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Repro > Non-Neoplastic Diseases of Female Repro Tract (Bala) > Flashcards

Non-Neoplastic Diseases of Female Repro Tract (Bala) Flashcards

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1
Q

Non-sexually transmitted organisms?

A

Actinomyces
M. tuberculosis
Candyda albicans

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2
Q

5 Most frequent vulvar infectious organisms in N America?

A
  1. HPV,
  2. HSV1 or 2
  3. gonococcal infection
  4. syphilis
  5. Candida albicans
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3
Q

Inflammation of vulva often causes:

A

itching (and the scratching then exacerbates the primary condition)

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4
Q

6 common causes of inflammation of the cervix?

A 
1 Chlamydia trachomatis
2 Trichomonas vaginalis
3 Candida
4 Neisseria gonorrhoeae
5 HSV 
6 HPV
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5
Q

How do cervical infections spread?

A

in an ascending fashion, the most severe of which is PID

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6
Q

What are the 2 ways to develop PID?

A
  1. primary infection of endometrium with subsequent spreading to adnexa
  2. organisms can be introduced via sexual intercourse
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7
Q

Organism(s) causing salpingitis

A

Neisseria gonorrhoeae

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8
Q

Organism(s) causing Skene gland adenitis

A

Neisseria gonorrhoeae

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9
Q

Organism(s) causing endometritis

A

Chlamydia trachomatis
Neisseria gonorrhoeae
Trich

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10
Q

Clinical presentation of Trichomonas Infection:

A
  1. Heavy often foamy, gray-green vaginal discharge
  2. mucosal irritation and itching
  3. painful sex
  4. painful peeing

**approx 25% of women are asymptomatic

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11
Q

Organism(s) causing cervicitis

A

Chlamydia trachomatis

Neisseria gonorrhoeae

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12
Q

How are protozoa detected?

A

cytological exam

**inflammatory cells + protozoa on/among squamous cells

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13
Q

Predisposing factors for Mycotic (Candida) Infection?

A

DM, pregnancy, oral contraceptives

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14
Q

Clinical presentation of Mycotic (Candida) Infection?

A
  1. White mucosal surface (due to small plaques) = “thrush”
  2. Curdy white vaginal discharge
  3. discomfort + itching

**only ~2% pts are symptomatic

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15
Q

~___% of women have a Candida infection.

A

10

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16
Q

Biopsy of Mycotic (Candida) Infection?

A

fungus does not penetrate the epithelium, but the submucosa is chronically inflamed

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17
Q

Candida infection can be diagnosed on:

A
  • -wet preparations

- -Pap smears

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18
Q

HSV incubation period?

A

1-3 weeks

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19
Q

Where do HSV vesicles develop?

A

vulva, vagina and cervix

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20
Q

HSV is common in what age group?

A

young

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21
Q

Characteristic cytology in HSV?

A

intra-nuclear steel-grey inclusions, multi-nucleation

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22
Q

What is the risk of HSV reactivation during pregnancy?

A

newborn may acquire fatal infection during passage through the birth canal

(**thus, need a c-section)

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23
Q

Histologically characteristic lesion for Molluscum contagiosum?

A

endophytic, crater shaped lesion with viral inclusion

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24
Q

What may result from a CMV infection?

A

spontaneous abortion

infection of the newborn

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25
PID can be caused by what organisms?
``` Gonococcus Chlamydia Mycoplasma enteric bacteria streptococci and staphylococci** ``` **in postpartum setting
26
Clinical presentation of PID:
vaginal discharge, pelvic pain, fever and adnexal tenderness
27
What is the chandelier sign?
prominent discomfort when the cervix is manipulated
28
What structures are typically involved in PID?
Vulva, vagina, cervix, endometrium and adnexa
29
Complications of PID? (5)
1. ruptures of tubo-ovarian abscess 2. peritonitis 3. sepsis 4. infertility 5. bowel obstruction from adhesions and fibrous bands
30
How is PID dx?
cytology specimen of acute pus-like exudate with evaluation of microbiology (which should be tested for anti-microbial sensitivity)
31
Spread of Gonorrheal PID?
ascending from vestibular glands >> vagina-cervix + endrometrium >> adnexa (+ovaries)
32
What is involved first in Gonorrheal infections?
periuthral glands and perivaginal glands
33
How does Gonorrhea reach the ovaries?
by spreading along mucosal surface of fallopian tubes
34
Complications of Gonorrheal PID?
infertility sepsis (+ endocarditis) peritonitis suppurative arthritis
35
PID, Gross Pathology?
mass-like conglomerates composed of inflammatory exudate, necrotic debris + fibrous tissue replacing the tubes and ovaries fibrovascular adhesions surrounding tube/ovaries
36
What causes the infectious complications associated with PID?
abscesses on ovaries/tubes can rupture causing peritonitis, sepsis or can turn into a sac containing clear fluid (hydrosalpinx)
37
What can result from the clearance of PID-related infection?
vascular adhesions (frozen pelvis) and strictures of fallopian tubes with consequent infertility
38
Ectopic Pregnancy is most common in...
in fallopian tubes
39
Clinical manifestation of Ectopic Pregnancy?
1. Sudden abdominal pain/acute abdomen 2. uterine bleeding 3. shock-like presentation * *about 6-12 weeks following previous menstrual period
40
What causes pain in ectopic preg?
trophoblast penetrates mucosa + muscularis wall; blood coming from the implantation site irritates the peritoneum (=pain)
41
What causes bleeding in ectopic preg?
growing embryo and placenta expand the lumen which eventually ruptures
42
How serious are ectopic pregnancies?
"life-threatening," so early detection is very important
43
Trx for ectopic pregnancies?
surgical or chemotherapeutic (Methotrexate) intervention
44
Histologically, how are the glands of proliferative endometrium characterized?
strait or slightly coiled pseudo-stratified mitotically active
45
Histologically, how is the stroma of proliferative endometrium characterized?
loose edematous mitotic figures
46
Histologically, how is proliferative endometrium characterized in the absence of ovulation?
Due to excessive prolonged estrogen stimulation: -endometrium remains in proliferative state - exhibits a disordered fragmented appearance - spiral arteries do not develop normally *when the estrogen level, breakthrough bleeding occurs
47
"The proliferative phase is dominated by"...
estrogen effect
48
"The secretory phase is dominated by"...
progesterone effect
49
Histologically, how is postovulation phase of secretory endometrium characterized?
basal secretory vacuoles decreasing mitotic activity simple epithelial layer
50
Histologically, how is Late phase of secretory endometrium characterized?
tortuous, dilated glands prominent secretory activity prominent stromal spiral arteries decidulization
51
Histologically, how are the glands of secretory endometrium characterized?
serrated | lack mitotic activity in the later stage
52
Histologically, how is the stroma of secretory endometrium characterized?
edematous first, than predecudual changes occur in order to accommodate the fertilized ovum
53
Luteal phase defect is caused by:
inadequate progesterone effect 2' to either: - -inadequate development - -early regression of corpus luteum
54
The diagnosis of Luteal phase defect is confirmed by:
endometrial biopsy, which shows an endometrium more than two days out of synchrony with the chronological day of menstrual cycle.
55
Luteal phase defect can cause:
infertility
56
Histologically, how is the menstrual phase of endometrium characterized?
features of regeneration Fibrin thrombi hemorrhage
57
Histologically, how is the stroma of menstrual endometrium characterized?
disintigration Leukocytic infiltration Extravasation of red blood cells into the stroma
58
Histologically, how is Postmenopausal (Atrophic) Endometrium characterized?
No evidence of proliferation or secretion
59
Histologically, how is the stroma of Postmenopausal (Atrophic) Endometrium characterized?
Dense, inactive
60
Histologically, how are the glands of Postmenopausal (Atrophic) Endometrium characterized?
Inactive | simple or cystic
61
How can the appearance of Postmenopausal (Atrophic) Endometrium be reversed?
exogenous hormones or hormones produced by tumors
62
Endometrial Hyperplasia: etiology?
prolonged, abnormally high estrogenic stimulation without progesterone effect
63
Conditions related to Endometrial Hyperplasia?
Stein-Leventhal syndrome perimenopause estrogen producing tumors obesity
64
Forms of Endometrial Hyperplasia?
simple with/without atypia | complex with/without atypia
65
Earliest changes of Endometrial Hyperplasia?
persistent or disordered proliferation Ciliation (which suggests tubal differentiation) glands > stroma (beyond 50%)
66
What is PTEN?
tumor suppressor gene, deletion and/or inactivation related to hyperplasia + carcinoma
67
How does a PTEN abnormality contribute to hyperplasia of endometrium?
unopposed estrogen increases PTEN production; inactivated PTEN = increased gland sensitivity to estrogen
68
How is estrogen over-stimulation treated?
1. trx of 1' cause | 2. large dose progestins
69
How is simple hyperplasia characterized?
Glandular crowding irregularly shaped glands with stroma (no cytologic atypia)
70
How is complex hyperplasia characterized?
marked glandular complexity and crowding scarce stroma (no cytologic atypia)
71
How is complex atypical hyperplasia characterized?
1. crowded glands 2. almost total loss of stroma between glands 3. cytological atypia 4. epithelial cells enlarged with prominent nucleoli and increased nuclear/cytoplasmic ratio
72
How is simple atypical hyperplasia characterized?
nuclei rounded, with prominent nucleoli | cellular atypia
73
___% of Complex Atypical Hyperplasia ___% of Complex Hyperplasia ___% of Simple Hyperplasia ...progress to endometrioid adenocarcinoma.
25% 3% <1%

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