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Dysplasia Dysplasia • Dysplasia – change of phenotype (size,shape and organization of tissue) • is a term used in pathology to refer to an abnormality of development.[1] This generally consists of an expansion of immature cells, with a corresponding decrease in the number and location of mature cells. Dysplasia is often indicative of an early neoplastic process. The term dysplasia is typically used when the cellular abnormality is restricted to the originating tissue, as in the case of an early, in-situ neoplasm Dysplasia are now usually referred as cervical intraepithelial neoplasia ( CIN) . They are regarded as mild, moderate or sever, depending on the degree of cytological atypia and also the thickness of the epithelium involved . CIN I : affecting the deepest 1/3 of the epithelium from the basal layer up ward CIN II : Affecting 2/3 of the thickness CIN III: Affecting full thickness HPV infection alone and CIN I are grouped together as ‘low – grad squamous intraepithelial Lesions (LSIL) and CIN II and CIN III as ‘high –grade SIL (HSIL) • Microscopic changes • Dysplasia is characterized by four major pathological microscopic changes: • Anisocytosis (cells of unequal size) • Poikilocytosis (abnormally shaped cells) • Hyperchromatism (excessive pigmentation) • Presence of mitotic figures (an unusual number of cells which are currently dividing). • Dysplasia is the earliest form of pre-cancerous lesion which pathologists can recognize in a pap smear or in a biopsy. Dysplasia can be low grade or high grade. The risk of low grade dysplasia transforming into high grade dysplasia, and eventually cancer, is low. Treatment is usually straightforward. High grade dysplasia represents a more advanced progression towards malignant transformation. • Invasive carcinoma is the final step in this sequence. It is a cancer which has invaded beyond the basement membrane and has potential to metastasize (spread to other parts of the body). Invasive carcinoma can usually be treated, but not always successfully. However, if it is left untreated, it is almost always fatal. • Carcinoma in situ, meaning "cancer in place", represents the transformation of a neoplastic lesion to one in which cells undergo essentially no maturation, and thus may be considered cancer-like. In this state, epithelial cells have lost their tissue identity and have reverted back to a primitive cell form that grows rapidly and with abnormal regulation for the tissue type. However, this form of cancer remains localized, and has not invaded past the basement membrane into tissues below the surface. Metaplasia • Metaplasia (Greek: "change in form") is the reversible replacement of one differentiated cell type with another mature differentiated cell type. The change from one type of cell to another may generally be a part of normal maturation process or caused by some sort of abnormal stimulus. In simplistic terms, it is as if the original cells are not robust enough to withstand the new environment, and so they change into another type more suited to the new environment. If the stimulus that caused metaplasia is removed or ceases, tissues return to their normal pattern of differentiation. Metaplasia is not synonymous with dysplasia and is not directly considered carcinogenic. •Causes • When cells are faced with physiological or pathological stresses, they respond by adapting in any of several ways, one of which is metaplasia. It is a benign (i.e. non-cancerous) change that occurs as a response to change of milieu (physiological metaplasia) or chronic physical or chemical irritation (pathological metaplasia). One example of pathological irritation is cigarette smoke that causes the mucus-secreting ciliated pseudo stratified columnar respiratory epithelial cells that line the airways to be replaced by stratified squamous epithelium, or a stone in the bile duct that causes the replacement of the secretory columnar epithelium with stratified squamous epithelium (Squamous metaplasia). Metaplasia is an adaptation that replaces one type of epithelium with another that is more likely to be able to withstand the stresses it is faced with. DEVELOPMENT OF THE PAP SMEAR • In 1928 George Papanicolaou initiated the a sampling of vaginal cells, speculating that these cells would predict which women develop cervical cancer. • Together with Dr Herbert Traut , published a monograph in 1947 that eventually resulted in Pap smears becoming the standard of care in cervical cancer screening • The procedure they outlined was modified in 1947 by Ayre,who collected cervical cells directly using a wooden spatula. • In1988 ,a workshop was held in Bethesda, Maryland, that provided a general consensus on how to read Pap smears and initial guidelines designed to decrease the variability among laboratories in reporting of result • A second workshop in 1991 modified these guidelines based on actual practice and clinical experience • The Bethesda 1988 and 1991 guidelines both emphasized delineating SQUAMOUS INTRAEPITHELIAL LESION ---Low grade {LSIL} and high grade {HSIL}----from atypical squamous cells of unclear significant {ASC—US}and normal Pap smears. The Bethesda 2001 consensus panel resulted in the following revisions in the terminology used to report Pap smear results: 1- Significant changes were made in the management of atypical squamous cells. The guidelines retained the and added the subcategory of “ atypical squamous cells favoring HSIL” [ASC-H] . ASC-US carries a moderately low incidence of CIN 2 or CIN 3 [10%] and very low incidence of cancer [0.1%],whereas ASC-H is associated with a much higher incidence of CIN 2 or 3. • 2- The Bethesda 2001 guidelines also eliminated the categories of “reactive change Pap smear” and “atypical squamous cells of unclear significance favoring reactive change Pap smear. • 3- AGC-US” atypical glandular cell of unclear significance ‘ was eliminated , primarily to avoid confusion with ASC-US. On average 44% of women with AGC-US have subsequent tissue examination that yields a diagnosis of cervical dysplasia, and cancer is diagnosed in 8%. • 4- The finding of AGC was made more specific in the 2001 guidelines with the inclusion of two categories:”AGC favoring neoplasia and “adenocarcinoma in situ”[AIS] Pap smear Technique and Interpretation • A- Frequency of screening: • 1- In USA the most recent recommendation is to screen for the first time 3 years after the onset of sexual activity Or before age 21 ,which ever comes first. • 2- ACOG recommends annual Pap smear screening / • AMERICAN CANCER SOCITY recommends every –other-year screening when using liquid –based cytology • 3- after age 30 , the interval between screening can be increased to 2-3 years . • 4- More frequent i.e. annual Pape smears are recommended for women : • a- using DSE • b - immunocompromised • c- previous history of stage 2 or 3 cervical intraepithelial neoplsia CIN D-- INTERPRETATION • The Bethesda guidelines recommend that 8000—12,000 squamous cells be obtained for conventional Pap smear but only 5000 cells for a liquid- based sample • Cells can obscured by blood , mucous and inflammatory cells • If more than 75% of the cells are obscured , the sample is inadequate and a new sample must be tested. • If 50—75% of the cells are obscured ,the sample is adequate but partially obscured. • The presence of endocervical cells [ at least 10] is recommended but not required in samples from women younger than 40 years of age but required from women older than 40 1---Negative result • NILM: negative for intraepithelial lesion or malignancy. • the normal cells; is optional for the pathologist to add information about other infection : • Candidiasis • Tricomoniasis • Herpes simplex virus • Bacterial vaginosis 2--ASC • The Bethesda guidelines regarding atypical squamous cells [ ASC ] emphasize the ability to distinguish between HSIL and LSIL . • Overall it is thought that 10– 30% of women with a finding of ASC on a Pap smear have underlying CIN grade 2 or 3 , and 0.1% may invasive cancer . • a--- ASC-US • It is estimated that 90- 95% of all finding of ASC fall into this category of ASC-US . • Women with a Pap smear result of ASC-US have a 5-7% of having CIN 2 and 3 and 39% of women with CIN 2 or 3 have a previous finding of ASC-US on Pap smear • ASC-US is associated with HPV in about 33- 67% of cases b- ASC-H The category of ASC-H describes atypical cells that are morphologically suspicious of HSIL but too few in number to qualify as HSIL . ASC-H is more highly associated with HSIL than ASC-US and is the most common precursor lesion for CIN . Follow –up of women with a finding of ASC-H leads to diagnosis of CIN 2 & 3 in 68%. 3--AGC • Atypical glandular cells is further differentiated according to whether the cells are : endocervical • Endometrial • Or not otherwise specified. • This finding is relatively rare ,occurring in 0.17- 1.8% of all Pap smear . • The presence of these cells has serious medical implications because women with a finding of AGC have a 9.7 times higher risk of progressing to CIN 2 • a : AGC favoring neoplasia : • This finding may correspond with high-grade lesions on tissue examination [27-96% of the time] b- Adenocarcinoma in situ [ AIS ] : It corresponds with high rates of advance lesions on tissue examination. A finding of AIS corresponds with high rates of advanced lesions on tissue examination 4– LSIL and HSIL • Studies have shown that the finding of LSIL is more variable and less reproducible than HSIL, and repeatable in only 80% of smear. Bethesda guidelines further specify [with features suspicious of invasion ] when histologic evidence supporting cancer is present. E- counseling women with abnormal Pap smear • Women with abnormal Pap smear findings should be counseled that HPV infection has been linked with the development of cervical cancer, and that HPV is the most common viral STD , affecting up to 70% of the sexually active population • Endometritis A- acute/ apart from infections at operations and by instrumentation it is either puerperal gonococcal The regrowth of new surface endometrium during each cycle prevents the persistence of any infection which not deep seated can be treated accordingly B- chronic : T.B Senile other causes It is a rare disease between the menarche and menopause because of regrowth of endometrium It is caused when the uterus is permanently injured or when there is a chance for its continuously infected like : foreign body Malignant disease of the uterus Infected polyp Retained gestational products Chronic salpingio-oopheritis Pelvic cellulitis from radiation Endometrial burn due to radiation • Microscopically there is large collection of plasma cells and f • Clinical features : 1- purulent discharge from the uterus 2- menorrhagia IN ANY SIGNS OF INFCETION ---- SEND FOR CULTURE TO EXCLUD T.B Treatment : find the cause and treat accordingly If there is wide spread infection then treat by hysterectomy Senile endometritis : The endometrium lose its resistance ,and not shed repeatedly It may be associated with senile vaginitis The endometrium infiltrated by macrophages known as foam cells the epithelium become destroyed lead to granulation tissue that lead to pus exudation if is collect in the cavity lead to pyomertra , because the cervix is narrow due to senility atrophied myometrium The uterus enlarge and become thin , pyrometera may cause squamous metaplasia or rarely ruptured spontaneously : • Clinical features: 1- purulent very offensive post menopausal discharge , some times bloody stained 2- Sometime intermittent discharge 3- uterus is enlarge D.D: 1- Ca of the uterus 2- if there is pyometra then DO dilatation of the cervix that lead to drainage of pus+ antibiotics for 1-2 weeks and then do curettage for DD Treatment : if the patient fit for surgery then hysterectomy after exclusion of Ca • UTERINE POLYPS 1- endometrial polyps usually multiple , and may be apart of hyperplastic endometrium, at menopause are single or few in number , Pathology : small, pink ,pale projecting from the endometrium ,some time has long stalk that make it projecting through the cervix or the vulva , atypical cellular changes or squamous metaplasia can occur ,adenocarcinoma can occur also • 2- fibroid polyp : sub mucosal fibroids can protrude in to the cavity or pass through the cervix into the vagina , its surface covered by endometrium ,it cause spasmodic dysmenorrhea ,menorrhagia , 3- Adenomayomatous polyp Contain smooth muscle + endometrial elements Usually coexist with adenomyosis ,causing heavy menses but regular, cramping , some time causing intermenstrual spotting ,malignant changes can occur with it • Placental polyp: It is rare ,due to organization of small retained pieces of placental tissue, it cause intermenstrual bleeding ,it may cause sever hemorrhage on removal , treated by excision , send for biopsy Asherman ΄s syndrome • When there is endometrial damage to endometrium ,the whole thickness , i.e. beyond the basal layer ,caused by : 1- excessive curettage for retained products , after miscarriage , for 2ndry PPH 2- T.B ,schistosomasis 3- ENDOMETRIAL RESCTION( ABLATION) It cause : it cause fibrosis and adhesion Hypo menorrhea, amenorrhea, infertility Treatment by : Resection by hysteroscopy + inert IUCD+ HRT Uterine fibroid • Definition: Uterine leiomyoma are benign tumors compose of uterine muscles plus fibrous connective tissue • It is common mass in uterus and body • It is present in 20% of all female • It is of unknown cause • It is may be found out side the uterine organ Vagina , broad ligament ,utero .sacral ligament, vulva, • Inevitably female sex hormones have been incriminated . Because it is rarely appear before puberty and after menopause , and there is a rapid growth during pregnancy, and frequently seen in condition associated with hyper estrongism that not antagonized by progesterone like anovulation , end . Polyp , endometrial hyperplasia, it is more in negros than in white women • Grossly : It is firm , round tumor in the uterine wall which is its self is hypertrophied it has a pseudo capsule which differentiate it from adenomyosis Since the blood supply at the periphery so the center is susptible to degenerative changes , ON cutting the tumor is solid, smooth, pinkish or white , the surface has whorl- like appearance Microscopically: It composed of groups & bundles of smooth muscle in a twisted whorl fashion ,with some connective tissue . Types: 1- intramural : the most common 2- sub serous myomas: projecting to wards the peritoneal cavity ± pedicle may reach a large size without producing symptoms 3-interligamantory tumor 4- sub mucosal 5-cervical FIBROIDS MAY BE SINGLE OR MULITIPLE Depending on size, number , location 1- Symptomless CLINICAL FEATUERS - Discovered accidentally by abdominal examination ,pelvic examination, U/S, laparotomy, 2- Abnormal uterine bleeding: heavy, prolong MAY be due to enlargement of uterine cavity by sub mucous fibroids ,or due to increase in vascularity, or due to necrosis of endometrium overlying the sub mucous myoma,frequently myoma may associated with polyps and endometrial hyperplasia 3- Intermenstrual bleeding in case of submucuse fibroid 4- pain: a- reappearance of dysmenorrhea ,congestive type, due to increase vascularity b- Backache incase of posterior fibroids of moderate size with retroversion c –colicky pain in case of sub mucous uterus d- torsion e- degenerative changes f- abdominal distention g- pressure symptoms: On venacava= edema On bladder = frequency Or dyspnea Degenerative changes: Due to either arterial , venous , or secondary infections or malignant transformation 1- hyaline degeneration 2- cystic degeneration 3-red degenerations 4- calcifications 5- necrosis 6- sarcomatous changes 7- infection Hyaline degeneration the tumor become soft ,and like jelly ,the cells fused together and become a structure less esonophilic mass Liquefaction may occur after menopause lead to cystic cavity FAT may be deposited in fibroid with release of fatty acids then undergo saponification ,Co3 and Po4 in blood react upon the soppy mass lead to deposition of CaCo3 and calcium phosphate ͢ Gritty on section of the tissue or Thin peripheral shall that can be seen by X -ray Necrosis Necrobiosis ( Red degeneration) a- diffuse b- local Usually in pregnancy or near menopause that lead to fibromyomatous pattern,( thrombosis of peripheral vessels, absence of cell nuclei, the blood vessels distended and become thin wall and engorged with R. B. C.s ,the tumor stained red and resemble raw meat ,it give fishy odor on cutting due to fatty acids, cystic degeneration may occur in the center and the cyst full with greasy brown debris Fatty degeneration Atrophy Torsion Sarcomatous changes that occur in 0.5% of fibroids, 2/3 of sarcoma of the uterus arise from uterine fibroids Infections Physical signs and differential diagnosis • Pelvic or abdominal mass D.D - Pregnancy - Ovarian tumor - endometrial or cervical polyp - Adenomyosis - Treatment 1- Conservative For small and no symptoms frequent U/S every 6 months . 2- surgical : myomectomy : a- laparotomy b- laparoscopy hysterectomy LH RH agonist Uterine artery embolisation ENDOMETRIAL HYPERPLASIA • What is endometrial hyperplasia? • Endometrial hyperplasia occurs when the endometrium, the lining of the uterus, becomes too thick. It is not cancer, but in some cases, it can lead to cancer of the uterus. • How does the endometrium normally change throughout the menstrual cycle? • The endometrium changes throughout the menstrual cycle in response to hormones. During the first part of the cycle, the hormone estrogen is made by the ovaries. Estrogen causes the lining to grow and thicken to prepare the uterus for pregnancy. In the middle of the cycle, an egg is released from one of the ovaries (ovulation). Following ovulation, levels of another hormone called progesterone begin to increase. Progesterone prepares the endometrium to receive and nourish a fertilized egg. If pregnancy does not occur, estrogen and progesterone levels decrease. The decrease in progesterone triggers menstruation, or shedding of the lining. Once the lining is completely shed, a new menstrual cycle begins. • What causes endometrial hyperplasia? • Endometrial hyperplasia most often is caused by excess estrogen without progesterone. If ovulation does not occur, progesterone is not made, and the lining is not shed. The endometrium may continue to grow in response to estrogen. The cells that make up the lining may crowd together and may become abnormal. This condition, called hyperplasia, may lead to cancer in some women. • When does endometrial hyperplasia occur? • Endometrial hyperplasia usually occurs after menopause, when ovulation stops and progesterone is no longer made. It also can occur during perimenopause, when ovulation may not occur regularly. Listed as follows are other situations in which women may have high levels of estrogen and not enough progesterone: • • Use of medications that act like estrogen • • Long-term use of high doses of estrogen after menopause (in women who have not had a hysterectomy) • • Irregular menstrual periods, especially associated with polycystic ovary syndrome or infertility • • Obesity • What risk factors are associated with endometrial hyperplasia? • Endometrial hyperplasia is more likely to occur in women with the following risk factors: • • Age older than 35 years • • White race • • Never having been pregnant • • Older age at menopause • • Early age when menstruation started • • Personal history of certain conditions, such as diabetes mellitus, polycystic ovary syndrome, gallbladder disease, or • thyroid disease • • Obesity • • Cigarette smoking • • Family history of ovarian, colon, or uterine cancer • What are the types of endometrial hyperplasia? • Endometrial hyperplasia is classified as simple or complex. It also is classified by whether certain cell changes are present • or absent. If abnormal changes are present, it is called atypical. The terms are combined to describe the exact kind of • hyperplasia: • • Simple hyperplasia • • Complex hyperplasia • • Simple atypical hyperplasia • • Complex atypical hyperplasia • What are signs and symptoms of endometrial hyperplasia? • The most common sign of hyperplasia is abnormal uterine bleeding. • Bleeding during the menstrual period that is heavier or lasts longer than usual • • Menstrual cycles that are shorter than 21 days (counting from the first day of the menstrual period to the first day of the • next menstrual period) • • Any bleeding after menopause • How is endometrial hyperplasia diagnosed? • Transvaginal ultrasound may be done to measure the thickness of the endometrium. Thick, it may mean that endometrial hyperplasia is present. • The only way to tell for certain that cancer is present is to take a small sample of tissue from the endometrium and study it under microscope. • This can be done with an endometrial biopsy, dilation and curettage, or hysteroscopy • What treatments are available for endometrial hyperplasia? • In many cases, endometrial hyperplasia can be treated with progestin. Progestin is given orally, in a shot, in an intrauterine device, or as a vaginal cream. • How much and how long the treatment take • it depends on age and the type of hyperplasia. • Treatment with progestin may cause vaginal bleeding like a menstrual period. • If there is atypical hyperplasia, especially complex atypical hyperplasia, the risk of cancer is increased. Hysterectomy • usually is the best treatment option if the patient do not want to have any more children. prevention of endometrial hyperplasia Taking estrogen after menopause, also need to take progestin or progesterone. If menstrual periods are irregular, birth control pills (oral contraceptives) may be recommended. They contain • estrogen along with progestin. Other forms of progestin also may be taken. • • If overweight present, losing weight may help. The risk of endometrial cancer increases with the degree of obesity