Repro Zaman: Female Genitourinary Tract; Kct

Front 1

What are the four stages of syphilis?

Back 1

1. Primary painless chancre w/ or w/o inguinal lymph node (often ignored & progresses to secondary form)
2. Secondary--systemic disease, condyloma latum (lesions on HANDS & SOLES of feet.
3. Latent
4. Tertiary--CNS, aorta.

Front 2

Describe the pathophysiology of H ducreyi.

Back 2

(gram negative bacillus).
Enters skin thru epithelial break (post minor trauma like sex)-->bacteria breach integument-->recruitment of keratinocytes, fibroblasts, endothelial cells, & melanocyte to secrete IL-6 & IL-8--> Hd cyto-lethal distending toxin secreted causing apoptosis & necrosis of human cells

Front 3

What is the role of IL-6 & IL-8 in the pathophysiology of H. ducreyi?

Back 3

IL-8: induces PMNs & macrophages to form intradermal pustules.
IL-6: stimulates T-cell IL-2 receptor expression, which, in turn, stimulates CD4 cells in region.

Front 4

How long does it usually take to get the palmar pustules of secondary syphilis post a primary syphilis in genitalia?

Back 4

6-8 weeks.

Front 5

Why do patients with H. ducreyi chancroids have a predilection of HIV?

Back 5

Macrophages in their ulcers have greater CCR5 & CXCR4 chemokine receptors, which are receptors for HIV entry, than normal cells.

Front 6

What is the difference b/w a chancroid & a chancre sore?

Back 6

-Chancroids have soft ragged edges & are full of pus
-Chancre sores have hard raised edges like a punched out lesion & are painless.

Front 7

Are chancroids seen more often in circumcised or uncircumcised males?

Back 7

uncircumcised.

Front 8

Describe the path of Granuloma inguinale & lymphogranuloma venereum (LGV).

Back 8

Caused by invasive serovars L1, L2,or L3 of Chlamydia trachomatis-->entry thru breaks of skin or across mucus membranes-->organism goes from site of inoculation down lymphatic channels to multiply w/in monocytes of lymph nodes it passes.

Front 9

Describe timing of the primary & secondary stages of LGV.

Back 9

-Primary stage:self-limited PAINLESS genital ulcer that occurs @ contact site 3-12 days or longer
---INFECTION SPREADS TO LYMPH NODES THRU DRAINAGE PATHS-->
-Secondary stage: happens 10-30 days to 6 months post primary stage.

Front 10

What are the clinical manifestations of LGV among males whose primary exposure was genital?

Back 10

Unilateral lymphadenitis & lymphangitis, often tender inguinal &/or femoral lymphadenopathy

Front 11

How does LGV present in females?

Back 11

Perimetritis (inflammation around uterus), salpingitis, lymphangitis & lymphadenitis in deeper nodes.
-Can get end-result(1-20 yrs later) of lymphatic obstruction: genital elephantiasis or esthiomene b/c of strictures or fistulas.

Front 12

What are the sx's of LGV that was transmitted thru anal sex?

Back 12

Lymphadenitis, lymphangitis, proctitis, inflammation limited to rectum (distal 10-12 cm. Possible anorectal pain, tenesmus (painful bowel mvmts w/ straining), rectal discharge, or proctocolitis, colonic mucosa inflammation extending to 12 cm above anus, proctitus, diarrhea, abdominal cramps, &/or perirectal or perianal lymphatic tissues inflammation.

Front 13

How is the diagnosis of LGV made?

Back 13

-Dx usually serologically (sensitivity of 80% after 2 wks, but may not be serotype specific, need to use culture--L1, L2, L3 cause LGV), exclusion of other causes of inguinal lymphadenopathy or genital ulcers.
-Culture w/ DFA TEST for L-type serovar of C trachomatis-->very sensitive & specific, not too available.
-PCR (Taqman analysis)-->takes 1 day to dx but many not be thorough enough.

Front 14

Describe the characteristics of Condyloma accuminatum (virus, strains, histo, locations.

Back 14

i) HPV --usually strains 6,11 (low #'s=more benign)
ii) Perianal, vulvar, vaginal
iii) Hyperkeratosis, papillomatosis, koilocytosis
iv) Low grade strains of HPV (6,11) give wart like condyloma;
-->High grade strains (16,18) give flat condyloma (organism is invasive b/c goes down & into skin surface).
Hence the more dangerous pre-malignant HPV assoc dysplasias often subtle & hard to ID.

Front 15

Describe the characteristics of a Bartholi gland cyst/abscess (size, cause, age of onset.

Back 15

a) Result from obstruction of Bartholin's duct. Cyst is 3-5 cm.
b) May develop secondary infection.
c) Common caused by N. gonorrhea, also E. Coli, Staph.
d) Commonly in reproductive years.

Front 16

Which glands become infected in the pre-menopause years and which post-menopause?

Back 16

Pre-Menopause: Bartholin's glands
Post-Menopause: Skene's glands

Front 17

What is the first step in developing a urethral caruncle & what will chronic irritation lead to?

Back 17

1st step in dev'ment: distal urethral prolapse (estrogen deficiency)
Chronic irritation: growth, hemorrhage, lesion necrosis.

Front 18

What is in the differential diagnosis for a urethral caruncle?

Back 18

Urethral diverticulum, urethral prolapse, urethral carcinoma, & periurethral gland abscesses.

Front 19

What does a Bartholin's gland infection look like on a gross specimen?

Back 19

Clear multicystic nodule, well circumscribed, easily removed during surgery.

Front 20

What does a urethral caruncle look like w/ microscopic examination?

Back 20

Like bed of granulation tissue covered w/ either squamous or transition epithelium. Infolding of epithelium may create papillary architecture. Inflammatory infiltration is common.

Front 21

With immunoperoxidase study, which cells are + for CD45?

Back 21

White blood cells

Front 22

Which immunoperoxidase study would indicate that the tissue was a carcinoma b/c it is found in epithelial cells & an epithelial process?

Back 22

Cytokeratin

Front 23

Which 2 immunoperoxidase studies are usually involved w/ adenocarcinomas of the colon & lover?

Back 23

CK7 & CK20

Front 24

HMB-45 & S-100 are positive in which type of cells?

Back 24

Neural type cells (melanocytes are closely related to neural type cells)

Front 25

What does vimentin positive indicate?

Back 25

Mesothelial primitive type cells--precursors to melanocytes.

Front 26

What is Breslow's thickness?

Back 26

Depth of invasion--usually measured by ocular microscopy, really invasive is >1cm.

Front 27

What are 4 characteristics of chronic dystophies of the vulva?

Back 27

a) Vulvar dystrophy
b) Leukoplakia
c) Keratosis
d) Kraurosis vulvae- vulvar atrophy & inflammation

Front 28

Define endometrisis.

Back 28

Non-neoplastic lesion, presence of endometrial tissue anywhere other than endometrial cavity.

Front 29

Describe the characteristics of accessory breast tissue. Where you can find this tissue?

Back 29

-Present anywhere along 'milk line'-->so can have primary primary breast CAall the way down to vulva;
-Enlarges during lactation
-Can give rise to breast-like neoplasms e.g. fibroadenoma, papillary hidradenoma.

Front 30

What is another name for a sebaceous cyst thats benign w/ keratinous material in center?

Back 30

Epidermal inclusion cyst.

Front 31

What are the characteristics Lichen sclerosis/Lichen sclerosis et atrophicus (40%) & how do you treat it?

Back 31

Female-post-menopausal;
a) Atrophy, narrowed introitus
b) thin epithelium (so can have trauma & bleeding)
c) Rx: anabolic steroids

Front 32

What is the male equivalent to Lichen sclerosis?

Back 32

Balanitis xerotica obliterans

Front 33

In a patient w/ HPV, microscopically when should you start to suspect carcinoma?

Back 33

When lesion becomes flat, invasion of basement membrane.

Front 34

What percent of Vaginal Intraepithelial Neoplasm (VIN) ( new term for vaginal dysplasia/carcinoma in situ) progresses to invasive CA?

Back 34

5-10%

Front 35

How do you make a diagnosis of VIN?

Back 35

Full thickness of epithelium involved w/ dysplastic cells but no evidence of invasion. May be assoc w/ leukoplakia or inflammation. If its assoc w/ a lot of inflammation, may be called Bowen's disease.

Front 36

VIN is associated w/ which serotypes of HPV?

Back 36

16 & 18. (also often multi-focal & assoc w/ CA elsewhere in genital tract)

Front 37

What is the most common vulval-malignancy (90-97%)? In what age group does it occur?

Back 37

Epidermoid (squamous cell) CA. Rare GYN tumor but most common here;
Older women (60y/o)

Front 38

What is the treatment for epidermoid (squamous cell) CA?

Back 38

Radial vulvectomy (bilateral vulvectomy & lymph node dissection). 60% have dz in lymph nodes @ surgery. Lots of lymphatic channels across midline, so need to do surgery. Often multi-focal CA.

Front 39

What are the three types of Paget's disease?

Back 39

1. Paget's dz of bone
2. Paget's dz of breast (nipple)
3. Extra-mammary Paget's dz of Vulva.

Front 40

Which cells are very characteristic of Paget's dz of the breast & extra-mammary Paget's dz of Vulva?

Back 40

large, clear mucin containing cells. In some pts this condition is assoc w/ underlying CA!!!!!

Front 41

What is the diagnosis & prognosis for someone with
Extramammary Paget's dz?

Back 41

Dz: 1. high degree of clinical suspicion
2. Skin biopsy

Prognosis: Catch early!! Dependant on early dx w/ definitive surgical tx.

Front 42

Which factor plays a role in predicting the risk of associated CA in a pt w/ EMPD?
Risk of genital EMPD? Perianal EMPD?

Back 42

-the anatomic location of the EMPD. 4-7% of pts w/ genital dz having CA. Perianal dz-->colorectal CA in 25-35%!!

Front 43

What is the second most common vulvar malignancy (2-5%)?

Back 43

Malignant melanoma.

Front 44

What is the prognosis of malignant melanoma?

Back 44

-Very malignant tumor of nevus cells w/ a 30% 5 yr survival.
-Prognosis depends on thickness of lesion (Breslow's thickness >1cm=poor, Clark's levels--levels3&4=poor)

Front 45

What does EMPD look like microscopically?

Back 45

Large vaculoated cells w/ dark nuclei.

Front 46

Do cancers metastasize to & from the vulva area?

Back 46

-mets usually from local sites (cervix, endometrium, colon, ovary)
-Vulvar CA can mets to other sites but rare
-can get ectopic breast tissue w/ ductal adenocarcinoma rarely & confused as mets.