Brainscape's Knowledge GenomeTM

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


See full index

Repro 2 > Final > Flashcards

Final Flashcards

1
Q

what are the fetal malpositions

A

presentation
position
posture

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

definition of presentation

A

signifies the relationship between the longitudinal axis of the foetus and the maternal birth canal

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

definiton of position

A

indicates the surface of the maternal birth canal to which the fetal vertebral column is applied

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

definition of posture

A

refers to the disposition of the movable appendage of the foetus

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

maternal causes of dystocia

A

failure of expulsive forces (uterine or abdominal causes)

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

primary uterine inertia

A
  • Are the onset of birth, (bitch, sow)
  • Fetus remains in intrauterine position

(uterinecontractions fail to be initiated)

Causes:
myometrial defect (overstretching, infection, degeneration, systemitc illness, hereditaty, small litter size)
biochemical deficiencies (E-P ratio, oxytocin, PGF, relaxin, Ca or glucose def)
oligamnion
premature parturion
envoronmetnal disturbances
condition - obsetiy/ malnutrition

  • Therapy : hand vaginal stimulation (Ferguson reflex), extraction of fetuss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

secondary uterine inertia

A

consequence of another case of dystocia

at first contractions are normla by thten myometrial exhaustation

cause = uterien damage or prolapse

therapy = eliminate cause, extract fetus, uterotonics in bithcn adn queen

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

abdominal causes of dysotica

A
  • Inability to strain
  • Causes : age, pain, debility, diaphragmatic rupture, tracheal / laryngeal damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

obstruction of birth canal

A

Bony pelvis
= Congenital = developmental abnormalities of the pelvis are generally rare in animals
= Acquired = fracture, diet, immaturity (juvenile pelvis), neoplasia, disease – exostosis (periostitis)

Soft tissue
= Vulva = congenital defect, fibrosis, immaturity
= Vagina =congenital defect, fibrosis, prolapse, cystocele (bladder, prolapse in vagina), neoplasia, prevaginal abscess, hymen
= Cervix = congenital defect (duplication – cervix duplex), fibrosis, failure to dilate – narrow cervical canal (4 degrees)
= Uterus = torsion, herniation, adhesion, stenosis of the horn or corpus

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

narrow pelvis

A

Interfere with the passage of a normally developed fetus

More common in non selective breeding + dwarf breeds

Pelvic inlet of the achondroplastic breeds of dog is flattened in brachycephalic breeds, is a common of dystocia

Therapy : mostly cesarean section, fetotomy

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

immature, juvenille pelvis

A

more common in sows, goats and cattle

Prematurely mated animals (the pelvis is not completely ossified)

Rachitis (most often in sow)

Therapy : mostly cesarean section, fetotomy

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

narrow vulva and vagina

A

o Most often in primiparous (heifers – overfat body condition)
o Prematurely mated animals (juvenile females)
o Insufficient serous infiltration of the soft parts of the canal
o Scar tissue, connective tissue – bar, wounds, persistent hymen (foals), congenital stenosis, edema of the vulva due to venous stasis
o Simultaneous appearance of a narrow vagina and vulva is possible
o Therapy : mostly operation – episiotomy

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

narrow vertical canal

A
  • Mostly in cows, sheep and goats
  • Disorder of the opening stage . fetal membranes
  • Hormonal insufficiency + Insufficient serous infiltration
  • Incomplete dilation of cervix in the ewe and doe goat (ringworm) -commonly associated with prolonged gestation and hypocalcemia, hypophosphatemia
  • Consequence of uterine torsion
  • Scar tissue, wounds, neoplasms
  • Protracted labour – 6-12 hours after rupture of the fetal membranes, involutionary processes
  • Degree of incompletely open cervix according to Götze
  • therapy: medically, manually
    = denaverine hydrochloride, misoprostol, fetotomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

stages of cervical canal

A
  • 1 =ring like cervix that adheres closely to the fetus, its hard and easily rupture during extraction of the fetus
  • 2 = only legs or head pass through the cervical canal
  • 3 = only 2-3 fingers or fists can be inserted into the cervical canal
  • 4 = cervical canal is closed (uterine torsion > 180 degree)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

dry birth canal

A
  • premature rupture, perforation of the amniotic membrane – leakage of the amniotic fluid
  • Prolonged birth, mucosal edema
  • Therapy: Fetal fluid supplements as substitutes for amniotic fluid
    o form of a water-soluble, cellulose-based obstetrical lubricant
    o a substitute such as soap (particularly soap flakes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

neoplasm in birth canal

A
  • Vagina, vulva
  • They can bleed and prolapse
  • Cysts, lipomas, papillomas, adenomas, carcinomas, mixed tumors
  • Neoplasms of the cervix are rare in livestock
  • They narrow the birth canal and make birth more difficult
  • Mare, cow, bitch
  • Therapy: operation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

dislocation of the gravid uterus

A
  • Torsion of the gravid uterus  uterus rotates about a longitudinal axis
  • Ventroversion, ventroflexion and retroversion, retroflexion  the uterus rotates around the axis that lies horizontally in front of the pelvis entrace
  • Lateroversion or lateroflexion  the uterus rotates around the axis that lies vertically in front of the pelvis entrace
  • Prolapse of the gravid uterus (Prolapsus uteri gravidi)  the uterus moves caudally in the direction of its longitudinal axis – due to heavy vaginal prolapse in cows (no special significance for birth)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ventroversion and ventroflexion

A
  • Gravid uterus is physiologically located on the ventral abdominal wall and ventroverted to a certain degree
  • If longitudinal axis of the uterus is vertically =pathology
  • Flexion of the gravid uterus more caudally – ventroflexion
  • Causes – older animals, in animals with lowered abdomen,overweight,. bicornual gestation in mare, ventral abdominal hernia, placental hydrops (mares)
  • Symptoms– during labour
  • Fetus is in transverse presentation (in front of the pelvis entrace)
  • Therapy – reposition of the gravid uterus (lifting the abdomen with a board or turning the animal on the back if lying down, fetal fluid supplements, reposition of malpresentation, Caesarean hysterotomy, fetotomy)
  • Epidural anesthesia!!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

lateroversion and lateroflexion of gravid uterus

A
  • Physiologically, gravid uterus is suppressed to the right side due to rumen in ruminants
  • The front part of the gravid uterus can be lateroverted, if going more caudally – lateroflexion (parts of the fetus remain in the dislocated part of the uterus and parturition is difficult)
  • Mostly in mares
  • Lateroversions are not problem during parturition as lateroflexions
  • Therapy – same as in ventroflexions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

retroversion and retroflexion of uterus

A
  • Physiologically in mares - the tips of the horns verted cranially and directed caudally (without any parts of the fetus)
  • Pathological – there are parts of the fetus in verted part of the uterus (e.g. legs to carpal or tarsal joint)
  • Mostly in mares
  • Therapy – sedation and lifting of the rear part of animal, rectally or vaginally pushing the front part of the uterus, fetal fluid supplements, fetotomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

torsion of gravid uterus

A
  • Rotation of pregnant uterus on its longitudinal axis to the left/right which leads to narrowing of the birth canal
  • Cow, rarely mare, small ruminants
    Cause
  • disposition (cattle) – anatomical relations, insufficient fixation of pregnant uterus
    Predisposing factors
  • excessive movements of the foetus/dam, decreased volume of fetal fluid, fall, kicking, relaxed ligaments, fetal overweight, cow tied in the barn for long period
    Features
  • ACW and CW (90-360o) <45 degrees is sufficient to result in dystocia
  • Either precervical or postcervical rotation
  • Torsio cornualis/ torsio cornuum uteri – place of rotation is one uterine horn or part of horn in small multiparous animals
    Signs
  • parurition not progressing, uneasiness and restless, vulvar lips uneven
    Diagnosis:
  • Vaginal: conically closed, shrinkage of front part of vagina, rotation of mucosa felt
  • Rectal: palpation of twisted horn and broad ligaments
    Prognosis:
  • depends on degree of torsion
    Therapy
  • return the uterus to its normal position
  • direct: to uterus with foetus
    o with extraction – turn foetus opposite to the torsion
    o kamer method – try to encourage the foetus to turn/turn ourselves
    o cämmer’s torsion fork with canvas cuffs – use of detorsion rod to correct a uterine torsion
    o auer-shreiner method: 3 forces simultaneously on uterus and foetus
    o snöborgs method: press abdominal wall (similar to above)
  • indirect: directed to mother’s body (in direction of torsion)
    o hold uterus in place and turn over cow (rolling)
  • C-section: when other methods don’t work, at long duration, foetus is dead and uterine rupture is possible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

endometritis in mares

A
  • Inflammation of uterus, differs in etiology, clinical manifestation and duration
  • The most common cause of subfertility and infertility
  • Every mare 5-15 years old, mates or AI in 3 consequetive estrus without conception thoroughly suspicious on endometritis

physiological endometritis after mating
PMIE
chronic endometirits
degenerative endometritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

physiological endometritis

A
  • Immediately after mating for AI
  • Uterine response on bacteria and proteins from semen
  • Resistent uterus overcome inflammation in 6-12h
  • Healthy endometrium overcome infection in 6-12h
  • Time frame 120 – 150h before embryo reaches uterus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

PMIE

A

Predisposing factors
= Inadequate evacuation of inflammation products, inadequate lymphatic drainage of uterus
= Poor contractibility of myometrium
=Bad overall conformation of mare
=Hormonal disbalance

occurs due to failure of natural defence mechanism
signs = vaginal discharge and inflammation

histroy = failure to conceive, irregular cyclicality

Treatment in estrus and post estrus with monitoring of mare – individual approach - flush uterus, repeat until clean
20IV ocytocin post flush
flush 4-6h post mating
cloprosenole but can influence CL

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

diagnosis of endometritis

A

Clinical (anamnestic, vaginal, rectal ultrasound)
Ultrasound – accumulation of fluid in uterus
= Fluid in utero 6h mating – normal
= Fluid in utero 12h or more after mating or AI = worrying
= Fluid in utero 24h or more after mating or Ai =endometritis

Laboratory (cytological, bacteriological)
= Cytological smear of endometrium or low volume flush
= Bacteriological cultivation of microorganism
=Proper evaluation based on combining both tests
= If in doubt, cytological smear more significant (number of neutrophilic leukocytes)

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

prevention of PMIE

A
  • Decrease number of mating or AI
  • Avoid mating out of full season
  • Ultrasound monitoring of ovulation
  • Start therapy immediately Induce ovulation with hCG or synthetic GnrH for LH (buserelin and deslorelin)
  • AI with extenders containing antibiotics
  • Minimal contamination technique
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

chronic endometritis

A

Untreated PMIE become chronic endometritis

cause = poor conformation, trauma, inadequeate vulva/cervical sphincter

bacteria = strep equi, e.coli, p.areuginosa, k.pneumonia

3 natural barriers:Rima vulve, vestibulo-vaginal ring and cervix

Diagnosis: history, vaginal, rectal, US, endoscopy, cytology

therapy:
surgical correction of anatomical defects (cassock, correction of urethral flow and correction of laceration)
ATB, flushes
for chronic mycotic = clotrimazole, amphotericin

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

pyometra as consequence of chronic endometirits

A
  • Multicausal etiology
    o Fibrotic cervix, adhesia of cervix
    o Chronic endometritis
  • No visible signs
  • Intermittent purulent discharge
  • Irregular cyclicity
  • Poor prognosis for future fertility
  • Uterus permanently damaged
  • Endometrium replaced with granulation tissue
  • Atrophy and fibrosis of endometrium
  • Recurrent disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

endometriosis

A
  • Direct link to early embryonic mortality and cervical fibrosis
  • Senile atrophy of uterine glands older pluriparous mares (>15g)
  • Endoscopic and PHD finding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

endometrial cysts

A
  • Lymphatic and real endometrial (usually due to drainage of lymph)
  • Doesn’t involve direct in fertility
  • Could disturb embryo mortality
  • Laser and caterisation during endoscopy, if indicated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

cause of infertility in cows

A

functional ovaires
displaying oestrus behaviour
narrow vagina
ovulation disorders
abortion
dystocia
detachment of placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

subfertility/reduced fertility in cow causes

A

acquired/ environmentally induced - more frequent, alimentary “starvation sterility”

congenital/hereditary - lower %, often incurable, lesions of sexual organs, inherited anestrous, sub oestrus, cysts

temporary (cysts, endometritis) and permanent (incurable)_

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

cause of sub fertility in cattle

A

physiologic disturbance path anatomic, infectious, management, nutritional, hormonal

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

what it sterility

A

an absolute inability to reproduce

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

infertility

A

considered (same as) sterility or denotes a delayed or irregular production of annual live calf

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

subfertility

A

most forms of functional infertility results in anestrus = failure of cows to display oestrus

inflammatory disease can compromise fertility

reduced fertility = heifers that don’t conceive in optimal period and cows that didn’t conceive until 150th PP

infertility - steriliy = heifers that due to hereditary, most often incurable lesion in the genitals cannot conceive

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

parameters most commonly used in fertility analysis and assessment are

A
  • Days open <90d
  • % of conception at first AI > 60%
  • Insemination index <1.5
  • Conception index 60%
  • Intercalving period – calving interval
  • Abortions (between 45-265 days of pregnancy) <3%
  • Age at first calving 24months
  • Culling rate and reasons for culling – indicator of the prevalence of subfertility in herds (reproduction problems, low production)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

impaired development of reproductive organs is due to

A
  • Absence of gonad stimulating action of the pituitary gland
  • Consequence of chronic diseases, deficient nutrition, very poor housing conditions of female calves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

infantilism

A

general developmental delay, including genitals
- can be the result of poor housing, deficient diet, chronic diseases - acquired!
- detected during gynaecological examination of heifers at breeding age (16-24 months)
- Clinical finding:
o poorly developed sexual organs (as in a calf) that are not active - vulva, vagina, uterus as in a calf
o Anestrus
o prone to obesity
o Dif. dg.: freemartins, ovarian hypoplasia, ovarian atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

freemartinism

A

most common non-inflammatory condition - 92% of heifers born to bull twins

results in infertility involving tubular reproductive tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are chimeras

A

individual animals that contain two cell types originating from separate zygotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

signs of freemartinsim

A

heifers have the bullish appearance and behaviour of male animals
vulva is small and shrivelled with very pronounced clit, urination is strong jet directed upwards

internal repro organs abnormal

rectally: cervix and uterus often missing

least masculinised form more common - hypo plastic ovaries, short vagina and absent cervix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

cause of freemartinism

A

day 28-30 of pregnancy = fusion of chorioallantoic part of placenta meaning common blood supply between twins

exchange of humeral and cellular elements between fetes –> 2 chimeras

testicular development occurs before ovaries I cows + antimullerian hormone from male inhibits growth of female

RBC, WBC, antimullerian germanitave embryonic stem cells androgens enter the female blood stream

50th day of feral development = initial freemartin development

75th day = masculinisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

diagnosis of freemartinism

A

clinic exam: rectal, length of vagina test
<7cm = freemartin, do chromosome testing if 7-14cm
false positive if persistent hymen
false negative if normal legnth

PCR = finds XX and XY in same animal, fast and accurate

karyotyping = blood lymphocytes in metaphase - spread and examine for XY cells

skin grafting - freemartin heifer will accept skin from male twin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

prognosis of freemartins

A

most female cattle that are blood chimeras are often sterile freemartins

barren so use for fattening - not for mating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

hermaphoriditism

A

mixing of sexual characteristics of both sexues in 1 individual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

type of hermaphrodism

A

ambiglandular
testicular
ovarian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

ambiglandular

A

bilateral = 1 testis + 1 ovary or 1 ovartestes on either

unilateral = testis and ovary/ ovotestes on 1 side and ovary or test on other

alternate = testis on 1 side, ovary on the other

rodents and pigs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

testicular

A

in goats, sheep, cattle and horse

only testis on both sides but external genitalisa resemble female

cause = androgen insensitivity
XY male and production of testosterone normal but due to intracellular androgen insensitivity - mesonephric duct system doesn’t develop

vagina = short or normal, no cervix, small or absent uterus and testes in normal ovary position

maybe inherited in cattle as X-linked trait

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

ovarian

A

cause = enzymopathies in steroid conversio
chromosomal factors
heterosexual twins in cows
more rare than testicular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

white heifer disease

A

segmental aplasia of mullein ducts

prenatal, hereditary, lack of development of portion of mullein duct system (except ovaries)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

signs of WHD

A

various degrees of aplasia of vagina, cervix, uterus and oxiducts

imperforate hymen - blockage of caudal part of 1 uterine horn
uterine unicorni –> accumulation of endometrial secretions in cranial horn that presses on bladder and rectum

animals are cyclic and develop cyclic structureus
maybe oviduct obstruction -> hydrosalpinx

recessive gene related

aplastic secretion usually a band of CT and muscle with no lumen, mucosal epithelium or glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

diagnosis of WHD + control

A

rectal palpation and vaginal exam

selective careful breeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

congenital repro problems (cow)

A

ovarian hypoplasia
congenital lesions on ovaries
abnormalities of uterine tubes
aplasia uteri
aplastic cervix
cervix duplex
uterus didelphys
vagina subsepta
hymen feminis persistens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

ovarian hypoplasia

A

hereditary and recessively transmitted to offspring

if unilateral - can conceive

if bilateral - not cyclic

partial = can conceive but will have a small reserve of follicles and stop cycling before being ready to mate

signs = small functionless ovaries with undifferentiated parenchyma, infantile genital tract and not cycling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

congenital lesions on ovaries

A

very easy to diagnose
hypoplastic ovaries don’t respond to eCG or GnRH so no oestrus

don’t use bulls with small, asymmetrical testes for breeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

abnormalities of uterine tubes, uterus and cervix

A

depending on site of aplasia cow is infertile of subfertile

partial/segmented aplasia more common than complete

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

aplasia uteri

A

= no uterus
in WHD, freemartin and hermaphoridte
if isolated portion of horn present secretions can accumulate which cause dilation and can be misdiagnosed as pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

hypoplastic cervix

A

vulnerable to ascending infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

cervix duplex

A

1 = duplication of lumen - each horn connects to vagina by separate canal-normal conception
2= 1 cervix opening in to a double of uteri sometimes 1 channel not patent

lower results with mating/AI
bulls transmit to 3-9% of offspring so exclude from breeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

uterus didelphys

A

complete absence of fusion of 2 paramesonpehric canals

AI in ipsilateral horn-conception and AI possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

vagina subsepta

A

= dorsoventral post cervical band and vertical vaginal bands

if adjacent to cervix - can interfere with sperm, calving or placenta passing

diagnosis = vag exam and palpation

therapy = pull as causally as possible and cut with scissors or fetotom knife

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

hymen feminis persistense

A

rare, increase in circular fold narrows vaginal entrance and interferes with mating
hereditatry
surgery not advised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

acquired repro problems cow

A

ovaritis
ovarian neoplasia
lesions of uterine tube
mucometra
uterine tumours
uterine adhesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

ovaritis (oophoritis)

A

very rare
cause = brucellosis, TB usually accidental finding PM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

ovarian neoplasia

A

rare
granulose cell tumours - looks like honeycomb on US

fibromas
GCT can produce ovarian steroids = anestrus or constant heat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

lesions of uterine tube

A

occlusion of lumen = secretion accumulation

hydrosalpin = congenital stenosis of infection

phyosalpinx = can occur to upper-inffection of hydrosalpin with t.pyogenes or ascending uterine infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

mucometra

A

rare consequence of untreated cystic ovaries

affected cows unable to conceive

thinning of uterus wall and degeneration of endometrium

differentiate from 9-11 weeks of pregnancy on rectal using US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

uterine tumours

A

rare in cattle - often in incidental finding but can affect fertility

rectal - can be mistaken for mummified foetus

leiomyoma, fibromyoma, fibroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

uterine adhesions

A

cause = perimetritis, uterine rupture, dystocia

signs = fibrous tags over surface animal often sterile

can involve omentum intestines, abdomen wall adhesions may after c-section

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

lesion of cervix

A

normal bacteria in caudal vagina, E.coli, strep, staph, T.pyo

inflammation post dystocia

cervicitis with puerperal metritiscommon if delayed uterine involution/ RFM

rare = laceration, fibrosis and obstruction of cervical canal –> infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

conditions of vagina, vestibule and vuvla

A

cysts of earth’s canal

obstretcial damage to perineum and vagina

laceration or bruising, scarring and distortion and fibrosis

next birth –> narrowing of birth canal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

urovagina

A

in cachet and old cows

prevalence in carols and holstein

pelvic and uterine ligaments loosen, anus and vulva moves forwards and vulva lies horizontally

vagina pulled cranially and hangs over edge of pelvis - urine leaks out of vulva and some goes into vagina

sometimes covers cervix –> endometritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

ovulatory conditions - cow (physiologically)

A

2-3 waves during cycle (wave 7-10d)

1st follicular waves 4th d pp
follicular recruitment 3-6 follicles 4mm
-> after recruitment, 1 follicle separates and grows until ovulation or atresia

biggest follicle secretes inhibit and oestrogen and blocks FSH so smaller follicles go into atresia

average diameter of ovulatory follicles = 14.8mm heifers, 17.4mm cows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

anovulatory conditions

A

follicle growth only until recruitement
> static ovaries <6mm, small ovaries

cause3 = severe malnutrition during puerperium
repeat checking + US to confirm

follicular growth only until 1 selection, but not to ovulatory size
v. common, small static ovary, no CL, but ovulatory size follicles
progesterone low
cause = NEB, suckling calves, disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

cause of anovulatory condition

A

NEB = increase NEFA, BHB and somatotropin, decreased insulin, IGF-1, leptin and glucose

leptin = decrease in correlation with frequency of LH pulses

interval until 1st ovulation PP coincides with exit from NEB

6 weeks pp - drop of 1 BCS tolerated
No LH > no ovulatory growth, no estradiol produced

pp anestrus= if esters not noticed 60 d after calving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

ovarian cyst cow

A

cysts = diameter > 2.5mcm but continues to grow and persist in absence of CL from follicle that didn’t ovulate (10d+)

benign = look like follicular cysts but don’t inhibit cycle/ovualtion/waves. CL present

most cysts disappear by 60d pp but some persist = chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

how to help with anovulatory conditions in cattle

A

improve energy status during transition period

prevent disase

decrease frequency of suckling to 1-2 x1d in beef cows

GnRH agonist, prostaglandins or progestogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

differential of ovarian cysts cattle

A

corpus hemorrhagicum
vaculoalted LC
non-ovarian cyst
abscess
tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

types of ovarian cyst in cattle

A

follicular
= thin wall, fluctuating, progesterone <1ng/ml. 15-45d post calving

luteal
= wall > 3mm, progesterone >1ng/ml formed from unovulatoed follicle and theca cells luteinise or formed from follicular cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

signs of ovarian cysts cattle

A

follicular = 80% anestrus, unequal esters or persistent anestrus, masculinisation
luteal = anestrus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

risk factors of ovarian cysts cow

A

dystocia, RFM, NEB, obesity, increased temp, older, feeding oestrogen type components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

cause of ovarian cysts cattle

A

neuroendocrine imbalance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

therapy of ovarian cyst cattle

A

follicular
= treat, don’t wait for regrression
= GnRH - leads to increase LH and lutenisation of cyst (oestrogen -> progesterone)
= then PGF2a 7-10d later + increase P4 - restores hypothalamic response to estradiol and ovualtion occurs
= 72% cows regain cyclicality in 28-30d post GnRH
= 20% remain in anestrus - P4 remains low during lutenisation and response of hypothalamus to estradiol doesn’t change
= intravag progesteagen for 9-12d = cyst regression + grow of follicular wave. Esters 7d after removal
= cyst aspiration

luteal
= PGF2a most effective
= GnRH or hCG good, but unsure what type of cysts
= GnRH then PGF2a 7-9d later, don’t rupture - haemorrhage and adhesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

prevention of ovarian cysts cow

A

decrease stress, treat infection, prophylactic GnRH 12-14d post birth

no effective treatment for multiple cysts so cull

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

persistent CL

A

anything that interiors with production or release of PGF2a

cause = uterine infections, insufficient involution, uterine abnormalities

treatment = PGF2a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

absent/ delayed ovulation

A

oestrus and ovualtion sized follicle that doesn’t ovulate and regress or ovulates late (normal 25-35h after esters)

delayed = 48 h between statrt of esters and ovulation

cause = insensitivity of hypothalamus to estradiol, weak LH surge

aetiology = NEB, heat, stress, increaction, fast metabolism

delayed ovulation = decreased conception due to old oocyte - improper fertilisation, poor development potential old sperm
Changes in uterine tube environment (slow passage of zygote)

-prevention = GnRH with/before AI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

inactive ovary

A

no cyclicality, small, oftenn flat follicles, no CL

cause = malnutrition, NEB, uterine infection

therapy = hormones eCG, rectal ovarian and uterine massage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

ovarian atrophy

A

small, hard, smooth ovaries without any formation

cause = prolonged non-stimulation of ovaries by hypothalamus - pituitary gland

aetiology = def Ca, P, Cu, Co, Fe, I , vitamin A, O, E, malnutrition, chronic disease, hoof problems, parasites

physiological atrophy = sterile

atrophy is high producing = atrophy lactations

therapy = treat primary cause GnRH, eCG, hCG, CIDR, vitamins, minerals, antiparasititics

don’t confuse with hypoplasia of ovaries (congenital and irreversible) –> will be no reaction after hormones, no germinative layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

bartholin gland cyst

A

= under mucosa of vestibule of vagina 2-10cm big, unilateral in older cows

cause = atresia/obstruction of excretory ducts

signs = disturb urination, interfere with mating, vaginitis

DD= tumour, prolapse, absecess

if puncture - amber liquid

treat = hold top of cyst and cut with scissors along wall of vagine rinse inside with 10% betaine

will reoccur if just punctured

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

pneumovagina

A

vulva not acting as a seal, aspiration of air and maybe faeces

leads to dilation of vagina and maybe uterus and bacterial contamination

cause = aging, vulva conformation, BCS, trauma

treat = none if mild, vulvoplastiy.caslick, treat underlying cause - BCS
AI to increase subfertility

prognosis = severe cases unlikely to breed successfully

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

tumours of vagina and vulva

A

fibropapillomas
= pedunculate, remove surgically

don’t affect fertility but can interfere with parturition

other tumours = rare
> SCC or lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

anestrus in cow

A

due to:
- pregnancy, persistent CL, ovarian cysts, anovulatory anestrus (normal)

anovulatory anestus.= normal-restoration of gonadotropin secretion and ovarian follicular activity occurs pp

pp anestrus = dairy cow not in heat by 60d pp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

true anestrus

A

cow not in heat because of inactive ovaries - in high yield cows and beef suckler cows

predisposition = stress, lameness, nutriton, breed, season

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

expression of estus

A

decrease in intensity of esters signs = increase number of cows in silent heat

high yield cows = decrease oestrogen conc = decrease intensity of heat signs

94
Q

silent heat

A

normal cyclic activity but weak abscent heat signs

cause = failure of oestrus detection, heat stress, erotism, def beta carotene, P, Cu, Co

95
Q

aids to detect oestrus

A

tail pain - removed when mounting
Lamar heat mount detector - clearer result than pain, turns red when mounted
heat watch
pedometers

96
Q

repeat breeder cow syndrome

A

= normally cyclic cow with no clinical abnormality which has failed to conceive after 3 successive insemination

97
Q

pathologic conditions of repeat breeder cow syndrome

A

subclinical endometritis
= chronic uterine damage

luteal deficiency
= insufficient progesterone so suboptimal growth of blastocyst so not enough IFN-1 for luteloysis

delayed ovulation
= extended follicular phase and decrease signs of oestrus
- increase progesterone concentration > allows follicular growth but postpones LH surge
- 2 wave cycles = old follicles

98
Q

treatment of repeat breeder cow syndrome

A

intrauterine ATB 10-12h post insemination
- uterus can recover before embryo arrives in uterius at day 4-5
- give GnRH at time of insemination

99
Q

cause and factors of repeat breeder cow syndrome

A

cause = unclear but mulitfactorial
-> cow, bull, environment

factors: age, genetics, infection of repro tract, nutrition, embryo mortality

100
Q

structural defects of sheep

A

karyotype alteraions
uncommon = aplasia/hypopalstia of ovaries/PMD, bilateral hydrosalpinx etc

intersexuality common in goats –> PIS -> always breed horned with non-horned to prevent

101
Q

EED small rum

A

asymptomatic absorption of embryo, no discharge

notice repeat breeding in longer period than normal (17d)

102
Q

infertility in ewess

A

fetal deeath
mummification - sterile, persists CL, resorption of liquid

macerate - infection, endometritis, purulent discharge, fatal death and emphyseam

bloody abortion - if occurs 45-70d of pregnancy - perivulvuar and tail area dirty with bloody discharge

103
Q

trauma in small rum

A

sheep= very resistant, maybe unnoticed

towards end of pregnancy - distended abdomen >5% abortion rate

most common cause = 3Ps
protector dog = too aggressive
pastor = too many sheep in truck
passage = narrow aisle

sheep need 50cm each at feeding station

104
Q

stress in small rum

A

housing, ventilation, flood

105
Q

functional factors in ewes

A

lower fertility at beginning and end of season - first few cycle anovulatory

don’t mate too early

cysts uncommon

first 2 weeks of pregnancy embryos not attached to uterus grow on secretion (uterotropha)

at 3 weeks placenta starts to develop .> placentomest 80-100

4-10 weeks placenta development, foetus grows slowly

106
Q

management factors in sheep

A

good esters detection and AI methods
proper implantation of male effect
1 ram to 30-50 ewes
flushing, hormones, BCS, feeding
avoid mixing pregnant and non-pregnant ewes

newborns need colostrum within 2-4h (IgG)

107
Q

male management

A

poor results if inexperience rams with maiden ewes

dont’ put male in repro programme too young

peak breeding = 3-4y
check testicles regularly

out of season = decrease libido, decrease sperm production and semen quality

108
Q

structural defects in goats

A

pallidness interest syndrome (PIS) = XX female to male intersexuality associated with polled goats

extreme = complete sex reversion

females with PIS = developmental abnormalities of sexual system

109
Q

functional factors in goats

A

irregular esters cycles and start and end of season

cystic ovarian disease in dairy breeders
- signs = persistent esters, nymphomania, short inter-oestrus interval
- follicles = >10mm, >10 d
- therapy = GnRH, 1500-2500IV hCG, 10d post PGF2a

repeated arbortion = probs also genetically induced by hyuperactivity of adrenal cortex

110
Q

pseudopregnancy

A

hydrometra, mucometra, cloud burts

accumulation of aseptic secretion within uterine lumen

signs = cyclic activity stops due to spontaneously persistent CL, abdomen distension, cloud burst at time of expected delivery, does looking for kids

diagnosis = US - no foetus or placetnomes and fluid in uterus

therapy = prostaglandins 2x in 12d

111
Q

RFM in goat

A

should be out within 3-4 h (12h+ RFM)

aetiology = infection, Se deficiency

signs = metritis, depression, fever, anorexia, foul smelling dishcarge

diagnosis = vaginal exam as goats eat placenta

therapy = intrauterine ATB, no manual removal, 5IV oxytocin few times per day, ATB parenterally penicillin if in time or oxytetracycline if disease
antitetatnus

112
Q

management factors of goats

A

optimal mating time

feeding - deficiency of Vitamin A, I or Mn

stress induced abortion. transport, chased by dog, weather

113
Q

sarannen esters synchro protocl

A

sponge placemat for 11 days
d9 = IM eCG + PGF2a at 2pm
d11= sponge removal at 2pm
d12 = estrus detection 24-36h post removal
d13= AI 43+- 2h after sponge removal at 9am
= 65%rate

114
Q

infections in goat

A

Q-fever
lepto
brucellosis
listeria
camplobacter
too
salmonella
chlamydia

115
Q

pregnancy toxeamie

A

cause = nutrition, toxemia, multiple fetus, BCS

unable to eat enough –> fat related –> converted to FA + glycerol for metal growth –> KB near birth –> abortion

toxemia due to too much metal metabolic products

signs = lethargy, muscle tremors, grinding teeth, opisthotonus, ataxia, coma, hypoglycaemia, ketonuria, increased BHBA, decrease Ca, increase K

therapy = bicarbonate, Ca, glucose precursos

No IV glucose due to hepatic lipipodsis + end of pregnancy insulin resistance

No PO glucose because digestion in ru,en causes FA formation

116
Q

toxic agents in sheep

A

can cause malformation or abortions

estrogenic herbs = contain phytoestrogens so cause edema, infertility, udder hypertrophy, abortio, genital proplase

overeating –> ruminal tympana –> increased abdomen pressure –> mechanincal abortion

teratogenic plants - alkaloids cross placenta and act on fetus

mycotoxins

nitrate and nitrites from fertilisers lead to hypoexmia of fetus

Cl cpompoudns, bromates, DMSO

legume - clover, alfalfa

117
Q

infectious agents - small rum

A

non-specific less important due to long anestrus afterr lambing (heal before next repro season)

RFM uncommon
bacterial/fungal = lesiosn with exudate between endometrium and choroid, diffuse or focal, edema, congestion, haemorrhage or vili necrosis. autolytic fetus

viral = macro no placental changes, fetus not autlytic

sample = fetus, placenta, vagina, maternal serum

negative fetal finding doesn’t exlcude infection becasue fetus becomes immunocompetent around 80d and doesn’t proceed antibodies befores

118
Q

specific infection in sheep

A

Q-fever
brucella
lepto
chlamydia
salmonela
toxo
campylobacter
listeria
pestivirus
schmallenberg Virus

119
Q

anestrus in pigs

A

esters 7 d post weaning normal -> weaning to esters interval 2-11 d

anestrus due to active, inactive or cystic ovaries

120
Q

gilt management

A

don’t induce esters if under 210d old and 105kg (puberty at 210d)
-> decreased maternal instincts, litter size and milk production

puberty can be delayed due to: breed, housing, nutrition, climate, stress

always correct nutrition and environment first before using drugs

breed gils at 250-260d old

120
Q

normal in pigs

A

return to esters <8%
abortion <2%
farrowing rate 95%
30 weaned/sow/year

121
Q

biological methods with pigs

A

flushing - protein and energ
supplements VitA, E and Se
male effects
h0use with cyclic sows

122
Q

hormonal estrus induction

A

gonadotropicn
PG600 = hCG + eCG + heat 3-6 d later

123
Q

second litter syndrome (pig)

A

mating at young age has no negative effect on 1st litter but decrease feed intake during 1st lactation has influence on 2nd litter size

124
Q

transport induced esters pig

A

for puberty stimulation too

in esters within 7 d post transport

125
Q

inducing ovulation in acyclic female (PIGS0

A

eCG/hCG –<estrus 3-6 d layer

regulating luteal phase in cyclic
- regumate 15-20mg/pig/d esters 2-8 d after last progesterone in pig

sows that return to esters within 21+/ 3d and fail to conceive = repeat breeders

EED if return to esters in 25d

126
Q

seasonal infertility - pig

A

anestrus

lower fertility end of summer and start of autumn

sigh program: 200lx 16h/day
improve nutrition, decrease stress and stocking density

therapy = gonadotropins

127
Q

empty/open sow

A

non-pregnay sows serviced again 6-d after 1st service

hsould be les than 1%
detect pregnancy 30 d post mating

128
Q

mycotoxins in pigs

A

in food or bedding
can impair fertility and cause abnormal development of fetuses

zearlenon - oestrogen mycotoxin -> repeat breeding, heat signs, vaginal and rectal prolapse, pseudopregnancy

129
Q

porcine parvovirus

A

on 60% of farms

infection:
d35= death and resorption
d35-70 = mummification
d7-114 = immunocompetence, maybe slight weakness of piglets

vaccinate gilts 2x before AI

130
Q

circovirus PCV2

A

oronoasla/horizojtal route of transmission

causes repro problems in sow herds

infects embryo after transplacental transmission

signs = embryonic and fetal death, loss of whole litter at any stage of pregnancy, mummification

vaccine available

131
Q

PRRS

A

rest disease in nurses and finishing pigs

possible transplacetnal transmission during early prengnayc

late term abortions, mummified foetuses, weak piglets

132
Q

Light programmes pig

A

to optimise fertility
200lux for 16h at eye level then 8hr darkness

lactational unit = 8h light, 16h dark
breeding unit = 16h light, 8h dark

133
Q

synchorno of estrus in gilts

A

regroup and place next to boar
synthetic progestaen PO for 14-18d + estrus in 4-6d

gonadotropins 1-2d after progestagen

134
Q

after weaning

A

PG600 directly after weaning to improve weak heat

progestagens to extend weaning - esters in interval to avoid 2nd litter syndrome

CL In pigs unresponsive until 12-24d post ovulation
natural CL regression due to endogenous PG at 14-17d

135
Q

timin of AI in pig

A

standing estrus lasts 48h
ovautlin 32h after start and lasts for 2-4h

sperm viable for 24h, ova 2-4

AI 0-24h before ovulation

2nd AI 12-24h after first

136
Q

embryonic and fetal death in pigs

A

embryonic = <30d of pregnancy.- stress, feeding, season, antural mechanism

fetal loss = mummification and stillbirth

preweaning mortality

stillbirth = dystocia, pregnancy duration, infection, parturition duration, interval between piglets, BCS, temp, human help

137
Q

management of lactation in pigs

A

prevent excessive weight loss during by optimising nutrition

decrease suckling to decrease metabolic burden andto increase repro rates

weight loss >12.5% = decreased farrowing rate and litter size

kskip a heat - serve at 2nd oestrus post weaning as better pregnancy rates and litter size

problems in lactational management if long wean -estrus period and poor 2nd litter

sows that become fat during prenugnac - decrease feed during lactation

poor lactation nutrition = decreased follicle development during and adter lactation, decrease ov rate, decrease ova quality and increase embryonic moortality

thin sows = prolonged wean-oestru, decreased preg rates and litter size

138
Q

induction of lactation estrus - pig

A

can be done in 70-90% of sows

success depends on parity and breed

pro = lactation period extend whilst sow is pregnant, allows piglets to be better developed when weaned

daily temporary removal of whole litter can induce estrus esp if with boar contact

139
Q

cystic obarian disease pig

A

persistent pathological filled fluid structures 20-300m each, can be mulitple

no LH surges so fillciels continue to grow

cause = stress, GnRH, therapy at wrong time, early induction of ovualtion after birth

diagnosis = US

cull as often poor repsonse to therapy

140
Q

vulvular discharge syndrome - pig

A

cause = overstocking, bedding, feral contamination, AI.mating

signs= white-grey secretion, bad smell

metritis = >100ml
cervicitis = not so much
vaginitis = less quality
bladder = >100ml at urination
take blood sample adn swab of discharge –> acitinobaculium suis

141
Q

post partum dysgalactia syndrome pigd

A

+ post mating endometritis
bacteria is usually from environment –>coliform

treatment = ampicillin, trimethoprim, fluids, NSAIDs, oxy

142
Q

pseudo lactation

A

physiological in bitch

prevalence = afgans, beagle, boxer and rare in cats

usually 1-3 m after oestrus but also 3-4 d post OVH in diestrus

143
Q

pathogenesis of pseudolactation

A

physiologically,i diestrus is similar between pregnant and non-pregnant bitches

trigger= progesterone decrease and prolactin increase, increase tissue sensitivity to prolactin
- different molecular types of prolactin with different bioactivity
- prolactin secretion in pituitary is under tonic inhibitory contorl of hypothalamus, mediated by direct inhibitory action of dopamine, or indirect serotonin (dopamine secretion suppressant)

144
Q

signs of pseudlactation

A

6-8 weeks after estrus and can last 30-90d

covert = no signs, physiologic condition

overt = divers signs

behavioural changes, physical changes in caudal mammary gland, aggression

often self limitig but can occur after every oestrus

145
Q

complications of pseudolactation and DD

A

rare - vomiting, anorexia, PUPD, tumours, mastitis, CEH

DD = rule out pregnancy, mastitis, tumour, pyometra

146
Q

diagnosis of pseudolactation

A

signs and histroy
hormonal tests no due to specific physiology of sexual cycle of bitch

147
Q

therapy of pseudolactation

A

mild = no treatment, prevent maternal behaviour, elizabethan collar

therapy if strong bevhaioural changes lasting longer than 4 weeks

drugs = antiprolactinemic, serotonin antaognist with dopamine eeffect I hgih dose (metergoline)
- dopamin agonist are prolactin inhibitors that exert effect by direct stimuatlion of dopamine D2 receptors
eg caergoline 5ug/kg PO for 7-9 d pergolide, bromcriptine

ovariohysterectomy is anestrus

no milking, tranquilliser but not phenothiazines

treat all bithces due to risk of mamary gland neoplasm

148
Q

what is feline mammary fibroepithelial hyperplasia

A

benign, progesterone assocaited fibroglandular proliferation or 1 more more mammary glands

can occur in males or females
most common in, intact cats 6m-13yr

when = 1-2 weeks after estrus or 2 w after hormonal therapy

149
Q

pathogenesis of feline mammary fibroepithelial hyperplasia

A

not completely understood

growth + development of mammary gland under progesterone control
-> progesterone in stromal and epithelial cells –> activation of specific cascade –> mammary gland proliferation

-> maybe changed regulation leads to disturbed response to progesterone

progesterone –> ductal branching
estrogen –> ductal elongation and bifurcation

progestogens cause stimulation and proliferation of epithelial cells and ductal canal to hyperplasia

high proliferative index

blood progesterone in normal conc

150
Q

pathomorpholical characteristics - feline mammary fibroepithelial hyperplasia

A

firm, well-circumscribed unencapsulated mass, solid and smooth

possible ulcerations and necrosis

micro=profieration of glandular, fibre - epithelial elements

151
Q

therapy and prognosis of feline mammary fibroepithelial hyperplasia

A

prognosis = good but relapse possible if no OBH

supportive therapy

treatment:
- OVH or ovariectomy = gold standard –> regression in 3-4 week, if not mastectomy

agleprisoton = competitivee progesterone antagonist 10mg/kg SC 1st then 3rd day, control day 7 repeat if needed, regression within 4-8 weeks

dopamine agonist for suppression of lactation
cabergoline for 5-7 days
bromocriptine 0.25mg/kg PO for 5-7 days side effects = ticks

152
Q

clinical findings of fibroepithelial hyperplasia

A

15-18cm excessive enlargement that appeared very rapildy

can be: bilateral whole chain enlargement asymmetric (non-pregnant) solitary mass in any gland

skin = tense and erytheamtous

palpation = firm, compact conssitency soft, gelatinous mass

lab = normal

large masses = problems walking
Greg queen = no milk, weak kittens

153
Q

complications of feline mammary fibroepithelial hyerplasi

A

mastitis in lactating queens

ulceration due to overstretched skin

maybe hemorrhagic/purulent exudate

increase temp, lethargy, anorexia

LN involvement

154
Q

diagnosis of mammary fibroepithelial

A

signs = spread of development
biopsy = FNA or excision - large amount of mitosis = false malignanyc

US - increased echogenicity
DD = neoplasia, FEH = bigger and softer

155
Q

congenital abnormalities in bithc

A

ovarian genesis rare and only affects fertility if bilateral

ovarian dysplasia in bithc with abnormal number of chromosomes

intersex - pseudohermaprhodites

vulvar hypoplasia and perivulvar deermatitis

156
Q

neoplasia in bitch

A

ovarian tumours uncommon, increase in older

granulosa cell tumour

uterine tumour uncommon - fibroeiomyoma

tumours of cervix rare

vagina and vestibule tumours more common - begging liopma etc

157
Q

transmissible venereal tumour - dog

A

affects vagina and external genitalia of bitch and penis in dog

transmission through coitus and sniffing and licing etc

lesions = friable, multilobulated max size after 5-7 weeks and can regress spontaneously within 6 months

metastasis uncommon

therapy = surgical debunking and them vincristine for 3-6 seeks
intratumoural injection with vincristine and interleukin 2

158
Q

hydro/muco/hematometra bitch

A

accumulation of sterile serous/mucoid fluid

diagnosis = unlarged uterus US/x-ray no systemic inflam (WBC normal)

treatment = ovariohystercotmy

hematometra = rodenticide toxicity, torson of uterine horn, rule out recent pregnancy

159
Q

cystic endometrial hyperplasia - bitch

A

acute/chronic post astral disease of adult intact bitches leading to inflammatory exudate in uterus

cause = repeat exposure of endometrium to progesterone

predisposing = 2 month diestrus

160
Q

secondary anestrus. -bitch

A

proonged interests period in failure to cycle 10-18 months of previous cycle

cause= silent heat, hypothyroidism, exogenous glucocorticoids
basenjis and wolf dogs = only 1 cycle per year

inducstion of estrus
- eCG, FSH, LH estrogen
- GnRH analogues
- dopamine agonists (cabergoline)

161
Q

pyometra

A

progesterone mediated uterine disease occurring during diestrous

bacterial infection with opportunistic organisms from vagina secondary to CEH

most common organism = e.coli

162
Q

types of pyometra

A

open
= 4-8 weeks post estrus, vulvar discharge, less systemically ill

closed
= abdo distension, minimal discharge, more systemic signs

163
Q

signs of pyometra

A

fever
hypothermia
dehydration

164
Q

lab and diagnosis of pyometra

A

lab
= neutrophilic (penia if endotoxemia)
= normocytic, normochromic aneamia
= WBC left shift
= azotemia, increased ALP and ALT
= hyperglobulinemia, hypoalbumineam

diagnosis = gen and gyno exam
x-ray or us

165
Q

therapy for pyometra

A

ovariohysterectomy

medical =have to be of breeding age, vital to program, open Cervi and not systemically ill

PGF2a dinoprosvt 2x 1d cloprotenol or alphaprostol fluids, pain relief, atb antipgroestins = no sidde effects compared to prostaglandins

166
Q

persistent anestrus dog

A

primary = lack of cycling by 24month old

dd= previos ovariohysterecotmy silent head
- > check serum progesterone conc every month, = presence of cantonal luteal tissue

therapy = FSH SC.IM for 6-8d

167
Q

hypothyroidism - dgo

A

can cause infertility by interfering with gamete maturation
-> thyroidd hormoens support granulosa cell function in developing follicles and are needed for normal placental trophoblast function

signs = irregular/proglonged interests period, prolonged proestrus decrease intensity/ducration of estrus, spotnaneous abortion, mummification, pups with low birth weight

diagnosis = fT4, canine TSH
treatment = thyroxine 2x1d
normal cycle in 4-6 m after adeuqate therapy

168
Q

causes of primary anestrus dog

A

persistent anestrus
hypothyroidism

systemic disease
hyperadrenocirticms
progesterone
ovarian aplasia
immune mediate oophoritis

169
Q

persistent estrus dog

A

combo of proestrus and estrus greater than 6 weeks

cause = presence of functional ovarian follicular cysts
granulosa cell tumour
PSS - due to delayed metabolism of hormones

170
Q

irregular estrus - dog

A

uterus needs 1390-150d for endometrial involution and repair

interestrus less than 4 months = usually infertile due to incomplete eenodmtrail repair

treatment = induce anestrus -> mibolerone, testosterone cyprionate IM

171
Q

split estrus - dog

A

most common at first and second estrus

signs = vulvar swelling, serosanginous discharge, no ovulation, follicles regress and proestrus signs disappear

cause = premature atresia and regression of follicles due to insufficient secretion of LH
-> normal estrus 1-3 weeks laterr
-> progesterone remains basal despite showin estrus signs

mate at correct time in relatio to OV

172
Q

vaginal prolapse dog

A

= protrusion of oedematous vaginal tissue into vagina lumen and through vulva lips

cause = unknown (no hyuperestrognism) but is due to estrogen sitimualtion during estrus and protestrus

1= slight.moderate eversion of vaginal tissue through vuvlar lips
2= prolaspe of cranial floor and lateral walls trhough vulvar lips
3= prolaspe of entire vaginal circumference as a donnut shaped mass

signs = discharge, dysruia, anuria

treatmet = can regreess spontaneously so keep clean and dry

surgery = for type 3 - circumferential excision of prolapsed tissue -> can recur so OVH

173
Q

anestrus in queen

A

physiological in autumn-winter

cause = inadequate photoperiod prevent follicular wavesa t start of mating season (need 14_h)

stress
congeintal abnormlaities (rare)
luteal cysts or neplasia (rare)

treatment
- induced estrus with FSH 2mg IM then 0.5-1mg IM each day for 4 more days
hCG IV
ovulation oof mature follicles with hCG 250iV IM or GnRH 25mg

174
Q

persistent estrus quee

A

lasts 2 follicular cycles but endocriniolgoical changes are normal

fertility decrease due to inadequate mating time

175
Q

follicular cyst queen

A

heat and signs for 21d+
treatment = 250-500 IV hog or 25mg GnRH
OVH

176
Q

anovulatory cycles queen

A

in half of queens bred only once

if not mated enough - no LH surge or mated in 1st 2 d in estrus

diagnosis = serum progesterone con

ovulation = when progesterone >1.5ng/ml

177
Q

pyometra queen

A

less common than in bithces
bacterial infection of uterus due to hormonal changes in cats

signs = variable, decreased appetite, PUPD, vomiting
pus contianing blood is open cervix

therapy = OVH
medical treatment maybe if open cervix not severely ill and for valuable breeding females

178
Q

end of season pregnancy rate depends on ( horse)

A

stallion fertility
mare fertiliyt
stud management
pregnancy mare manageemtn

179
Q

reasons for fertility failure in hrse

A

no conception -> fails to cycle, normal cycle but no conception

conception but loss befroe check

early pregnancy but loss post day 11 diangosis

abortion (up to day 300)

stillbirth or non-viable foal

180
Q

causes of infertility/subfertility in horse

A

structural
- inherited
- injuries to genital tract
- age related deegeneration of ovaries and endometrium (defective bulva most common problem)

infectious
- endometritis, metritis, pyometra

functional
- no oestrus behaviour
- shortened lutal phase
- ovulatory dysfunction/multiple ovulation

181
Q

ovary problems in horses

A

no follicular growth

ovulatory failure

poor oocyte quality

chromosomal abnormality

182
Q

oviduct problem in horse

A

blockage
infection/inflammation
failure to pick up oocyte
poor environment

183
Q

uterus problem in horse

A

infection/inflammation
fibrosis
poor environment
mechanical problem

184
Q

cervix problems - horse

A

tears
adhesion
fibrosis
inflammation

185
Q

vagina, vulva and vestibule problems in horse

A

urine pooling
air
vaginitis
foreign material

186
Q

breeding soundness exam In horsse

A

age, health, history, BCS, repro history

exam external genitalia and mammary gland

palpation + US of internal tract

vaginal insepction - cervical function

endometrial fucntion - bactiology and cytology

endometrial biopsy
hysteroscopy
endocrine exam
further exams - karyotyping

187
Q

urine pooling horse

A

more common in older mares

urine enters cervix during estrous and can pass into uterus causing endometritis and infertility

treatmetn = correct predispoing factors, uterine lavage, urethral extension surgrey –> vaginaloplasty of transverse folds

188
Q

perineal laceration in horse

A

= rectovaginal fistula (cloaca)

cause = dystocia in young maiden mares due to rigidity of birth canal

first aid = debridement, cleaning and hemostasis, parenteral broad spec ATB for 5 days, NSAIDs and tetanus jab daily cleaning + monitor uterine involution

can do elective surgery at least 10 weeks post birth, if foal survives bss done after weaning

surgery = modified Goetze technique –> stage 1 repair = appropriate stripping of mucodsal surface, residual shelf between rectum and vagina in mobilised and fixed as caudally as possible

189
Q

persistent hymen - horse

A

can cause accumulation of fluid within vagina and uterus due to impaired natural drainage

rupture with scalpel

190
Q

granulosa theca cell tumour -in hourse

A

age 5-9 y old

signs = behaviour changes, anestrus, lymphoma, clitoral enlargement, aggressiveness

diagnosis = rectal + US - 7-40cm, spherical mass with honeycomb/multicystic appearance
hormonally active AMG >4ng/ml

therapy = unilateral ovariectomy
prognosis = good, most return to normal cyclic activity

191
Q

fibrosis of cervix in horse

A

older mare
cervix can’t relax properly during esturus so fluid accumulates in uterus –> post breeding e
endometritis common

192
Q

ovarian cyst adenoma In horse

A

unilateral
not hormonally active –> anestrus

193
Q

endometrial biopsy - mare

A

biopsy = taking piece of uterus surface to detect inflammation or degenetation

indication = prepurchase exam, barren mare, past infertility, abortion, pyometritis or mares needing repro surgrey

when = estrus - cervix in open and more easily penetrated and mare more resistant to endometritis
diestrus = endometrial glands more active and may give better picture of their function

194
Q

categories of endometrial biopsy mare

A

I : normal pathologic changes, small and sparsely scattered, foaling rate 80-90%, factors affecting foaling rate = overall management

IIA: mild changes, 50-80%, overallmanagement and endometria changes

IIB: moderate changes, 10-50%, “”

III: severe changes, widespread inflammation, scarring, atrophy of glands in physiological breeding season, 0-10%, severe changes in endometrium

195
Q

endocrine diagnostic of ovarian function - mare

A

progesterone
- normal range <1.0ng/ml oestrus, anestrus
- >1.0ng/ml diestrus, pregnancy, persistent CL

estradiol 17B
- no significance

testosterone
- 20-45pg/ml = increase in estrus, transitional phase

anti-mullerian hormone
- 0.1-4ng/ml = no changes in normal mare , >4ng/ml = GTCT

196
Q

twins in mares

A

number 1 cause of abrtion (in late pregnancy - 7 months +)

1 twins = breed, older mares, heredtiary repeatable
- check for twins at 14-18d (before fixation) 30d (before cups

if to term 25% live birth, 14% live to 2 weeks

twins between 5-30days –> manual destruction terminate wit PGF2a

between 35-70days -> terminate with PGF2a transvaginal US guided allantocentesis (TUGA)

197
Q

EED - mares

A

causes = uterine pathology
fibrosis –> uterine gland failure (need secretion to support embryo due to delayed placental attachment)

if allowed, can do ET

progesterone supplemtnation

diagnosis = palpation, hormonal assay, best = US, check GSD, CRL and FHR

= loss of conceptus before organogenesis is complete
- embryo <40d
- fetus >40d
- early fetal deeath 40-150d
- abortion from 300th d
- stillbirth 300-320 need ICU

198
Q

gestational age measurement in horse

A

AV = amnionic vesicle diameter

GSD = gestational sal diameter

CRL = crown-rump length

head length

eye length

trun diameter

FHR = fetal heart rate

199
Q

infectious infertility in horse (signs)

A

irregular cycle, anestrus, mated tail and crsuty hair on rum, white exudate, red mm

200
Q

primary causes of abortion in horse

A

twins
herpesvirus
placentitis

201
Q

older mares

A

less pregnancy rates, less oocytes/mebyros collected

less EED

oviductal embryos smaller and of lesser quality

uterine embryos - decreased collection rates and quality and delayed development

15-20y = shorter follicular phase, smaller follicles, more double ovulation

20y+ = longer follicular pahse, intermitten ovulation, failure to ovulate

202
Q

failure of ovulation in horse

A

no apparent, problem with oestrus

doppler US - increased blood flow in follicular wall, sudden appearnace of echogenic particles in follicular fluid

203
Q

hemorrhagic anovulatory follicle in horse

A

cause = older age, late in breeding season, post induction of luteolysis, moves with bushings, NSAID or glucocorticoids drug

pathogen = impaired prostaglandin synthesis in follicular wall inhibits ovulation

conception not possible as oocyte stays in follicle

DD = GTCT

90% will form CL/ lutenisation –> spontaneously or induction with PGF2a
10% won’t lutenist -> can take 6-8weeks, no echogenic particles on US, no P4 < 1ng/ml in blood, no inhibitor effect on cycle disappears in weeks-months

rare= development of ovrian hematoma –> abdomen disteress, blood in abdo

no therapy

oestrus reoccurs spontanelously

induce luteolysis with PGF not before 8 days after start of lutenisation

prophylaxis = no induction of esturs and ovulation when follicles of preov size aresent

204
Q

causes of anestrus in horse

A

winter anestrus/spring transition
lactation anesturs
siletn heat
multiple ovulations
dietrus ovulation
recent steroid aministraiotn
GTCT
persists CL
-> therapy PGF2a

abortion post d35-> eCG secreted by endometrial cups

205
Q

endometrial swab in horse

A

need :clean uterine culture: for some stallions prior to breeding

culture and ctyology

when = late oestrus best because uterine flora decreaes with increase in estrogen

206
Q

dog mammary tumour stage

A

use elston and ellis (Nottingham) method

–> tubule formation 1-3, nulclear pleomorphism 1-3 mitotic counts 1-3

total 3-5= grade 1, 6-7= grad 2 , 8-11 = grade 3 all is malignant

increased malignancy = decreased survival

207
Q

cats mammary tumour staging

A

modified methdos
same grades of malignancy

208
Q

grades of tumour

A

1= well-differentiated carcinoma
2= moderaltey differentieated
3= poorly differentiated carcinoma

209
Q

TNM classification

A

T = primary tumour size

T1 = <3cm (d), <1cm (cats)
T2= 3-5cm 1-3cm
T3 = >5cm. >3cm
T4 = inflammation

N = lymph node invovlement
N0 = no mets (cyto/histo)
N1 = mets to ipsilateral LN
N2 = mets to contralateral LN

M= metastatic disease
M0 = no distant
M1 = distant mets

210
Q

molecular classification of tumour

A

immunohistochemicl markers.in canine mamary neoplasms
-> ER, PR, HER2, p63, P-cadherin

molecular subtypes
- Lumina A = best prognosis
Luminal B
basal like = poor prognosis
tripple negative ER, PR, HER

211
Q

prgnosis of tumour

A

positive.= small breeds (benign), males, ER + PR expression

negatives = >3cm, ulceration, LN involvment, mets, lymphovascualr infiltration

dogs 2 year survival = 75-90%, >3cm = 14m
cats stage 1/2 - 12-29m
4=1m
<3cm post op = 9 months

212
Q

treatment of tumour

A

surgery
adjuvant jormone, chemo, radiatio, desmopressin, anti-cox2 treatemtn
not without surgery

anti-cox 2 inhibitors
- selective = firocoxib
- non-selectve meloxicam
in combo with chemo
for IMC = improved quality of lif

213
Q

mammary tumour bitch

A

unspayed
influence of sex hromones/castration
<50% malignant
<25% mets to lungs

214
Q

mammary tumour queen

A

lower prevalence than bithces
influence of sex hormones/castration
>90% malignant
mets to lung

215
Q

mammary gland

A

= modified apocrine sweart gland, tubuloalveolar gland
- parenchyma (alveoli)
> simple columnar secretory epithelium lined with my-epithelial cells, covered by basal lamine
stoma = CT
ducts = lactiferous, papillary
vessels and verse

216
Q

vascularisation of mammary gland

A

T1+T2 = cranial superficial epigastric, lateral thoracic and intercostal arteries
A1 = cranial superficial epigastric with anastomses to caudal one
A2 + 1 = caudal superifical epigastric

veins follow artery pattern but small veins cross the midline = potential depostion of maligant cells in adjacetn gland

AT1 = cranial thoracic
T2 = caaudal thoracic
A1 cranial abdomina
A2 caudal abdomianl
I inguinal

217
Q

lymphatic drainage (bitch)

A

axillary LN = both thoracic
superficial inguinal = caudal abdo + inguinal gland

cranial abdo gland can be axillary +/or superifical inguinal

in neoplasic thoracic glands - superficial cervixal or ventral thoracic LN involved

both abdo glands drained by axillary, superficial inguinal + popliteal

inguinal drained big popliteal lymph lymph centre

218
Q

IVEP

A

in vitro embryo production (IVEP)
-> in vitro maturaion, in vitro fertilisation, in vitro culture

oocytes from slaughterhouse
- aspiratie follicles 2-8mm -4-12 ooytes/ovary
- transport to lab-saline and ATB
- 32-37oC within 2 h

oocytes from live animals
- transvaginal follicle aspiration 2-8mm - ovum pick up
- stimulated (FSH or eCG) or unstimulated cows

219
Q

equipment for opu

A

opu device
US with sector probe
needle guiding syste
vacuum pump

220
Q

application of opu

A

alternative to MOET - 100 embryos/year/donor

calves from more bulls

can get offspring from infertile but, important cows

221
Q

grading oocytes

A

G1 = compact cumulus - oocyte complexes (COCs) unexpanded cumulus mass with >3 layers of cells, homogenous, evenly granular ooplasma

G2= COCs with 2-3 layers of cells, homogenous, evenly gradnular ooplasma

G3= partially/wholly denuded oocytes with expanded or scatteed cells or with an irregular and dark ooplasm

G4 = expandded or scattered cumulus cells

222
Q

in vitro maturation

A

G1 + G2
media, gonadotropins, esrtadiol, cystamine for 24hr at 39oC + 5% CO2

expansion of COCs and resumption of meiosis

maturation rate = % metaphase II oocytes, average of 85-90%

223
Q

risk factors for mammary tumours

A

age
= risk increase wihth age (median 8y)

breed + genetic
= poodles, English sprigner, GSD, maltese, yorkiie
= no common genetic mtatuion found yet but BRCA 1+2 genes involve in English springer spangles= beagles = familial susceptibility

hormones and growth factors
= castration = best way to prevent
= befreo 1st heat = 0.5% risk
= before 2nd heat = 8%
= befoer 3rd heat = 26%
= preventative effect 0 after 4yr old
= number of pregnancies = no influencee
= more than 3 pseudolactation = incrase risk due to mechanic compression of acini and release of carcinogenic free radical

COX-2 expressin
- in jhumans
= cox-1 = in many tissues
= cox 2 - not innormal cells, induced by growht factors, inflam, oncogens, more frequent In malignancy

diet
= thin at 9-11 months old, decrease risk
obesity = decrease serum globulin - increased serum estrogen

adipose tissue = inreased estradiol production
high intake red meat

224
Q

molecular pathogenese sin tumours

A

stem cells
= primary places of neoplastic transformation

estrogen
= growth factor production, direct genotoxic effect

progesterone
= synthesis of GH + it’s receptors(effects on mammary gland

225
Q

mammary tumour in cats

A

rare
10-12 yr old
2x higher risk in siamese
high mortality and almost always malignant
OVH in 1st year = 90% preventive

226
Q

mammary tumour signs

A

1 or more nodules in mammary gland

usually clinically health
severity of signs depemnds on extent and location of metastasis
-> lungs , live,r bone, brain, spleen, kidney, skin, eye

227
Q

initial work up for tumour

A

age, age at OVH
history = duration of signs, repro cycles, lactation, progetsterone therapy

general condition and physical exam –> look at all mam glands in dorsal recumebcny and check LN

228
Q

diagnosis of mamary tumour

A

blood and biochem
x-ray of thorax, CT will see 1mm

US
FNA + cytology = prediction of malignancy. 4 sampes per mass. good to differentiate from mastocytoa

check LN - biopsy/FNA for staging

229
Q

treatment of mammary tumour

A

surgery = gold standard

exception = inoperable, higly metastic tumours or IMC

230
Q

surgeries for mammary tumour

A

lumpectomy
simple mastectomy
regional mastectomy
unilateral
bilateral mastectomy

231
Q

classification of tumour

A

epithelial
- simple adenoma/carcinoma -> invasive but good pronosis if completely removed
- epithelial and myoepithelial -> complex adeoma/carcinaoma > rare metasasis, prognosis semi good if compleelt removed

mesenhycma
- fibroadenoma/fibrosarcona, less than 5% of all mammary tumours
combo of epithelial and mesenchyma - very aggresive and poor prognosis

232
Q

repro tract formation

A
  • Epithelial and primordial germ cells migrate to the sexually undifferentiated gonad
  • At the beginning of development, there are two channel systems: Wolffian and paramesonephric (Müller)
  • Normally one goes and the other continues. In male fetuses= Wolff canals
  • Anti-Müller hormone from testes = regression of Müller channels
  • Müller canals develop into the fallopian tube, uterus, cervix, and vagina
  • The formation of the external genitalia is influenced by the hormone gonads

Repro 2 (4 decks)

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