Female Genital system and Breast Flashcards
1
Q
- Disease of vulva and vagina:
VULVITIS
A
= inflammation of the vulva (external female genital organs)
CAUSES:
- HPV: condyloma acuminata + valvular intraepithelial neoplasia
- HSV-2: papule progress to vesicle and converge to ulcers. Painful.
- Syphilis: T.pallidum, primary chancre
- Candida albicans: vulvovaginatis, small white patches with leucorrhea + itching
- Gonorrhea: N.gonorrhea, suppurative infection of vulvovaginal glands
2
Q
- Disease of vulva and vagina:
CONTACT DERMATITIS
A
- vulvar pruritus
- reactive inflammation to exogenous stimulus - irritant or allergen
3
Q
- Disease of vulva and vagina:
LICHEN SCLEROSUS
A
- non-neoplastic epithelial disorder
- thinning of epidermis + loss of rete pegs, hydraulic degeneration of basal cells, superficial hyperkeratosis + dermal fibrosis
- smooth, white plagues
- autoimmune reaction
- most common in post-menopausal women
4
Q
- Disease of vulva and vagina:
LICHEN SIMPLEX CHRONICUS
A
- non-neoplastic epithelial disorder
- end stage of inflammatory dermatoses
- epidermal thickening, expansion of stratum granulosum, hyperkeratosis
- looks like leukoplakia
- epithelium show increased mitotic activity, no atypia
5
Q
- Disease of vulva and vagina:
CONDYLOMAS AND LOW GRADE VIN
A
= anogenital warts 1. Condyloma lata: - flat moist lesion, 2nd syphilis 2. Condyloma acuminata: - elevated papillary lesion - anywhere on anogenital surface - histo: perinuclear cytoplasmic vacuolization with nuclear angular pleomorphism + koilocytosis TREATMENT: - CO2 laser - podophyllin
6
Q
- Disease of vulva and vagina:
HIGH GRADE VIN + CARCINOMAS
A
- women >60 years
- 90% squamous cell cc, rest are adenocarcinomas, melanomas, basal cell cc.
1. HPV associated: - younger patiens, smokers
- HPV (16 and 11)
- in situ changes
2. Non-HPV associated: - older women
- preceded with years of non-neoplastic epithelial changes
- epithelium display dyskeratic cells, angular budding, basal keratinization
⇒ labia majora, minora, clitoris
⇒ matastasize to regional LN
TREATMENT: - excision
- radical vulvectomy
- prognosis: 5 year survival ⇒ 50-75%
7
Q
- Disease of vulva and vagina:
EXTRAMAMMARY PAGET
A
- form of intraepithelial carcinoma
- no underlying carcinoma (unlike Paget disease of breast)
- red, scaly, crusted plaque - may appear as inflammatory dermatosis
- Histo:
- large epitheloid cell infiltrate the epithelium
- abundant granular cytoplasm
- occasional vacuoles containing mucin
8
Q
- Disease of vulva and vagina:
BARTOLIN’S CYST
A
- formed when glands are blocked ⇒ fluid-filled cysts
- often secondary to gonorrhea ⇒ abscess ⇒ obstruction of duct
- painful, huge cyst
- women age 40 or more
- associated with accessory breast tissue
- may have mucocele like changes
TREATMENT: - excise in old
- marsupialize
9
Q
- Disease of vulva and vagina:
ANGIOMYOFIBROBLASTOMA
A
- benign vulvar tumor
- well-circumscribed, 0,5-12cm
- alternating hyper- and hypo cellular area
- spindle cells, plump stromal cells, no atypia
- rare/ no mitotic figures
Positive stains: vimetin, desmin mesenchymal tumor
10
Q
- Disease of vulva and vagina:
VAGINITIS
A
= inflammation of vagina- transient and non-serious
- produces leucorrhea ⇒ vaginal discharge
CAUSES:
- C.albicans: vulvovaginitis, white discharge
- Trichomonas vaginalis:
* large, flagellated ovoid protozoa
* purulent discharge
* inflammation of superficial squamous mucosa
* strawberry cervix
* treatment: metronidazole
- other fungi and bacteria
11
Q
- Disease of vulva and vagina:
VAGINAL INTRAEPITHELIAL NEOPLASIA AND SQUAMOUS CELL CARCINOMA
A
- women >60 years old
- VIN is a precursor lesion associated with HPV infection
- invasive squamous cell cc is associated with presence of HOV DNA
12
Q
- Disease of vulva and vagina:
VAGINAL CLEAR CELL ADENOCARCINOMA
A
- young women in late teens-early 20s
- mothers took diethylstilbestrol during pregnancy
- location: cervix, vaginal mucosa
- benign lesions, vaginal adenomas appear as red granular foci + lined by mucus secreting or ciliated columnar cells ⇒⇒ clear cell adenocarcinoma arise
13
Q
- Disease of vulva and vagina:
SARCOMA BOTRYOIDES
A
- rare primary vaginal cancer
- infants, children <5 years
- also in urinary bladder + bile ducts
14
Q
- Pathology of cervix:
CONGENITAL ANOMALIES OF CERVIX
A
- due to failure of Müllerian ducts to fuse or develop after fusion
GYNATRESIA: absence of vagina ⇒ lack of müllerian ducts to unite
DOUBLE VAGINA: partial failure of Müllerian ducts to fuse
⇒ partial septate vagina
⇒ rudimentary second vagina
15
Q
- Pathology of cervix:
CERVICITIS
A
= inflammation of cervix with mucopurulent vaginal discharge - infectious/non-infectious cervicitis CAUSES: - Chlamydia trachomantis - Ureaplasma urealyticum - Trichomonas vaginalis - Candida spp - Neisseria gonorrhea - HSV-2 - HPV - streptococcus, staphylococcus, enterococcus, e.coli
16
Q
- Pathology of cervix:
CERVICAL INTRAEPITHELIAL NEOPLASIA CIN
A
- detected by etiologic examination - Pap smear
- may begin as low-grade CIN ⇒ higher grade, or begin as high-grade
CIN 1: mild dysplasia with koilocytotic atypia
CIN2: moderate dysplasia with progressive atypia in all layers of the epithelium
CIN 3: severe dysplasia and carcinoma in situ with diffuse atypia and loss of maturation
SIL1/SIL2
17
Q
- Pathology of cervix:
CIN epidemiology + pathogenesis
A
- peak incidence of CIN: 30 yrs
- peak incidence of carcinoma: 45 yrs
RISK FACTORS:- early age at first intercourse
- multiple partners
- persistent infection by high risk HPV
- smoking
- immunodeficiency
- HPV detected in precancerous lesions: 16, 18, 45, 31 ⇒ viral genome integrated into host genome, expressed large amount of E6 and E7 proteins ⇒ block tumor suppressor genes p53 and RB
18
Q
- Pathology of cervix:
INVASIVE CARCINOMA OF CERVIX
A
TYPES OF CANCER: 1. squamous cell cc (75%) 2. adenocarcinoma 3. small cell neuroendocrine cc CLINICAL COURSE: - diagnosed early with Pap smear - preinvasive phase ⇒ white area - symptoms: leukorrhea, hemorrhage, painful intercourse, dysuria PROGNOSIS: - stage 0: 100% - stage 1: 90% - stage 2: 82% - stage 3: 35% - stage 4: 10%
19
Q
- Pathology of cervix:
SQUAMOUS CELL CARCINOMA OF CERVIX
A
- peak incidence: 45-55 yrs
- treatment:
- surgery
- radiation therapy
- radioactive implants
- pelvic extenteration
20
Q
- Pathology of cervix:
ADENOCARCINOMA OF CERVIX
A
- usually in situ
- Symptoms: vaginal bleeding, pelvic pain
- metastasis: pelvic LN, upper abdomen, ovaries, diastant organs
- morphology: exophytic mass, ulcerated plaque, barrel shape, well differentiated, papillary, endometrioid
- prognosis:
- S1: 79%
- S2: 37%
- S3: <9%
21
Q
- Endometritis, endometrial hyperplasia, endometriosis:
ENDOMETRITIS pathogenesis
A
= inflammation of endometrium
- associated with retained products of conception ⇒ miscarriage, delivery, foreign body
- retained tissue act as nest for infection
- removal of foreign body ⇒ resolution
22
Q
- Endometritis, endometrial hyperplasia, endometriosis:
ENDOMETRITIS classification
A
- acute/ chronic⇒ predominant neutrophilic or lymphoplasmacytic response
- chronic endometritis ⇒ plasma cells
- acute endometritis caused by n.gonorrhea, c.trachomatis, mycoplasma
- histo: neutrophilic infiltrate in superficial endometrium and glands
23
Q
- Endometritis, endometrial hyperplasia, endometriosis:
ENDOMETRITIS clinical course
A
- fever
- abdominal pain
- menstruational abnormalities
- infertility
- ectopic pregnancy
24
Q
- Endometritis, endometrial hyperplasia, endometriosis:
ENDOMETRIAL HYPERPLASIA etiology
A
= excessive proliferation of endometrial cells
- excess of estrogen relative to progestin ⇒ hyperplasia ⇒ preneoplastic
- failure of ovulation
- prolonged administration of estrogenic steroids
- estrogen producing ovarian tumors
- granulosa-theca cell tumor
- obesity
25
83. Endometritis, endometrial hyperplasia, endometriosis:
| ENDOMETRIAL HYPERPLASIA classification
- classified according to crowding of endometrial cells + atypia
1. simple hyperplasia
2. complex hyperplasia
3. atypical hyperplasia
- can become autonomously proliferating ⇒ giving rise to carcinoma
- risk of developing carcinoma depend on severity of hyper plastic changes + cellular atypia
26
83. Endometritis, endometrial hyperplasia, endometriosis:
| ENDOMETRIOSIS general + pathogenesis
= condition in which endometrial glands and stroma appears outside the endometrium
- multifocal and may involve tissue in the pelvis
PATHOGENESIS:
1. Regurgitation theory
- menstrual black flow through fallopian tubes with subsequent implantation
- menstrual endometrium viable + survives when injected into anterior abdominal wall
- cannot explain lesions in LN, skeletal muscle + lungs
2. Metaplastic theory
- endometrial differentiation of coelomic epithelium
- cannot explain endometriotic lesions in lungs or LNs
3. Vascular or lymphatic dissemination
- explains extra pelvic or lymph involvement
27
83. Endometritis, endometrial hyperplasia, endometriosis:
| ENDOMETRIOSIS clinical course
- depends on distribution of lesions
- extensive scarring of oviducts and ovaries ⇒ discomfort in lower abdomen ⇒ sterility
- pain on defecation
- painful intercourse
- dysuria
- dysmenorrheal and pelvic pain due to intrapelvic bleeding and periuterine adhesions
28
84. Tumors of the endometrium and myometrium:
| ENDOMETRIAL POLYPS
- sessile, hemispheric lesions, 0,5-3cm
- histo: composed of endometrium resembling basal layer with small muscular arteries
- normal endometrial architecture but dilated glands
- stromal cells monoclonal + have cytogenic rearrangement at 6p21 ⇒ neoplastic
- occur usually at time of menopause
- clinical significance: production of abnormal uterine hemorrhage, + cancer risk
29
84. Tumors of the endometrium and myometrium:
| ENDOMETRIAL CARCINOMA pathogenesis
- women 55-65 yrs
1. Premenopausal women with estrogen excess ⇒ endometriod carcinoma of endometrium
- risk factors: obesity, DM, HT, infertility, estrogen therapy, estrogen secreting tumor
- frequently arise from endometrial hyperplasia
- similar appearance to normal endometrial glands
- Hereditary nonpolyposis colon cancer syndrome ⇒ DNA mismatch repair gene
- Cowden syndrome ⇒ mutation in PTEN, KRAS, B-catenin
2. Older women with endometrial atrophy ⇒ serous carcinoma of endometrium
- atrophy or polyp as background
- mutation in p53, PTEN, DNA mismatch
30
84. Tumors of the endometrium and myometrium:
| ENDOMETRIAL CARCINOMA clinical course
- marked leukorrhea + irregular bleeding
- erosion + ulceration of endometrial surface
uterus may be enlarged
- prognosis:
* S1: 90%
* S2: 30-50%
* S3/4: <20%
31
84. Tumors of the endometrium and myometrium:
| ENDOMETRIAL CARCINOMA morphology
ENDOMETRIOID CARCINOMA:
- resembles normal endometrium
- mucinous, tubal and squamous differentiation
- originate in mucosa + infiltrate myometrium
- metastasize to regional LN
SEROUS CARCINOMA:
- small tufts and papillae
- much greater cytologic atypia
- poorly differentiated cancers - aggressive
32
84. Tumors of the endometrium and myometrium:
| LEIOMYOMA general
- benign tumor of smooth muscle of myometrium
- cause: genetic factors, estrogens + oral contraceptives
- monoclonal tumors
- chromosomal abnormalities can be found
- symptoms: menorrhagia
- rarely transform into sarcomas
33
84. Tumors of the endometrium and myometrium:
| LEIOMYOMA morphology
- sharply circumscribed, firm, grey-white mass with whorled cut surface
- localization:
* intramural ⇒ embedded in myometrium
* submucosal ⇒ beneath the endometrium
* subserosal ⇒ beneath serosa
- foci of ischemic necrosis + area of hemorrhage and cystic softening
- can become densely collagenous and calcified
- histo: whorling bundles of smooth muscle cells
34
84. Tumors of the endometrium and myometrium:
| LEIOMYOSARCOMA
- arise de-novo from mesenchymal cell of myometrium
- solitary tumors
- recurrence is common
- metastasize to lungs
MORPHOLOGY:
- bulky masses infiltrating uterine wall
- soft, hemorrhagic, necrotic
- histo: wide range of differentiation
- tumor necrosis + cytologic atypia + mitotic activity
35
85. Non-neoplastic diseases of the ovary and fallopian tubes:
FOLLICLE AND LUTEAL CYSTS
- harmless lesions originate in unruptured graafian follicles
- multiple cysts + develop underneath serosal covering
- small and filled with clear serous fluid ⇒ can achieve 4-5cm ⇒ pelvic pain
- first lined by granulosa cells or luteal cells but pressure causes atrophy
- cysts rupture ⇒ intraperitoneal bleeding
36
85. Non-neoplastic diseases of the ovary and fallopian tubes:
POLYCYSTIC OVARY DISEASE
```
STEIN-LEVENTHAL SYNDROME
- multiple cystic ovaries + dense fibrous capsule
- leading cause of female sub fertility
SYMPTOMS:
- oligomenorrhea
- hirutism
- infertility
- obesity
⇒ secondary to excessive production of estrogen
⇒ excessive production of androgens
⇒ high concentration of LH
⇒ low concentration of FSH
MORPHOLOGY:
- ovaries twice the size, grey-white, filled with subcortical cysts 0,5-1,5cm
- histo: thickened fibrotic tunica
```
37
85. Non-neoplastic diseases of the ovary and fallopian tubes:
SALPINGITIS
```
= inflammation of fallopian tubes
CAUSE:
- gonorrhea
- chlamydia
- mycoplasma hominis
- coliforms
- strepto- and staphylococci
SYMPTOMS:
- fever
- lower abdominal pain
- pelvic masses
- adherence of tube to ovaries ⇒ tubo-ovarian abscess / tubo-ovarian complex
- adherence to tubal plicae ⇒ luminal culsde-sac ⇒ risk for ectopic pregnancy
```
38
85. Non-neoplastic diseases of the ovary and fallopian tubes:
ECTOPIC PREGNANCY
- mostly implant in the fallopian tube
- mortality of tubal pregnancy at isthmus or within uterus is higher ⇒ increased vascularity ⇒ internal hemorrhage
- caused by combination of retention of the embryo within the fallopian tube due to impaired embryo-tubal transport and alteration in tubal environment allowing early implantation to occur
39
85. Non-neoplastic diseases of the ovary and fallopian tubes:
PRIMARY ADENOCARCINOMA OF FALLOPIAN TUBES
- papillary, serous or endometrioid origin
| - increased in women with BRCA mutation
40
85. Non-neoplastic diseases of the ovary and fallopian tubes:
HEMATOSALPINX
- bleeding into fallopian tube
| - often caused by ectopic pregnancy
41
86. Ovarian tumors:
| PATHOGENESIS
RISK FACTORS:
- nulliparity
- family history
- unmarried women
- oral contraceptives reduces risk
- familial cause⇒ mutation in BRCA, KRAS, HER2/NEU
42
86. Ovarian tumors:
| SURFACE EPITHELIAL TUMORS
- arise from coelomic mesothelium that covers surface of ovary
- with repeated ovulation + scarring ⇒ epithelium into cortex⇒ small epithelial cyst ⇒ can undergo metaplasia and neoplastic transformation into epithelial tumors
43
86. Ovarian tumors:
| SEROUS CYSTADENOMA
- women 30-40yrs
- smooth glistening cyst wall; papillary tumors have papillary projections on outer surface or protruding into cystic cavity
- histo: small, multi lobular, simple papillary processes
44
86. Ovarian tumors:
| SEROUS BORDERLINE TUMOR
- younger women, often pregnant
- rarely malignant
- 1/3 bilateral
45
86. Ovarian tumors:
| SEROUS CYSTADENOCARCINOMA
- malignant cystic tumor of surface epithelial cells
- 5 year survival ⇒ 70%
- 2/3 bilateral
- solid, hemorrhagic, necrotic
- histo: nuclear atypia, stratification, glandular complexity, branching papillary folds, frequent mitoses, stromal invasion
- Psammon bodies: calcium concentration + concentric laminations
- frequent loss of heterozygosity of p53 and BRCA1
46
86. Ovarian tumors:
| MUCINOUS TUMORS
- the epithelium contains mucin-secreting cells
- less likely malignant
- larger size, often unilateral. filled with sticky, gelatinous fluid rick in glycoproteins
47
86. Ovarian tumors:
| MUCINOUS CYSTADENOMA
HISTOLOGY:
- tall, columnar, nonciliated cells
- basal nuceli
- intracellular mucin
- endocervical type epithelium
48
86. Ovarian tumors:
| MUCINOUS BORDERLINE TUMORS
HISTOLOGY:
- resembles villous or tubular adenomas of intestines
- endocrine cells common
- noninvasive with intraglandular or intracystic epithelial proliferations
49
86. Ovarian tumors:
| MUCINOUS CYSTADENOCARCINOMA
- mostly ovarian metastases
- stromal cells
- distant metastases rare
- unilateral, >10cm, smooth capsule, cystic and solid areas
- Histo: stromal invasion, more solid growth, atypia, stratification
50
86. Ovarian tumors:
| ENDOMETRIOID TUMORS
- solid or cystic
- mass projecting from wall of an endometriotic cyst filled with chocolate-colored fluid
- histo: formation of tubular glands within linings of cystic spaces
- usually malignant
51
86. Ovarian tumors:
| BRENNER TUMOR
- uncommon, solid, unilateral
- abundant stroma with nests transitional-like epithelium
- nests are cystic + lined by columnar mucus-secreting cells
- smoothly encapsulated + grey-white
52
86. Ovarian tumors:
| TERATOMA
- children + young adults
- usually benign (the younger the patient ⇒ more likelihood for malignancy)
BENIGN CYSTIC TERATOMA:
- differentiation of totipotent germ cells ⇒ mature tissue: ectoderm, endoderm + mesoderm
- formation of cyst lined by epidermis with adnexal appendages ⇒ "dermoid cyst" ⇒ contain hair, sebaceous glands, teeth, cartilage, bone etc.
- might cause infertility
IMMATURE MALIGNANT TERATOMA:
- age: 18yrs
- bulky, solid and punctuated by areas of necrosis
- Histo: immature differentiation
- foci of neuroepithelial differentiation ⇒ aggressive + metastasize
53
86. Ovarian tumors:
| CHORIOCARCINOMA
- age: 30yrs
- unilateral
- identical to placental tumor
- hemorrhagic focus
- give metastasis early
- resistant to chemotherapy
54
86. Ovarian tumors:
| DYSGERMINOMA
- age: 20-30 yrs
- mostly unilateral
MORPHOLOGY:
- solid, cords of clear cells separated by fibrous bands
- stroma: lymphocytes + granuloma
- malignant
- radiotherapy
55
86. Ovarian tumors:
| SEX CORD STROMAL TUMORS
```
- derived from ovarian stroma
GRANULOSA CELL TUMOR:
- differentiation towards follicular granulosa cells
- women >15yrs
- associated with hyperestrogenism
- symptoms:
* precocious puberty in children
* metorrhagia
* endometrial hyperplasia/ carcinoma
* breast fibrocystic changes
- prognosis: 10yr survival >90%
- Histo: small, bland, cuboidal to polygonal cells + Call-Exner Bodies
```
56
86. Ovarian tumors:
| GRANULOSA-THECAL CELL TUMOR
- sex cord stromal tumor
- any age, postmenopausal
- unilateral
- morphology: variable size, grey-yellow, cystic spaces
- theca cells ⇒ estrogen ⇒ endometrial / breast cc.
57
86. Ovarian tumors:
| THECOMA-FIBROMA
- sex cord stromal tumor
- any age
- unilateral
- solid grey
- rarely malignant
- hormonally inactive ⇒ ascites, hydrothorax
58
86. Ovarian tumors:
| SERTOLI-LEYDIG CELL TUMOR
- sex cord stromal tumor
- any age
- unilateral
- solid, small ⇒ testis like
- rarely malignant
- masculinization, defeminization
59
86. Ovarian tumors:
| CLINICAL FEATURES OF OVARIAN TUMORS
```
⇒ lower abdominal pain
⇒ abdominal enlargement
⇒ increased pressure on other organs
⇒ ascites
⇒ CA-125 present
```
60
87. Pathology of pregnancy:
| PLACENTAL INFLAMMATIONS AND INFECTIONS
1. Ascending infections through birth canal:
- bacterial infection ⇒ premature birth + premature rupture of membrane
- chorio-amnion show polymorphonuclear leukocytic infiltration with edema + congestion of vessels⇒ "acute chorioamnionitis"
- infection can involve umbilical cord + placental villi
- e.g. Candida albicans
2. Hematogenous infection:
- vilitis ⇒ vili infected
- e.g. syphilis, TBC, listeriosis, toxoplasmosis + viruses
Transplacental ⇒ TORCH complex
61
87. Pathology of pregnancy:
| ECTOPIC PREGNANCY
= implantation of fertilized ovum in abnormal site
- location: oviducts, ovaries, abdominal cavity
- causes: chronic inflammatory changes in oviduct, intrauterine tumor, endometriosis
- rupture of ectopic pregnancy ⇒ abdominal pain, acute abdomen, shock
62
87. Pathology of pregnancy:
| GESTATIONAL TROPHOBLASTIC DISEASE GTD general
- group of pregnancy related disorders arising from trophoblasts
- tumors:
* hydatidiform mole
* invasive mole
* choriocarcinoma
- increase in hCG
63
87. Pathology of pregnancy:
| HYDATIDIFORM MOLE
- voluminous mass of swollen, cystically dilated chorionic villi
- vili covered by atypical chorionic epithelium
- age: before 20s, after 40s
Subtypes:
1. Complete:
* does not permit embryogenesis
* all chorionic vili are abnormal, cells are diploid
* empty egg fertilized by 2 spermatozoa ⇒ diploid with only paternal cells
2. Partial:
* early embryo formation ⇒ contain fetal parts
* some normal chorionic vili, cells triploid
* normal egg fertilized by 2 spermatozoa ⇒ triploid with predominance of paternal cells
64
87. Pathology of pregnancy:
| INVASIVE MOLE
- complete moles, more invasive locally, no metastasis
- retains hydrophilic vili ⇒ penetrate uterine wall deeply
- local spread to broad ligament may occur
- Histo: epithelium hyperplastic + atypical changes, proliferation of cuboidal + syncytial components
- difficult to remove completely
65
87. Pathology of pregnancy:
| CHORIOCARCINOMA
- aggressive malignant tumor
- arises from gestational chorionic epithelium or totipotent cells in gonads
- age: <20s, >40s
- arise in complete hydatidiform mole or after abortion
- symptoms:
* bloody, brownish discharge
* rising titer of hCG
* absence of uterine enlargement
- Metastasis to lungs, vagina, brain, liver and kidneys
- treatment: chemotherapy
66
87. Pathology of pregnancy:
| PREECLAMPSIA/ ECLAMPSIA
= development of HT + proteinuria and edema in third trimester
- mostly in first pregnancy of women older than 35yrs
- symptoms:
* convulsive seizures
* DIC
PATHOGENESIS:
- inadequate development of spiral arteries ⇒ bad blood flow to placenta
- musculoskeletal walls of arteries are retained and remain narrow
CONSEQUENCES:
- placental hypoperfusion ⇒ infarct
- reduced elaboration of vasodilators by trophoblasts ⇒ HT
- ischemic placenta ⇒ DIC
- renal function impaired
67
88. Inflammation and fibrocystic changes of breast:
| ACUTE MASTITIS
= inflammation of breast tissue
- develop when bacteria get access to tissue via ducts
- cause: S.aureus
- single/multiple abscesses + acute inflammatory changes
68
88. Inflammation and fibrocystic changes of breast:
| MAMMARY DUCT ECTASIA
- nonbacterial chronic inflammation of breast + thickening of breast secretions
- ductal dilation + rupture ⇒ inflammation
- leads to induration of breast substance + retraction of nipple
69
88. Inflammation and fibrocystic changes of breast:
| TRAUMATIC FAT NECROSIS
- causes a mass
| - harmless and uncommon
70
88. Inflammation and fibrocystic changes of breast:
| FIBROCYSTIC CHANGES general
- due to exaggeration and distortion of normal cyclical menstrual cycle breast changes
- arise during reproductive period, may persist after menopause
71
88. Inflammation and fibrocystic changes of breast:
| FIBROCYSTIC CHANGES types
1. Non-proliferative patterns:
CYSTS AND FIBROSIS:
- increase in fibrous stroma + dilated ducts + formation of cysts
- stroma⇒ compressed fibrous tissue
2. Proliferative patterns:
EPITHELIAL HYPERPLASIA:
- proliferative lesions in ductules, terminal ducts and lobules of breast
- some mild and orderly, some more atypical + high risk for malignancy
SCLEROSING ADENOSIS:
- marked intralobular fibrosis + proliferation of small ductules and acini
- minimal risk for malignancy
72
88. Inflammation and fibrocystic changes of breast:
| RELATIONSHIP OF FIBROCYSTIC CHANGES TO BREAST CARCINOMA
1. Minimal or no increased risk of breast cc:
- fibrosis, cystic changes, apocrine metaplasia, mild hyperplasia, fibroadenoma
2. Slightly increased risk:
- moderate hyperplasia, ductal papillomatosis, sclerosing adenosis
3. Significantly increased risk:
- atypical hyperplasia, ductular or lobular
73
89. Tumors of breast:
| FIBROADENOMA
- arise from CT and epithelium
- morphology: small, solid, rubbery, noncancerous, harmless lump composed of fibrous + glandular tissue
* Pericanalicular FA: ducts are open with regular structure + surrounded by fibroblastic stroma
* Intracanalicular FA: ducts compressed by stromal proliferation ⇒ star-shaped structure
- cause: increased estrogen activity
- age: young women - 30yrs
CLINICAL FEATURES:
- solitary, discrete, movable mass
- enlarge late in menstrual cycle + pregnancy
- regress after menopause
- never become malignant
74
89. Tumors of breast:
| PHYLLODES TUMOR
- arise from periductal stroma
- grow large, become lobulated and cystic
- threatening change: increased stromal cellularity with anaplasia + high mitotic activity
- remain localized
- cured by excision
- only most malignant ones metastasize
75
89. Tumors of breast:
| INTRADUCTAL PAPILLOMA
- benign epithelial tumor growing in finger-like fronds inside a duct
- middle aged women
- solitary lesions in principal lactiferous ducts or sinuses
- multiple papillomas ⇒ might become malignant
- clincial: serous/bloody nipple discharge
76
89. Tumors of breast:
| ADENOMA
- rare
- arise from epithelium
- tubular and lactating adenoma: young women
- nipple adenoma: all ages
⇒ may ulcerate the skin
77
89. Tumors of breast:
| CARCINOMA epidemiology
1. Geographic factors
2. Age: more in older women
3. Genetics and family history:
⇒ specific inherited mutations: BRCA-1, BRCA-2
⇒ Li-Fraumeni syndrome (p53)
⇒ Cowden disease (PTEN)
4. Exogenous estrogen
5. Oral contraceptives
6. Obesity
7. Alcohol
8. Smoking
9. Ionizing radiation
10. Menarche at young age or menopause at old age
11. Benign breast disease
12. Late age of 1st pregnancy
78
89. Tumors of breast:
| CARCINOMA pathogenesis
1. Genetic changes:
- familial heriditary syndromes (Li-Fraumeni, Cowdens)
- overexertion of HER2/NEU protooncogene
- amplification of RAS and MYC genes
- mutation in tumor suppressor genes p53 and RB
- hypermethylation of estrogen receptors
2. Hormonal influences:
- increased estrogen
3. Environmental variables:
- irradiation + exogenous estrogen
79
89. Tumors of breast:
| CARCINOMA spread of breast cancer
- through lymphatics and hematogenous channels
- LN metastasis
* outer quadrant + central ⇒ axillary LN
* inner quadrant ⇒ LN along internal mammary arteries
- distant dissemination later ⇒ lungs, bones, liver, adrenals (+brain, spleen, pituitary)
80
89. Tumors of breast:
| CARCINOMA prognosis
1. Size of the primary carcinoma
2. Lymph node involvement and number of LN
3. Distant metastasis
4. Grade of the carcinoma
5. Histologic type of carcinoma
6. Presence or abcense of estrogen or progesterone receptors
7. Proliferative rate of cancer
8. Aneuploidy
9. Overexpression of HER2/NEU
81
89. Tumors of breast:
| STAGING OF BREAST CANCER
STAGE 0: 5yr survival ⇒ 92%
- DCIS
- LCIS
STAGE 1: 5yr survival ⇒ 87%
- invasive carcinoma 2 cm, no nodal involvement
STAGE 2: 5yr survival ⇒ 75%
- invasive carcinoma 5cm without nodal involvement
STAGE 3: 5yr survival ⇒ 46%
- invasive carcinoma with nodal involvement
STAGE 4: 5yr survival ⇒ 13%
- any breast cancer with distant metastasis
