Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Repro - Pathology > Female Genital Tract > Flashcards

Female Genital Tract Flashcards

1
Q

What is Trichomonas?

A

large flagellated protoza, transmitted sexually

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the gross pathology of Trichomonas?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Who are prone to get candida infxns

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are clinical presentation of a trichomonas infxn

A

pruritus, malodorous, dyspareunia, dysuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the gross pathology of candida

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the micro patholgoy of candida infxn

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where can HSV be latent

A

sacral ganglion and trigeminal ganglion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the gross pathology of HSV

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the micro pathology of HSV

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can Chlamydia cause?

A

cervicitis, endometritis, salpingo-oophoritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can gonorrhea cause?

A

skene gland adenitis, endometritis, salpingitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the most common STDs in USA

A

HPV, HSV, GC, Syphilis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are common non-STIs

A

C. Albicans, Actinomyces, Mycobacterium TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 2 etiologies for a pelvic inflammatory disease

A
  1. Ascending inflammatory polymicrobial infxn

2. primary endometrial infxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are common bugs that cause PID from an ascending infxn

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

Periurethral/perivaginal glands – Bartholin Glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the most common and most severe infxn in women

A

PID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the pathology of GC infxn

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the pathology of a polymicrobial infxn

A

signs of inflammations in deeper layers; less mucosal involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When does a cancer usually arise from an HPV infxn

A

when the HPV is integrated into host DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What effects do E6 and E7 have on host cells

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how can you distinguish btwn the endocervix and the vagina pathologically

A

Endocervix – blood vessels are more prominent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the gross pathology of condyloma acuminata

A

fungating/exophytic lesions w/ bizarre vessels and hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the microscopic pathology of the spectrum of CIN?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What immunostain can you do to look at the mitotic activity for CIN

A

Ki67

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How can you dx CIN/CIS

A

Schiller Test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does the Schiller test do

A
  1. applying acetic acid will reveal abnormal mucosa - shows dysplastic cells
  2. applying iodine turns normal cells brown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are some features of CIN

A

maturation arrest, blurred/missing distinction of basal cell layer, loss of cellular orientation, polarity, increased N:C ratio, hyperchromatic epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the spectrum of HPV related neoplasm

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where are various HPV’s found in a cell

A
  • 6 and 11 = episomally

- 16 and 18 = integrated into host DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the risk factors for CIN?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are precancerous lesions to cervical squamous cell carcinoma

A

CIN 3, CIS, HSIL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What indicates Koilocytes

A
  1. increased mitotic activity
  2. irregular nuclear membrane
  3. Raisinoid nucleus
  4. Cytomegaly
  5. peripheral halo
  6. stippled/coarse chromatin
38
Q

What is the microscopic pathology of cervical SCC

A

nest of invading squamous cells, mayhaps vascular/lymphatic invasion; desmosplastic reaction, keratin pearls

39
Q

What is the epidemiology of cervical SCC

A
  • 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
Q

What is the staging of cervical SCC

A
  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
Q

What is the treatment for early stage vs advanced stages of cervical SCC

A

Early stage - hysterectomy

Late stage - hysterectomy plus radiation

42
Q

How can prevention be done for cervical SCC

A

vaccines containing virus-like particles –> no HPV pre-cancerous lesions of invasive carcionma

43
Q

what is the best prognostic factor for cervical SCC

A

tumor stage

44
Q

What mediates the phases of them menstrual cycle?

A
  1. Proliferative - Estrogen
  2. Secretory - Progesterone
  3. Menstrual - progressive decrease in P and E
45
Q

What is the pathology for the proliferative phase

A
  • straight glands and pseudo-stratified epithelium
  • Edematous stroma: spindle cells w/ decreased cytoplasm and increased mitotic rate
  • NO mucin production
46
Q

What is the pathology of the secretory phase

A
  • 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
Q

what is the pathology of the menstrual phase

A
  • extravasation of RBC into stroma and leukocyte infiltration into stroma
  • fibrin thrombin and disintegrated glands/stroma
48
Q

What is the basis of dz in the endometrium

A

prolonged estrogen exposure – excessive proliferation – fragmented; upon decrease estrogen –> break-through bleeding

49
Q

What is the microscopic pathology of menopause

A

inactive simple/cystic glands - essentially atrophic endometrium

  • inactive fibrous-appearing dense stroma
  • no evidence of proliferation or secretion
50
Q

What is endometrial hyperplasia

A

increased gland/stroma ratio from gland proliferation

51
Q

What is the etiology of endometrial hyperplasia

A

increased E stimulation w/ decreased P effects

  • PCOS
  • Perimenopause
  • E- producing tumors
  • Obesity
52
Q

What is the pathogenesis of endometrial hyperplasia

A
  1. Inactivation of PTEN TSG - increases PTEN = decreased AKT activity
  2. Normally, E increases PTEN
53
Q

What is the pathology of simple adenomatous endometrial hyperplasia +/- atypia

A
  • ciliation suggests tubual differentiation
  • increased gland/stroma ratio w/ variation in size/shape of glands; decreased stroma compared to normal; glandular crowding
54
Q

What is the pathology of complex adenomatous endometrial hyperplasia +/- atypia

A
  • increased crowding of glands w/ scanty stroma in btw the glands; back to back glands
55
Q

What is the pathology of atypical hyperplasia

A

Classic cellular atypia - rounded identical cells (loss of polarity) w/ increased N:C ratio

56
Q

what has a greater risk for endometrium carcincoma: simple of complex?

A

Complex proliferation has 25%

57
Q

What is the MC gyn cancer

A

Endometrial adenocarcinoma, occurs in post-menopausal

58
Q

What is the grading of endometrial adenocarcinoma

A

Grade 1 : well differentiated
Grade 2 : moderately differentiated
Grade 3 : no architecture

59
Q

What is the pathogenesis of endometrial adenocarcinoma

A

no PTEN TSG gene

60
Q

What is malignant mixed mullerian tumor

A

malignany endometroid cells of adenocarcinoma + sarcomatous components (striated muscle, bone, adipose)

61
Q

What is leiomyoma

A

benign smooth muscle neoplasm – Fibroids

MC tumor in women, regresses after menopause

62
Q

What is the gross pathology of a leiomyoma

A

Sharply circumscirbed but not encapsulated; multiple— undergoes dystrophic calcification and hyalinization thus called Fibroids. Rounded

63
Q

What is the micro pathology of leiomyoma

A

White whorled bundles of SM cells, spindle-shaped smooth muscle, eosinophilia, cigar-shaped nuclei

64
Q

What is the presentation of a leiomyoma

A

bleeding/camping/loss of pregnancy (compresses uterus) and increased urination (compresses bladder)

65
Q

What is a leiomyosarcoma

A

malignant SM neoplasm, nuclear atypia, increased mitotic figures and increased necrosis

66
Q

What is the 2nd MC gyn cancer

A

Ovarian neoplasia

67
Q

What are the clinical presentations of ovarian cancer

A
  1. ad pain
  2. GI/urinary symptoms
  3. vaginal bleeding
68
Q

When are most ovarian cancers found

A

not until metastasis. It’s benign in young women and malignant in old women

69
Q

What is the most common ovarian cancer

A

surface epithelium tumors - 65%
Germ cell - 20%
Sex Cord - 10%
Mets - 5%

70
Q

What are the surface epithelium tumors

A

serous tumors, mucinous tumors, endometroid tumors, transitional cell tumors

71
Q

What is the etiology of surface epithelium tumors

A

neoplastic transformation of coelomic epithelium associated w/ increased E exposure and BRCA +

72
Q

What is a cystadenocarcionma

A

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
Q

What is a cystadenoma

A

Large, simple cyst

* cubodial to low columnar, ciliated

74
Q

What is the pathology of mucinous ovarian tumor

A

Can be HUGE; tall columnar epithelium w/ apical mucin and absent cilia. forms sticky gelatinous glycoprotein-rick fluid

75
Q

What is the pathology of endometroid ovarian tumor

A

presence of tubular glands

76
Q

What is the pathology of Brenne tumor

A

transitional cell adenofibroma

* nests of transitional epithelium as seen in lining of bladder, contains mucinous glands at the center

77
Q

What is the epidemiology of germ cell ovarian cancers

A

common in kids - malignant

* if in adults - benign

78
Q

What is the pathology of a teratoma

A
  • 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
Q

What is the pathology of dysgermninoma – F version of a seminoma

A

large vesicular walls w/ clear cytoplasm; central nuclei; lymphocytes; granulomas

80
Q

What is the pathology of a yolk sac tumor

A

Rich in AFP

Schiller-Duval Bodies – glomerular - looking central blood vessel surrounded by endodermal germ cells

81
Q

What is the pathology of Granulose-theca cell tumors

A
  • mustard yellow from increased androgen production, areas of necrosis
  • coffee bean shaped nuclei and Call Exner bodies (immature follicle formation)
82
Q

What is the presentation of a granulose-theca cell tumor

A

In kids - precocious puberty
In adults - post-menopausal bleeding
* secretes inhibin and calretinin (neruonal protein)

83
Q

what is the pathology of Leydig-Sertolid cell tumor

A

gross - gray/golden brown

Micro - tubules composed of sertoli/leydig cells

84
Q

What is the presentation of Leydig cell tumor

A

increased androgens so masculinzation

85
Q

What is adenomyosis

A

benign endometrial gland/stroma w/in myometrium

86
Q

What is the pathology of adenomyosis

A

Gross = enlarged soft uterus, hemorrhagic cystic

Micro - proliferative glands

87
Q

what is endometriosis

A

benign endometrial glands/stroma outside the uterus

88
Q

What is the pathogenesis of endometriosis

A
  1. retrograde menstrual implantation
  2. vascular dissemination
  3. metaplasia
89
Q

What is the most common site

A

Ovaries – chocolate cyst

90
Q

What are the symptoms of endometriosis

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions