Repro 5 Flashcards

1
Q

List 4 peripartuient/prepartum problems in female

A
  1. Uterine displacement = prepubic tendon rupture
  2. Vaginal prolapse
  3. Uterine torsion (horses)
  4. Hydrops allantois/amnii
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2
Q

List 7 parturient/intrapartum problems in the female

A
  1. Foetal dystocias (not covered here)
  2. Uterine torsion (cattle)
  3. Incomplete cervical dilation
  4. Uterine inertia
  5. Haemorrhage
  6. Perforations/lacerations
  7. Eclampsia
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3
Q

List 5 Postparturient/ Postpartum problems in the female

A
  1. Uterine prolapse
  2. Infections
    1. Endometritis
    2. Metritis
    3. Pyometra
    4. Salpingitis/pysalpinx
  3. Subinvolution of placental sites (SIPS)
  4. Retained foetal membranes
  5. Cystic ovarian disease
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4
Q

Uterine displacement what is it, how occur and what leads to

A

○ AKA prepubic tendon rupture (doesn’t actually rupture) - actually uterine haemorrhage
○ Ventral herniation -> uterus move through the tearing of the abdominal cavity
§ Separation or tearing of prepubic tendon and musculature - structural defect
§ Rapid progression to entire ventral abdomen
§ Painful ventral swelling
○ Alters uterine conformation and hinders normal foetal expulsion
§ Normally foetus on gently slope, now have to do a sharp turn and lost abdominal musculature to push the baby out

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5
Q

Uterine displacement what most common in, treatment options and prognosis

A
  • More common in older draft mares
    ○ Not common in athletic breeds (thoroughbreds or standardbreds)
  • Treatment
    ○ Abdominal support and reducing activity
    ○ Induced or assisted or elective C-section - traditionally
    ○ Conserve approach -> wait and let mare foal may result in better mare and foal prognosis
  • Prognosis is poor for survival of both dam and foetus
    ○ Prognosis of foetus depends on when during gestation this occurs -> generally very premature and doesn’t survive
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6
Q

How to tell the different between vaginal and uterine prolapse

A

Uterus -> have caruncles

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7
Q

Vaginal prolapse what common in, what else may prolapse, what stage of pregnancy, why and does it occur again

A

○ Older ruminants and pigs -> generally after having a few babies
○ +/- cervix
○ Usually late pregnancy
§ Increased abdominal pressure and relaxed perineal musculature (relaxin)
§ More common in obese animals or with twins
§ Predisposed by increased oestrogens
□ Including phytoestrogens
○ Often recurs at parturition and subsequent parturition
§ If not valuable probably cull the animal

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8
Q

Uterine torsion in horses, what stage of gestation, what predisposed by and results and treatment

A

○ Horses mid-late gestation (from 8 months)
○ Predisposed by
§ Foetal movement
§ Slipping/falling
§ Trauma
§ Hilly terrain
§ In horses often associated with colic (effect of rolling) -> uterine torsion cause colic or colic cause uterine torsion???
○ >180degree rotation causes uterine and foetal vascular compromise
§ Dystocia (cervical torsion)
§ Infarction/necrosis
§ Foetal death
Treatment
- Horses treated surgically by flank incision and correction of torsion
○ Put on exogenous progesterone for a couple of weeks (or until 320 day of gestation

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9
Q

Uterine torsion in cattle what stage of gestation occur, why occur, predisposed by the two types and what torsion in small animals

A
  • most commonly found at time of parturition
    § Broad ligament attachment unstable in late pregnancy
    □ As uterus swells with pregnancy the broad ligament attachment moves around the underside of the uterus
    ® Predispose to twists of the uterus -> torsion
  • Can occur clockwise or anti-clockwise
    ○ Determine by looking at vulva and rectal palpation with confirm direction
    Small animals may have segmental torsion
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10
Q

What are the 4 steps in correcting a uterine torsion in cattle and what may be needed

A
  1. Cow placed on the side of torsion (right torsion on right side)
  2. Plank is placed in the flank
  3. One person of 70-90Kg should stand on the plank while the cow is rolled over her back with help of ropes attached to her feet
  4. Checked rectally if the torsion has been resolved
    - If move to the wrong direction can tear the broad ligament -> need to know which way the torsion is
    A C-section is still often necessary if the cervix is not sufficiently dilated to deliver the calf vaginally -> still worth a try
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11
Q

Hydrops allantois what is it, clinnical signs in cattle, how to diagnose via palpation, prognosis and treatment

A
  • Bilateral distention, apple shaped (different from bloat, which is usually just distention of the left side) - distention on both side
    ○ Fluid accumulation in the allantois -> the placenta isn’t doing its job
  • Cow is sick (anorexic, down, weak, decreased rumen motility)
  • If only tight uterine wall can be palpated and no fetal parts or placentomes, a diagnosis of hydrops allantois is made
  • Prognosis is poor for cow’s life and fertility.
    ○ Treatment can be either induction or C-Section with slow release of fluid (cow should receive fluid replacement therapy)
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12
Q

Hydrops amnii/hydramnios what is it, what due to, characteristics, results, prognosis and treatment

A

extension of the amnion via amniotic fluid
- due to a defective calf, usually attributed at least partly to a defect in swallowing of amniotic fluid by the calf (calf generally swallows the amniotic fluid to decrease the amount)
- Cow is pear shaped (c.f. apple shape in hydrops allantois).
- Characterized by a gradual accumulation of highly viscous fluid during the last half of gestation
○ The placenta is normal
○ Usually fetus and placentomes can be palpated
○ The cow is usually clinically otherwise unaffected.
○ The pregnancy usually goes to term, and frequently a small, deformed fetus is delivered.
- Postpartum metritis is uncommon (unlike hydrops allantois).
- The prognosis is good for life and fertility.
- No treatment is required -> The cow may be allowed to go to term or induced to calve

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13
Q

Incomplete cervical dilation what species most common in, what called in sheep, pathogensis and what sheep predisposed by

A

○ Mostly ruminants particularly in sheep (50% dystocias)
§ Called ringwomb in sheep
§ Ruminant cervix highly collagenous, very thick barrier if not relaxed
○ Pathogenesis poorly understood
§ Hormonal imbalance, Hypocalcemia and hypophosphataemia proposed as risk factors
□ Involved with muscular movement and dilation
§ Sheep predisposed by previous vaginal prolapse
□ Scaring and fibrosis around cervix

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14
Q

Uterine contraction what primers the uterus and positive and negative hormones and therefore what could cause uterine inertia

A
Oestrogen priming of the uterus 
	- Therefore occur with decrease 
Negative with progesterone 
	- Therefore occur with increase 
Positive with prostaglandin and oxytocin
	- Therefore occur with decrease
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15
Q

Uterine inertia what are the 2 types, common in, due to and causes

A

1) Primary inertia
§ Common in multiparous animals
§ Due to inadequate myometrial contraction
§ Causes
□ Hypocalcaemia/hypomagnesaemia
□ Overdistension/under-distension of the uterus
® perfect stretch for maximum contraction
□ Increased progesterone
□ Decreased oxytocin, prostaglandin or oestrogen
2) Secondary inertia
§ Due to myometrial exhaustion
§ Any cause of dystocia that causes prolonged myometrial contracture

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16
Q

Foaling what is important in terms of ensuring a easy delivery

A
  • Generally come out one leg first then other close behind as the shoulders are broad and cannot fit across together
  • Therefore if pulling foal through should pull one leg at a time
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17
Q

Haemorrhage during parturition where does it occur, 3 clinical signs, treatment and prognosis

A
  • Bleeding into broad ligament after uterine artery rupture
    ○ Can stop the bleeding by the broad ligament blocking the rupture
    ○ If bleed into the abdomen then problem but generally clot themselves
  • Clinical signs
    ○ Colicky post foaling
    ○ High heart-rate
    ○ Prolonged CSF
  • Treatment
    ○ Keep quiet
    ○ Tranexamic acid -> reduce enzymatic destruction of fibrin and fibrinogen -> help form the clot
    ○ Maybe fluid replacement
  • Prognosis
    ○ Either self-limiting or not (dying)
    ○ If survive recommend that don’t breed again (increased risk of occurring again)
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18
Q

Lacerations/perforations during parturition where occur, what can result from and how to fix

A
  • Vulvar and vestibular lacerations are quite common and usually do not require repair if they only involve the mucosa
    ○ If submucosa involved, immediate suturing is indicated to prevent contamination
  • Recto-vaginal perforation
    ○ Foot comes through anus leads to recto-vaginal fistula -> generally not too much of an issue
    § Try to push back through and give epidural (to stop the pushing) IF CANNOT
    □ Cut through recto-vaginal shelf itself with a scalpel (preferable to a tear)
  • Third degree perineal laceration; tear of vulva, perineal body and anal sphincter -> creates cloaca
  • Fix via surgery -> want to do surgery after healing and oedema has gone down therefore the season is lost for that mare
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19
Q

Necrotic vaginitis following trauma during dystocia what can lead to and how to avoid this

A
  • If very bad can lead to adhesions in the vagina -> infertile
  • Therefore need to stop these adhesions from occurring by giving intramammary antibiotics via rectal sleeve and breaking down the adhesions (needs to be done everyday)
  • Also if very bad should give antibiotics systemically
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20
Q

Uterine prolapse what most common in, result from, predisposed by, 3 main consequences and prognosis

A

○ Older ruminants (dairy cows and ewes)
○ Caused by excessive abdominal straining, uterine inertia and/or contractile dysrhythmia
§ Therefore anything that causes this will result in
○ Predisposed by
§ Prolonged dystocia
§ Retained placenta
§ Postparturient hypocalcaemia
○ Consequences
§ Infarction
§ Endometritis/Metritis
§ Urinary/intestinal obstruction
- Poor prognosis for future fertility and guarded for survival
○ Replacement might be possible if hind-end of mare can be elevated and the organ Is not necrotic
§ Chance of recurrence is not great so if properly corrected no serious long term effects

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21
Q

What are the 6 steps in the treatment of uterine prolapse of a cow and what disease need to treat first

A
  • Epidural anaesthesia is helpful to prevent straining
    1. Tip of pelvis cranially by placing the cow in “frog leg” position and elevate the uterus
    ○ Aid in replacing the uterus and may help empty the bladder if it is trapped
    2. Generally the placenta is removed only if loose
  • More trauma is caused to the endometrium by manually removing the placenta than by leaving some attached to the uterus
    3. Sugar, glycerol, or other hyperosmolaric substances are sometimes used to reduce the oedema in the uterus and shrink it down
    4. Oxytetracycline powered or other broad spectrum antibiotics are sprinkled on the uterus before replacement of uterus
    5. Complete replacement is essential to prevent continues straining and reoccurrence
    ○ Need to ensure the uterine horns are inverted (use old wine bottle)
    6. Wait until you get it into place then give oxytocin (after replacement)
    ○ If give before uterus will contract down and make the job more difficult
    Important to treat milk fever first before replacement because that is a life-threatening condition
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22
Q

Endometritis what are the 2 main mechanisms of transmission and what causes in cattle and horses and were the 3 consequences

A

1) Venereal disease
□ Cattle: Trichomoniasis, brucellosis (EXOTIC), leptospirosis, campylobacteriosis
□ Horses: Taylorella equigenitalis (contagious equine metritis – EXOTIC)
2) Ascending infection -> most important
□ Predisposed post-partum due to retained membranes, uterine trauma/prolapse, immunosuppression
□ Cattle: Trueperella pyogenes, Fusobacterium necrophorum, other anaerobes
□ Horses: Streptococcus zooepidemicus, Pseudomonas aeruginosa, coliforms
Consequences
§ Mild cases resolve spontaneously
§ May persist chronically and cause endometrial damage
§ Foetal loss and/or infertility

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23
Q

Metritis what are the 4 main consequences

A
§ Infertility
§ Uterine rupture and peritonitis
§ Abscessation/adhesions
§ Sepsis (especially horses)
□ Susceptible to laminitis
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24
Q

Pyometra in cattle define, clinical signs results and treatment

A

○ Accumulation of purulent material in the uterus due to persistent corpus luteum and continued progesterone secretion
○ Cattle (and dogs, but different pathogenesis)
○ Develops after oestrus cycle
○ Often clinically silent
§ Cervix closed so no exudate
§ Uterus doughy on palpation
§ Affected animal infertile
○ Difficult to treat
§ Can try to give an injection of prostaglandin (but problem persists so will have same problem next time)
§ Therefore often culled

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25
Q

Salpingitis/pyosalpinx what is it, how present, what results in and causes

A

○ Inflammation of the uterine tube
§ Pyosalpinx: segmental pus accumulation due to obstructed drainage
○ Usually bilateral
§ Uterine tube highly susceptible to damage and secondary stenosis/occlusion
§ Infertility common -> very serious
○ Cause
§ Usually extension from metritis/endometritis
§ Some pathogens (Ureaplasma, Mycoplasma) may specifically localize in uterine tube

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26
Q

Subinvolution of placental sites what species and age, what lead to, what result in and 3 treatment options

A

○ Subinvolution of placental sites
§ Young bitches (<3 years old)
§ Persistent haemorrhagic discharge (lochia) due to failure of uterine involution
□ Discharge >6 weeks post-partum suggestive
§ Trophoblasts fail to regress and invade uterine wall - act as psuedomalignancy
□ Uterine perforation may occur
§ Potentially fatal iron-deficiency anaemia results from persistent discharge
Treatment
1. In light case-> nothing, as it often self-limiting
2. In more severe cases: oxytocin (1-2IU every 2-4 hours) and methergine (2 to 4 drops ever 6-8 hours)
3. In case the dog does not respond or life-threatening haemorrhage occurs, ovariohysterectomy is recommended

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27
Q

Retained foetal membranes what are the main species affected, defined at what duration in cattle and consequences in cattle

A

○ Mostly an issue in cattle (6-8% of calving), rarely horses and other species
○ Incomplete placental expulsion >12 hours post-partum
Consequences in cattle
○ Typical persist for 6-10 days until autolytic dehiscence occurs
○ Uncomplicated RFMs do not cause significant systemic effects
§ Milk decrease in milk production
○ Provide niche for development of metritis - only time will see as sick
§ Wicking ascending infection

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28
Q

Retained foetal membranes in horses when an issue, consequences and treatment

A
  • LIFE-THREATENING EMERGENCY
    ○ Normally released within 1 hour, retained if not released within 4-6 hours
    § Antibiotics required after 6 to 8 hours
    ○ Attend if FM not passed 4 hours post foaling
  • Life-threatening consequences
    ○ Laminitis, septicaemia, toxic shock and death
    ○ Septic/toxic metritis happens fast
    Treatment
    How to remove membranes
    ○ Should never be removed just by traction
    § Risk of trauma, haemorrhage and severe uterine damage
    ○ Can get a hold of the RFM and wrap them into a cord and the apply VERY LIGHT traction while feeling rectally where they are attached
    § That area can then be massaged rectally and often the membranes will be released
    ○ After the membranes are released, uterus is flushed with copious amounts of fluid (saline or ringer’s solution) for days until fluid is clear
    ○ Oxytocin is continued for another 24-48 hours in order to aid uterine involution
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29
Q

What are 6 predisposing factors to retained foetal membrane

A
  1. Dystocia
    § Causes uterine inertia
    § Villous edema impairs separation of interdigitation
  2. Abortion/premature birth/induced labor
    § Imparied hormonal signalling and decreased collagenase secretion
  3. High progesterone/low oestrogen
    § Imparis prostaglandin secretion, decreased post-partum contractility
  4. Placentitis
    § Villous edema and thickening impairs separation of interdigitation
  5. Hypocalcaemia
    § Uterine inertia
  6. Vitamin E/selenium deficiency
    § Possibly impaired uterine contraction???
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30
Q

Eclampsia what species observed in, clinical signs, treatment and prevention

A
  • Observed mainly in toy breeds with large litter <38 days post-partum
  • Clinical signs
    ○ Tremors, nervousness, salivation; late stage: opisthortonus
  • Treatment
    ○ Calcium IV to effect, oral calcium supplementation, wean puppies if >4 weeks
  • Prevention
    ○ Adequate Ca:P ratio per partum
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31
Q

Cystic ovarian disease what species present in, what develops from, result in and causes

A

○ Cattle (esp dairy) and pigs
§ NOT HORSES
○ Anovulatory ovarian follicles that become cystic
○ Follicular cysts may be incidental finding or cause disease
○ Cause
§ Impaired ovulatory hormonal signalling
□ Proposed mechanism include
® Decreased pituitary sensitivity to oestrogen stimulus
® Decreased follicular hormonal receptors
□ Predisposed by periparturient stresses
® Dystocia
® Retained foetal membranes
® Ketosis

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32
Q

What are the two forms of ovarian cyst, what need to distinguish between, how

A
1) Follciular cysts 
○ Need to distinguish between follicular cyst from preovulatory follicle 
§ Distinguished based on 
□ Size (>17-25mm in cows, >20mm in sows)
□ Persistence 
2) Luteinized cyst 
○ Need to distinguish luteinized ovarian cysts from cystic corpora lutea 
§ Cystic corpora lutea have: 
□ Has undergone ovulation but has fluid retention 
□ Thicker wall 
□ Focal protrusion on one side 
- Site of ovulation
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33
Q

what are the 2 main effects of Cystic ovarian disease

A

1) Anovulatory infertility - main problem
2) Persistent hormonal secretion
□ Oestrogen
® Persistent oestrus/nymphomania
® Oedema and enlargement of uterus, cervix and vulva
® Hydrometra/mucometra
® Bone marrow suppression - oestrogen is myelotoxic
□ Androgens
® Masculinization
□ Progesterone (Luteinized cysts)
® Predisposed to uterine infection and pyometra

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34
Q

What are the 3 stimulus for the stretching reflex

A
  • Stretching of the vagina
  • Stretching of the cervix
  • Suckling of the puppies already born
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35
Q

Rabbit gestation length and what are they called when born

A
  • Gestation length of 30 days
  • Altricious
    ○ Their skin is without pigment or hair at birth
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36
Q

Acepromazine and Morphine what important with dystocia

A

Acepromazine
- Not an analgesic
- Likely to cause hypotension, with an associated reflex tachycardia
Morphine
- Does cross the placenta
○ Results in depressed post-natal respiratory drive

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37
Q

What are 3 sings of hypocalcaemia and 2 hormoens involved with mobilizing stored calcium

A

Signs of hypocalcaemia
- Generalised skeletal muscle twitching
- Absence of straining when vagina distended with a speculum
- Failure to deliver a pup after two or more hours
Hormones involved with mobilising stored calcium
- Parathyroid hormone
- Cholecalciferol

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38
Q

Define Puerperium and what occurs in this time

A
puerperium
- The time between birth until reproductive function is restored
○ What occurs during this time 
	§ Lactation
	§ Uterine Involution
	§ Return of ovarian cyclicity
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39
Q

Uterine involution define and what are the 4 overlapping processes

A

Uterine Involution
- changes in the uterus that result in returning the organ to normal size after parturition
(reduction in the increase in collage and smooth muscle that has occurred due to pregnancy)
4 overlapping processes
1. Myometrial contractions and expulsion of lochia
2. Necrosis and sloughing of tissues
3. Repair and growth of surface epithelium
4. Removal of bacterial contamination

40
Q

What are the 4 main steps in uterine involution in the cow and the time frames

A
  1. Myometrial contractions and expulsion of lochia (uterine fluid, placental fragments, caruncles)
    - Combination of exsanguination, placental maturation and strong contractions needed to separate the placentomes
    - Contractions subside in a couple of days
    ○ Myometrial cell size drops 700um to 200um in days
  2. Necrosis and sloughing of tissues
    - Takes days
  3. Repair and growth of surface epithelium
    - Repair of inter-caruncular regions usually by day 8
    - Caruncular regions vary often by day 20 but can be delayed
  4. Removal of bacterial contamination
    Bacterial contamination is common
41
Q

Bovine uterine involution what is the primary stimulus, what are the 2 main phases in terms of speed of changes with gravid horn and cervix changes and how long does the whole process take

A
  • Primary stimulus for change during period is removal of foetus
  • Uterine contractions continue for several days although reduce in regularity, frequency & amplitude (occur at 3 – 4 minute intervals)
  • Initial rapid phase of involution followed by slower subsequent changes
  • Diameter of gravid horn halved by 5 days & length halved by 15 days
  • Cervix constricts rapidly – within 10 -12 hours of normal birth impossible to insert hand into uterus; at 96 hours will admit just two fingers
    ○ Complete process from 26 – 52 days (changes after 25 days imperceptible)
42
Q

Bovine uterine involution elimination of bacterial contamination, how occur, normal cow when sterile, main mechanism of elimination and other roles

A
  • Immediately post-partum vulva relaxed & cervix dilated – allows entry of a wide range of bacteria into vagina and uterus
  • Very high bacterial contamination rate in 1st 20 – 30 days post-partum
  • In normal, healthy cows uterus should be sterile by 6 – 8 weeks
  • Main mechanism of elimination – phagocytosis by migrating leukocytes
  • Persistence of uterine contractions (4 days), sloughing of caruncular tissue & uterine secretions important in expulsion process
  • Early return to cyclical activity probably also plays an important role
43
Q

What are the 5 main things that can prolong uterine involution in cattle

A
  1. Prolapse uterus
  2. Retained foetal membranes
  3. Metritis
  4. Endometritis
  5. Pyometra
44
Q

Retained foetal membranes what is the normal steps in the expulsion of membranes and therefore what are the risk factors involved in developing this

A

Main steps involved in expulsion of the membranes:
1. Maturation of the placenta
2. 2Exanguination of the foetal side of the placenta after the blood supply is cut off (which causes physical shrinkage)
3. Uterine contractions (causing distortion)
Risk Factors
- Slow calvings, dystocia (slows exanguination)
- Low energy (causes slow calvings!)
- Low Calcium (smooth muscle contraction)
- Infection (slows maturation)

45
Q

What are 6 ways to diagnose endometritis in cattle

A

1) Observe vaginal discharge
2) Rectal palpation – not v. accurate (Uterus thinwalled)
3) Vaginoscopy – cervical, vaginal discharge
4) Metricheck
○ Scrap along the bottom of the vagina and pull back
§ Look at discharge and rate accordingly
5) (Ultrasound – uterine fluid)
6) (Biopsy – cumbersome, deleterious results to uterus sometimes)

46
Q

What is the typical incidence of uterine infections between calving - 24, 16-30dpp, 31-45dpp and 46-60dpp

A
Time	Infected 
Calving to 25pp	90%
Day 16-30pp	78%
Day 31-45pp	50%
Day 46-60pp	9%
47
Q

What are hte main risk factors for endometritis

A
- Balance between bacteria and immunity
○ disruption of neutrophil function
○ type of bacteria eg penicillinase
○ progesterone administration
○ glucocorticoid administration
○ hygiene of calving environment
- RFMs or Metritis
- Stillbirth or calf dies within 24 hours
- Twins
- Dystocia
- Milk Fever
- Vulval discharge
- Calving induction
48
Q

Uterine involution in the cow what are factors increase and decreasing the rate and why important

A

Factors Affecting Process
- Increased Rate
○ Age – involution more rapid in primiparae than pluriparae
○ Season – probably more rapid in spring & summer
○ Climate – heat stress can inhibit speed of involution
- Delayed Rate
○ Periparturient abnormalities – dystocia, RFM, hypocalcaemia, twins & metritis can delay involution
○ Delayed return to cyclical ovarian activity – can slow process by possibly delaying healing
Why important
- Delayed uterine involution can increase the time to pregnacy by months
- Very important economically

49
Q

Uterine involution in the ewe how long does it have

A
  • 5 month gestation and generally only produce a lamb

○ Not a huge issue with fertility as joining after a few months to resolve

50
Q

Uterine involution in the horse, when can they be ready to conceive, how long for expelling foetal membranes, what makes quicker than cow, how long does it take and describe fertility on foal heat

A
  • Very efficient process in the mare
  • Can deliver 50kg foal & be ready to conceive within 2 weeks
  • Foetal membranes typically expelled about 60 minutes after foaling
  • Lochial discharge relatively slight & usually ceases in 24 – 48 hours
  • Crypts or microcaruncles are located within endometrium unlike the cow - caruncles are outgrowths that must be sloughed
    ○ Quicker
  • In uncomplicated pregnancy & parturition uterus is grossly normal in size & fluid content 7days post-foaling & histologically complete by day 14
  • Foal heat (begins 5-12 days after foaling) pregnancy rates comparable to breeding on subsequent cycles in mares that have uncomplicated birth and involution process
51
Q

Uterine involution in the sow how rapid, when does regeneration occur and at what stage does return oestrus generally occur

A
  • Rapid initial uterine weight loss occurs in first 5 days
  • Involution complete by 28 days
  • Regeneration of epithelium starts day 7 & complete by day 21
  • Return to oestrous & ovulation usually occurs after weaning - generally later the time of weaning shorter the time interval to 1st oestrous
52
Q

Uterine involution in the bitch and queen rate of involution, how long till foetal membranes passed, is there discharge present and how long does the whole process take

A
  • No hurry – dogs only cycle every 6 months
  • Rate of involution similar to other species – uterine horns restored to pregravid size by 4 weeks
  • Most canine placentas passed with puppy or 5 – 10 minutes after birth
  • Lochial discharge immediately post-partum very noticeable – green colour to bloodstained mucoid discharge within 12 hours
  • Complete endometrial involution takes about 12 weeks
  • At 3 months slight pigmented bands representing former placentation sites may be grossly observed in endometrium
53
Q

How does foetus receive and get rid of oxygen and nutrients

A

○ O2-blood delivered to the foetus via the umbilical vein

○ De-O2-blood returned to placenta via the umbilical arteries

54
Q

Oxygen tension in the foetus what are the normal levels and level in foetus and what does this result in

A

○ Normal arterial PO2 is approximately 100 mmHg
§ PO2 in umbilical vein in foetus is approximately 55 mmHg
○ Foetal haemoglobin has increased affinity for O2
○ Tissue oxygen levels in the foetus are very low

55
Q

How does the blood in the foetus bypasss the lungs

A

○ Foramen ovale-shunts blood from right to left atria -> bypass the lungs
○ Ductus arteriosus-shunts blood from the pulmonary artery to the aorta -> ensure complete bypass of the lungs

56
Q

How does the change in the lungs at birth occur

A
  • At birth, flow of O2-blood from the placenta stops!
    ○ Increase in systemic vascular pressures -> increases pressures in the left side of the heart
  • Hypoxia causes reflex gasping and expansion of the lungs with air
    ○ Decrease in pulmonary vascular pressures -> decreases pressures in the right side of the heart
57
Q

List 3 things that occurs at birth to the foetal circulation if everything goes right or if things go wrong

A

If everything goes right…
• Increasing pressure within the left atrium closes the foramen ovale
• Increased O2-haemoglobin saturation (ie: increased blood O2content) causes constriction of ductus arteriosus
• Entire volume of blood from the right ventricle enters the pulmonary artery and directed to the lungs
But, if things go wrong…
• Patent ductus arteriosus(PDA)
• Occasionally see a reversion to foetal circulation in very sick neonates
• Failure of the ductus venosus to close is an uncommon cause of porto-systemic shunts

58
Q

Why is colostrum so important for some species, how does antibodies get into colostrum and what can give if neonate doesn’t get enough

A

Importance
○ Agammaglobulinaemic at birth - no antibodies at birth - immunologically naïve
§ Lack opsonins for proper antigen processing
- Immunoglobulins concentrated in mammary gland by receptor-mediated transfer
○ Begins several weeks before parturition
○ Colostral IgG concentrations can be 5-10-times higher than maternal serum concentrations
○ Only provides antibodies against antigens to which the dam has been exposed
- Can give plasma transfusion if doesn’t receive enough

59
Q

How do neonates absorb antibodies within colostrum, how long for, when make their own and reach significant levels and when are maternal anitbodies gone

A
  • Neonate has specialized enterocytes that absorb large molecules by pinocytosis
    ○ Maximum rate of immunoglobulin absorption occurs in the first few hours of life
    ○ Absorption of macromolecules by this process has ceased by 24 hours of age
  • Immunoglobulins produced by the neonate become detectable within the first 1 or 2 weeks of life
    ○ Do not reach significant levels for several months
  • Half-life for (equine) maternal antibodies is approximately 20-30 days and most have gone by 6-months of age
    § Implications for vaccine programs
60
Q

List and describe 3 reasons for failure of the passive transfer of antibodies

A
  1. Failure to ingest a sufficient quantity of colostrum
    - Orphans, Rejected or abandoned neonates
    - Too weak to stand (e.g., prolonged dystocia)
    - Unable to stand (e.g., contracted tendons)
    - Unable or lack of desire to suckle (e.g., hypoxic-ischaemicencephalopathy - hypoxic injury)
  2. Ingestion of poor quality colostrum (low IgG content)
    - Premature lactation (placentitis in mares)
    - Premature parturition (inadequate udder development)
    - Ingestion of grasses infected with specific endophytes(fescue associated agalactiain mares)
  3. Failure to absorb colostral components from gut lumen
    - Seen occasionally in premature or dysmature neonates
    - Delayed ingestion of colostrum
61
Q

What are the main way to determine the adequacy of passive transfer and level that is adequate in horses

A
  • Usually measure or estimate IgG concentration
  • Direct and indirect measures
  • Qualitative, semi-quantitative and quantitative assays
  • ELISA or antibody-based assays are generally species specific
    >800 mg/dL considered adequate for foals
    § Different species has different ideal values
62
Q

How does maternal nutrition relate to feotal nurition and what does that influence

A

1) Birth weight is often reduced when dams are malnourished
○ Low birth weight neonates are likely to be more susceptible to adverse environmental conditions
○ Impaired heat conservation
- Weak at birth -> impaired ability to consume colostrum and, subsequently, adequate volumes of milk
○ Immunity
○ Starvation
2) *Over-feeding increases foetal growth (and causes deposition of fat within the pelvic canal) -> increased risk of dystocia

63
Q

How does climatic conditions affect neonatal mortality and how try to overcome this

A
  • Neonatal mortality increases with decreasing ambient temperature and with increasing precipitation:
    ○ Greater (relative) surface area
    ○ Evaporation of amniotic fluid
    ○ Limited caloric reserve
  • Newborn animals have stores of brown fat
    ○ Stores rapidly depleted in cold weather if unable to consume enough milk
64
Q

What are 6 factors that can increase neonatal mortality

A
  1. Presence of sick animals
  2. Mixing age groups
  3. High population density
  4. Inadequate cleaning of stalls or pens between animals
    ○ Porous materials
    ○ Older buildings
  5. Poor personal hygiene
  6. Sharing equipment
65
Q

What historical evens make a high risk mare

A
○ Unhealthy uterine environment
○ Repeated breedings
○ Abortion or premature birth
○ Premature placental separation
○ Placentitis
- Previous dystocia
○ Contracted tendons
- Prolonged pregnancies
○ 344 days (320-350 days)
- Previous sick foals
66
Q

What events during pregnancy makes a high risk mare

A
- Premature lactation
○ Loss of colostrum
- Disease during gestation
○ Reduced O2-content/delivery
○ Prostaglandin elaboration
○ Recurrent colic
- Excess abdominal enlargement:
○ Hydrops(amnii, allantois)
○ Body wall defects
- Prolonged gestation
67
Q

What events during parturition makes a high risk

A
  • Poor udder development
  • Dystocia (horses):
    ○ Stage I:30 min to 4 hours
    ○ Stage II: 20-30 min
    ○ Stage III: 30 min to 3 hours
  • Premature placental separation
  • Meconium staining
  • Abnormalities of the placenta
    ○ Weight/Gross/Microscopic
68
Q

Define serve, cover, submission/submitted and return to service

A

Service
- what is done by the male
Cover
- Same as “serve” but in horses
Submission/submitted
- like “service” but from the female point of view
Return to service
- Animals do not all become pregnant after a single “service”
- Polyoestrus animals that don’t conceive will cycle again and are said to “return”

69
Q

Thorougbreds what is their arbitary birthday, mating season starts when, and what is timeframe to do stuff

A
  • Thoroughbreds have an arbitrary birthday 1st Aug
    ○ (Standardbreds 1st September)
  • Mating season starts 1st September
  • Born earlier = age/size advantage
    ○ Melbourne foals may do better born August than July!
  • Aim to get mare pregnant ASAP after Sep 1
    ○ Mares have a “foal heat” at ~10 days
    ○ Then oestrus approx every 21 days
    ○ Foal heat may be less fertile
    § Check with ultrasound/culture a few days post-partum
    Without risk factors, 78-85% chance of pregnancy
70
Q

What are 4 main risk factors for later return in mares and the 2 consequences

A

1)Time since foaling
○ Incomplete uterine involutio, Endometritis
2) Mare cycling abnormalities
- Photoperiod, nutrition, climate etc
3) Stallion problems
○ Numerous
4) Problems with the timing of mating
○ Covered elsewhere
Consequences of later return - important
- If a foal is born later in the season
1) It may be smaller than its competitors at 2yo
2) The mare may be difficult to get pregnant early next season

71
Q

What must the cow do first before returning to service

A
○ Calve
○ Clean Up (endometritis)
○ Start Cycling (post-partum anoestrus)
○ Be detected on heat - especially for artificial insemination 
○ Be Inseminated
○ Conceive
○ Stay Pregnant
72
Q

Post-partum anoestrus in cattle what is needed for ovulation and why doesn’t it occur in this stage

A
  • In order to ovulate, follicles require stimulation by FSH (early) and LH (later)
  • LH stimulation is deficient in post-partum anoestrus cows
    ○ Direct effect: Low energy availability decreases LH pulsatility
    ○ Indirect effect: effects of LH on the ovary are synergistic with IGF-I in blood
73
Q

What is IGF-1 role with ovulation, how is this decreased and what occurs postpartum in cattle

A

GH in the liver produces IGF-1 which primes the ovary to increase its response to LH -> ovulation
Post-partum anoestrus
1) Energy balance, nutrition, disease and aging decrease GH in liver from forming IGF1
2) without as much IGF-1 LH doesn’t work as well on the ovary
3) no cycling of the ovary and follicular growth

74
Q

What are the 7 factors that contribute to fertility

A
  1. Cows
  2. Bulls
  3. Nutrition
  4. Diseases
  5. Facilitates
  6. Heat detection
  7. Lameness
  8. Calving patterns
75
Q

List and define the 5 rates that describe reproduction performance in cattle and which used to describe at farm level

A
  1. Submission Rate
    - % cows submitted in first 21 (or 30) days
    ○ One cow can be submitted multiple times still only counts as 1
  2. Conception Rate
    - % cow pregnant per 100 inseminations
  3. Pregnancy Rate
    - % of the herd pregnant after a given time
  4. 6 week in calf rate - industry standard
    - % of the herd pregnant after 6 weeks of joining
    ○ Typical herd will have 50% 6 week in calf rate
  5. Empty rate - industry standard
    - % herd empty (after a given no of weeks – 12or 20)
    4 and 5 rate of farms
76
Q

6 important factors that can optimise fertility on the farm

A
  1. Calving Pattern
  2. Condition Score (Nutrition)
  3. Heat Detection
  4. AI Technique
  5. Growing Heifers
  6. Bulls
77
Q

Calving pattern how does it affect fertility in herds

A

CALVING PATTERN
○ 6-8 weeks - dairy farm optimal
§ Cows that calf within the first 6 weeks have 6 weeks to recover before joining
§ Later calvers are harder to get in calf quickly so only smaller conception rates
- Time since calving is a major determinant of fertility -> longer time since calf higher conception and submission rate (more fertile)

78
Q

How does condition score affect herd fertility

A

Post-partum period all cows loss weight due to the small size of rumen (needs to spread out again) and therefore getting energy from fat stored on the body until can eat enough to fulfill the requirements - energy balance -> THEN START CYCLING
- better condition score higher submission and conception rate

79
Q

Heat detection how does it affect herd fertility

A
  • The first couple of heats are harder to detect
  • Many Holsteins on heat for less than 3 hours
  • Cows will only stand to be mounted if it’s convenient
  • Cows cycling at the wrong time of day can be missed
  • The use of “heat detection aids” is common
  • synchronise the cattle to avoid these issues
80
Q

What cow level factors decrease fertility

A
  • Calving trouble
  • Twins
  • Retained foetal membranes
  • Lameness before MSD
  • Timing of AI
81
Q

List 4 consequences of late calvers in dairy cattle

A

○ Sub-optimal nutrition
○ May have shorter lactation
○ Smaller, more at risk calves
○ Decreased fertility next year - calve later next year

82
Q

List 6 consequences of late calvers in beef cattle

A
  • Average weight of progeny is lighter
  • Not worth as much at sale
  • Need more old cows because more heifers don’t meet critical mating weights
  • Cows less likely to get in calf
  • Affects following year - hard to cut back the calving interval by simply having shorter joining periods
  • End up with older herd
83
Q

List 4 diseases of the ovary

A
  1. Aplasia/hypoplasia
  2. Ovarian cyst
  3. Oophoritis
  4. Ovarian neoplasia
84
Q

List 7 diseases of the uterus

A
  1. Hydrosalpinx
  2. Developmental anomalies
  3. Hydrometra/mucometra
  4. Adenomyosis
  5. Cystic endometrial hyperplasia
  6. Pyometra (bitch)
  7. Uterine neoplasia
85
Q

List the 3 diseases of the vagina/vulva

A
  1. Vaginitis/vulvitis
  2. Vaginal hyperplasia
  3. Vaginal/Vulval neoplasia
86
Q

List the 4 developmental cysts in teh ovary

A

1) Paraovarian
2) cystic rete ovarri
3) epithelial inclusion cysts
4) cystic subsurface epithelial structures

87
Q

Paraovarian and cystic rete ovarii what are they, how arise and clinical significance

A

Developmental cysts of ovary
1. Paraovarian
○ Mesonephric/paramesonephric duct remnants
§ Significant only if on the fimbriae where may obstruct passage of ovum
2. Cystic rete ovarii
○ Develop from remnant of rete ovarii
○ Within in the ovary but can protrude outwards
○ Incidental

88
Q

Epithelial inclusion cysts and cystic surface epithelial structures what are they, common in which species, how occur and clinical significance

A

Developmental cysts of the ovary
Epithelial inclusion cysts
○ Common in mares
○ Occur at ovulation fossa
○ May impair subsequent ovulation
§ Ovulation of follicle within cyst or obstruct
4. Cystic subsurface epithelial structures
○ Bitches
○ Cystic expansion of epithelial invaginations
○ May become neoplastic

89
Q

Persistent anovulatory follicles in mares when occur, what occurs and what results in

A
  • Occur during transition between anoestrus and oestrus cycling
    ○ Follicles develop, but don’t ovulate
    ○ Typically undergo haemorrhage
    ○ Spontaneously resolve, but timing unpredictable
    § Results in irregular cycling during transition periods
    § Some may persist into the anoestrus period
90
Q

Oophoritis what species common in and what result from generally

A
- Rare except in birds 
○ Usually systemic infection 
§ Pyogenic bacteria
§ Tuberculosis 
Viruses - FIB, BVD
91
Q

What are the 3 ovarian neoplasms

A

1) germ cell neoplasia - gametes
2) sex cord-stromal neoplasia - endocrine cells and stroma
3) ovarian epithelial (acutally mesothelium) neoplasia

92
Q

Germ cell neoplasms bengin or malignant, 2 types and examples within

A
  • Benign
    1) Undifferentiated
    ○ Dysgerminoma
    § Analogous to seminoma in males
    § Large pleomorphic (anaplastic) round cells - high mitotic rate
    □ Although anaplastic generally correlated to malignancy rare in this case
    2) Differentiated
    ○ Teratoma (can occur in any organ)
    § Differentiation includes two or more germinal layers
    □ Ectodermal epithelium
    ® Skin and hair
    □ Endodermal epithelium
    ® GI tract, liver, lung
    □ Mesoderm
    ® Bone, cartilage, muscle
    § Forms mosaic of different well-differentiated tissue types -> Tend to get all 3 germinal layers
93
Q

Sex cord-stromal neoplasia within the ovary wheat species most common, 2 common types, character and what can they form

A
  • All species but very common in mares
  • Most common types (may be mixed)
    ○ Granulosa cell tumour
    ○ Theca cell tumour
  • Usually benign
  • Form polycystic structures lined by granulosa and/or theca cells
94
Q

Sex cord-stromal neiplasia what do they produce and what effects do they have based on these products

A
- Hormonally active 
○ Oestrogens (granulosa cell tumour) 
§ Persistent oestrus/nymphomania 
§ Bone marrow suppression 
○ Inhibin (granulosa cell tumour) 
§ Anoestrus 
§ Atrophy of contralateral ovary 
○ Androgens (thecal cell tumour)
§ Masculinization
95
Q

Ovarian epithelial (actually mesothelium) neoplasia what dervied from, what species most common in, type of growth and character

A
  • Derive from ovarian lining
  • Most common in the bitch
  • Papillary and cystic growth
  • Usually malignant (ovarian carcinoma)
    ○ Peritoneal carcinomatosis
    ○ Lymphatic metastasis
    § Ascites due to lymphatic obstruction is often the first clinical sign observed
96
Q

Hydrosalpinx what is it, results and what caused by

A
  • Accumulation of serous fluid on uterine tube
  • Bilateral - infertile due to failure of movement
  • Caused by stenosis of uterine tube
    ○ Trauma during rectal manipulation
    ○ Congenital segmental aplasia
    ○ Low-grade salpingitis (pyosalpinx more common)