(From Middle Robbins, by Brian Buschman)
Return to Semester Four Goodies
Return to The
Unofficial Ross Page
Lichen sclerosis is a thinning of the skin of the vulva. It is most often in post-menopausal women. There is some tie to cancerous change.
1) Condylomas are warts on the anogenital area. They may be condyloma lata (which have become rate) from secondary syphilis or condyloma acuminata from HPV 6 or 11.
2) Valvular carcinoma is mostly seen in older women and is a result of HPV 16 and 18. They usually come after vulvar intraepithelial neoplasia (VIN). VIN III is carcinoma in situ.
3) Extramammory Paget’s disease is a dysplasia in the epithelia that shows perinuclear halo cells.
4) Melanoma of the vulva is a very aggressive neoplastic tumor. Prognosis is related to depth of invasion.
Cervicitis is caused by many things. Vaginal erosions are a normal migration of the cervical columnar epithelium down to the vagina. IT will go back up but in the meantime will appear inflamed but is not really. The most common microorganism to cause cervical inflammation is C. trachomatis.
1) Endocervical polyps are a factor of inflammation and are covered by the same mucus secreting epithelia.
2) Cervical intraepithelial neoplasia (CIN) is related to HPV 16, 18, 31 or 33. They code for genes that inactivate p53 and Rb. It leads to proliferative cells that are non-invasive.
3) Invasive C of the cervix is the evil end product of CIN 10-15 years later. It may be seen in one of three forms:
a. Funguating (cauliflower-like)
b. Ulcerative
c. Infiltrative where it goes deep inside and may even involve the bladder or the rectum.
Adenomyosis is the growth of the endometrium down into the myometrium.
Endometriosis is the spread of endometrial tissue to other pelvic locations besides the uterus. These parts undergo the same monthly cycles so they lead to intrapelvic bleeding and therefore bruising if near the skin. It often leads to sterility.
Most gynecologic problems that present have to do with abnormal bleeding. Causes include:
1) Anovulation causes glandular hyperplasia with minimal stromal development because of increased estrogen in relation to progesterone levels. This causes lack of support of rupture of spiral A’s.
2) Inadequate luteal phase messes up normal progesterone secretion and sence cycle.
3) Contraceptive indeed bleeding.
Endometrial hyperplasia is a result of excess estrogen production and administration which is not balanced by progesterone. It causes glandular hyperplasia inconsistent with stromal hyperplasia. It causes bleeding and can lead to carcinoma.
Endometrial polyps made of stroma covered by columnar epithelial are benign cysts that often develop of the time of menopause.
Leiomyomas are smooth muscle cells that form tumors. Their growth is related to estrogens. They are monoclonal. They can grow out on a stalk and even attach to other organs.
Leiomyosarcoma do NOT come from leiomyomas but from mesenchymal cells. They are solitary tumors. They may invade the uterus, project out or masquerade as leiomyomas. Recurrence is common after resection.
Endometrial carcinoma is the MC cancer of the female genital tract. It’s risk is based on estrogens. They can infiltrate the wall or grow into the lumen of the uterus. Eventually either will fill the uterus and spread out.
Clinical signs are bleeding in a post-menopausal woman.
Fallopian tubes are rarely the site of primary disease. Most fallopian tube problems are salpingitis spread from PID.
The ovaries have few problems other than neoplasm. Follicle cysts develop from extra large/high-pressure cysts.
Polycystic ovaries result in overproduction of androgens and LH.
1) Serous Tumors are tumors of the ovarian coverings. They show cysts that are filled with serous fluid/mucus. They have psammoma bodies (calcified concretions). Those with low malignant potential do not invade the ovary. Others do. Spread is contiguous. Ascites is seen with seeding of ovarian tumors.
2) Mucous tumors are similar to serous tumors but they have NO psammoma bodies and are mucus producing. They come from the endocervical mucosa.
If they metastisize or rupture the pelvis develops, pseudomyxoma peritonei where it becomes filled with the mucus.
Enometrioid tumors develop from an endometriotic cysts and form a glandular pattern similar to the endoneurium. They are malignant.
Serous cystadenomas may develop with more fibrous stroma in which case they are called a cystadenofibroma.
Brenuer rumors are urinary like stuff. They have transitional epithelia that resembles that of the urinary tract. It may come from the epithelia of the ovary or from reminanents of urinary tissue within the ovary.
Teratomas may be:
1) Benign (mature) cystic tetratomas that show all germ layers, have a calcified focus, are filled with sebaceous secretions, have matted hair and there might be teeth from them. They are only emergencies if they undergo torsion. That makes them mature is that they show great differentiation.
2) Immature malignant tetratomas are very different from immature tetratomas. Cells are more undifferentiated, do not show hair, teeth and such. They often metastasize.
Most placental inflammations are ascending spread of vaginal flora. Sometimes they may come to the placenta in the blood but not often.
These are tumors of the trophoblast.
1) Hydatidiform moles are enlargements of the chorionic villi where a complete hydatidiform mole leads to no room for fetal parts and a partial one leads to some fetal parts. They are detected by vaginal bleeding around the 3rd month and show no heart sounds or fetal parts. They have elevated hCG.
2) Invasive moles are like hydatidiform moles but they are invasive. They go deep into the walls, leave the uterus and may embolize. They do not metastasize (even though they do spread). If a woman is treated for a hydatiform mole but still has elevated hCG levels than it is probably an invasive mole.
3) Choriocarcinoma is a very malignant tumor of the chorionic epithelium. The more risky the pregnancy (young/old material age, etc) the higher the rate of choriocarcinoma. It appears in the blood with elevated hCG especially the b-subunit.
It has great prognosis these days compared with the past.
In the 3rd trimester patients many develop hypertension, proteinuria and edema called preelampsia. If it leads to convulsive seizures then it is called eclampsia. It can lead to DIC that blocks organs and is fatal.
It is seen in placentas with hyoperfusion from undilated spiral A’s. It’s process is:
1) Placental hypoperfusion (ie baby infarcts)
2) Reduced PGI1, PGE2 and NO leading to relative vasoconstriction and hypertension.
3) Ischemic placenta makes thromboplastic stuff causing DIC.
Return to Semester Four Goodies
Return to The
Unofficial Ross Page