lined by benign epithelium form a lymphoid follicle (not specific pattern)

impt in differential dx of vaginal bleeding (b/c also in differential is endometrial ca)

Other infections not shown: gonococcus, chlamydia, syphilis, CMV, schistomiasis, TB



pap smear

see squamous cells but also see lymphocytes; see branching tree looking thing (that's the fungus)

be weary of STDs increasing in senior citizens



pap smear

see bluish glandular thing with flagellum which is the parasite

Herpes Simplex Virus


pap smear

cell crowded with ground glass nuclei (multinucleated cell)

NO CURE just there are vaccines in antivirals to control trials breakouts

HPV Cervical Premalignancy and Malignancy

HPV causes cervical cancer but NOT all HPV infections cause cancer; HPV is often species and site specific; causes many types of warts; has many subtypes; genital tract subtypes related to cervical cancer; epidemiology of genital HPV infecton: not usually seen prior to sexual activity; likelihood of infection directly related to number of sexual partners, young age at first intercourse, and male's sexual partners; same risk factors for cervical precancer and cancer; Majority of cervical cancers occur in the transitional zone; pts with lesions get colposcopy (use dissecting microscope and put vinegar on the cervix => lesions turn white and then biopsy the lesions) pap smear with viral subtyping little if any undifferentiated cells, limited to bottom layers of epithelium (action is near surface); hallmark: koilocyte (enlarged, dark irregular nucleus with perinuclear cytoplasmic clearing (halo) with "hard" edge

CIN1 / LGSIL (low grade squamous intraepthelial lesion)

low overall risk of progression; most regress

can have any low risk HPV (6, 11, 42, 44) OR high risk HPV (16, 18, 31, 33)

includes flat condyloma and low grade dysplasia; this is a productive HPV lesion (i.e. cell is a factory making more HPV virus => halo)

CIN2/ HGSIL (high grade squamous intraepthelial lesion)

high risk HPV subtypes ONLY (16, 18, 31, 33) much higher risk high risk HPV of persistence subtypes and progression ONLY (16, 18, 31, 33)

undifferentiated cells and mitoses up to middle layers of epithelium


full thickness undifferentiated cells and mitoses, qualitatively worse cellular features, look for mitoses (in all layers) - bottom image = squamous lining transformed into high grade lesion and is tracking backwards to replace endometrial gland; cytology: higher nuclear: cytoplasmic ratio than LGSIL (dark angry looking nuclei in sm cells)

includes high grade dysplasia and carcinoma in situ

Squamous Carcinoma

ulcerated or fungating mass originating in transformation zone; often large since pt not screened; can present with vaginal discharge / + LN; high risk subtypes

fungating mass (looks like mushroom); red = glandular tissue; white = squamous tissue

invasive histologic pattern (local tissue destruction)

surgery and radiation

stage most impt for prognosis - ca much worse when reaches pelvic wall (stage III, 35% 5 yr survival vs 75% for stage II); morbidity greater from direct extension rather than mets incidence appears to be rising

endocervical adenocarcinoma

goes through in situ phase but progression not as well understood

associated with HPV 18 (18 can also cause squamous cancers)

pap smears (not as effective at detecting as they are at detecting squamous lesions)

glandular cells become dysplastic => ca

Uterine Pathology
Ovulatory Causes of Infertility not common limited to bacterial infections that arise after delivery or miscarriage

acute endometritis

bleeding, discomfort, pain

PNMs and eosinophils invade glands and stroma


chronic endometritis

abnormal bleeding, pain, discharge, infertility

PLASMA CELLS in stroma, some bleeding

etiology: retained products of conception, IUD associated infections, TB; most common in setting of PID dx: culture, detect gonoccocal DNA or RNA, endocervical contents; Tx: ascending infection that begins in vulva or vagina; common; with ectopic pregnancy - can get

PID: Gonorrhea

pelvic pain, adnexal tenderness, fever, vaginal discharge complications

cervical envolvement common (asymptomatic), preferentially

abscess formation in fallopian tube

islands of inflammatory cells (PNMs, lymphos, macros) in

PID: Chlamydia

infects same sites as gonorrhea but recurrent with milder infections = symptoms and common less acuity

chlamydia = obligate intracellular pathogen; exists in 2 forms: 1) elementary body (infectious but NEVER divides) & 2) reticulate body (divides but not infectious); often recog by persistence of symptoms after tx gonorrhea - ** other PID pathogen = enteric bacteria composed of mature smooth muscle (looks ressection of like myometrium) fibroid, cauterization, hysterectomy


endometrial bleeding, infertility, heaviness, pain

4 locations: intramural, subendometrial, subserosal, pedunculated

dx: need to see gross masses then look at histo

very well demarcated, located in myometrium

most common tumors in women; estrogen responsive


menometrorrhagia (irregular and heavy menses), colicky dysmenorrhea, dyspareunia, pelvic pain (esp during menstrual period)

spongy looking myometrium from endometrial glands/stroma

endometrial glands/stroma in myometrium (surrounded by smooth muscle)

presence of endometrial glands and stroma w/in myometrium; 20% of women


depends on location involved; common complaints: dysmenorrhea, dyspareunia, pelvic pain, menstrual irregularities, infertility (30-40% women)

rarely shows features (mets and invasion) similar to malignant tumors => serious complications; distribution: ovaries, uterine ligaments, rectovaginal septum, pelvic peritoneum, laparatomy scars; associated with ovarian malignancies (clear cell carcinoma & endometrioid carcinoma)

dx: cytology needs pigemented macrophages and blood, stroma, and glands (need 2 out of 3) AND clinical hx

chocolate cysts when ovaries

have to see endometrial glands AND stroma mixed with diff tissue type; hemosiderin laden macrophages (from blood)

DUB (dysfunctional uterine bleeding)

clinical term for uterine bleeding not caused by any underlying organic (structural) abnormality; common at menarche and perimenopausal

presence of endometrial glands and stroma outside uterus; dx of women in reproductive life; 10% women; theories: 1) regurgitation theory 2) metaplastic theory 3) vascular or lymphatic dissemination theory functional disturbance; most cases have no cause but are from anovulatory cycle; when cause: from 1) endocrine disorder 2) primary lesion of ovary (PCOS) 3) generalized metabolic disorder (eg DM)

clinically infertile low progesterone; endometrial bx: Inadequate Luteal inadequate corpus luteum formation => (irregular secretory endometrium lags in Phase (ovulatory low progesterone => can't maintain ovulatory cycles), histological charac (eg. Day 26 has dysfunctional endometrium increased bleeding subnuclear vacuoles) bleeding) or amenorrhea Uterine most common female genital cancer; post-menopausal women (median age 58); cause unknown but E plays a role; tamoxifen => 3x risk increase Malignancies: for uterine ca (in uterus, tamoxifen is agonist) Endometrial Carcinoma

Endometriod Carcinoma

phenotype: nulliparous, obese, younger, DM, HTN, late onset menopause, irregular or post- 5x risk to get well- pre and post menopausal differentiated menopausal bleeding endometrial ca women at risk arising in background of complex hyperplasia with atypa, low grade

bx and endometrial curettage (to r/o polyps, hyperplasia, leoimyomas), frequently ER/PR+

pink, polyploid looking mass kind of looks like curdled milk

well diff = glands w/ no intervening stroma, complex glands with infoldings (cribiform); poorly diff = solid mass of tumor w/ some good outcome glands; nuclei &long term jumbled, round, survivial prominent nucleoli, clearing of chromatin (atypia features); squamous differentiation: pink-keratin part of tumor background appears atrophic; complex branching papillae (w/ pink fibrovascular core) lined by pleomorphic cells with high nuclear grade; tumor cell tufts; psammoma bodies (calcifications); histo identical to ovarian serous ca, no hyperplasia

Classical Pathway (type 1) endometroid is most common, others: adenocarcinoma with squamous differentiation, mucinous, squamous; estrogen related prototype; almost always p53 NEGATIVE

phenotype: multiparous, thin, older, poorly irregular or postpost differentiated Serous Carcinoma menopausal menopausal deeply invasive bleeding women lesions (myometrium), high grade

bx and endometrial curettage; POSITIVE for p53 & ER/PR -

poor prognosis (widespread lymphovascular permeation)

alternate pathway (type II) - type of alt is clear cell; nonhormonal prototype; precursor = EIC (endometrial intraepithelial carcinoma) - in situ replacement of benign endometrial glandular epithelium by malignant cells;

Clear Cell Carcinoma

aggressive, high stage, poor prognosis

architectural pattern: solid, papillary, tubular, cystic; atypical nuclei see clear cell w/ clearing of cytoplasm (might be eosinophilic)

4% of endometrial ca

Uterine Sarcomas Stromal Nodule (BENIGN)

3-5% of uterine malignancies (w/ mixed tumors)

premenopausal women Low Grade Endometrial Stromal Sarcoma

worms distinctive gross appearance / may extend beyond uterus

malignant endometrial stroma; clusters of sm uniform cells infiltrate myometrium & fill lymphatics; minimal atypia & mitoses; cells look bland & haphazardly arranged, sm & hyperchromatic nuclei significant atypia with mitoses, hemorrhage & necrosis common; nuclei = pleomorphic, prominent nucleoli,

Undifferentiated Endometrial Sarcoma (formerly high grade endometrial stromal sarcoma)

post menopausal

aggressive - most have spread beyond uterus at dx dev indep from leiomyomas ; incidental dx = presumed leiomyoma


post-menopausal bleeding, uterine enlargement, average age = 53 abdominal pain, constipation, urinary frequency

malignant smooth muscle; firm and white hypercellular tumor that's w/ spindle cells hemorrhagic w/ in fasicular some necrotic pattern; areas pleomorphic cells, chromatic nuclei, mitoses

Mixed Tumors Adenofibroma (BENIGN) Adenomyoma (BENIGN)

malignant epithelium and stroma


recurrence and distant mets after many years

polyploid mass

epithelial component resembles proliferative endometrium is BENIGN; stromal w/ slit-like glands; mitoses component is MALIGNANT

Carcinosarcoma (MMMT = malignant mixed mullerian tumor)

elderly pts with pelvic pain and bleeding

glandular component usually endometrioid ca; stroma can be homologous (differentiation same as uterus bulky mass w/ endometrial hemorrhage and smooth muscle necrosis or stroma) or heterogenous (diff from uterus mesenchymal from elsewhere like fat, cartilage, skeletal muscle large polyploid lesions in endometrial cavity

BOTH epithelial and non-epithelial poor prognosis (5 components = year survival = 18MALIGNANT; 39%); uniformly mets to LN = aggressive epithelial (carcinoma mets not sarcoma)

Endometrial Polyps (BENIGN)

localized proliferation of glands and stroma; see thick walled BVs and fibrotic stroma (pink); cystic dilated glands w/ normal sized glands scattered btwn; fibrotic background + stroma

Endometrial Hyperplasia

diffuse proliferation of glands and stroma; result of prolonged estrogen stimulation via anovulatory cycles, obesity, hormone-producing ovarian tumors (ex. granulosa cell tumor); progression of "untreated" atypical hyperplasia to endometrioid adenocarcinoma numerous glands that look crowded but simple and tubular; increased abundance of glands compared to background stroma; nuclei are still well oriented, they're elongated, no prominent nucleoli

Simple Endometrial Hyperplasia w/o Atypia

Simple Endometrial Hyperplasia w/ Atypia

simple b/c glands are still round and tubular (NOT branching); ATYPIA: nuclei are rounding up, chromatin is clearing out in some places, nuclei look crowded / jumbled, prominent nucleoli

Complex Endometrial Hyperplasia w/ Atypia

glands look complex - not round and tubular; ATYPIA: nuclei jumbled, rounding up in some places, chromatin clearing, lose orientation to BM

most likely to be associated with or progress to endometrial cancer

Ovarian Pathology Non-Neoplastic Cystic Changes / Lesiosn Fallopian Tube Disorders Primary Ovarian Tumors Follicle Derived: cystic follicle (< 3cm) & follicular cyst ( > 3cm); corpora-lutea derived: cystic corpus luteum (< 3cm) & corpus luteum cyst (> 3cm); epithelial inclusion cyst Infections (PID); Endometriosis; Tubal Pregnancy (common site = ampulla); Tumors (adenocarcinoma - BRCA mutation; TIC (tubal intraepithelial carcinoma) 3 categories: 1) surface epithelial tumors (65-70%) 2) germ cell tumors (15-20%) 3) sex cord-stromal tumors (5-10%)

Surface Epithelial Benign: cystadenoma, cystadenofibroma; Borderline: serous borderline tumor, mucinous borderline tumor; Malignant: serous carcinoma, mucinous carcinoma, endometrioid carcinoma, clear cell carcinoma Tumors Serous: cyst collapses (looks like a tent); when full, it's full of clear fluid; cauliflower like growth can be seen; Mucinous: find many cysts inside (daughter cysts), looks like jelly -> mucin cystic (unilocular or multilocular); monolayer lining on BM; serous: cuboidal, ciliated cells; mucinous: columnar cells w/ copious apical mucin


cytsic + adenoma; serous or mucinous; papillary or not; neoplastic part = epithelium

Borderline Tumors : Serous Type

cystic with nodular buds, excrescences can grow on ovarian surface; very solid looking (b/c of more overgrowth and proliferation)

epithelial proliferation -> stratification; hierarchy papillary architecture (looks like tree trunk w/ branches); mild to moderate cellular atypia

have mixed features: not quite benign or malignant (clinically and hist), more proliferative (m); NO INVASION (b) (but may have local spread to peritoneal surface); can met to LN, can recur, rarely => death (b)

Ovarian Carcinoma

screening: pelvic exam, ultrasound, CA-125 (more sensitive than tend to be specific; marker relatively most cases = in blood); genetic asymptomatic; cause testing for affect women >40 unknown BRCA1/2 yo carriers => prophylactic bilateral salpingooophorectomy

Hereditary Ovarian Carcinoma

most cases associated w/ family hx, BRCA1/2: younger age at dx AD, high penetrance

ugly cells prognosis not so 8th most common (obvious good b/c it's hard cancer but 5th killer malignant to detect early (in US), more than features), 80% of malignant stromal ovarian tumors = invasion; varied epithelial tumors; growth patterns protective factors: (serous: oral contraceptives, solid with or papillary, gland multiparity, tubal w/o cysts, bulky forming, solid; ligation; risk factors: (usually) - looks mucinous/endo nulliparity, hereditary fleshy metrioid/ clear predisposition cell: gland forming or solid; psammoma bodies (concentric calcifications) approx 10% of ovarian cancers; BRCA = tumor suppressor gene; "two hit" theory -> 1) inherited germline mutation of one copy of gene, 2) somatic mutation of backup copy of gene; loss of suppressor fxn => dev of tumor

Germ Cell Tumors

derived from transformed germ cells (follicles / oocytes); most common tumors in young women (<20 yo); ovarian teratoma: aberrant differentiation of totipotent cells to any/all germ layers (ecto/endo/mesoderm) hasn't been fertilized; analogous to seminoma starts to look like embryo

dysgerminoma embryonal carcinoma

choriocarcinoma yolk sac tumor (endodermal sinus tumor)

increased bHCG increase serum AFP schiller-duval body (looks glomeruloid) composed of mature elements histo evidence from all germ of all 3 germ layers (teeth, layers hair, etc) see thyroid tissue like colloid composed of immature (embryonic or fetal-like) elements from any/all germ layers; blue surgery, adjuvent staining; see immature chemotherapy neuroepithelium (left pic) and immature mesenchyme (right)

similar to placenta

Teratoma: Mature Cystic Teratoma (dermoid cyst)

peak incidence 2040

most common benign ovarian germ cell tumor but may have malignant transformation to squamous cell carcinoma struma ovarii: mature thyroid tissue predominantly; carcinoid tumor

Teratoma: Monodermal (or highly specialized)

Teratoma: Immature

very rare in women >30

malignant; graded by amt of immature neuroepithelium

Sex-Cord Stromal Tumors

tumors derived from ovarian stroma (developed from sex cords of the embryo); may be hormonally active; Classification: fibroma, thecoma (fibrothecoma), granulosa cell tumor, sertoli-leydig cell tumor classic looking "coffee bean fleshy and cystic nuclei" nuclei looking; with cleared out hemorrhagic; center and line yellowish in down middle; color Call-Exner Bodies cellular, bland spindled solid, firm, tanfibroblasts; yellow mass collagen bundles

can present with hyperestrinism Ovarian Granulosa (tumor Cell Tumor hormonally active)

low grade malignancy; occurs at any age (2/3 post menopausal)

tumors recaptiulating granulosa cells of follicle; at risk for endometrial carcinoma


most common sex cord tumor; no hormonal activity; can be associated with Meigs syndrome & Gorlin Syndrome


may present with hyperestrinism

uniform, solid consistency; yellowish

spindle looking for fibroma part and epithelioid for thecoma part

tumors recapitulating theca cells of follicles; rare to exist as pure form (commonly with fibroma - fibrothecoma; may produce estrogen => hyperestrinism => risk of endometrial hyperplasia or carcinoma

Ovarian Metastatic most common origin = non-mullerian primary - colon > breast > stomach; endometrial carcinoma = most common mullerian origin Tumors Krukenberg Tumor Pseudomyxoma Peritonei Prostate Benign Prostate Pathology bilateral ovarian mets abdominal cavity full of mucin regulation of prostate growth mainly by T (and DHT by conversion) elevated PSA levels possible with hyperplasia and inflammation can present with urinary tract obstruction due to compression and increased muscle extremely tone => common in men hesitency, >50 dribbling, frequency, nocturia, urgency, hydroureter, hydronephrosis fever, tenderness of prostate (b/c it's infectious in etiology) transurethral resection of prostate (TURP) glandular: stroma is reduced and and suprapubic glands are enlarged, have prostatectomy; 5projections (papillae) protruding alpha reductase into lumen due to hyperplasia; inhibitor stromal: rarely find glands, (finasteride => spindle nuclei and abundant inhibits action of eosinophilic cytoplasma (look T); alpha 1 receptor similar to smooth muscle cells) antagonist to relax the smooth muscle (stromal cells) PNMs fill prostatic glands antibiotics => microabcesses not many PNMs, lot's of lymphocytes and plasma cells signet-ring carcinoma commonly from GI primary appendical origin

Benign Prostatic Hyperplasia (BPH)

can have elevated PSA

enlargement of prostate gland by stromal or glandular proliferation and nodular formation; etiology: androgens & estrogens

Prostatitis: Acute

etiology: typically bacterial infection can be due to inability to cure acute prostatitis (can flip back to acute => alterations back and forth); many cases it's noninfectious

Prostatis: Chronic

Prostatis: Granulomatous

aggregate of histiocytes and lymphocytes form a nodule


etiology: hereditary factors (~9% of prostate ca); racial difference (genetic and environmental probs); sex hormones (T and androgen receptors, Malignnat Prostate which are very sensitive to T so can also activate w/ lower amts of T); dietary fat (free radicals, sex hormone production); PSA Screening: low sensitivity & specificity - high preoperative PSA =. poor prognosis; use Gleason Grading (predominant grade + second most predominant grade) Pathology higher score => worse prognosis pathogenesis poorly understood but recurrent spreads fusions of lymphovascularly; TMPRSS2 to very slow growing can go to bones ERG or cancer => many (relatively ETV1 => don't present common => brings clinically increase alkaline androgenic phosphatase) ERG under control of T => more androgens (in ~50% of ca) low power (architecture): tumor glands = sm or intermediate (opposite of BPH where glands or stroma are BIGGER); decrease in stroma; infiltrative; cancerous glands most commonly infiltrate btwn benign glands; diagnosed ca in high power: loss of basal cells; enlarged nuclei w/ clumping men; higher incidence in AA; chromatin; prominent nucleoli; helpful features: perineural invasion, crystalloids (pink rectangular material in lumen), acidic mucin (looks blue b/c very acidic so picks up basic dye which is blue) high grade PIN => cytological features similar to carcinoma but no invasion; still have stroma; nuclei with very big prominent nucleoli detection: DRE, trans-rectal ultrasound (TRUS), PSA (4-10ng/mL - 25-35% w/ ca; >10ng/mL - 50% w/ ca), decrease in free PSA (<10% total PSA) increases chance for detection of ca (specificity); PSA velocity (measure PSA over time to see trend in changes); PSA density (PSA value versus volume of prostate); management: observation, surgery (radical prostatectomy), radiation (external beam, brachytherapy), hormonl therapy (blocking T via orchiectomy, inhib GnRH, inhib androgen synthesis, inhib androgen binding to receptor, inhib 5 alpha reductase - finasteride), chemotherapy (for hormone-resistant ca) precancerous cellular proliferation of prostatic ducts and acini


Prostatic Intraepithelial Neoplasia (PIN) Testicular Pathology Abnormal Gonadal Fxn not gone through puberty, no secondary sexual hair, genitalia anosmia almost prepubescent, sm testicular volume

Kallman's Syndrome


give GnRH replacement OR give gonadotropins (LH first to get T up b/c need intratesticular T to make sperm, then give FSH => spermatogenesis)

hypogonadotropic hypogonadism from missing GnRH neurons

gynecomastia from T being low but potentially T tx options: 1) injectible very small firm estrogen still being higher fasting testosterone enanthate every 2-4 testes, very tall, made; prolactin is glucose; FSH = weeks; 2) transdermal testosterone high in labs from normal male hair Klinefelter's karyotype = HIGH; LH = patches, change daily; 3) transdermal high LH => high E pattern, normal Syndrome 47, XXY HIGH; T= T cream, apply daily; 4) oral penis, female => high prolactin; LOW; substituted T, methyl T (not as obesity pattern, elevated prolactin = good, hepatotoxic) gynecomastia gonadotropins b/c HIGH trying to stimulate testes to make sperm elevated temperature => lowered sperm Mediterranean counts Fever source can be exogenous (i.e. steroids) or endogenous (i.e. CAH) but => Excess Androgens suppression of gonadotropins and aspermia causes of testicular atrophy: cryptorchidism, progressive atherosclerosis, inflammatory orchitis, hypopituitarism (low FSH and LH), generalized Benign Conditions malnutrition, irradiation, prolonged administration of anti-androgens (prostate ca), exhaustion atrophy (high levels of FSH), primary failure of of Testes genetic origin (eg. Klinefelter) progressive Testicular descent most descend atrophy and occurs in 2 phases: spontaneously into incomplete fibrosis of 1) abdomen to pelvic scrotum w/in first descent of testes testicle => brim (MIF) 2) pelvic tends to be year; orchioplexy by major sites = inferitility; brim to scrotom unilateral; rarely 2 years old: surgical inguinal canal or cause not well changes start to (androgens); Cryptorchidism associated with placement of testis higher up in understood take place at 2 relatively common: defined hormonal into scrotal sac => scrotum yo; BM looks 1% of 1 yo; risk of disorder improved fertility (intraabdominal = thick, infertility; 5-10x (not guaranteed) rare) interstitium increased risk of and may decrease looks testicular ca (in both risk of testicular ca prominent testes) children (congenital urinary associated w/ tract anomalies) - gram neg UTIs (urethritis, rods; young adults: G and C; acute inflammation => mixed cystitis, prostatits) adults: e coli and pseudomonas; inflammatory infiltration (PNMS, Inflammation of => secondary mumps (viral): >20% of adults lymphocytes, eosinophils); w/ TB Testis involvement of => orchitis; syphilis => orchitis see caseating granulomas (necrosis, testis / w/o epididymitis; TB: begins in giant cells, hyaline) epidydimu;s; can epididymis and may spread to form abscess tesis

granulomatous orchitis

unilateral enlargement (+/probably middle aged men pain) - may mimic autoimmune tumor may be associated w/: incomplete descent, atrophy, defective scrotal ligaments venous occulsion +/arterial compromise

granulomas present diffusely throughout testis, confined to seminiferous tubules; macrophages, plasma cells, lymphocytes congestion, enlargement, hemorrhage, infarction/necr osis surgical emergency: orchioplexy; need can be in association to manually untwist w/ strenuous w/in 6 hours or physical activity lose testis

Vascular Disturbances (Testicular Torsion) Tumors Germ Cell Tumors

pain, enlarged testis

most common tumor in men 15-35; incidence is increasing (maybe environmental); most common in white males (5:1 compared to blacks); 95% are germ cell tumors; lymphoma is common in older men; testicular cancer associated with testicular dysgensis syndrome seminomatous includes: seminoma & "spermatocytic seminoma" ; non-seminomatous includes: embryonical carcinoma, yolk sac tumor, choriocarcinoma, teratoma; LDH (lactate dehydrogenase) - can be used to assess tumor burden Placental Alkaline Phosphatase (PLAP) peak incidence: 30s sheets of uniform cells ("fried eggs"); bulky, lobulated large masses; round/ovoid homogenous; nuclei; surgery (radical tan, fleshy; prominent orchiectomy) + usually devoid of nucleoli; clear radiation hemorrhage/nec cytoplasm; rosis - "potato lymphocytes; neoplasm" fibrous separations (+/) crowded sheets of cells; architectural formations (papillary, glandular, bulky or small chemotherapy + tubular); ugly tumors, orchioectomy + cells (lg hemorrhage, retroperitoneal LN pleomorphic necrosis dissection cells, hyperchromatic nuclei, prominent often mult nucleoli) most common germ cell tumor (~50%); frequently occurs pure; variants: typical (~85%), anaplastic (~5-10%); spermatocytic: << 5%; usually low stage at dx; spread initially to LN


Embryonal Carcinoma

peak incidence: 20-30s


more aggressive than seminoma (VERY impt to distinguish); rare in pure form

Yolk Sac Tumor

well circumscribed tumor w/ pale alpha feto yellow mucoid protein in serum cut surface; can have hemorrhagic and cystic foci looks kind of like placenta; elevated bHCG areas of hemorrhage and necrosis

"lace-like" reticular architecture; "SchillerDuval" bodies; stains for AFP synctiotrophobl ast and cytotrophoblast ; nuclei with prominent nucleoli and pink cytoplasm

most common in children <3 yo; very rare in adults


can present with gynecomastia

most aggressive; rare in pure form; early mets

painless/ painful enlargement; chemotherapy + metastases with clinically occult or tumor derived from see evidence of orchioectomy + unapparent tumors; extragonadal Teratoma one or more germ diff tissue types retroperitoneal LN signs/symptoms; lung or layer dissection retroperitoneal LNs physiologic conditions: medical: DM, CAD, neurologic disorder (ex. MS), renal failure, vulvovaginal atrophy, infections, alcoholism, drug abuse, heavy smoking, incontinence; hormonal: iatrogenic (OCPs, Depo Provera, etc), cancer tx, hair loss tx; drugs: antilipids, antipsychotics, benzos, bariburates, anti-HTN, anti-reflux, phenytoin, TCAs, SSRIs, alcohol, antihistamines, anticholinergics, amphetamines, narcotics; psychologic Sexual Disfunction causes: predisposing factors: family attitudes to sexuality, inadequate sex education, traumatic sexual experiences; precipitants: psychiatric illness, childbirth, infidelity, dysfxn in partner / prob in relationship; maintaining factors: anxiety, poor communication, lack of foreplay, depression, dysfxn in partner, poor sexual info, prob in general relationship Female Disorders persistently or recurrently deficient Hypoactive Sexual (or absent) sexual fantasies and desire for sexual activity, which Desire Disorder causes personal distress persistent or recurrent inability to attain, or to maintain until completion of the sexual activity, an Female Sexual Arousal Disorder adequate lubrication/swelling response of sexual excitement, which causes personal distress persistent or recurrent delay in, or Female Orgasmic absence of, orgasm following normal excitement phase, which causes Disorder distress don't need to distinguish btwn women who are aroused mentally by non-genital stimuli from those who are not aroused by any stimuli limitations of this def: women with female orgasmic disorder often have sexual arousal disorder; often it's intensity of orgasm that has diminished => distress


recurrent or persistent genital pain associated with sexual intercourse, which causes distress recurrent or involuntary spasm of musculature of outer 1/3 of vagina that interferes with sexual intercourse recurrent or persistent genital pain associated with noncoital sexual stimulation

penile-vaginal movement of intercourse may be impossible b/c of pain from partial or complete penile entry


"muscular spasm" has never been documented; reflexive muscle tightening, fear of vaginal entry, and pain w/ its attempt are characteristic

Noncoital Sexual Pain Disorder

Male Disorders deficient or absent sexual fantasies judgement must and desire for be made by sexual activity, Hypoactive Sexual clinician taking which causes Desire Disorder into account pts distress and can't age and life be accounted for circumstances by other physical dx recurring inability to achieve or maintain an erection until Male Erectile completion of sexual activity, which Disorder causes distress; can't be accounted (impotence) for by other medical condition delay or absence of orgasm must be judged following normal by clinician Male Orgasmic excitement or taking into acct Disorder sexual activity; pts age and life must be persistent circumstances or frequent & => distress

evidence suggests that relationship issues and/or sexual trauma in childhood may play role; also life stressors and other interpersonal difficulties

tx includes discovering and resolving underlying conflict or life difficulties

prognosis: course can be consistent or periodic; i.e. can get remission if life stressors reemerge

short of other physiologic cause, usually a result of 'performance anxiety' or fears of not being able to achieve or maintain an erection often thought of as beginning in adolescence or early adulthood b/c sexual intimacy becomes related with a negative life event or aspect

tx for non-medical management = 'Sensate Focus' (involves progression of sexual intimacy typically over several weeks ultimately leading to penetration and orgasm) tx includes working through the underlying issues; therapists also use behavioral techniques like sensate focus

medical causes must be ruled out first; prognosis: very good with high success rates medical cause must be r/o first (including using substances); prognosis is very good

premature ejaculation

Sexual Aversion Disorder

ejaculation with minimal sexual stimulation before or shortly after penetration and before person wishes it; must be persistent or frequent & => distress when presented persistent or w/ sexual recurring aversion opportunity, pt to or avoidance of may get panic sexual activity that attacks or => distress extreme anxiety recurrent or persistent genital pain ass. w/ sex

relationship stress, novelty of new relationship, anxiety, issues related to control and intimacy can all play role in its dev

tx involves relaxation training, education, and working through underlying issues; if its due to new relationship, difficulty will resolve as relationship matures tx involves discovering and resolving underlying conflict or life difficulties tx: resolve underlying sexual and relationship issues

medical causes must be r/o first (including substance use); prognosis is good prognosis: varies but increases w/ ability to gain insight and work through issues that => disorder need to r/o other medical conditions first (including substance use); prognosis: varies


relationship issues and/or sexual trauma in childhood may play role relationship of this can be dx in disorder w/ males or females victims of rape and sex abuse