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Repro - Pathology > Female Genital Tract > Flashcards

Female Genital Tract Flashcards

1
Q

What is Trichomonas?

A

large flagellated protoza, transmitted sexually

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2
Q

What is the gross pathology of Trichomonas?

A

cervical and vaginal mucosa is covered in yellow/green/gray frothy discharge; strawberry cervix

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3
Q

Who are prone to get candida infxns

A

DM, Pregnancy, OCP users. This is NOT sexually transmitted

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4
Q

What are clinical presentation of a trichomonas infxn

A

pruritus, malodorous, dyspareunia, dysuria

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5
Q

What is the gross pathology of candida

A

Thrush; cottage-cheese vagina –> white exudate forming small plaques on muscoal surfaces

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6
Q

what is the micro patholgoy of candida infxn

A

fungus doesn’t penetrate epithelium; submucosa is chronically inflamed; branched hyphae on KOH

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7
Q

Where can HSV be latent

A

sacral ganglion and trigeminal ganglion

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8
Q

What is the gross pathology of HSV

A

painful vesicles on vulva, vagina, and cervix –> erodes into painful ulcers

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9
Q

What is the micro pathology of HSV

A

enlarged multinucleated cells w/ nuclear inclusions seens w/ Tzanck smear

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10
Q

What can Chlamydia cause?

A

cervicitis, endometritis, salpingo-oophoritis

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11
Q

What can gonorrhea cause?

A

skene gland adenitis, endometritis, salpingitis

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12
Q

What are the most common STDs in USA

A

HPV, HSV, GC, Syphilis

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13
Q

What are common non-STIs

A

C. Albicans, Actinomyces, Mycobacterium TB

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14
Q

What are the 2 etiologies for a pelvic inflammatory disease

A
  1. Ascending inflammatory polymicrobial infxn

2. primary endometrial infxn

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15
Q

What are common bugs that cause PID from an ascending infxn

A

GC, CT, Mycoplasm
Enteric Bacteria
Streptococci, Staphylcocci in postpartum setting

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16
Q

Wha tis the most common site of the initial inflammation of a GC infxn

A

Periurethral/perivaginal glands – Bartholin Glands

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17
Q

What is the most common and most severe infxn in women

A

PID

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18
Q

How does GC cause PID

A
  1. it travels up to the fallopian tubes and causes Acute cervicitis –> endomitritis –> supparrative salpingitis
  2. tubes then fill w/ pus (pyosalpinx) –> chronic follicular salpingitis –> hydropsalpinx –> fused fimbfria and tube strictures form ( can cause infertility)
  3. The inflammation spills from the fimbriated end of the tube onto ovary (acute salpingo-oophoritis–> Tube- ovarian abscess)
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19
Q

How do polymicrobial infxns causes PID

A

they spread via lymphatics or venous bloos, there is less contact spread via mucosa and more involvement of deeper layers

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20
Q

What is the pathology of GC infxn

A

increased mucosal involvement w/ congestion of PMNs, lymphocytes, plasma cells –> necrotic debris/fibrous tissue

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21
Q

What is the pathology of a polymicrobial infxn

A

signs of inflammations in deeper layers; less mucosal involvement

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22
Q

What are some complications of PID (mainly GC)

A

Peritonitis, adhesions/fibrous bands –> bowel obstruction
Sepsis –> arthritis, meningitis, endocarditiis
Infertility (from adhesions and strictures)

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23
Q

Why does HPB affect the cervix?

A

1 the squamocolumnar junctions at cervix presents physiologic metaplasia w/ immature metaplastic squamous cells that are susceptible to HPV

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24
Q

When does a cancer usually arise from an HPV infxn

A

when the HPV is integrated into host DNA

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25
What effects do E6 and E7 have on host cells
1. E6 degrades p53 via ubiquitin dependent proteolysis 2. E7 inactivates Rb * this results in increased p16INK4a and increased Cyclin E = increases lifespan of epithelial cells --> koilocytic changes --> condyloma or cancer can occur
26
how can you distinguish btwn the endocervix and the vagina pathologically
Endocervix -- blood vessels are more prominent
27
What is the gross pathology of condyloma acuminata
fungating/exophytic lesions w/ bizarre vessels and hemorrhage
28
What is the microscopic pathology of the spectrum of CIN?
1. CIN 1 - dysplasia limited to basal layer only 2. CIN 2 - dysplasia in lower 1/3 and middle 1/3; superficiallt there is still epithelial differentiation 3. CIN 3 - dysplasia in all layers + little epithelial differentiation 4. CIS - complete dysplasia w/ no epithelial differentiation
29
What immunostain can you do to look at the mitotic activity for CIN
Ki67
30
How can you dx CIN/CIS
Schiller Test
31
What does the Schiller test do
1. applying acetic acid will reveal abnormal mucosa - shows dysplastic cells 2. applying iodine turns normal cells brown
32
What are some features of CIN
maturation arrest, blurred/missing distinction of basal cell layer, loss of cellular orientation, polarity, increased N:C ratio, hyperchromatic epithelium
33
What is the spectrum of HPV related neoplasm
1. CIN 1 : mild dysplasia; large cells w/ bi/multinucleated cells 2. CIN 2 : moderate dysplasia; higher N:C ratio 3. CIN 3: severe dysplasia; small cells; very high N:C ratio 4. Carcinoma in situ * CIN 1 = LSIL * * CIN 2+3+CIS = HSIL
34
Where are various HPV's found in a cell
- 6 and 11 = episomally | - 16 and 18 = integrated into host DNA
35
What are the risk factors for CIN?
- 2/3 of graduating college women are HPV+ 1. persistent HPV 16/18 infxn 2. Young age of first intercourse 3. OCP 4. ISP 5. HLA subtypes 6. Multiple sexual partners 7. Smoking
36
What are precancerous lesions to cervical squamous cell carcinoma
CIN 3, CIS, HSIL
37
What indicates Koilocytes
1. increased mitotic activity 2. irregular nuclear membrane 3. Raisinoid nucleus 4. Cytomegaly 5. peripheral halo 6. stippled/coarse chromatin
38
What is the microscopic pathology of cervical SCC
nest of invading squamous cells, mayhaps vascular/lymphatic invasion; desmosplastic reaction, keratin pearls
39
What is the epidemiology of cervical SCC
- 2nd MC cancer of women, 8th overall - 50% cases are fatal - Pap smears significantly decrease progression of disease - MC age of HPV infxn - 20 yrs old
40
What is the staging of cervical SCC
1. Stage 1a - microinvasive w/out metastasis or vascular invasion (3 vs 5 mm) Stage 1b - tumor invasion grossly visible ( 4 cm is cutoff for 1b1 and 1b2 Stage 2 - extends beyond cervix but not to pelvic wall and upper 2/3 vagina Stage 3 - lower 1/3 vagina (IIIa) and invades pelvic wall --> hydronephrosis/non-functioning kidney (IIIb) Stage 4 - urinary bladder/rectum in 4a; invades beyond true pelvis in 4b
41
What is the treatment for early stage vs advanced stages of cervical SCC
Early stage - hysterectomy | Late stage - hysterectomy plus radiation
42
How can prevention be done for cervical SCC
vaccines containing virus-like particles --> no HPV pre-cancerous lesions of invasive carcionma
43
what is the best prognostic factor for cervical SCC
tumor stage
44
What mediates the phases of them menstrual cycle?
1. Proliferative - Estrogen 2. Secretory - Progesterone 3. Menstrual - progressive decrease in P and E
45
What is the pathology for the proliferative phase
* straight glands and pseudo-stratified epithelium * Edematous stroma: spindle cells w/ decreased cytoplasm and increased mitotic rate * NO mucin production
46
What is the pathology of the secretory phase
* Early/post ovulation - basal secretory vacuoles w/ decreased mitotic rate; simple epithelial layer * Late - tortuous, corkscrew dilated glands w/ increased secretion of mucin, spiral arteries, and decidulization
47
what is the pathology of the menstrual phase
* extravasation of RBC into stroma and leukocyte infiltration into stroma * fibrin thrombin and disintegrated glands/stroma
48
What is the basis of dz in the endometrium
prolonged estrogen exposure -- excessive proliferation -- fragmented; upon decrease estrogen --> break-through bleeding
49
What is the microscopic pathology of menopause
inactive simple/cystic glands - essentially atrophic endometrium - inactive fibrous-appearing dense stroma - no evidence of proliferation or secretion
50
What is endometrial hyperplasia
increased gland/stroma ratio from gland proliferation
51
What is the etiology of endometrial hyperplasia
increased E stimulation w/ decreased P effects - PCOS - Perimenopause - E- producing tumors - Obesity
52
What is the pathogenesis of endometrial hyperplasia
1. Inactivation of PTEN TSG - increases PTEN = decreased AKT activity 2. Normally, E increases PTEN
53
What is the pathology of simple adenomatous endometrial hyperplasia +/- atypia
* ciliation suggests tubual differentiation * increased gland/stroma ratio w/ variation in size/shape of glands; decreased stroma compared to normal; glandular crowding
54
What is the pathology of complex adenomatous endometrial hyperplasia +/- atypia
* increased crowding of glands w/ scanty stroma in btw the glands; back to back glands
55
What is the pathology of atypical hyperplasia
Classic cellular atypia - rounded identical cells (loss of polarity) w/ increased N:C ratio
56
what has a greater risk for endometrium carcincoma: simple of complex?
Complex proliferation has 25%
57
What is the MC gyn cancer
Endometrial adenocarcinoma, occurs in post-menopausal
58
What is the grading of endometrial adenocarcinoma
Grade 1 : well differentiated Grade 2 : moderately differentiated Grade 3 : no architecture
59
What is the pathogenesis of endometrial adenocarcinoma
no PTEN TSG gene
60
What is malignant mixed mullerian tumor
malignany endometroid cells of adenocarcinoma + sarcomatous components (striated muscle, bone, adipose)
61
What is leiomyoma
benign smooth muscle neoplasm -- Fibroids | MC tumor in women, regresses after menopause
62
What is the gross pathology of a leiomyoma
Sharply circumscirbed but not encapsulated; multiple--- undergoes dystrophic calcification and hyalinization thus called Fibroids. Rounded
63
What is the micro pathology of leiomyoma
White whorled bundles of SM cells, spindle-shaped smooth muscle, eosinophilia, cigar-shaped nuclei
64
What is the presentation of a leiomyoma
bleeding/camping/loss of pregnancy (compresses uterus) and increased urination (compresses bladder)
65
What is a leiomyosarcoma
malignant SM neoplasm, nuclear atypia, increased mitotic figures and increased necrosis
66
What is the 2nd MC gyn cancer
Ovarian neoplasia
67
What are the clinical presentations of ovarian cancer
1. ad pain 2. GI/urinary symptoms 3. vaginal bleeding
68
When are most ovarian cancers found
not until metastasis. It's benign in young women and malignant in old women
69
What is the most common ovarian cancer
surface epithelium tumors - 65% Germ cell - 20% Sex Cord - 10% Mets - 5%
70
What are the surface epithelium tumors
serous tumors, mucinous tumors, endometroid tumors, transitional cell tumors
71
What is the etiology of surface epithelium tumors
neoplastic transformation of coelomic epithelium associated w/ increased E exposure and BRCA +
72
What is a cystadenocarcionma
large white/tan fleshy tumow w/ papillary projections and cystic areas. * pathology --- tall columnar ciliated/non-ciliated epithelial cells filled w/ serous fluid * Psammomma bodies
73
What is a cystadenoma
Large, simple cyst | * cubodial to low columnar, ciliated
74
What is the pathology of mucinous ovarian tumor
Can be HUGE; tall columnar epithelium w/ apical mucin and absent cilia. forms sticky gelatinous glycoprotein-rick fluid
75
What is the pathology of endometroid ovarian tumor
presence of tubular glands
76
What is the pathology of Brenne tumor
transitional cell adenofibroma | * nests of transitional epithelium as seen in lining of bladder, contains mucinous glands at the center
77
What is the epidemiology of germ cell ovarian cancers
common in kids - malignant | * if in adults - benign
78
What is the pathology of a teratoma
* at least 2/3 layers * mature benign - hair, bone, teeth, brain, tissue,etc * immature malignant - resembles embryonal tissue, increased risk * struma ovarii - always unilaterla, functional
79
What is the pathology of dysgermninoma -- F version of a seminoma
large vesicular walls w/ clear cytoplasm; central nuclei; lymphocytes; granulomas
80
What is the pathology of a yolk sac tumor
Rich in AFP | Schiller-Duval Bodies -- glomerular - looking central blood vessel surrounded by endodermal germ cells
81
What is the pathology of Granulose-theca cell tumors
* mustard yellow from increased androgen production, areas of necrosis * coffee bean shaped nuclei and Call Exner bodies (immature follicle formation)
82
What is the presentation of a granulose-theca cell tumor
In kids - precocious puberty In adults - post-menopausal bleeding * secretes inhibin and calretinin (neruonal protein)
83
what is the pathology of Leydig-Sertolid cell tumor
gross - gray/golden brown | Micro - tubules composed of sertoli/leydig cells
84
What is the presentation of Leydig cell tumor
increased androgens so masculinzation
85
What is adenomyosis
benign endometrial gland/stroma w/in myometrium
86
What is the pathology of adenomyosis
Gross = enlarged soft uterus, hemorrhagic cystic | Micro - proliferative glands
87
what is endometriosis
benign endometrial glands/stroma outside the uterus
88
What is the pathogenesis of endometriosis
1. retrograde menstrual implantation 2. vascular dissemination 3. metaplasia
89
What is the most common site
Ovaries -- chocolate cyst
90
What are the symptoms of endometriosis
related to site 1. infertility - primary complaint 2. fibrous adhesion/strictures impair fallopian tubes 3. Painful defecation in pouch in douglas etc

Repro - Pathology (5 decks)

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