Female Reproductive Pathology Flashcards

1
Q

what are the portals of entry for infection of the female repro system

A
  1. ascending infection
  2. hematogenous
  3. direct injury
  4. trans-neural (herpesvirus)
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2
Q

what are the defense mechanisms of the female reproductive tract

A
  1. physical (anatomic)
  2. innate/adaptive immunity
  3. hormones
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3
Q

physical barriers to infection of the female repro system

A
  • normal conformation
  • stratified squamous epithelium
  • ciliary movement and mucus production
  • epithelial tight junctions
  • muscular contraction
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4
Q

effects of progesterone on immunity

A

closes cervix
decreases immune response of the uterus

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5
Q

effects of estrogen on immunity

A

opens cervix
increases immune response of the uterus

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6
Q

is the non pregnant uterus resistant or non resistant to infection

A

highly resistant

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7
Q

what route of entry most commonly affects the ovaries/oviduct

A

hematogenous spread

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8
Q

what route of entry most commonly affects the uterus

A

ascending infection

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9
Q

what is the common response to injury by the ovary

A

lymphocytic inflammation

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10
Q

what is the common response to injury by the oviduct

A

edema + inflammation –> scarring + obstruction –> cystic dilation

leads to hydrosalpinx or pyosalpinx

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11
Q

what is the common response to injury by the uterus

A
  • accumulation of fluid/pus
  • endometrial scarring –> infertility
  • hormonal stimulation –> cystic endometrial hyperplasia
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12
Q

what are disorders of sexual development

A

disorders resulting from sex chromosome/gene mutations

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13
Q

XY SRY positive

A

pseudohermaphrodite with mutation of AMH-R

ex. persistent Müllerian duct syndrome

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14
Q

XX SRY negative

A

true hermaphrodite w/ male and female gonads

ex. polled intersex syndrome

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15
Q

freemartins

A

androgenization of a normal female fetus

caused by exposure of a female twin to hormones produced by the male twin due to anastomosis of allantoic blood vessels
- only occurs in twins with 1 M and 1 F

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16
Q

is the male twin affected in freemartinism

A

NO/minimally affected

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17
Q

incomplete development of mullerian ducts

A

aplasia/hypoplasia of uterus, ducts, ovaries, etc

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18
Q

segmental aplasia of paramesonephric ducts

A

part of the PM ducts does not develop - can affect any part of the duct

leads to absent/reduced vagina, cervix, uterine body, and horns

SEVERE - can cause insufficient PGF2a production in ruminants (local luteolysis) resulting in ability to regress the corpus luteum

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19
Q

ovarian agenesis

A

leads to lack of ovarian tissue in one or both ovaries

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20
Q

ovarian duplication

A

separate origination or splitting of a developing ovary leading to ovarian remnant syndrome

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21
Q

ovarian hypoplasia

A

small ovaries with a lack of follicles; unable to ovulate

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22
Q

vaginal cysts

A

cysts that develop in the wall of the vagina; arise from remnants of the mesonephric ducts

caused by inflammation or hyperestrogenism

23
Q

ovarian/paraovarian cysts

A

cysts derived from Graafian follicles or epithelium

24
Q

epithelial inclusion cysts

A

cysts located around the ovulation fossa and prevent ovulation

leads to cystic dilation

occurs in HORSES

25
subsurface epithelial structures (SES)
no clinical significance UNLESS leading to polycystic ovarian disease --> hyperestrogenism --> myelotoxicity occurs in CARNIVORES
26
cystic ovarian follicles
larger than normal follicles caused by stress --> ACTH --> excess cortisol --> inhibits GnRH --> dec. LH or LH-receptors --> no LH surge --> no ovulation --> no pregnancy --> no luteinization --> no new cycle --> follicle continues growing only significant if the follicle does NOT ovulate (no ovulation scar/papilla) leading to prolonged open days treat with PGF2a or chorionic gonadotropin + GnRH to induce luteolysis
27
cystic ovarian degeneration
cystic ovarian follicles in ruminants that are >2.5 cm and persist for 10+ days without the formation of a corpus luteum
28
luteinized cysts
anovulatory luteinized follicular cysts that develop from follicular cysts due to delayed/insufficient release of LH - component of COD in ruminants - clinically significant if not ovulating
29
cystic corpus luteum
corpus luteum with cystic center unknown cause - usually incidental
30
ovarian hematoma
extremely large corpus hemorrhagicum occurs in HORSES (do not get follicular cysts normally) can rupture and lead to abdominal hemorrhage
31
hydrosalpinx
cystic dilation/fluid accumulation in the oviduct only clinically significant if bilateral (can get normal oocyte transit in unaffected horn)
32
endometrial atrophy
loss of ovarian function leading to atrophy of the endometrial endothelium - normal in anestrus - abnormal with malnutrition, cachexia, and disorders of sexual development leads to inability to sustain pregnancy from loss of surface area for nutrient/gas exchange
33
how is endometrial atrophy diagnosed
endometrial biopsy graded 1, 2, 3 based on degree of severity (high, reduced, low chance of successful delivery of a live foal)
34
endometrial hyperplasia
local or generalized regions of epithelial hyperplasia caused by hormonal overstimulation or chronic mechanical irritation (GCTs, estrogenic plants) leads to reduced fertility, predisposes to infection, hypotonicity (dystocia/prolapse), estrogen priming of dogs followed by progesterone occurs in SHEEP, COWS, CATS, DOGS
35
mucometra/hydrometra
mucus/fluid accumulation in the uterus caused by a congenital or acquired obstruction of the uterine outflow tract when cervix is open - seen with hyperestrogenism and CEH predisposes to infection
36
endometrial polyps/papillomas
localized, pedunculated, hyper plastic nodules of endometrial stroma occurs in OLD DOGS, CATS, COWS (fibropapilloma) usually concurrent with CEH
37
oophoritis
inflammation of the ovary caused by hematogenous spread of bacteria/viruses occurs in BIRDS, REPTILES, uncommon in mammals
38
uterine inflammation
ascending bacterial infection of the uterus while the cervix is open occurs in: - ruminants: postpartum - carnivores: diestrus (progesterone) - equine: post-mating
39
what does an open and closed cervix predispose to
open: infection closed: pyometra
40
endometritis
inflammation of the endometrium leads to: 1. PGF2a release + progesterone priming --> premature lysis of CL --> shortening of estrus cycle 2. erosion/scarring of endometrium --> decrease PGF2a release --> persistent CL
41
metritis
inflammation of all uterine layers
42
pyometra
infection of the uterus with dilation and accumulation of pus in the uterine lumen caused by endometritis/metritis occurs in RUMINANTS, DOGS, CATS - cows: prevents PGF2a release --> retained CL --> mimics pregnancy - dogs/cats: caused by CEH --> pyometra syndrome (CL always present)
43
what is diagnostic of pyometra in dogs/cats
presence of a CL
44
genital herpesvirus infection
venereally spread virus the ONLY external genitalia pathology that causes a gross lesion occurs in most species lesion: death of mucosal epithelial cells leading to vesicles --> rupture --> erosions
45
ovarian neoplasia categories
sex cord stromal tumors germ cell tumors epithelial tumors
46
granulosa theca cell tumors
benign tumors of the sex cords/follicles unilateral benign hormonally functional diagnostics: AMH levels occurs in HORSES, DOGS
47
what hormonal changes occur with GCTS
produce inhibin, testosterone, estrogen, and AMH inhibin --> inhibits FSH --> contralateral testicular atrophy testosterone --> male behaviors estrogen --> constant estrus
48
epithelial tumors
cyst adenomas, ovarian carcinomas, ovarian adenocarcinomas carcinomas: can lead to carcinomatosis (direct lateral extension) occurs in DOGS
49
dysgerminomas
germ cell neoplasia of the ovaries occurs in all species but RARE
50
uterine neoplasia categories
smooth muscle tumors, endometrial tumors, venereal tumors
51
leiomyomas
smooth muscle tumor; can occur in cervix, vagina, and uterus well demarcated, unencapsulated, spheric, variable sized benign or malignant occurs in all species
52
endometrial carcinoma
malignant tumor of the endometrium unknown cause occurs in COWS, RABBITS
53
canine transmissible venereal tumors (TVT)
contagious neoplasm of DOGS originates from histiocytes (monocytes/macrophages) transmissible by any contact - engrafts due to down regulation of MHC expression