Reproductive System Pathology_FM Breast and FM Reproductive Systems

Marc Imhotep Cray, MD
Photo: Color-enhanced scanning electron micrograph of a human spermatocyte fertilizing an oocyte; From: Seeley’s Anatomy & Physiology 10th ed New York, NY: McGraw-Hill 2010

Learning Outcomes cont.
2
Breast:
1. List the inflammatory breast lesions and discuss their etiology.
2. Describe the morphology of the inflammatory breast lesions with
special reference to breast abscess, duct ectasia and fat necrosis.
3. List the proliferative breast lesions and discuss their etiology.
4. Describe the morphology of the proliferative breast lesions with
special reference to fibrocystic changes.
5. Explain the relationship between fibrocystic changes of the breast
and breast cancer.
6. Classify breast tumors
By the end of this sequence the learner will/should be able to:

Female Breast Learning Outcomes cont.
3
7. Describe the morphology of the benign breast tumors with special
reference to fibroadenoma and intraductal papilloma
8. List the risk factors of breast cancer
9. List the histological classification of breast cancer.
10.Explain the prognostic factors of the breast cancer with special
reference to: stage at the time of diagnosis, histological features &
Estrogen-receptor status
11.Describe the gross and microscopic features of different breast
carcinoma with special reference to: in situ ductal carcinoma, in situ
lobular carcinoma, invasive duct carcinoma, invasive lobular
carcinoma & Paget’s disease of the breast.

Learning Outcomes cont.
4
Female genital system:
1. Describe acute and chronic cervicitis.
2. Describe the pathogenesis, risk factors, clinical features and
morphology of squamous cell carcinoma of cervix.
3. Describe the terms used in dysfunctional uterine bleeding and list
its causes.
4. Describe endometritis with special references to various forms of
endometritis.
5. Define endometriosis; explain the theories of endometriosis and
its morphology and complications.
6. Describe endometrial polyps.
FM Reproductive Anatomy_ The Noted Anatomist

FM Genital System Learning Outcomes cont.
5
7. Describe the three types of endometrial hyperplasia.
8. Describe risk factors, etiology, clinical features, morphology and
pathogenesis of endometrial carcinoma as well its morphology.
9. Describe the morphology and clinical features of leiomyomas of the
uterus.
10.List the differences between leiomyoma and leiomyosarcoma of
the uterus.
11.Classify tumors and tumor like lesions of the ovary
12.Describe the pathogenesis and morphology of surface epithelium
tumors, teratomas and granulose theca cell tumors

Female Breast Pathology
6

Female Breast Functional Anatomy
7
 Functional unit of breast is lobule supported by a specialized
intralobular stroma
 Inner luminal epithelial cells produce milk during lactation
 Basally located myoepithelial cells have contractile function to aid
in milk ejection
 Ducts are conduits for milk to reach the nipple
Size of breast is determined primarily by interlobular stroma
increases during puberty and involutes with age
Each normal constituent is a source of both benign and malignant
lesions

Normal breast, gross
8
Klatt EC. Robbins and Cotran Atlas of Pathology, 3rd Ed. 2015.

Breast, mammogram
9
 A mammogram uses a small amount of x-radiation to
visualize the breast parenchyma
 This mammogram shows normal pattern of
lactiferous sinuses and ducts. There is one suspicious
density ( ), however, which could be a carcinoma or
just an area of pronounced sclerosis with fibrocystic
changes
 A mammogram is a useful screening tool to find such
lesions and to determine need for further workup
 A mammogram may detect lesions that are not
palpable
 Women in their 30s begin to have some involution of
lobules and adjacent stroma, and breast tissue
becomes more radiolucent from an increased
composition of adipose tissue replacing fibrous
stroma and lobules

Marc Imhotep Cray, MD 10
Normal breast, microscopic

Origins of breast disorders
Kumar, V; Abbas AK (Eds.), Robbins Basic Pathology, 10th Ed. Philadelphia: Elsevier, 2018; Fig.19.22, 736.
 Benign epithelial lesions include
intraductal papillomas that grow in
sinuses below nipple & epithelial
hyperplasia that arises in lobules
 Malignant epithelial lesions are
mainly breast carcinomas, which may
remain in situ or invade into breast
and spread by metastasis
 Specialized intralobular stroma
(green) cells may give rise to
fibroadenomas and phyllodes
tumors, whereas interlobular stroma
(red) may give rise to a variety of
rare benign and malignant tumors

Clinical Presentations of Breast Disease
12
Predominant symptoms and signs of diseases of breast are pain,
inflammatory changes, nipple discharge, “lumpiness,” or a palpable mass
Kumar, V; Abbas AK (Eds.), Robbins Basic Pathology, 10th Ed. Philadelphia: Elsevier, 2018; Fig.19.23, 737.

Risk Factors for Breast Cancer Development
13
Not Modifiable Modifiable
Age Body mass index
BRCA germline mutations Diet
Family history Alcohol
Chest radiation Exogenous estrogen
Race/ethnicity Exercise
Height Smoking
Age at menarche Reproductive history
Age at menopause Age at first full-term delivery
Breast density Lactation
Atypia on prior breast biopsy
Redrawn after Rubin R and Strayer DS Eds. Rubin’s Essential of Pathology:, 6th Ed., 2014, Pg. 536.

Clinical Presentations of Breast Disease:
Key Points
14
 Symptoms affecting breasts are evaluated primarily to
determine if malignancy is present
 Regardless of symptom, underlying cause is benign in majority of
cases
 Breast cancer is most commonly detected by palpation of a
mass in younger women and in unscreened populations and
by mammographic screening in older women

Vignette #1
15
A 30-year-old woman presents to your clinic complaining of bilateral, diffuse
breast pain. Her last menstrual period was 2 weeks ago and she says that she has
felt several painful masses in both breasts during her self-examination in the
shower. She is very concerned because she has a sister-in-law, who was recently
diagnosed with breast cancer. On physical examination, you notice multiple,
palpable masses on both breasts but no changes to the overlying skin. After taking
a detailed history, you learn that the patient does not drink or smoke, has no
immediate family members with a history of breast cancer, and there has been no
nipple discharge. You order a fine needle aspiration cytology, which reveals an
aspirate suggestive of a cyst. You reassure the patient that the lesion is benign and
recommend that she avoid trauma to the affected regions and wear a brassiere
that gives good support and protection.
What is the Diagnosis?

Fibrocystic Changes of the Breast
16
Etiology and Epidemiology: Caused by hormonal imbalance (increased estrogens
and/or decreased progesterones); Peak incidence is between 25 and 50 years old
Pathology:
Four histologic types:
1. Cystic: multiple fluid-filled cysts appear blue (blue-dome cyst) cysts lined by
polygonal cells with eosinophilic granular cytoplasm that are similar to
apocrine epithelium (apocrine metaplasia), may see papillary projections of
cystic epithelium;
2. Epithelial hyperplasia of breast duct: increase in number of epithelial layers
in terminal duct lobules resulting in irregular lumens;
3. Stromal fibrosis: hyperplasia and fibrosis of breast stroma;
4. Sclerosing adenosis: increased number of acini, stromal fibrosis

Fibrocystic Changes of the Breast cont.
17
Clinical Manifestations: Presents with diffuse breast pain (midcycle tenderness)
and multiple, palpable lesions, often bilateral; no changes in overlying skin or
nipple; rapid fluctuation in size of masses is common
Treatment: Symptom management with pain control
NB: Fibrocystic changes are most common breast disorder
 Cystic and stromal fibrosis represent no increased risk for carcinoma, but
 Epithelial hyperplasia and sclerosing adenosis do carry a mildly increased
risk

Fibrocystic changes, gross

Fibrocystic changes, microscopic

Sclerosing adenosis, microscopic

Epithelial hyperplasia, microscopic

Normal lactating breast, microscopic

Acute mastitis, microscopic

Breast abscess, gross

Vignette #2
28
A 21-year-old African American woman presents to the clinic
complaining of a large mass in her left breast. She has no immediate
family members with breast cancer. On physical examination,
you notice that the mass is round, rubbery, mobile, and nontender.
It is approximately 4 cm in diameter. You order a needle biopsy that
shows a combination of connective tissue and cystic spaces taking on
a leaflike appearance. You inform the patient that this lesion is most
often benign, but nevertheless you suggest that she be treated with a
local excision to remove the growth.

Benign Tumors of the Breast
29
Epidemiology: Fibroadenoma (FA): Occurs in women < 40; tends to occur more
frequently and at a younger age in African American women; Phyllodes tumor
(PT): Occurs most commonly after the age of 50; Intraductal papilloma (IP):
Occurs in middle-aged women
Pathology:
 FA: Gross: small, mobile, rubbery, firm mass with sharp, well-circumscribed
edges; Microscopic: fibroblastic stroma surrounding cystic and glandular
spaces; may regress after menopause and demonstrate calcifications.
 PT: Gross: large, bulky mass of connective tissue and cysts; Microscopic:
cystic spaces on cut section of stroma contains leaflike projections from cyst
walls; leaflike appearance on breast surface; 5%–10% undergoes malignant
change with atypia (cystosarcoma phyllodes).
 IP: Gross: arising from major lactiferous ducts; Microscopic: proliferation of
ductal epithelial tissue in papillary growth manner; apocrine metaplasia

Benign Tumors of the Breast cont.
30
Clinical Manifestations: FA and PT: Increased size and tenderness of
mass with pregnancy or menstrual cycle; no overlying skin changes; no
lymphadenopathy; no nipple retraction
IP: Presents with nipple discharge
Treatment:
FA: No treatment or simple excision
PT: Local excision with wide margin; can recur after resection
IP: Simple excision
Of note: Phyllodes tumor and intraductal papilloma
carry a mildly increased risk of breast carcinoma

Fibroadenoma, gross

Fibroadenoma, microscopic

Phyllodes tumor, microscopic

Phyllodes tumor, mammogram
34
 This mammogram shows a bright, solid
10-cm rounded mass lesion consistent
with a phyllodes tumor
 It still has discrete margins, similar to a
fibroadenoma, but is much larger
 The biologic behavior of a phyllodes
tumor is difficult to predict, and it may
recur locally, but rarely are there high-
grade lesions that can metastasize
 Tend to occur at an older age than do
fibroadenomas, most commonly in sixth
decade

Intraductal papilloma, microscopic

Vignette #3
36
A 50-year-old woman presents to your clinic after finding a mass on the upper
outer quadrant of her left breast. After taking a thorough history, you learn that
her mother died from breast cancer and her maternal aunt was also diagnosed
with breast cancer at an early age. The patient started her period at age 11, did
not bear any children, and has not been through menopause. On physical
examination, she is markedly obese and you notice retraction of the skin and the
nipple on her left breast. You locate the mass in question during your breast
examination and find that it is fixed, hard, and nontender. The mass was not
present on her last mammogram dating back 2 years. You also feel palpable
axillary lymph nodes. You schedule the patient for an immediate mammography
and needle biopsy to confirm your suspicions.

Breast Carcinoma
37
Etiology and Epidemiology:
Risk factors include:
 Family history of first-degree
relative with breast cancer at
young age (highest risk),
 Autosomal dominant
inheritance of mutations in
BRCA1 or BRCA2 gene,
 female gender,
 Increased age,
 Early first menarche,
 Delayed first pregnancy,
 Nulliparity,
 Late menopause,
 Radiation exposure, and
 exogenous estrogen use

Breast Carcinoma Epidemiology cont.
38
 Breast carcinoma is the most common malignancy of women globally
(excluding nonmelanoma skin cancer) and causes majority of cancer deaths
in women
Incidence in United States decreased slightly in 2002 and then stabilized
 changes attributed to a decrease in use of postmenopausal hormone
therapy and a plateau in number of women undergoing mammographic
screening
 Worldwide incidence and mortality is increasing at an alarming rate
 major factors underlying this trend in developing countries are thought to
be social changes that increase breast cancer risk—specifically, delayed
childbearing, fewer pregnancies, and reduced breastfeeding—combined
with a lack of access to optimal health care

Breast Carcinoma Pathology
39
 Almost all breast malignancies are adenocarcinomas (>95%)
 In the most clinically useful classification system, breast cancers
are divided based on expression of hormone receptors:
 estrogen receptor (ER) and progesterone receptor (PR)—and
 expression of human epidermal growth factor receptor 2 (HER2,
also known as ERBB2 & HER2/neu), into three major groups:
• ER positive (HER2 negative; 50%–65% of cancers)
• HER2 positive (ER positive or negative; 10%–20% of cancers)
• Triple negative (ER, PR, and HER2 negative; 10%–20%
of cancers)
NB: These three groups show striking differences in patient
characteristics, pathologic features, treatment response,
metastatic patterns, time to relapse, and outcome

Age and incidence of breast cancer subtypes
40
 The three hormone receptors
expression groups of the
previous slide show striking
differences in
 patient characteristics,
 pathologic features,
 treatment response,
 metastatic patterns,
 time to relapse, and
 outcome Kumar, V; Abbas AK (Eds.), Robbins Basic Pathology, 10th Ed. Philadelphia:
Elsevier, 2018; Fig.19.26, 740.

FM Breast Anatomy
41

Breast Carcinoma Pathology cont.
42
1. Infiltrating ductal carcinoma: Tumor cells arranged in cords,
islands, or glands embedded in dense fibrous stroma; may arise
from ductal carcinoma in situ (DCIS)
2. Intraductal comedocarcinoma: Sheet of tumor cells confined
within duct; central necrosis; periductal fibrosis with inflammation
3. Inflammatory: Lymphatic involvement of overlying skin
4. Paget disease: Paget cells (large cells w clear halo of pale
cytoplasm) extend from ducts and invade epidermis of nipple;
underlying ductal adenocarcinoma within subareolar excretory
ducts always present

Breast Carcinoma Pathology cont.
43
5. Infiltrating lobular: Often multiple and bilateral; cells line up
(Indian file) with tumor cells surrounding lobule in target fashion;
signet ring cells; may arise from lobular carcinoma in situ (LCIS)
after many years
6. Medullary: Solid sheets of cells with large nucleoli in scant
stroma; lymphocytic infiltrate
7. Mucinous (colloid): Pools of extracellular mucin surrounding
tumor cell clusters; gelatinous consistency
Note: Breast carcinoma is second most
common cause of cancer death among women

Breast Cancer Morphology
44
 Most common location of tumors within breast is in upper
outer quadrant (50%), followed by central portion (20%)
 About 4% of women with breast cancer have bilateral primary
tumors or sequential lesions in the same breast
 Breast cancers are classified morphologically according to
whether they have penetrated the basement membrane
• Those that remain within this boundary are termed in situ
carcinomas, and
• those that have spread beyond it are designated invasive
carcinomas

Breast Cancer Morphology cont.
45
In classification, above main forms of breast carcinoma are as follows:
A. Noninvasive
1. Ductal carcinoma in situ (DCIS)
2. Lobular carcinoma in situ (LCIS)
B. Invasive
1. Invasive ductal carcinoma (includes all carcinomas that are not of a special
type)-70% to 80%
2. Invasive lobular carcinoma- 10% to 15%
3. Carcinoma with medullary features-5%
4. Mucinous carcinoma (colloid carcinoma) -5%
5. Tubular carcinoma-5%
6. Other types
Adapted from: Kumar, V; Abbas AK (Eds.), Robbins Basic Pathology,
10th Ed. Philadelphia, Pa : Elsevier, 2018;742.

Noninvasive (in Situ) Carcinoma
46
 Two morphologic types of noninvasive breast carcinoma: ductal
carcinoma in situ (DCIS) and lobular carcinoma in situ (LCIS)
“ terms ductal and lobular are misleading, as both types of CIS are thought to
arise from cells in terminal duct that give rise to lobules*”
 By definition, both "respect" the basement membrane and do
not invade into stroma or lymphovascular channels
• DCIS has a wide variety of histologic appearances, including solid,
comedo, cribriform, papillary, micropapillary, and "clinging" types
*From: Kumar, V; Abbas AK (Eds.), Robbins Basic Pathology, 10th Ed. Philadelphia: Elsevier, 2018;743.

Carcinoma in situ.
(A) Lobular carcinoma in situ (LCIS).
(B) Ductal carcinoma in situ (DCIS). DCIS partially involves the lobule in the lower half of this photo
and has completely effaced the upper lobules, producing a ductlike appearance.
(C) Mammographic detection of calcifications associated with DCIS.
47
Kumar, V; Abbas AK (Eds.), Robbins Basic Pathology, 10th Ed. Philadelphia: Elsevier, 2018; Fig.19.28,743.

Vignette #4
48
A 49-year-old woman presents to your office concerned about a rash
on her left nipple that has developed over the past month. The rash is
itchy, but painless. On physical examination, you find a large
eczematous-like patch over the left nipple as well as a fixed mass in
the left breast. You perform both a skin biopsy as well as a needle
biopsy of the mass. When the skin biopsy reveals large cells with a
clear halo of pale cytoplasm invading the epidermis, you become
certain that the biopsy of the mass will reveal carcinoma of the breast.

Breast Carcinoma cont.
49
Clinical Manifestations: Painless, usually fixed, hard, nontender mass
often found in upper outer quadrant of breast; retraction of overlying
skin and nipple; palpable axillary lymph nodes
 Infiltrating ductal carcinoma: Firm, fixed, fibrous mass
 Inflammatory: Red, swollen, hot, painful to touch, orange-peel
appearance of skin
 Paget disease: Itchy, scaly, painless, eczematous patches on nipple
 Medullary: Soft, fleshy-consistency mass
Lab findings: Paraneoplastic syndrome with secretion of PTH-related
peptide may lead to hypercalcemia
Imaging: Mammogram with microcalcifications, spiculated or
enlarging mass

Breast Carcinoma cont.
50
Treatment:
 Surgery and radiation therapy;
 Chemotherapy;
 Hormonal therapy (tamoxifen or aromatase inhibitors) for
patients with cancer cells expressing estrogen receptor in their
nuclei (ER/PR+);
 Biologic therapy Trastuzumab (herceptin) for patients with
HER2/neu expression
NB: Metastasis occurs to lymph nodes, lung, liver, and bone.

Ductal carcinoma in situ, microscopic

Lobular carcinoma in situ, microscopic

Paget disease of breast, microscopic

Invasive ductal carcinoma, microscopic

Invasive ductal
carcinoma, gross
and mammogram

Infiltrating ductal carcinoma, gross
and mammogram

Breast Carcinoma Key Points Summary
57
 The lifetime risk of developing breast cancer for an American woman is 1 in 8.
 A majority (75%) of breast cancers are diagnosed after the age of 50.
 The major risk factors for developing breast cancer are related to hormonal
factors and inherited susceptibility.
 About 12% of all breast cancers are caused by identified germline mutations;
BRCAI and BRCA2 genes account for one-half of the cases associated with
single-gene mutations.
 DCIS is a precursor to invasive ductal carcinoma and is most often found on
mammographic screening as calcifications.
 When carcinoma develops in a woman with a previous diagnosis of untreated
DCIS, it is usually is an invasive ductal carcinoma in the same breast.

 LCIS is both a marker of increased risk and a precursor lesion.
 When carcinoma develops in a woman with a previous diagnosis of LCIS, two-
thirds are in the same breast and one-third is in the contralateral breast.
 Invasive carcinomas are classified according to histologic type and biologic
type: ER-positive/HER2-negative, HER2-positive, and ER/PR/HER2-negative
(triple-negative). The biologic types of cancer have important differences in
patient characteristics, grade, mutation profile, metastatic pattern, response to
therapy, time to recurrence, and prognosis.
 Prognosis is dependent on the biologic type of tumor, stage, and the availability
of treatment modalities.
Breast Carcinoma Key Points Summary (2)

Ovaries and Uterus Pathology
59

Normal internal genitalia, gross
60

Normal internal genitalia, radiograph
61

Normal fallopian tube, microscopic
62

Normal adult ovary, microscopic
63

Normal ovary, microscopic
64

Corpus luteum, gross
65

Menstrual cycle capsular summary:
 Menstrual cycle is divided into follicular phase and luteal phase
Ovulation defines transition between these two phases
 During follicular phase, gonadotroph cells of anterior pituitary gland
secrete LH and FSH in response to pulsatile GnRH stimulation
 Circulating LH and FSH promote growth and maturation of ovarian follicles
 Developing follicles secrete increasing amounts of estrogen
 At first, estrogen has an inhibitory effect on gonadotropin release Just
before midpoint in menstrual cycle, however, estrogen exerts a brief
positive feedback effect on LH (LH Surge) and FSH release This is
followed by follicular rupture and release of an egg into fallopian tube
 During second half of cycle, corpus luteum secretes both estrogen and
progesterone
 Progesterone induces a change in endometrium from a proliferative to a
secretory type
 If fertilization and implantation of a blastocyst do not occur within 14 days
after ovulation corpus luteum involutes secretion of estrogen and
progesterone declines, menses occurs, and a new cycle begins
Cairo CW, Simon JB, Golan DE. (Eds.). Principles of Pharmacology:
The Pathophysiologic Basis of Drug Therapy. LLW, 2012.

Hormonal Control of the Menstrual Cycle, Animation.
67
Online Version

Menstruation terminology
68
 Dysmenorrhea= Pain with menses often associated with
endometriosis
 Oligomenorrhea > 35-day cycle
 Polymenorrhea < 21-day cycle
 Metrorrhagia= Frequent or irregular menstruation
 Menorrhagia= Heavy menstrual bleeding > 80 mL blood loss or > 7
days of menses
 Menometrorrhagia= Heavy, irregular menstruation

Vignette #5
69
A 45-year-old woman presents to the clinic complaining of vague
abdominal pain for the past 4 days. She describes her pain as more of
a pelvic pressure that is generalized bilaterally. Her last menstrual
period was 2 weeks ago and she states that she has regular menstrual
cycles. She denies the possibility of pregnancy and is currently not
taking oral contraceptives. She has not had any changes in digestive
functions and denies any nausea, vomiting, constipation, or diarrhea.
She has no family history of ovarian cancer. When an ultrasound
confirms your suspicions, you place the patient on oral contraceptive
pills, believing that her symptoms will disappear in 2 months, and you
schedule her for a follow-up ultrasound.

Ovarian Cysts
70
Etiology and Epidemiology:
 Follicular (F) cyst: Associated with hyperestrinism and endometrial
hyperplasia; most common cause of ovarian enlargement; mostly found
during menstrual years
 Corpus luteum (CL) cyst: Found during menstrual years
 Theca-lutein (TL) cyst: Associated with choriocarcinoma, hydatidiform
moles, and clomiphene (synthetic gonadotropin) therapy
Pathology
 F: Often bilateral; distention of unruptured Graafian follicle; lined by
granulosa cells
 CL: Often unilateral; contains clear fluid; lined by yellowish luteal cells with
cytoplasmic lipid droplets; may hemorrhage into persistent mature corpus
luteum
 TL: Often bilateral and multiple; lined by luteinized theca cells

Ovarian Cysts cont.
71
Clinical Manifestations: All may be asymptomatic or present with
pelvic pressure/pain or vague GI discomfort
 F: Pain not associated with menstruation
 CL: Delayed menstruation
 TL: Amenorrhea
Lab findings:
hCG elevated as a result of trophoblastic proliferation
Treatment:
 F: Often disappears with 2-month regimen of oral
contraceptives; follow with serial ultrasounds; laparoscopic
removal if persistent
 CL and TL: Cyst removal or unilateral oophorectomy

Vignette #6
72
A 30-year-old white woman presents to the fertility clinic with her husband,
complaining of the inability to conceive. The couple has already checked the
husband’s sperm motility and count, which are within the normal range. The
patient informs you that she has not menstruated for the last 4 months and that
she has had a very irregular and sporadic menstrual cycle all of her life. You
perform a physical examination, finding that the patient is obese with an
inordinate amount of facial hair. She denies any abnormal uterine bleeding. You
order serum studies that show elevated plasma LH and testosterone and
decreased FSH levels. Based on these findings, you inform the patient that
weight reduction will be the most effective treatment for restoring ovulation
and that adjunct therapy with clomiphene can aid in ovulation.

Polycystic Ovarian Syndrome (Stein-Leventhal
Syndrome)
73
Etiology and Epidemiology: Etiology unclear, but it is believed that a dysregulation
of enzymes involved in androgen biosynthesis may be caused by increased LH
secretion thereby resulting in excessive production of androgens; associated
with obesity, Cushing syndrome, congenital adrenal hyperplasia, genetic
predisposition, and androgen-secreting adrenal tumors
Common endocrine disorder affecting 2%–5% of women during reproductive age
Pathology and Pathophysiology:
Pathophysiology: Increased androgen production causes anovulation, multiple
follicular cysts, and theca cell hyperplasia
Gross: Ovaries enlarged; pearly white thickened ovarian capsule; multiple cysts
Microscopic: Cysts have granulosa cell layer and luteinized theca cells; cortical
stromal fibrosis

PCOS cont.
74
Clinical Manifestations: Amenorrhea; infertility; obesity; hirsutism (in
70%); insulin resistance with increased risk of diabetes; virilism;
increased risk of breast and endometrial carcinoma
Lab findings: Increased LH, decreased FSH, increased testosterone,
evidence of insulin resistance
Treatment: Weight loss; oral contraceptives; metformin for insulin
resistance; gonadotropin analogs; ovulation induction with clomiphene

Polycystic ovary, MRI
75

Polycystic ovarian syndrome, microscopic
76

Vignette #7
77
A 40-year-old woman presents to the emergency room with
generalized abdominal pain and pelvic pressure. After taking a more
complete history, you learn that she has not passed stool for the last
3 days and vomited this morning. She tells you that the pain has
been steady over the last week. You order an abdominal/pelvic CT
scan, which is inconclusive, but does demonstrate bilateral
enlargement of the ovaries. The patient is taken to the operating
room for an exploratory laparotomy that shows extensive mucinous
ascites, cystic epithelial implants on the peritoneal surfaces, and
several adhesions. You believe that the patient’s mucinous peritoneal
involvement is caused by her ovarian condition.

Ovarian Tumors of Surface Epithelium Origin
78
Epidemiology: Usually occurs in women > 20 years of age
Pathology:
 Serous cystadenoma: Bilateral, benign cyst with fallopian tube-like epithelium
 Papillary serous cystadenocarcinoma: Bilateral, malignant cysts lined by
stratified atypical epithelium; papillary growth; psammoma bodies
 Mucinous cystadenoma: Multilocular, benign cysts with columnar cells filled
with mucin
 Mucinous cystadenocarcinoma: Malignant tumor with mucus-secreting
atypical columnar epithelium; loss of gland architecture; necrosis
 Brenner tumor: Benign tumor with nests of cells resembling bladder
transitional epithelium interspersed in fibrous stroma
 Endometrioid tumor: Malignant tumor resembling endometrium
Clear cell tumor: Rare, malignant tumor composed of sheets of clear cells

Ovarian Tumors of Surface Epithelium
Origin cont.
79
Clinical Manifestations: Mild, nonspecific abdominal discomfort;
malignant forms may present with weakness, weight loss, and
anorexia; pseudomyxoma peritonei (intraperitoneal accumulation of
mucinous material) is associated with mucinous cystadenocarcinoma
Lab finding: Elevated CA-125 in ovarian carcinomas
Treatment: Tumor removal; oophorectomy or hysterectomy;
chemotherapy
Of note: Ovarian epithelial tumors make up 75% of ovarian tumors.

Serous cystadenoma, gross
80

Serous
cystadenoma,
MRI and CT
image

Multiloculated ovarian tumor, gross
82

Cystadenoma, serous, mucinous, microscopic
83

Borderline serous tumor, microscopic
84

Borderline tumor, gross
85

Cystadenocarcinoma & peritoneal
metastases, CT images
86

Cystadenocarcinoma, gross
87

Cystadenocarcinoma, microscopic
88

Endometrioid tumor, microscopic
89

Brenner tumor, microscopic
90

Vignette #8
91
An 18-year-old white woman is admitted to your gynecologic service with a 1-
month history of increasing abdominal pain and a rapidly enlarging pelvic
mass. While admitting the patient, you perform a bimanual pelvic examination
that reveals a left ovarian mass. This finding is consistent with the admitting
note and was confirmed by abdominal/pelvic CT, which showed that the left
ovary was twice as large as the right ovary. Serum studies demonstrate an
elevated AFP level. There is no inguinal lymph node involvement and no signs
of metastasis on imaging studies. Based on your findings, you perform a
unilateral oophorectomy and send the diseased ovary for pathologic analysis.
Histology shows glomerulus-like structures composed of a central blood vessel
enveloped by germ cells within a space similarly lined by germ cells. These
histologic bodies confirm your suspected diagnosis and you start the patient
on combination chemotherapy

Ovarian Tumors of Germ Cell Origin
92
Etiology and Epidemiology: Risk factors include nulliparity, positive family history
of ovarian cancer, mutations in BRCA1 and BRCA2 genes and high expression of
HER2/neu oncogene; Occurs most commonly in children and young adults (except
for teratomas, which can occur at all ages)
Pathology:
 Dysgerminoma: Malignant unilateral tumor comprised of large vesicular cells
with clear cytoplasm and central nuclei; analogous to male testicular seminoma
 Yolk sac tumor: Malignant tumor with Schiller-Duval bodies (glomerulus-like
structure composed of central blood vessel enveloped by germ cells)
 Choriocarcinoma: Aggressive and malignant tumor with areas of necrosis and
hemorrhage composed of neoplastic syncytiotrophoblasts and cytotrophoblasts
 Teratoma: 90% of germ cell tumors; mature teratomas (dermoid cysts) are
benign; immature are malignant ; Histology: structures from all germ layers.
 Struma ovarii: Unilateral ovarian teratoma composed of thyroid tissue

Ovarian Tumors of Germ Cell Origin cont.
93
Clinical Manifestations: Mild, nonspecific abdominal discomfort;
struma ovarii may lead to hyperthyroidism
Lab findings: Increased AFP (yolk sac), increased hCG (choriocarcinoma)
Tx: Tumor removal; oophorectomy or hysterectomy; chemotherapy
Note: Germ cell tumors make up 25% of ovarian tumors

Mature cystic teratoma, gross

Mature cystic teratoma, CT image

Mature cystic teratoma, microscopic

Dysgerminoma, gross

Dysgerminoma, microscopic

Vignette #9
99
A 12-year-old girl is brought into the emergency room because of
heavy vaginal bleeding. The child is also complaining of GI discomfort
and pelvic pressure. She states that she had her last menstruation 2
weeks earlier and she is not sexually active. Her first menstruation was
at the age of 10. On physical examination, the child appears to have
undergone precocious puberty. A pelvic examination reveals a
palpable right ovarian mass, which is confirmed by a CT scan. Serum
studies show a significantly increased level of circulating estrogen.
When a biopsy reveals distinctive, gland-like structures filled with an
acidophilic material, you worry that this patient may have an
increased risk of developing endometrial carcinoma later in life if this
mass is not removed.

Ovarian Tumors of Sex Cord–Stromal Origin
100
Etiology and Epidemiology: Risk factors include nulliparity, positive family
history of ovarian cancer, mutations in BRCA1 and BRCA2 genes, and high
expression of HER2/neu oncogene; Affects all age groups
Pathology and Pathophysiology:
 Ovarian fibroma-thecoma (OFT): Secretes estrogen; tumor composed of
round lipid-containing cells in addition to well-differentiated fibroblasts
 Granulosa cell tumor (GCT): Secretes estrogen causing endometrial
hyperplasia/carcinoma in adults; characterized by Call-Exner bodies (small
follicles filled with eosinophilic secretions) and small cuboidal, deeply
stained granulosa cells arranged in anastomotic cords
 Sertoli-Leydig cell tumor (SLCT): Secretes androgens; tumor composed of
Sertoli or Leydig cells interspersed with stroma

Ovarian Tumors of Sex Cord–Stromal Origin cont.
101
Clinical Manifestations: Mild, nonspecific abdominal discomfort
 OFT: Presents with Meig syndrome (triad of ovarian tumor,
ascites, and hydrothorax)
 GCT: Vaginal bleeding from endometrial hyperplasia; cystic
disease of breast; endometrial carcinoma
 SLCT: Virilism
Lab findings: Increased estrogen levels (OFT and GCT)
Treatment: Tumor removal; oophorectomy or hysterectomy;
chemotherapy
Note: Ovarian sex cord–stromal tumors are rare

Granulosa–theca cell tumor, gross

Granulosa cell tumor, microscopic

Thecoma-fibroma, gross

Thecoma-fibroma, microscopic

Vignette #10
106
A 31-year-old woman presents to the clinic complaining of abnormal
vaginal bleeding. She states that her last menstrual period was 1
week ago and that she has not experienced abnormal bleeding
before. Her past medical history is notable for two prior episodes of
pelvic inflammatory disease in the last year. She has also been trying
to conceive for the last year without success. On pelvic examination,
redness and inflammation of the cervix is visible, but no discharge is
apparent. You obtain an endometrial biopsy, which you suspect will
show plasma cells along with macrophages and leukocytes in the
glandular lumen. You begin empiric antibiotic therapy to prevent
possible sequelae from the suspected diagnosis.

Endometritis
107
Etiology:
 Acute endometritis: Caused by trauma, Staphylococcus aureus and
Streptococcus species; usually occurs after delivery or miscarriage;
 Chronic endometritis: Caused by granulomatous disease, chronic PID,
postpartal or postabortal states, and TB
Pathology:
Endometrium: Plasma cells seen with macrophages and lymphocytes
Clinical Manifestations:
Acute: Presents with inflammation after delivery or miscarriage
Chronic: Presents with abnormal vaginal bleeding, pain, discharge, and infertility
Treatment: Antibiotic Tx (helps to prevent other sequelae, such as salpingitis)
Of Note: Endometrial polyps are masses composed of endometrial tissue within
endometrial cavity  occur in women older than 40 years of age and may result in
uterine bleeding, but are usually benign

Acute endometritis, microscopic

Chronic endometritis, microscopic

Granulomatous endometritis, microscopic

Vignette #11
111
A 24-year-old woman presents to the clinic complaining of increased
pain and bleeding during menstruation. Her last three
menstruations have been accompanied by increasing intensity of
cramping and larger amounts of blood. She tells you that her
menstrual cycle has been irregular for the last 6 months. After
taking a complete history, you learn that she has been having
increased pelvic pain with intercourse. On pelvic examination, you
palpate fixed, bilateral ovarian masses and an MRI reveals chocolate
cysts on the ovary. You begin the patient on oral contraceptives and
you suggest surgical removal of the masses if the pain persists.

Endometriosis
112
Etiology and Epidemiology: Etiology unknown, but thought to be
caused by a combination of genetic, hormonal, and immune factors;
Afflicts 10% of women, usually between the ages of 20 and 30
Pathology:
 Gross: Non-neoplastic nodules, composed of endometrial tissue in
abnormal locations outside the uterus, including ovary (most
common), uterine ligaments, rectovaginal septum, and pelvic
peritoneum; presence of chocolate cysts on ovaries that have
resulted from cyclic bleeding (menstrual type) of ectopic
endometrial tissue
 Microscopic: Endometrial glands; endometrial stroma; presence of
hemosiderin pigment

Endometriosis cont.
113
Clinical Manifestations: Presents with fixed, palpable, bilateral
ovarian masses, pain during menses (dysmenorrhea), and pain during
intercourse (dyspareunia); menstrual irregularities may lead to
infertility presenting complaint of 30%–40% of pts.
Treatment: Oral contraceptives; progesterone; danazol; GnRH;
surgical removal/coagulation (cauterization) of lesion
Note: Adenomyosis is endometriosis within the myometrium and
usually presents with uterine enlargement and irregular bleeding

Adenomyosis, MRI

Adenomyosis, gross

Adenomyosis, microscopic

Endometriosis, gross

Endometriosis, microscopic

Endometrial polyp, gross

Vignette #12
121
A 35-year-old African American woman presents to the clinic
complaining of more frequent menstrual periods and profuse
menstruation. She also complains of increased weakness and fatigue
during her menstruations. On physical examination, you find a firm
abdominal mass in the pelvic region. When questioned, she states
that she was aware of the mass, but she notes that the mass often
only appears during menstrual periods. When a biopsy of the mass
reveals whorled bundles of smooth muscle cells, you reassure this
patient that her condition is unlikely to proceed to malignancy.

Leiomyoma (fibroids)
122
Etiology and Epidemiology: Etiology unknown, but chromosomal abnormalities
have been found in tumor cells; Most common benign neoplasm of female
genital tract; Most commonly seen in women of reproductive age with an
increased incidence in African Americans
Pathology:
Gross: Multiple, enlarged, irregular, heterogenous tumors in the myometrium
(intramural), beneath endometrium (submucosal), or beneath serosa
(subserosal); tumor is estrogen-sensitive with its size increasing during pregnancy
and decreasing with menopause
Microscopic: Whorled pattern of smooth muscle bundles; rare mitoses in muscle
cells, although cellular atypia and giant cells may be present

Leiomyoma (fibroids) cont.
123
Clinical Manifestations: Profuse menstruation; frequent menstrual periods;
acute or recurrent pelvic pain; urinary frequency (owing to compression of
bladder); infertility
Lab findings: Iron deficiency anemia (owing to blood loss)
Treatment: Myomectomy or hysterectomy; uterine artery embolization
Note: Also called uterine fibroids, leiomyomas do not progress to
leiomyosarcomas
 Leiomyosarcomas are fleshy, irregular tumors with areas of necrosis and
hemorrhage that arise de novo and may protrude from cervix
 Leiomyosarcomas are more prevalent among African Americans, are
malignant, and can be treated with combination chemotherapy

Leiomyomata, gross

Uterine fibroids as seen during laparoscopic
surgery
125
https://commons.wikimedia.org/wiki/File:Uterine_fibroids.jpg

Leiomyomata, MRI and CT image

Leiomyoma, microscopic

Leiomyosarcoma, gross

Leiomyosarcoma, microscopic

Vignette #13
130
A 60-year-old woman presents to the clinic with postmenopausal
vaginal bleeding. After taking a complete history, you learn that she is
nulliparous and suffers from type 2 diabetes, which is well-controlled
with diet and insulin. On physical examination, the woman is obese
and has a blood pressure reading of 150/96. You decide to perform a
PAP smear as well as an endometrial biopsy. Based on the patient’s
presenting signs and medical history, you are worried that you might
find well-defined gland patterns lined by malignant stratified
columnar epithelial cells on endometrial biopsy.

Endometrial Carcinoma
131
Etiology and Epidemiology: Risk factors include unopposed estrogen use,
obesity, diabetes, HTN, nulliparity, and late menopause
Peak incidence is between 55 and 65 years of age
Endometrial carcinoma is most common gynecologic malignancy
Pathology: Typically preceded by endometrial hyperplasia
Gross: Localized polypoid tumor or diffuse tumor involving entire endometrial
surface
Microscopic: Adenocarcinoma characterized by well-defined gland patterns lined
by malignant stratified columnar epithelial cells; may see some squamous cells

Endometrial Ca. cont.
132
Clinical Manifestations: Presents with postmenopausal vaginal bleeding,
leading to early diagnosis; may cause obstruction of cervix with collection of pus
(pyometra) or blood (hematometra) presenting with lower abdominal pain
Treatment: Total hysterectomy and bilateral salpingo-oophorectomy; radiation
therapy
Important Note:
 Endometrial hyperplasia is abnormal endometrial gland proliferation caused
by excess estrogen (eg, polycystic ovarian syndrome, estrogen-secreting
ovarian tumor, estrogen replacement therapy)
 It manifests clinically with postmenopausal vaginal bleeding  may lead to
endometrial cancer depending on degree of atypia

Endometrial atypical hyperplasia, microscopic

Endometrial carcinoma, gross

Endometrial carcinoma, gross (2)

Endometrial carcinoma, type I, microscopic

Endometrial carcinoma, type II, microscopic

Vignette #14
138
A 42-year-old woman presents to the clinic complaining of postcoital
bleeding and vaginal discharge. She complains of a 3-month history of
spotting in her underwear after intercourse and an odorous vaginal
discharge that is not purulent. Her social history is significant for past
practice of prostitution and her past medical history is significant for
several STDs that were appropriately treated. She has not had a
routine PAP smear in over 10 years. After a PAP smear reveals
abnormal cells, you perform a cervical biopsy, worrying that you may
find invasive malignant cells in the cervix and adjacent koilocytosis.
You fear that the patient will need to undergo a hysterectomy with
possible adjunct radiation therapy if your suspected diagnosis is
confirmed.

Dysplasia, Carcinoma in Situ, and Squamous
Cell Carcinoma of the Cervix
139
Etiology and Epidemiology: Associated with human papilloma virus (HPV) types
16, 18, 31, and 33, early age of first intercourse and multiple sexual partners
Occurs most commonly between the ages of 30 and 45
Pathology: Cervical dysplasia: Involves squamocolumnar junction; characterized
by cells with hyperchromatic nuclei, irregular nuclear contours, and scant
cytoplasm; epithelial growth begins at basal layer extending outward; classified as
Cervical Intraepithelial Neoplasia (CIN) Subtypes Grades I-III (or Squamous
Intraepithelial Lesions Low-grade to High-grade )
 CIN I (LSIL) is characterized by atypical undifferentiated cells only in lower third
of epithelium, whereas
 CIN II (HSIL) superficial layer of cells still shows differentiation and koilocytosis
 CIN III (HSIL) has atypia through > 2/3 thickness of epithelium, koilocytotic
change usually is absent

Dysplasia, Carcinoma in Situ, and Squamous
Cell Carcinoma of the Cervix (2)
140
Pathology cont:
Cervical carcinoma in situ (CIS): Dysplastic cells extending through entire
epithelium, but without invasion of basement membrane
Invasive cervical carcinoma (ICC):
Gross: can be exophytic, ulcerating, or infiltrating mass
Microscopic: usually squamous cell carcinoma with large cells and keratinization;
can be adenocarcinoma or undifferentiated carcinoma; arises from preexisting
CIN at squamocolumnar junction; non-neoplastic epithelial cells often
demonstrate koilocytosis (assoc. w. HPV infection)
Koilocytes, also known as halo cells, are a type of epithelial cell that develops
following a human papillomavirus (HPV) infection; They are structurally different
from other epithelial cells, in that, their nuclei are an irregular size, shape, or color

Natural History of Squamous Intraepithelial
Lesions (SILs)
141
Lesion Regress Persist Progress
LSIL (CIN I) 60% 30% 10% (to HSIL)
HSIL (CINII,III) 30% 60% 10% (to carcinoma)*
*Progression within 10 years. LSIL, Low-grade SIL; HSIL, high-grade SIL
Redrawn after Kumar V and Abbas AK. Robbins and Cotran Basis Pathology, 10th Ed. Philadelphia: Saunders, 2018, Fig. 19.1 , Pg. 718.
Remember:
Cervical Intraepithelial Neoplasia (CIN) Subtypes Grades I-III (or Squamous Intraepithelial Lesions
Low-grade to High-grade )
 CIN I (LSIL) is characterized by atypical undifferentiated cells only in lower third of epithelium,
whereas,
 CIN II (HSIL) superficial layer of cells still shows differentiation and koilocytosis
 CIN III (HSIL) has atypia through > 2/3 thickness of epithelium, koilocytotic change usually is absent

Three Stages of squamous intraepithelial lesions (SIL)
Spectrum of squamous intraepithelial lesions (SIL) with normal squamous epithelium for
comparison: LSIL with koilocytotic atypia; HSIL w progressive atypia in all layers of the
epithelium; and HSIL w diffuse atypia and loss of maturation (carcinoma in situ, far right image)
Kumar V and Abbas AK. Robbins and Cotran Basis Pathology, 10th Ed. Philadelphia: Saunders, 2018, Fig. 19.6 , Pg. 719.

Cytologic features of squamous intraepithelial
lesion (SIL) in a Papanicolaou Smear
Superficial squamous cells may stain either red or blue.
(A) Normal exfoliated superficial squamous epithelial cells. (B) Low-grade squamous intraepithelial lesion (LSIL).
(C and D) Both high-grade squamous intraepithelial lesions (HSILs). Note the reduction in cytoplasm and the increase in
the nucleus-to-cytoplasm ratio as the grade of the lesion increases. This observation reflects progressive loss of cellular
differentiation on surface of cervical lesions from which these cells are exfoliated
Kumar V and Abbas AK. Robbins and Cotran Basis Pathology, 10th Ed. Philadelphia: Saunders, 2018, Fig. 19.7 , Pg. 719.

Dysplasia, Carcinoma in Situ, and Squamous Cell
Carcinoma of Cervix (3)
144
Clinical Manifestations: ICC: Irregular vaginal bleeding; postcoital
spotting; cervical ulceration; nonpurulent discharge; dysuria; invasive
disease can obstruct ureters and lead to renal failure
Treatment ICC: Hysterectomy; radiation therapy; prevention with
HPV vaccine
NB: Screening for cervical cancer with PAP smears should begin 3
years after intercourse and no later than age 21 and continue every
1–3 years until age 70

Normal cervix, gross

Normal cervix, microscopic

Normal cervical transformation zone, microscopic

Chronic cervicitis, gross

Chronic cervicitis, microscopic

Cervical squamous metaplasia, microscopic

Human papillomavirus effect, microscopic

Cervical squamous dysplasia, Pap smear

Cervical squamous carcinoma, Pap smear

Squamous cell carcinoma, gross

Squamous cell carcinoma, gross (2)

Squamous cell carcinoma, gross (3)

Vignette #15
157
A 27-year-old woman presents to the emergency room with lower
abdominal pain, chills, fever, and a purulent vaginal discharge. After
taking a history, you learn that she has had multiple sexual partners
over the last year and has not practiced safe sex. She states that the
pain started 3 days ago with subsequent fevers, chills, and night
sweats. On physical examination, she is febrile with a temperature of
102.4°F. Pelvic examination is significant for cervical motion
tenderness with foul-smelling, purulent, cervical discharge. Her
pregnancy test is negative. You admit the patient to the hospital and
you begin her on IV cefoxitin plus doxycycline while awaiting the
results of her endocervical culture.

Pelvic Inflammatory Disease
158
Etiology and Epidemiology: Common causes include Chlamydia trachomatis
(subacute), Neisseria gonorrhoeae (acute), Gardnerella vaginalis, and
Trichomonas vaginalis; Usually occurs in young, nulliparous, sexually active
women with multiple partners
Pathology: Fallopian tubes: Edematous tubal serosa with fibrin covering;
purulent exudate in lumen; collections of pus may form a pyosalpinx or
degrading pus may form a hydrosalpinx (water-filled fallopian tubes)
Infection can also involve the ovaries and other pelvic structures

PID cont.
159
Clinical Manifestations: High fever; lower abdominal pain; cervical motion
tenderness (chandelier sign); purulent cervical discharge; RUQ pain indicates
perihepatitis (Fitz-Hugh-Curtis syndrome); Salpingitis is a risk factor for ectopic
pregnancy, infertility, chronic pelvic pain, and adhesions
Treatment: Antibiotics effective against causative organism
Note: Ectopic pregnancy occurs most often in fallopian tubes, but may also
occur in ovary, abdominal cavity, or cervix
 Risk factors include salpingitis, endometriosis, and tubal ligation
 Clinical manifestations include severe abdominal pain 6 weeks after LMP
and elevated hCG which is lower than normal for pregnancy stage

Pathogenesis of gonococcal infections
160
 Neisseria gonorrhoeae is a gram-negative diplococcus whose
surface pili form a barrier against phagocytosis by neutrophils
 Pili contain an immunoglobulin A (IgA) protease that digests
IgA on luminal surface of mucous membranes of urethra,
endocervix and fallopian tube thereby facilitating
attachment of gonococci
 Gonococci cause endocervicitis, vaginitis and salpingitis
 In men, gonococci attached to mucous membrane of urethra
cause urethritis and, sometimes, urethral stricture
 GC may also attach to sperm heads and be carried into the
fallopian tube Penetration of mucous membrane by
gonococci leads to stricture of fallopian tube, pelvic
inflammatory disease (PID) or tuboovarian abscess
Rubin R and Strayer DS Eds. Rubin’s Pathology: Clinicopathologic Foundations of
Medicine, 6th Ed. Baltimore: Lippincott Williams & Wilkins, 2012; Fig. 9.18, 394.
Click for large view

Gonorrhea of the fallopian tube
Cross-section of a “pus tube” shows
thickening of wall and a lumen swollen
with pus
Rubin R and Strayer DS Eds. Rubin’s Pathology: Clinicopathologic Foundations of
Medicine, 6th Ed. Baltimore: Lippincott Williams & Wilkins, 2012; Fig. 9.19, 394.

Acute salpingitis, microscopic

Tubo-ovarian abscess, gross

Ectopic pregnancy, gross

Vignette #16
165
After vaginally delivering a newborn from a 32-year-old woman, you
find the mother to be hemorrhaging an abnormally large amount of
blood. You recall that she has had one previous C-section and
extensive scarring. Given the amount of blood after delivery and the
abnormal gross appearance of the placental remnants, you believe
that the patient’s pregnancy was complicated by a defective decidual
layer that allowed the placenta to attach directly to the myometrium.
You call the operating room to set up for an emergency hysterectomy,
which you believe may be necessary to control the patient’s massive
hemorrhage.

Placental Attachment Abnormalities (Abruptio Placentae,
Placenta Previa, Placenta Accreta)
166
Etiology:
Abruptio placentae: May be associated with DIC; increased risk with smoking,
cocaine, and hypertension
Placenta accreta: Predisposed by prior C-section scars or endometrial
inflammation
Placenta previa: Predisposed by prior C-section scars
Pathophysiology:
Abruptio placentae: Premature separation of placenta
Placenta accreta: Defective decidual layer allows placenta to attach directly to
myometrium
Placenta previa: Attachment of placenta to lower uterine segment or cervix;
may occlude cervical os; may coexist with placenta accreta

Placental Attachment Abnormalities cont.
167
Clinical Manifestations:
Abruptio placentae: Painful uterine bleeding usually during third trimester; can
result in fetal death
Placenta accreta: Massive hemorrhage after delivery
Placenta previa: Painless bleeding in any trimester; premature labor
Treatment:
Abruptio placentae: Immediate fetal delivery; control of maternal bleeding
Placenta accreta: Hysterectomy may be necessary to stop bleeding
Placenta previa: Bed rest; possible hospitalization

Vignette #17
168
A 31-year-old pregnant woman is brought to the emergency room
complaining of headaches and blurred vision of 1-week duration. She
is currently 32 weeks into her first pregnancy. On physical
examination, you find edema of the face and lower extremities. Her
blood pressure is 160/100, but she has no prior history of
hypertension. Laboratory studies show a mild thrombocytopenia,
elevated AST and ALT, and significant proteinuria. Based on these
findings, you admit the patient for immediate bed rest, close
monitoring, and blood pressure control. You tell the patient that it is
possible that you may need to deliver her baby early in order to treat
the patient’s current condition.

Preeclampsia and Eclampsia
169
Etiology and Epidemiology: Risk factors include preexisting hypertension,
diabetes, chronic renal disease, autoimmune disorders, or twin gestation
Affects 7% of pregnant women usually during the third trimester of a woman’s
first pregnancy
Pathology and Pathophysiology: Placenta: Evidence of infarct; presence of
retroplacental hematomas; decreased vascularity; fibrinoid necrosis
 Pathophysiology: Intrinsic defect in invading cytotrophoblast leads to
remodeling of uterine vasculature and resulting placental ischemia;
decreased placental perfusion induces vasoconstrictive effects leading to
toxemic hypertension in susceptible women

Preeclampsia and Eclampsia cont.
170
Clinical Manifestations: Preeclampsia: Triad of hypertension, proteinuria, and
edema; associated Sx include headache, blurry vision, and abdominal pain
Eclampsia: Preeclampsia triad plus seizures, altered mentation, hyperreflexia,
and possibly DIC
Lab findings: Thrombocytopenia, elevated LFTs, hyperuricemia, hemolytic anemia
Treatment: Preeclampsia: Delivery of fetus as soon as possible; bed rest; salt
restriction; treatment of hypertension
Eclampsia: Medical emergency; treat with IV magnesium sulfate and diazepam;
delivery of fetus
NB: HELLP syndrome refers to hemolysis, elevated LFTs, and low platelets and is a
severe form of preeclampsia (Video on HELLP syndrome & “USMLE”)

THE END
See next slide for further study.
171

Companion Tools and Resources (online)
172
Discipline (Pathology) Track Folder
 Reproductive Pathology
Organ Systems Track Folders
 M and FM Reproductive System & FM Breast
 Pregnancy, Childbirth, & the Puerperium
Textbooks:
Kumar V and Abbas AK. Robbins and Cotran Basis Pathology, 10th Ed.
Philadelphia: Saunders, 2018.
Rubin R and Strayer DS Eds. Rubin’s Essential of Pathology:, 6th Ed.
Baltimore: Lippincott Williams & Wilkins, 2014.

Reproductive System Pathology_FM Breast and FM Reproductive Systems

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