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

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

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
Q

PID can be caused by what organisms?

A 
Gonococcus
Chlamydia
Mycoplasma
enteric bacteria
streptococci and staphylococci**

**in postpartum setting

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26
Q

Clinical presentation of PID:

A

vaginal discharge, pelvic pain, fever and adnexal tenderness

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27
Q

What is the chandelier sign?

A

prominent discomfort when the cervix is manipulated

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28
Q

What structures are typically involved in PID?

A

Vulva, vagina, cervix, endometrium and adnexa

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29
Q

Complications of PID? (5)

A
  1. ruptures of tubo-ovarian abscess
  2. peritonitis
  3. sepsis
  4. infertility
  5. bowel obstruction from adhesions and fibrous bands
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30
Q

How is PID dx?

A

cytology specimen of acute pus-like exudate with evaluation of microbiology (which should be tested for anti-microbial sensitivity)

31
Q

Spread of Gonorrheal PID?

A

ascending from vestibular glands&raquo_space; vagina-cervix + endrometrium&raquo_space; adnexa (+ovaries)

32
Q

What is involved first in Gonorrheal infections?

A

periuthral glands and perivaginal glands

33
Q

How does Gonorrhea reach the ovaries?

A

by spreading along mucosal surface of fallopian tubes

34
Q

Complications of Gonorrheal PID?

A

infertility
sepsis (+ endocarditis)
peritonitis
suppurative arthritis

35
Q

PID, Gross Pathology?

A

mass-like conglomerates composed of inflammatory exudate, necrotic debris + fibrous tissue replacing the tubes and ovaries

fibrovascular adhesions surrounding tube/ovaries

36
Q

What causes the infectious complications associated with PID?

A

abscesses on ovaries/tubes can rupture causing peritonitis, sepsis or can turn into a sac containing clear fluid (hydrosalpinx)

37
Q

What can result from the clearance of PID-related infection?

A

vascular adhesions (frozen pelvis) and strictures of fallopian tubes with consequent infertility

38
Q

Ectopic Pregnancy is most common in…

A

in fallopian tubes

39
Q

Clinical manifestation of Ectopic Pregnancy?

A
  1. Sudden abdominal pain/acute abdomen
  2. uterine bleeding
  3. shock-like presentation
    * *about 6-12 weeks following previous menstrual period
40
Q

What causes pain in ectopic preg?

A

trophoblast penetrates mucosa + muscularis wall; blood coming from the implantation site irritates the peritoneum (=pain)

41
Q

What causes bleeding in ectopic preg?

A

growing embryo and placenta expand the lumen which eventually ruptures

42
Q

How serious are ectopic pregnancies?

A

“life-threatening,” so early detection is very important

43
Q

Trx for ectopic pregnancies?

A

surgical or chemotherapeutic (Methotrexate) intervention

44
Q

Histologically, how are the glands of proliferative endometrium characterized?

A

strait or slightly coiled
pseudo-stratified
mitotically active

45
Q

Histologically, how is the stroma of proliferative endometrium characterized?

A

loose
edematous
mitotic figures

46
Q

Histologically, how is proliferative endometrium characterized in the absence of ovulation?

A

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
Q

“The proliferative phase is dominated by”…

A

estrogen effect

48
Q

“The secretory phase is dominated by”…

A

progesterone effect

49
Q

Histologically, how is postovulation phase of secretory endometrium characterized?

A

basal secretory vacuoles
decreasing mitotic activity
simple epithelial layer

50
Q

Histologically, how is Late phase of secretory endometrium characterized?

A

tortuous, dilated glands
prominent secretory activity
prominent stromal spiral arteries
decidulization

51
Q

Histologically, how are the glands of secretory endometrium characterized?

A

serrated

lack mitotic activity in the later stage

52
Q

Histologically, how is the stroma of secretory endometrium characterized?

A

edematous first, than predecudual changes occur in order to accommodate the fertilized ovum

53
Q

Luteal phase defect is caused by:

A

inadequate progesterone effect 2’ to either:

  • -inadequate development
  • -early regression of corpus luteum
54
Q

The diagnosis of Luteal phase defect is confirmed by:

A

endometrial biopsy, which shows an endometrium more than two days out of synchrony with the chronological day of menstrual cycle.

55
Q

Luteal phase defect can cause:

A

infertility

56
Q

Histologically, how is the menstrual phase of endometrium characterized?

A

features of regeneration
Fibrin thrombi
hemorrhage

57
Q

Histologically, how is the stroma of menstrual endometrium characterized?

A

disintigration
Leukocytic infiltration
Extravasation of red blood cells into the stroma

58
Q

Histologically, how is Postmenopausal (Atrophic) Endometrium characterized?

A

No evidence of proliferation or secretion

59
Q

Histologically, how is the stroma of Postmenopausal (Atrophic) Endometrium characterized?

A

Dense, inactive

60
Q

Histologically, how are the glands of Postmenopausal (Atrophic) Endometrium characterized?

A

Inactive

simple or cystic

61
Q

How can the appearance of Postmenopausal (Atrophic) Endometrium be reversed?

A

exogenous hormones or hormones produced by tumors

62
Q

Endometrial Hyperplasia: etiology?

A

prolonged, abnormally high estrogenic stimulation without progesterone effect

63
Q

Conditions related to Endometrial Hyperplasia?

A

Stein-Leventhal syndrome
perimenopause
estrogen producing tumors
obesity

64
Q

Forms of Endometrial Hyperplasia?

A

simple with/without atypia

complex with/without atypia

65
Q

Earliest changes of Endometrial Hyperplasia?

A

persistent or disordered proliferation
Ciliation (which suggests tubal differentiation)
glands > stroma (beyond 50%)

66
Q

What is PTEN?

A

tumor suppressor gene, deletion and/or inactivation related to hyperplasia + carcinoma

67
Q

How does a PTEN abnormality contribute to hyperplasia of endometrium?

A

unopposed estrogen increases PTEN production; inactivated PTEN = increased gland sensitivity to estrogen

68
Q

How is estrogen over-stimulation treated?

A
  1. trx of 1’ cause

2. large dose progestins

69
Q

How is simple hyperplasia characterized?

A

Glandular crowding
irregularly shaped glands with stroma
(no cytologic atypia)

70
Q

How is complex hyperplasia characterized?

A

marked glandular complexity and crowding
scarce stroma
(no cytologic atypia)

71
Q

How is complex atypical hyperplasia characterized?

A
  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
Q

How is simple atypical hyperplasia characterized?

A

nuclei rounded, with prominent nucleoli

cellular atypia

73
Q

___% of Complex Atypical Hyperplasia
___% of Complex Hyperplasia
___% of Simple Hyperplasia
…progress to endometrioid adenocarcinoma.

A

25%
3%
<1%

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