Pathology Morphology Repro And Endo

Front 1

Acute Cervicitis

Back 1

Cervix is congested, swollen with profuse purulent discharge.

There are acute inflammatory cells, erosion, and reactive epithelial changes.

There is a polymorphonuclear infiltrate and there may be loss of the epithelial lining (cervical erosion).

Front 2

Chronic Cervicitis

Back 2

This includes inflammation, usually mononuclear cells, with lymphocytes, macrophages, and plasma cells. Necrosis and granulation tissue may also be present.

Morphology: Some patterns are:

Cervical erosion: The cervical mucosa of the external os desquamates and the columnar epithelium of the endocervix extends down and covers the denuded area. The transparent columnar epithelium (columnar metaplasia ) shows the underlying hyperaemic tissue. So, the os appears intense red and bleeds easily on touch

Squamous metaplasia:The subcolumnar reserve cells undergo squamous metaplasia due to chronic inflammation.

Cervical Dysplasia: Epithelial repair leads to atypia or dysplasia of repair.

Nabothian follicles: As the squamous epithelium overgrows, it obstructs crypt openings, with accumulation of mucus in deeper crypts to form mucous cysts (nabothian follicles)

Endocervical Polyps which may produce spotting of blood / vagina

Leucorrhea

Front 3

Cervical Intraepithelial Neoplasia (CIN):

Back 3

It may be either raised (acuminatum) or macular (flat condyloma).

The atypical cells show increased in N/C ratio; pleomorphic nuclei; loss of polarity; increased mitotic figures, including abnormal mitoses; and hyperchromasia –in other words, they take on some of the characteristics of malignant cells.

It is divided into three stages:

CIN I: mild dysplasia in the lower layers with koilocytotic atypia (viral cytopathic effect)

CIN II : Involvement of more layers of the epithelium

CIN III: Involvement of full thickness of the epithelium

Front 4

Cacrinoma of Cervix

Back 4

Gross

Fungating (or exophytic) is most common,

Ulcerating, and

Micro:

Infiltrating cancer.

95% of cancer cervix is squamous cell carcinomas

5 % of cancer cervix is: Adenocarcinoma

Front 5

Staging of Carcinoma

Back 5

Stage 0:Carcinoma in situ (CIN III).

Stage I:Carcinoma confined to the cervix.

Stage II: Extends beyond the cervix but not pelvic wall and involves the vagina but not the lower third.

Stage III. Carcinoma has extended onto pelvic wall and the lower third of vagina.

Stage IV. Carcinoma has extended beyond the true pelvis or has involved the mucosa of the bladder or rectum. This stage includes those with metastatic dissemination.

Front 6

(Pelvic Inflammatory Disease)

Gonorrhea

Back 6

It is characterized by acute suppurative inflammation which occurs in ascending order in the superficial mucosa and submucosa of urethra, Bartholin’s glands, vagina (rare) ,cervix , uterus (rare) and fallopian tubes:

Urethritis, Paraurthritis -Bartholin's gland, vaginitis, cervisitis , endometritis, acute supprative salpingitis, Salpingio-oophiristis

Tubo-ovarian abscess

Pyosalpinx

Hydrosalpinx

Front 7

Pueperal Infection:

Back 7

Def: Infection of uterus after labour or abortion.

Agents: polymicrobial eg. Staphylococci, streptococci, coliform bacteria, and Clostridium perfringens.

Gross:

Uterus: bulky, soft and flabby.

Endometrium: congested and ulcerated.

Cavity: contains necrotic tissue and purulent exudate.

Cut section: myometrium shows septic thrombophlebitis of veins.

Micro:

1.

Front 8

Tumors of Vulva:

Leukoplakia

Back 8

opaque, white, scaly, plaque-like mucosal thickenings.

Microscopically : there is epithelial hyperplasia (acanthosis) and hyperkeratosis of the overlying skin.

Front 9

ToV

Benign:

Condyloma Acuminatum:

Back 9

Gross-frequently multiple but may be solitary; often coalesce;

-frequently multiple but may be solitary; often coalesce;

-involve perineal, vulvar, and perianal regions as well as the vagina

-lesions are identical to those found on the penis and around the anus in males.

Micro:

There is branching tree-like proliferation of stratified squamous epithelium with a fibrovascular core.

-Acanthosis, parakeratosis, hyperkeratosis and koilocytosis are seen

Front 10

ToV

Malignant:

) Vulvar Intraepithelial Neoplasia (VIN)

Back 10

Vulvar Intraepithelial Neoplasia denotes dysplasia of the vulvar epithelium.

Front 11

ToV

Malignant:

Carcinoma:

Back 11

They begin as small areas of epithelial thickening that resemble leukoplakia.

Gross:

Firm, indurated, exophytic tumors or ulcerated lesions.

Microscopy:

Usually squamous cell carcinomas

Spread:

Early: The inguinal, pelvic, iliac, and periaortic lymph nodes are most commonly involved.

Late lympho-haematogenous dissemination involves the lungs, liver, and other organs.

Front 12

ToV

Malignant:

Extramammary Paget's Disease

Back 12

Presents as a pruritic red, crusted, sharply demarcated, map-like area on the labia majora.

The diagnostic microscopic feature is the presence of large, anaplastic tumor cells (Paget’s cells) within the epidermis.

-In contrast to Paget’s disease of the nipple, in which 100% of patients show an underlying ductal breast carcinoma, vulvar lesions are confined to the epidermis of the skin.

Front 13

ToVagina:

Premalignant and Malignant Neoplasms

Vaginal Intraepithelial Neoplasia

Squamous cell Carcinoma:

Adenocarcinoma (clear cell carcinoma):

Embryonal Rhabdomyosarcoma (sarcoma botryoides) :

Back 13

Gross: polypoid, rounded, bulky masses that sometimes project out of the vagina

-Grape-like clusters (hence the name “botryoides”)

Microscopy: consists of malignant embryonal rhabdomyoblasts.

-The tumor cells are small and have oval nuclei, with small protrusions of cytoplasm from one end like a tennis racket.

Spread: invade locally and cause death by penetration into the peritoneal cavity or by obstruction of the urinary tract.

Front 14

Endometrial Hyperplasia

Back 14

a) Simple hyperplasia (cystic or mild hyperplasia),

mild irregularity in gland shape with cystic alterations.

evolves into cystic atrophy in which the epithelium and stroma become atrophic.

b) Complex hyperplasia (adenomatous hyperplasia without atypic

Increase in the number and size and crowding of glands of varying sizes

“Budding” of glands with finger-like processes

No cytological atypia.

c) Atypical hyperplasia, or adenomatous hyperplasia with atypia:

This is a higher grade of hyperplasia.

Increased glandular crowding, irregular epithelial lining and stratification are present.

There is cellular atypia with cytomegaly, loss of polarity, hyperchromatism, prominence of nucleoli, increased N/C ratio and increased mitosis .

Front 15

Adenomyosis

Back 15

Gross: enlargement of the uterine wall with numerous small cysts.

Microscopy: irregular nests of endometrium, within the myometrium, separated from the basalis by at least 2 to 3 mm.

Clinically: During the menstrual cycle, hemorrhage within these areas results in menorrhagia, colicky dysmenorrhea, dyspareunia, and pelvic pain.

Front 16

Endometriosis

Back 16

-The foci of endometrium undergo the cyclic menstrual changes with periodic bleeding.

-This produces nodules with a red-blue to yellow-brown appearance.

-There are extensive fibrous adhesions between tubes, ovaries, and other structures and obliteration of the pouch of Douglas.

-The ovaries may become distorted by large cystic spaces (3 to 5 cm in diameter) filled with brown blood debris to form so-called “chocolate cysts”.

-The histologic diagnosis of is made, if two of the three following features are seen: Endometrial glands, stroma, and hemosiderin pigment.

Front 17

Tumors of Uterus:

Benign:

Endomytrial polyp

Back 17

-sessile masses of variable size that project into the endometrial cavity.

-may be single or multiple

-usually 0.5 to 3.0 cm in diameter but occasionally large and pedunculated.

-may be asymptomatic or may cause abnormal bleeding if they ulcerate

-Rarely, adenocarcinomas may arise within endometrial polyps.

Histologically- two types,

formed of normal endometrium

formed of hyperplastic endometrium (more common)

mostly cystic variety

may develop in association with generalized endometrial hyperplasia

are responsive to effect of estrogen but not progesterone.

Front 18

ToU

Leiomyomas:

Back 18

Gross: sharply circumscribed, discrete, round, firm, gray-white,vary in size from small to massive tumors that fill the pelvis.

found in the myometrium of the corpus

within the myometrium (intramural),

just beneath the endometrium (submucosal) or

Beneath the serosa (subserosal).

Secondary changes in leiomyomas (fibroids):

1.Degenerations as hyaline and myxomatous degenerations.

2. Red degenerations: this is ischaemic necrosis and haemorrhage e.g. during pregnancy.

3. Atrophy and fibrosis after menopause.

4. Uterine haemorrhage due to necrosis of the covering endometrium.

5. Malignant change (leiomyosarcoma): very rare.

Cut section: whorled pattern of smooth muscle bundles

Large tumors may show areas of yellow-brown to red softening (red degeneration).

Histologically: interlacing bundles of smooth muscles and fibrous tissue.

Front 19

ToU:

Carcinoma of the Endometrium:

Back 19

. Localised polypoid pattern

2. Diffuse Pattern.

) Adenocarcinomas (about 85%)

-Well-defined gland patterns lined by malignant columnar epithelial cells.

-Classified as:

Well differentiated (grade 1)

-easily recognizable glandular patterns;

Moderately differentiated (grade 2)

- glands mixed with solid sheets of malignant cells;

Poorly differentiated (grade 3),

Solid sheets of cells with no glands and a greater degree of nuclear atypia and mitotic activity.

2) Adenoacanthoma: Squamous elements most commonly are histologically benign in appearance (called also adenocarcinoma with squamous metaplasia when associated with well-differentiated adenocarcinomas.

3) Adenosquamous carcinomas: Less commonly, moderate or poorly differentiated endometrioid carcinomas contain squamous elements that appear frankly malignant.Such tumors have also been termed “adenosquamous carcinomas” if more than 10% of the tumor is squamous.

Front 20

Staging of endometrial adenocarcinoma is as follows:

Back 20

Stage I. Carcinoma is confined to the corpus uteri itself.

Stage II. Carcinoma has involved the corpus and the cervix.

Stage III. Carcinoma has extended outside the uterus but not outside the true pelvis.

Stage IV. Carcinoma has extended outside the true pelvis or has obviously involved the mucosa of the bladder or the rectum.

Front 21

2-Malignant Mixed Mesodermal Tumors (Mixed Müllerian Tumors):

Back 21

Malignant mixed müllerian tumors (MMMTs) consist of endometrial adenocarcinomas in which malignant mesenchymal (stromal) differentiation takes place. They are called mixed tumors because they consist of malignant glandular and stromal (sarcomatous) elements, and the latter tend to differentiate into a variety of malignant mesodermal components, including muscle, cartilage, and even osteoid.

Front 22

3-Leiomyosarcomas:

Back 22

These uncommon malignancies arise de novo directly from the myometrium or endometrial stroma, which undergoes smooth muscle differentiation. Their origin from a pre-existing leiomyoma is a controversial issue, and most believe that such occurrences are extremely rare.

Front 23

(FP inflammatory)

Acute Salpingitis

Back 23

Morphology: It is characterized by hyperemia and edema of the tube. The external surface is covered by a fibrinopurulent exudate, and the lumen contains pus.

Suppuration may extend to produce an abscess that involves the tube and ovary (tubo-ovarian abscess).

Front 24

Gestational Placental Infections:

Back 24

Morphology - uterine curettage specimen shows the following microscopic picture:

Focal areas of decidual necrosis, with intense neutrophilic infiltration

Thrombi within decidual blood vessels,

Areas of hemorrhage and markedly edematous placental villi

Fetal parts may or may not be present

Front 25

Ectopic Pregnancy

Back 25

a shock like state with signs of an acute abdomen.

Morphology:

hematosalpinx /tubal hematoma – the tube is filled with blood

Placental tissue can be seen invading the tubal wall which is the cause of tubal rupture and hemorrhage into the peritoneum

Front 26

DIC and Toxamia

Back 26

Morphology: placenta shows infarcts, fibrinoid necrosis in uterine vessels & thrombi. There is increased retroplacental hematoma formation.

The liver /brain /heart / anterior pituitary: show areas of hemorrhage and necrosis & fibrin thrombi in the capillaries.

The kidney shows diffuse glomerular lesions

Front 27

Periductal Mastitis

Back 27

Microscopically: the main feature is the extension of keratinising squamous epithelium to an abnormal depth into the opening of the nipple ducts. Keratin gets trapped in the ductal system and causes dilatation and rupture of the duct. If secondary infection occurs, acute inflammation sets in with abscess and fistula formation.

It is common in smokers because Vitamin A deficiency associated with smoking along with toxic substances in tobacco smoke affect the differentiation of ductal epithelium, leading to the disease.

Complications may be:

Abscess formation

Fistulous tract opening onto the skin

Squamous metaplasia of the epithelium.

Front 28

Mammary duct Ectasia

Back 28

Morphology: dilatation of lactiferous ducts due to marked chronic granulomatous inflammatory reaction of the tissue. The dilated ducts are filled with granular debris, and lipid laden macrophages and lymphocytes. Later on, fibrosis may produce skin and nipple retraction.

Front 29

Non-proliferative breast changes

(fibrous changes)

Back 29

Morphology: many histological changes are seen –

1. Cyst formation - small cysts formed by the dilatation of lobules

2. Epitheliosis - epithelial proliferation and formation of papillae

3. Fibrosis - proliferation of fibrous tissue

4. Adenosis- increase in the number of acini per lobule

Front 30

PROLIFERATIVE BREAST DISEASE WITHOUT ATYPIA

Fibroadenoma

Back 30

a) Pericanalicular fibroadenoma: proliferation of both fibrous tissue and ducts is seen, where the lumen of the ducts remain patent/open.

b) Intracanalicular fibroadenoma: the proliferating fibrous tissue compresses the lumina of the duct, which appear slit- like and obliterated.

Front 31

PROLIFERATIVE BREAST DISEASE WITH ATYPIA

Back 31

Morphology: it is a cellular proliferation which resembles ductal carcinoma in situ (DCIS) or lobular carcinoma in situ (LCIS) but lacks sufficient features for a diagnosis of carcinoma in situ, as the cells are not completely monomorphic, or they fail to completely fill the spaces like in ductal carcinoma in situ.

Front 32

MANIFESTATIONS OF BREAST DISEASE

Back 32

Breast mass: any breast mass should be regarded as breast cancer until proved otherwise

Nipple changes and discharge: recent nipple inversion, flattening, or retraction can be associated with cancer. Nipple discharge may be milky, serous or bloody

Skin changes: may be present in advanced cancer of the breast. Infiltration of the skin can cause tethering/ dimpling of the skin over the mass, followed by ulceration. Extensive involvement of dermal lymphatics results in lymphedema which produces thickening of skin and a pitted appearance known as ‘peau d’ orange’, due to its resemblance to orange peel.

Distinctive clinical presentation as in Paget’s disease of the nipple:

It presents as an eczematous change in the nipple and areola. Microscopically- carcinoma cells are present in the epidermis. The cells are large with abundant cytoplasm. In most cases the underlying breast shows ductal carcinoma

Front 33

In Situ non invasive

Ductal carcinoma in situ (DCIS)

Back 33

It is a neoplastic proliferation of ductal epithelial cells

the basement membrane is intact

it does not metastasise if present in pure form.

Gross: produces a hard mass composed of thick cord like structures with necrosis and calcification, which is detectable by mammography

Front 34

Invasive Ductal

Back 34

Retraction of nipple in late stages

Peau d’orange change in surface of the skin

Breast maybe smaller than normal

Localised hard mass, often fixed

Gross morphology: hard, gritty, greyish white mass. Yellowish white streaks are present due to deposition of elastic tissue (elastosis) in the tumor. Microscopically: the tumor is composed of small groups and cords of cells separated by dense fibrous stroma. Malignant cells show anaplastic features and mitotic activity.

Front 35

Adrenal Cushing:

causes

Back 35

primary hypothalamic pituitary diseae associated with hypersectiono f ACTH

Hypersecretion of cortisol by an adrenal adenoma, carcinoma, nodular hyperplasia

Secretiono of ectopic ACTH by nonedmdpcrine neoplasm

Most are exopgenous glucocoritcoid administration

Front 36

Cushing

Morphology

Back 36

main leison found in pituitary and adrenal glands

due to high levels of endogenous /axogenous glucocorticoids termed: Crooke Hyaline change -normal granular basophilic cytoplasm replaced by homogenous lightly basophilic material. the result of accumulation of intermediate keratin filaments in cytoplasm.

the morphology of adrenal glands depend on cause of hypercortisolism some :

Cortical atrophy

Diffuse and nodular hyperplasia

Functional adenoma / rarely carcinom