branimira

Question 1

maternal causes of dystocia

Answer 1

failure of expulsive forces (uterine or abdominal causes)

Question 2

primary uterine inertia

Answer 2

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

Question 3

secondary uterine inertia

Answer 3

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

Question 4

abdominal causes of dysotica

Answer 4

Inability to strain
Causes : age, pain, debility, diaphragmatic rupture, tracheal / laryngeal damage

Question 5

obstruction of birth canal

Answer 5

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

Question 6

narrow pelvis

Answer 6

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

Question 7

immature, juvenille pelvis

Answer 7

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

Question 8

narrow vulva and vagina

Answer 8

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

Question 9

narrow vertical canal

Answer 9

• Mostly in cows, sheep and goats
• Disorder of the opening stage .
• 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

Question 10

stages of cervical canal (narrow cervical canal according to goetze)

Answer 10

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)

Question 11

torsion of gravid uterus

Answer 11

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

Question 12

endometritis in mares

Answer 12

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

Question 13

physiological endometritis

Answer 13

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

Question 14

PMIE

Answer 14

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

Question 15

diagnosis of endometritis

Answer 15

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)

Question 16

prevention of PMIE

Answer 16

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

Question 17

chronic endometritis

Answer 17

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

Question 18

pyometra as consequence of chronic endometirits

Answer 18

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

Question 19

endometriosis

Answer 19

Direct link to early embryonic mortality and cervical fibrosis
Senile atrophy of uterine glands older pluriparous mares (>15g)
Endoscopic and PHD finding

it’s a degenerative chronic condition demonstrated by fibrosis within the endometrions
- irreversible
- severity increases with age
- diagnosis = biopsy
- it’s caused by growht and spread of tissue similar to the endometrium or uterine lining outside of the uterine cavity

Question 20

endometrial cysts

Answer 20

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

Question 21

cause of infertility in cows

Answer 21

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

Question 22

freemartinism

Answer 22

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

results in infertility involving tubular reproductive tract

Question 23

what are chimeras

Answer 23

individual animals that contain two cell types originating from separate zygotes

Question 24

signs of freemartinsim

Answer 24

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

Question 25

cause of freemartinism

Answer 25

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

Question 26

diagnosis of freemartinism

Answer 26

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

Question 27

prognosis of freemartins

Answer 27

most female cattle that are blood chimeras are often sterile freemartins barren so use for fattening - not for mating

Question 28

hermaphoriditism

Answer 28

mixing of sexual characteristics of both sexues in 1 individual

Question 29

type of hermaphrodism

Answer 29

ambiglandular testciular ovarian

Question 30

ambiglandular

Answer 30

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

Question 31

testicular

Answer 31

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

Question 32

ovarian

Answer 32

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

Question 33

congenital repro problems cow

Answer 33

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

Question 34

ovarian hypoplasia

Answer 34

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

Question 35

congenital leiosns on ovaries

Answer 35

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

Question 36

cervix duplex

Answer 36

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

Question 37

uterus didelphys

Answer 37

complete absence of fusion of 2 paramesonpehric canals AI in ipsilateral horn-conception and AI possible

Question 38

vagina subsepta

Answer 38

= 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

Question 39

acquired repro problems co

Answer 39

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

Question 40

urovagina - cow

Answer 40

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

Question 41

ovarian cyst cow

Answer 41

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

Question 42

how to help with anovulatory conditions in cattle

Answer 42

improve energy status during transition period prevent disase decrease frequency of suckling to 1-2 x1d in beef cows GnRH agonist, prostaglandins or progestogens

Question 43

differentials of ovarian cysts cattle

Answer 43

corpus hemorrhagicum vaculoalted LC non-ovarian cyst abscess tumour

Question 44

types of ovarian cyst cattle

Answer 44

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

Question 45

signs of ovarian cyst cattle

Answer 45

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

Question 46

risk factor of ovarian cyst cow

Answer 46

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

Question 47

cause of ovarian cyst cattle

Answer 47

neuroendocrine imbalance

Question 48

therapy of COD cattle

Answer 48

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

Question 49

prevention of ovarian cyst cow

Answer 49

decrease stress, treat infection, prophylactic GnRH 12-14d post birth no effective treatment for multiple cysts so cull

Question 50

absent or delayed ovulation

Answer 50

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

Question 51

ovarian atrophy

Answer 51

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

Question 52

bartholin gland cyst

Answer 52

= 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

Question 53

penumovagina

Answer 53

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

Question 54

RBC

Answer 54

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

Question 55

pathologic conditions of RBC

Answer 55

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

Question 56

treatment of RBC

Answer 56

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

Question 57

cause and factors of RBC

Answer 57

cause = unclear but mulitfactorial -> cow, bull, environment factors: age, genetics, infection of repro tract, nutrition, embryo mortality

Question 58

trauma in small rum

Answer 58

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

Question 59

pseudopregnancy in goats

Answer 59

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

Question 60

pregnancy toxaemia

Answer 60

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

Question 61

pseudolactation

Answer 61

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

Question 62

pathogenesis of pseudolactation

Answer 62

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)

Question 63

signs of pseudolactation

Answer 63

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

Question 64

complications and dd of pseudolactation

Answer 64

rare - vomiting, anorexia, PUPD, tumours, mastitis, CEH DD = rule out pregnancy, mastitis, tumour, pyometra

Question 65

diagnosis of peudolactation

Answer 65

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

Question 66

treatment of pseudolactation

Answer 66

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

Question 67

what is feline mammary fibroepithelial hyperplasia

Answer 67

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

Question 68

pathogenesis of FEH

Answer 68

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

Question 69

pathomorphological characteristics of FEH

Answer 69

firm, well-circumscribed unencapsulated mass, solid and smooth possible ulcerations and necrosis micro=profieration of glandular, fibre - epithelial elements

Question 70

therapy and prognosis of FEH

Answer 70

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

Question 71

clinical findings of FEH

Answer 71

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

Question 72

complications of FEH

Answer 72

mastitis in lactating queens ulceration due to overstretched skin maybe hemorrhagic/purulent exudate increase temp, lethargy, anorexia LN involvement

Question 73

diagnosis of FEH

Answer 73

signs = spread of development biopsy = FNA or excision - large amount of mitosis = false malignanyc US - increased echogenicity DD = neoplasia, FEH = bigger and softer

Question 74

congenital abnormalities in bitch

Answer 74

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

Question 75

transmissible venereal tumour dog

Answer 75

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

Question 76

cystic endometrial hyperplasia - bitch

Answer 76

acute/chronic post estral disease of adult intact bitches leading to inflammatory exudate in uterus cause = repeat exposure of endometrium to progesterone predisposing = 2 month diestrus

Question 77

pyometra

Answer 77

progesterone mediated uterine disease occurring during diestrous bacterial infection with opportunistic organisms from vagina secondary to CEH most common organism = e.coli

Question 78

types of pyometra

Answer 78

open = 4-8 weeks post estrus, vulvar discharge, less systemically ill closed = abdo distension, minimal discharge, more systemic signs

Question 79

signs of pyometra

Answer 79

fever hypothermia dehydration

Question 80

lab and diagnosis of pyometra

Answer 80

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

Question 81

therapy for pyometra

Answer 81

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

Question 82

split estrus dog

Answer 82

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

Question 83

vaginal prolapse dog

Answer 83

= 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

Question 84

pyometra queen

Answer 84

ess 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 female

Question 85

endometrial biopsy mare

Answer 85

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

Question 86

categories of endometrial biopsy mare

Answer 86

I : (NONE) healthy mares, no pathologic chcanges or any existing changes foaling rate 80-90% IIA: (MILD) small changes, slight to moderate inflammatory changes, 50-80% IIB: (MODER)figrotic changes are more severe, inflammation is more widespread, 10-50% III: (SEVERE)severe changes, widespread inflammation, scarring, atrophy of glands in physiological breeding season, 0-10%, severe changes in endometrium more fibrotic nests

Question 87

endometrial swab in horse

Answer 87

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

Question 88

dog mammary tumour stage

Answer 88

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

Question 89

cats mammy tumour staing

Answer 89

modified mnethods sam grade of malignacy

Question 90

grades of tumour

Answer 90

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

Question 91

TNM classification

Answer 91

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

Question 92

treatment of tumour

Answer 92

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

Question 93

mammary tumour bitch

Answer 93

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

Question 94

mammary tumour queen

Answer 94

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

Question 95

vascularisation of mammary gland

Answer 95

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

Question 96

lymphatic drainage

Answer 96

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

Question 97

risk factors for mama tumours

Answer 97

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

Question 98

molecular pathogenesis in tumours

Answer 98

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

Question 99

mammary tumours in cats

Answer 99

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

Question 100

mammary tumour signs

Answer 100

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

Question 101

initial work up for tumour

Answer 101

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

Question 102

diagnosis of mamary tumour

Answer 102

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

Question 103

treatment for mammary tumour

Answer 103

surgery = gold standard exception = inoperable, higly metastic tumours or IMC

Question 104

classification of tumour

Answer 104

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

Question 105

benefits of ET

Answer 105

faster genetic progress offspring from old/injured animals increased milk production in dairy herd increased farm income through embryo sales (easier to transport and than live animals) preserves superior genetics/endangered species

Question 106

limitations of ET

Answer 106

decreased genetic diversity expensive and time consuming success rates less than AI not all potential donors respond well

Question 107

MOET

Answer 107

multiple ovulation embryo transfer embryos flushed from donor and transferred to recipient goal = obtain maximum number of genetically superior embryos in minimal amount of time

Question 108

MOET select donor cow

Answer 108

based on produceer preference has to be reproductively sound (no birthing difficulties, normal cycles etc) disease free, appropriate BCS etc

Question 109

MOET superovaulation of donro

Answer 109

9-11d after heat, give FSH, LH to induce ovulation could give prostaglandins to cause estrus in 48-60h 85% of donors average 5 transferable embyros purified FSH 2x1d for 4-5d

Question 110

MOET insemination of donor

Answer 110

2-3 x at 12 h intervals 12h after onset of standing heat semen put in body of uterus

Question 111

MOET flushing embryos

Answer 111

7d after start of estrus rectal US to assess superovulatory response (CLs) and give epidural use a foley catheter, collection flask and flushing fluid

Question 112

MOET selection and preparation of recipients

Answer 112

young dairy cows in good BC - repro sound in heifer - 15m+, 350kg+ - cheap and better for synchro but possible calving problmes syncorhinsed with PGF, gestated or Ovsynch

Question 113

MOET transfer of embyros

Answer 113

load embryo in 0.25ml insemiahtion straw and low into ET gun palpate recipient to see which ovary has CL and transfer to ipsilateral uterine horne transfer within 8hr after flushing (can be frozen)

Question 114

steps of MOET

Answer 114

select donor cow superovualtion of donor cow insemination of donor cow flushing embyros evaluate embyros selection and preparation of recipient transfer of embyros

Question 115

APGAR

Answer 115

immediately for calves within 1-3 mins for foals 2 = best A= appearance P=pulse G=grimace A=activity R= respiration scores 7-8 = vital 4-6 danger 0-3 avital

Question 116

calves APGAR

Answer 116

activity = check pupils and interdigital reflex grimace 0=nothing 1= decreased 2= active = check head movements under cold water respiratory 0= nothing 1= arrhytmic 2= rhythmic MM 0= pale/blue 1= cyanotic 2= pink

Question 117

puppies APGAR

Answer 117

pulse 0= <180 1= 180-220 2= >220 respiration 0= none or <6 1= 6-15 2= >15 reflexes 0= no 2= present MM 0= cyanotic 1= pale 2= pink

Question 118

fetotomy

Answer 118

operations performed on fetus to decrease size by divison/removal of parts for vaginal delivery partial or total

Question 119

when to do fetotomy

Answer 119

dead fetus emphysematous fetus fetus toobig/pelvis too narrow fetus has abnormality irreducible/incorrect 3Ps

Question 120

fetus alive?

Answer 120

pinch toes/poke eyes -move away put finger in mouth - sucke check retail tone - should contract

Question 121

kill fetus

Answer 121

use finger knife to cut vascular structures on neck or umbilicus faster and less painful = head decapitation with fetotomy wire

Question 122

after care, after fetotomy

Answer 122

remove every piece of fetus, check uterus for cuts/another calf, remove placenta, oxytocin, ATB locally or systemic if infected

Question 123

advantage of fetotomy

Answer 123

little assistance needed lower cost less intense post op avoids excessive maniupulation

Question 124

disadvatntaghe of fetotomy

Answer 124

possible laceration of birth canal exhaustion of dam injury of vet

Question 125

types of cut in fetotomy

Answer 125

transverse = section perpendicular to long axis of fetotome oblique = section oblique to long axis of fetotome longitudinal = section parallel to long axis of fetotome

Question 126

method of fetotomy

Answer 126

subcutaneous/intrafetal = remove enough parts of limbs to decrease size of fetus lost of physical strength needed and time consuming percutaneous/extrafetal method

Question 127

danish (zagreb) method

Answer 127

anterior longitudinal presentaiton head removal oblique section of forelimb, next and part of thorac section of pelvis or fetal trunk bisection of pelvis

Question 128

causes of dystocia

Answer 128

FETAL oversized dfetus congenital abnormality abnormal orientation MATERNAL birth canal pathologies felt membrane abnormalitis placenta problems

Question 129

why od pregnancy termination

Answer 129

unwanted mating bithc too young/old bitch health proglems litter of no value

Question 130

4 mechanism of preg termination

Answer 130

changing estrogen-progesteroen relation - estrogen or glucocorticoids inhibition of luteal function - PGF or dopamine agonists blocking progesterone synthesis by inhibiting steroidogenesis - epostan blocking progesteron activity on receptor leve - aglepriston

Question 131

inflammatory mamary carcinoma

Answer 131

rare, locally aggressive, fast growing, highly malignant,highhlt metastatic form of mammary tumour that affects humans and dogs 7.6% of mmamary tumours in dogs are IMC

Question 132

IMC histologically

Answer 132

high grade carcinoma with dermal lymphatic invasion anapaestic carcinoma tubular, solid or mixed high % of VEGF immunoreactive tumour cells meaning angiogenic and metastatic potential

Question 133

forms of IMC

Answer 133

primary = animals without history of previouss mamary nodules secondary = with history of previous mammary tumour post surfical or non-post surgical

Question 134

signs of IMC

Answer 134

edema, eryhtema, ucleration, warmth, firmness, pain maybe lymphadema of limbs uni or bilateral can mimic severe mastitis and dermatitis occurs in luteal phase of cycle due to progesteornr

Question 135

metastasis of IMC

Answer 135

bladder ovaries and uterus rrrely to lung, liver bone and kdinsye

Question 136

treatment of IMC

Answer 136

surgery not recommended palliative care adjuvant theray chemo, cox-2inhibitors v.poor prgonsosi - 60 days

Question 137

pregnancy termination in cats

Answer 137

less common oestrogen’s PGF2a (dinoprost and cloprostenol) dopamine agonist (cabergoline) antiprogestin

Question 138

surgical castration

Answer 138

gonadectomy OVH long term problems; obesity, rinary incontiencne, endocrine disorders, behaviour changes, neoplasia

Question 139

non-surgical castraton

Answer 139

why= inconvenient estrus timing, pyometra management, contraception least invasive - separate male and female contraction havs to be: safe, cheap, efficient and easily applied

Question 140

hormones for contraception

Answer 140

progestogens androgens GnRH agonist GnRH antagonist

Question 141

chemicals for contraceptiojn

Answer 141

zinc gluconadte ca chloride chlorhexiidne gddigluconate hypertonic saline

Question 142

progestogens

Answer 142

most frequently used method in male animals = prevents sexually related behaviour eg spraying

Question 143

contraceptive effect of progestogens

Answer 143

negative feedback effect on hypothalamus + pituitary -> prevents stimulation of follicle growth and ovulation (continuous high conc suppress FSH+ LH production) impede movement of sperm and eggs to site of fertilisation interfere with implantation

Question 144

side effects of progestogens

Answer 144

depend on type, dose, duration and age of animal less if given in anestrus and small doseas increase appetite, weight gain, lethargy, alopecia, adrenocortical suppression, acromegaly symptoms uterine pathology - CEH, pyometra mammary gland neoplasia

Question 145

medroxyprogesterone acetate

Answer 145

long lasting injection 2mg/kg SC or 5mg PO for 21d max return to estrus in 2-9 months most adrogenic and immunosuppresivem

Question 146

melengestrol acetate

Answer 146

temporary estrus suppression (can be used with GnRH agonist) 2.2mg/kg PO for 8 d early in proestrus 2-4w administration during anestrus antiadrogenic, antiestrogenic, cortisol agent

Question 147

contraception GnRH (agonist)

Answer 147

- suppression of GnRH  suppresses reproductive steroid hormones therefore behaviour worry over effect on non-target tissue pros = good for male and female suppression estrus behaviour reversbiel conc = initial inducement of estrus and increase in temp (due to FSH and LH) slow onset and variable duration injection or SC implant

Question 148

deslorelin

Answer 148

implant for male (females and cats too) 4.7mg for 6m, 9.4mg for 12 m dose dependent time for return to feritlity

Question 149

nafarelin

Answer 149

18.5mg SC implant -> 2ug/kg/day SC last 8-11 mo after removal of implant im bitches and 3 year in cats

Question 150

GnRH antagonsit

Answer 150

block GnRH receptors on pituitary cells without causing initial stimautlion of sexual behaviour expensive - peptide on non-peptide molecules generations: detirelix, acilin, degarelix, cetrorelix pros = suppression for short time, suppresses estrus behaviour, reversible non-peptides = cheaper and can be given PO, effect starts quicklyy cons = frequent applciation reversible no depo or long acting formaultions first gen can cause histamine reaction in dogs not in early pregnancy (LH) 2nd gen = luteal suppression + preg termination 3rd gen= preg termination and progesterone, decrease without side effects

Question 151

melatonin

Answer 151

for cats PO for 30-35d - implant better short tem suppression -> 2-4 months, reversible, caution - initial induction of esters 12-18mg

Question 152

prostaglandins

Answer 152

luteolytic and utertonic action natural = dinoprosvt. synthetic = cloprostenol dinoprosvt = dose dependent side effects: hyper salivation, decreased HR, vomiting, that stops 1 h after admin, gradually increase dosage cloprostenol = more potent but decreased side effects, from 200-120d

Question 153

dopamine agonist

Answer 153

effect D2 receptors -> decrease prolactin secretion -> decrease progesterone decrease prolactin -> luteolytiss bromocriptine = strong effect,ataxia and omiting cabergoline = more efficient in smaller dose, milder side effects, movre peicfi cD2 receptors agonist and eodesn’t cross BBB as easy, efficient after 30d,

Question 154

combined therapy

Answer 154

D2 agonists and PGF2a -> 100% effective from day 25+, less side effects, don’t have to give everyday , cabergoline PO aglespristone and PGF misopristol = synthetic analogue of PGE, intravaginal - causes cervical dilation combo with anglepirston = abortion in shorter duration (6d)